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Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

Adult-Gerontology Acute Care Practice Guidelines

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

Catherine Harris, Ph D, MBA, AGACNP, is an associate professor of graduate programs and a faculty in the Acute Care Nurse Practitioner Program at Thomas Jefferson University in Philadelphia. She earned her Ph D in nursing at the University of Pennsylvania and an MBA from Drexel University before becoming credentialed as an acute care nurse practitioner at Thomas Jefferson University in Philadelphia. Dr. Harris specializes in neurocritical care, having presented extensively on ischemic and hemorrhagic stroke. She has been a mentee for the Fellows of the American Association of Nurse Practitioner Mentorship Program and has won numerous research grants in neurocritical care and global health.

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

Adult-Gerontology Acute Care Practice Guidelines Catherine Harris, Ph D, MBA, AGACNP Editor

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

Copyright © 2020 Springer Publishing Company, LLC All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior permission of Springer Publishing Company, LLC, or authorization through payment of the appropriate fees to the Copyright Clearance Center, Inc., 222 Rosewood Drive, Danvers, MA 01923, 978-750-8400, fax 978-646-8600, info@copyright. com or on the Web at www. copyright. com. Springer Publishing Company, LLC 11 West 42nd Street New York, NY 10036 www. springerpub. com Acquisitions Editor : Suzanne Toppy Compositor : diacri Tech, Chennai ISBN: 978-0-8261-7004-0 e-book ISBN : 978-0-8261-7005-7 18 19 20 21 22 / 5 4 3 2 1 The author and the publisher of this Work have made every effort to use sources believed to be reliable to provide information that is accurate and compatible with the standards generally accepted at the time of publication. Because medical science is continually advancing, our knowledge base continues to expand. Therefore, as new information becomes available, changes in procedures become necessary. We recommend that the reader always consult current research and specific institutional policies before performing any clinical procedure. The author and publisher shall not be liable for any special, consequential, or exemplary damages resulting, in whole or in part, from the readers' use of, or reliance on, the information contained in this book. The publisher has no responsibility for the persistence or accuracy of URLs for external or third-party Internet websites referred to in this publication and does not guarantee that any content on such websites is, or will remain, accurate or appropriate. Library of Congress Cataloging-in-Publication Data Names: Harris, Catherine AGACNP, editor. Title: Adult-gerontology acute care practice guidelines / [edited by] Catherine Harris, Ph D, MBA, AGACNP. Description: New York, NY : Springer Publishing Company, LLC, [2019] | Includes bibliographical references and index. Identifiers: LCCN 2019015624 |ISBN 9780826170040 |ISBN 9780826170057 (ebook) Subjects: LCSH: Geriatric nursing. |Intensive care nursing |Older people-Medical care. |Nurse practitioners. Classification: LCC RC954. A38 2019 |DDC 618. 97/0231-dc23 LC record available at https://lccn. loc. gov/2019015624 Contact us to receive discount rates on bulk purchases. We can also customize our books to meet your needs. For more information please contact: sales@springerpub. com Publisher's Note :New and used products purchased from third-party sellers are not guaranteed for quality, authenticity, or access to any included digital components. Printed in the United States of America.

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

To Matthew, My beautiful little boy, you are always in my heart, and I am so proud of you! Mom and Dad, Thank you for your encouragement and always being there for me.

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

vii Contents Contributors xi Reviewers xv Foreword Harrison Reed, MMS, PA-C xvii Preface xix Organization xxi What Is Different About This Book xxiii Acknowledgments xxv Introduction xxvii I. ACUTE CARE GUIDELINES BY SYSTEM 1. ENT Guidelines Conjunctivitis 3 Pharyngitis 5 Rhinosinusitis 8 2. Pulmonary Guidelines Acute Respiratory Distress Syndrome 11 Asthma 14 Chronic Obstructive Pulmonary Disease 17 Pleural Effusions 22 Pneumonia 24 Pulmonary Embolism 27 Restrictive Lung Disease 30 3. Cardiac Guidelines Acute Coronary Syndromes 35 Angina 40 Arrhythmias 43 Dyslipidemia 48 Heart Failure 50 Hypertension 55 Pericardial Effusions 57 Valvular Heart Disease 60 4. Gastrointestinal Guidelines Acute Abdomen 67 Cirrhosis 72 Drug-Induced Liver Injury 75 Gastroesophageal Reflux Disease 76 Gastrointestinal Bleeding 78 Hepatitis-Alcoholic 81 Hepatitis-Autoimmune 82 Hepatitis A 83Hepatitis B 84 Hepatitis C 85 Inflammatory Bowel Disease 86 Nonalcoholic Fatty Liver Disease 89 Pancreatitis 90 Peptic Ulcer Disease 93 5. Nephrology Guidelines Acute Kidney Injury 95 Benign Prostatic Hypertrophy 99 Chronic Kidney Disease 101 Hematuria 104 Hypercalcemia 107 Hyperkalemia 109 Hypermagnesemia 111 Hypernatremia 112 Hyperphosphatemia 115 Hypocalcemia 116 Hypokalemia 117 Hypomagnesemia 119 Hyponatremia 120 Hypophosphatemia 124 Metabolic Acidosis 125 Nephrolithiasis 127 Nephrotic Syndrome 129 Prostatitis 131 Pyelonephritis 133 Urinary Incontinence 135 Urinary Tract Infection 138 6. Neurology Guidelines Anoxic Brain Injury 141 Brain Death 142 Headaches 144 Intracerebral Hemorrhage 147 Ischemic Stroke/Cerebrovascular Accident 150 Contents Share: Adult Gerontology Acute Care Practice Guidelines-

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

viii Status Epilepticus 152 Transient Ischemia Attack 155 7. Targeted Temperature Management Guidelines Fever Management 157 Hypothermia or Targeted Temperature Management After Cardiac Arrest 160 8. Endocrine Guidelines Adrenal Insufficiency 165 Diabetes Mellitus—Type 1 167 Diabetes Mellitus—Type 2 170 Diabetic Ketoacidosis 175 Hyperglycemic Hyperosmolar State 177 Metabolic Syndrome 179 Pheochromocytoma 180 Prediabetes 181 Thyroid Disorder—Euthyroid Sick Syndrome 183 Thyroid Disorder—Hyperthyroidism 184 Thyroid Disorder—Hypothyroidism 186 Thyroid Disorder—Myxedema Coma 187 Thyroid Disorder—Thyroid Storm 188 9. Psychiatric Guidelines Bipolar Disorder 191 Major Depressive Disorder 194 Posttraumatic Stress Disorder 196 Schizophrenia 198 Substance Use Disorders 200 Psychiatric Patient Medical Clearance 201 10. Infection Guidelines Colitis: Infective 203 Encephalitis 206 Endocarditis: Infective 208 Influenza 212 Meningitis 214 Necrotizing Fasciitis 217 Osteomyelitis 218 Peritonitis 220 Systemic Inflammatory Response Syndrome (SIRS)/Bactermia/Sepsis 223 Septic Arthritis 227 Tuberculosis 230 11. Peripheral Vascular Guidelines Acute Limb Ischemia 235 Aortic Vessel Disease: Aneurysms of the Aorta 237 Carotid Artery Disease 239 Peripheral Artery Disease: Lower Extremity 242 Peripheral Artery Disease: Upper Extremity 243 Peripheral Vascular Disease 245 Thoracic Outlet Sydnrome 249 12. Hematology Guidelines Anemia 251 Bleeding Diatheses 254Coagulopathies 257 Deep Vein Thrombosis 258 Sickle Cell Crisis 261 13. Oncology Guidelines Brain/Central Nervous System Malignancies 265 Breast Cancer 266 Gastrointestinal Cancers: Colorectal Cancer 269 Gastrointestinal Cancers: Gastric Cancer 271 Gastrointestinal Cancers: Hepatic Cancer 273 Gastrointestinal Cancers: Pancreatic Cancer 275 Gynecologic Cancers: Cervical Cancer 276 Gynecologic Cancers: Endometrial Cancer 277 Gynecologic Cancers: Ovarian Cancer 279 Head and Neck Cancers 280 Leukemias: Acute Leukemias 281 Leukemias: Chronic Leukemias 284 Leukemias: Myelodysplastic Syndromes 287 Leukemias: Myeloproliferative Neoplasms 289 Lung Cancer 291 Lymphomas: Hodgkin Lymphoma 293 Lymphomas: Non-Hodgkin Lymphoma 294 Multiple Myeloma 296 Sarcoma 298 Skin Cancer 299 14. Immune System, Connective Tissue, and Joints Guidelines Back Pain 303 Compartment Syndrome of the Lower Leg 305 Joint Pain 308 Osteoarthritis 311 Rheumatoid Arthritis 312 Spondyloarthropathies 314 Systemic Lupus Erythematosus 315 Vasculitis-Variable Vessel 319 Vasculitis-Small Vessel 320 Vasculitis-Medium Vessel 323 Vasculitis-Large Vessel 324 15. Dermatology Guidelines Atopic Dermatitis 327 Cellulitis 329 Seborrheic Dermatitis 331 Stasis Dermatitis 333 16. Geriatric Guidelines Delirium 335 Dementia 338 Falls 340 Urinary Incontinence 343 17. Trauma Guidelines Chest Trauma 347 Penetrating Chest Injuries 349 Penetrating Intracranial Injuries 350 Shock 352 Spinal Cord Injuries 354 Traumatic Brain Injury 357Contents

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

ix II. PERIOPERATIVE CONSIDERATIONS 18. Preoperative Evaluation and Management Scope of Chapter 361 Considerations 361 Care Principles 362 Medication Management 364 19. Perioperative and Intraoperative Management Scope of Chapter 367Considerations 367 Care Principles 370 Medication Management 372 20. Postoperative Evaluation and Management Scope of Chapter 373 Outcomes 373 Wound Management 375 Medication Management 377 III. PROCEDURES Ankle-Brachial Index Measurement 381 Arterial Lines 383 Bone Marrow Aspiration and Biopsy 387 Bronchoscopy 391 Central Venous Access 394 Chest Tube Insertion 404 Chest Tube Removal 407 Digital Nerve Blocks 409 Extracorporeal Membrane Oxygenation 411 Endotracheal Intubation 415 Endotracheal Extubation 419 External Ventricular Drain 421 Intraosseous Vascular Access 423Long Leg Casting 425 Lumbar Puncture 429 Peripherally Inserted Central Catheter Placement 432 Reduction of the Ankles 435 Reduction of the Fingers 437 Reduction of the Hip 440 Reduction of the Patella 442 Reduction of the Shoulder 444 Splinting 446 Synovial Fluid Aspiration 451 Thoracentesis 454 Transpyloric Feeding Tube Placement 457 IV. SPECIAL TOPICS End-of-Life Considerations 461 Health Prevention and Screening 467 Hemodynamic Monitoring Devices 482Telemedicine in Acute Care 489 Transitional Care 493 APPENDIX Normal Laboratory Values 501 Index 515 Contents

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

xi Contributors Dana A. Albinson, MSN, BSN, AGACNP Adult-Gerontology Acute Care Nurse Practitioner Thomas Jefferson University Hospital Philadelphia, Pennsylvania Frank O. Amanze, MSN, AGACNP-BC, CFRN, CCRN, PHRN, NRP Nurse Practitioner Thomas Jefferson University Philadelphia, Pennsylvania M. Kamran Athar, MD Assistant Professor of Medicine and Neurological Surgery Thomas Jefferson University Hospital Philadelphia, Pennsylvania Ponrathi Athilingam, Ph D, RN, ACNP, FAANP, FHFSA Associate Professor, College of Nursing University of South Florida Tampa, Florida Asha Avirachen, MSN, BSN, AG, ACNP Adult-Gerontology Acute Care Nurse Practitioner Department of Neurosurgery, Hospital of University of Pennsylvania Philadelphia, Pennsylvania Suzanne Barron, MSN, RN, CRNP, FNP Adult and Gerontology Acute Care Nurse Practitioner Thomas Jefferson University Philadelphia, Pennsylvania Karen A. Beaty, MPAS, PA-C Physician Assistant MD Anderson Cancer Center Houston, Texas David Bergamo, MSPAS, PA-C, AAHIVS Physician Assistant Infectious Disease Associates and Christiana Care Health System Christiana, Delaware Amy Blake, MSN, FNP-BC Family Nurse Practitioner Team Health Hospitalist & Post Acute Care Wilmington, Delaware Ann E. Burke, MSN, CRNP, FNP-BC Nurse Practitioner Thomas Jefferson University Hospital Philadelphia, Pennsylvania Dana Cafaro, MS, PA-C Associate Program Director & Assistant Professor Thomas Jefferson University Physician Assistant Program Atlantic City, New Jersey E. Mone ́e Carter-Griffin, DNP, RN, ACNP-BC Associate Chair for Advanced Practice Nursing University of Texas at Arlington Arlington, Texas Alexis Chettiar, Ph D, MSN, RN Director of Quality Improvement Center for Elders' Independence Oakland, California Christine M. Chmielewski, MS, CRNP, ANP-BC, CNN-NP Nephrology Nurse Practitioner Thomas Jefferson University Hospital Philadelphia, Pennsylvania Kelly Cimino, MSN, RN, CRNP, AG ACNP-BC Nurse Practitioner Thomas Jefferson University Philadelphia, Pennsylvania Jennifer Coates, DNP, MBA, ACNP-BC, ACNPC Critical Care Nurse Practitioner Drexel University Philadelphia, Pennsylvania Lisa Coco, MSN, CRNP, CDE Nurse Practitioner Thomas Jefferson University Philadelphia, Pennsylvania Courtney Connolley, MSN Nurse Practitioner Thomas Jefferson University Philadelphia, Pennsylvania Heather Warren Cook, MSN, RN, AGACNP-BC Acute Care Nurse Practitioner Hospital of the University of Pennsylvania Philadelphia, Pennsylvania Contributors

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

xii Jane S. Davis, DNP, MSN, BSN, CRNP University of Alabama at Birmingham Birmingham, Alabama Erin Michelle Dean, MS, PA-C, RD Physician Assistant Department of Surgical Oncology, MD Anderson Cancer Center Houston, Texas Michele De Castro, MSN, CRNP Nurse Practitioner Division of Hospital Medicine, Thomas Jefferson University Philadelphia, Pennsylvania Jingyi Deng, MSN, RN-BC, AGACNP-BC Cardiac Surgery Nurse Practitioner Lankenau Medical Center Philadelphia, Pennsylvania Jessica S. Everitt, Pharm D Assistant Professor University of Mississippi Medical Center Jackson, Mississippi Susan F. Galiczynski, MSN, RN, CRNP, CEN Nurse Practitioner Crozer-Chester Medical Center Philadelphia, Pennsylvania Alexis C. Geppner, MLS (ASCP), PA-C Physician Assistant MD Anderson Cancer Center Houston, Texas Bridget Gibson, CRNP, Adult Acute Care, MSN, BSN Neurocritical Care Nurse Practitioner Thomas Jefferson University Philadelphia, Pennsylvania Debra Hain, Ph D, APRN, AGPCNP-BC, FAANP, FNKF Professor/Nurse Practitioner Florida Atlantic University, Chrisitne E. Lynn College of Nursing and Cleveland Clinic Florida, Department of Nephrology Boca Raton, Florida Catherine Harris, Ph D, MBA, AGACNP Associate Professor Thomas Jefferson University College of Nursing Philadelphia, Pennsylvania Carey Heck, Ph D, CRNP, AGACNP-BC, CCRN, CNRN Assistant Professor, Director, AGACNP Program Thomas Jefferson University, College of Nursing Philadelphia, Pennsylvania Shannon B. Holloway, MHS, PA-C Physician Assistant MD Anderson Cancer Center Houston, Texas John Hurt, MPAS, PA-C Director of Clinical Education Samford University Physician Assistant Program Birmingham, Alabama Alicia John, MSN, RN, CNS Advanced Practice Provider Kingwood Medical Center Houston, Texas Cynae Johnson, DNP, MSN, WHNP-BC Advanced Practice Provider MD Anderson Cancer Center Houston, Texas Swetha Rani Kanduri, MD Assistant Professor of Medicine University of Mississippi Medical Center Jackson, Mississippi Kiffon M. Keigher, MSN, APN, ACNP-BC Program Manager, Acute Care Nurse Practitioner Advocate Aurora Health Park Ridge, Illinois Alison M. Kelley, MSN, AGACNP-BC Critical Care Nurse Practitioner Emory University Hospital Atlanta, Georgia Karthik Kovvuru, MD Assistant Professor of Medicine University of Mississippi Medical Center Jackson, Mississippi Kathryn Evans Kreider, DNP, APRN, FNP-BC, BC-ADM Assistant Professor of Nursing Duke University Durham, North Carolina Megan Krug, MHS, PA-C Physician Assistant Dana Farber Cancer Institute Boston, Massachusetts Monique Lambert, DNP, APN, ACNP-BC, FAANP Anesthesia Critical Care Northshoure University Health Care System Skokie, Illinois Sarah L. Livesay, DNP, RN, ACNP-BC, ACNS-BC, FNCS, FAHA Associate Professor Rush University, Department of Adult Health and Gerontological Nursing Chicago, Illinois Kristopher R. Maday, MS, PA-C Program Director, Associate Professor University of Tennessee Health Science Center Physician Assistant Program Memphis, Tennessee Shawn Mangan, MSN, RNFA, ANP-C, AGACNP-BC Acute Care Surgery/Trauma Intensive Care Unit Nurse Practitioner Thomas Jefferson University Hospital Philadelphia, Pennsylvania Contributors

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

xiii Amelita B. Marzan, MS, APRN, FNP-C, OCN Advanced Practice Provider MD Anderson Cancer Center Houston, Texas Sijimol Mathew, MSN, ACNP-BC Advanced Practice Provider MD Anderson Cancer Center Houston, Texas Juan A. Medaura, MD Assistant Professor of Medicine University of Maryland Medical Center Baltimore, Maryland Heather H. Meissen, MSN, ACNP, CCRN, FCCM, FAANP Program Director NPPA Critical Care Residency Emory Healthcare Atlanta, Georgia Rose Milano, DNP, MS, BSN, RN, ACNP-BC Assistant Professor Rush University College of Nursing Chicago, Illinois Robin Miller, DNP, MPH, ACNP-BC Assistant Professor of Clinical Nursing Oregon Health & Science University Portland, Oregon Robin Miller, MSN, FNP-BC, AGACNP-BC Nurse Practitioner Thomas Jefferson University Hospital Philadelphia, Pennsylvania Divya Monga, MD Division of Nephrology University of Mississippi Medical Center Jackson, Mississippi Madeleine Nguyen-Cao, PA-C Physician Assistant MD Anderson Cancer Center Houston, Texas Karen Sheffield O'Brien, Ph D, RN, ACNP-BC Assistant Professor University of St. Thomas and Memorial Hermann Sugar Land Nurse Practitioner Houston, Texas Dominick Osipowicz, MSN, CRNP, AGACNP-BC Nurse Practitioner Christiana Care Health System Newark, Delaware Jennifer W. Parker, Ph D, MSN, BSN Acute Care Nurse Practitioner University of Pennsylvania Health System West Chester, Pennsylvania Joanne Elaine Pechar, MSN, ANP-BC, AGACNP-BC Acute Care Nurse Practitioner Department of Penn Orthopedics, Pennsylvania Hospital Philadelphia, Pennsylvania Cheryl Pfennig, MSN, RN, NP-C, AOCNP Advanced Practice Registered Nurse, Surgical Oncology MD Anderson Cancer Center Houston, Texas Allyson Price, MPAS, PA-C Physician Assistant MD Anderson Cancer Center Houston, Texas Rae Brana Reynolds, Ph D, RN, ACNP-BC Manager, Advanced Practice Providers MD Anderson Cancer Center Houston, Texas Monica Richey, MSN, ANP-BC Nurse Practitioner Northwell Health New York, New York Courtney Robb, MS, RN, CRNFA, FNP-C Nurse Practitioner MD Anderson Cancer Center Houston, Texas Allison Rusgo, MHS, MPH, PA-C Assistant Clinical Professor Drexel University Philadelphia, Pennsylvania Annamma Sam, Ph D, WHNP-BC Advanced Practice Provider MD Anderson Cancer Center Houston, Texas Leigh A. Samp, MPAS, PA-C Physician Assistant MD Anderson Cancer Center Houston, Texas Laura A. Santanna Lonergan, MHS, PA-C Physician Assistant Pennsylvania Hospital Philadelphia, Pennsylvania Syed Omar Shah, MD, MBA Assistant Professor of Neurology and Neurological Surgery Thomas Jefferson University Hospital Philadelphia, Pennsylvania Christina Shin, PA-C Physician Assistant Rush University Chicago, Illinois Ruth Anne Skinner, DNP, ACNP-BC, C-NP, CNRN ACNP Lead Faculty College of Nursing & Health Care Professions, Grand Canyon University Phoenix, Arizona Mary Rogers Sorey, MSN, RN, ACNP Assistant Professor Division of Nephrology, Vanderbilt University Medical Center Nashville, Tennessee Contributors

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

xiv Cara M. Staley, MSN, RN-BC, AGACNP-BC Vascular Surgery Nurse Practitioner Thomas Jefferson University Hospital Philadelphia, Pennsylvania Jerrad M. Stoddard, MS, MA, PA-C Physician Assistant Texas Oncology Round Rock, Texas Frances M. Stokes, DNP, RN, ACNP-BC, CMNL Nurse Practitioner Intensivist Austin, Texas Julie Stone, MSN, RN, ACNP-BC, BC-ADM Endocrinology Nurse Practitioner Ascension St. Vincent Heart Center Indianapolis, Indiana Siji Thomas, ACNP, OCN Acute Care Nurse Practitioner MD Anderson Cancer Center Houston, Texas Nicole Thomer, MSN, AG-ACNP Nurse Practitioner, Neuro Critcal Care Thomas Jefferson University Hospital Philadelphia, Pennsylvania Melissa Timmons, PA-C Physician Assistant MD Anderson Cancer Center Houston, Texas Amber Tran, MSN, CRNP, FNP-BC Family Nurse Practitioner Department of Dermatology and Cutaneous Biology, TJU Philadelphia, Pennsylvania Fiona Unac, MN, NP, GDip AL&T Nurse Practitioner Radiology Department, Soldiers' Memorial Hospital Hastings, New Zealand Dawn Vanderhoef, Ph D, DNP, PMHNP, FAANP Assistant Professor and Academic Director Vanderbilt University School of Nursing Nashville, Tennessee Susan Varghese, MSN, RN, ANP-C Adult Nurse Practitioner MD Anderson Cancer Center Houston, Texas Valerie F. Villanueva, MSN, RN, FNP-BC Supervisor, Advanced Practice Providers MD Anderson Cancer Center GYNONC and Reproductive Medicine Houston, Texas Catherine Wells, DNP, ACNP, CNN-NP, FNKF Assistant Professor Division of Nephrology, University of Mississippi Medical Center Jackson, Mississippi Mary L. Wilby, Ph D, MSN, MPH, RN, CRNP, ANP-BC Assistant Professor, Nurse Practitioner Track Coordinator La Salle University Philadelphia, Pennsylvania Joseph Willmitch, MSPAS, PA-C, DFAAPA Director of Clinical Education University of Tennessee Health Science Center Physician Assistant Program Memphis, Tennessee Danielle Zielinski, MSN, BSN, RN, ACNP-BC Acute Care Nurse Practitioner Northwestern Medicine, Neurosurgery Chicago, Illinois Kim Zuber, MS, PAC Executive Director American Academy of Nephrology Pas Oceanside, California Contributors

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

xv Reviewers M. Kamran Athar, MD Assistant Professor of Medicine and Neurological Surgery Thomas Jefferson University Philadelphia, Pennsylvania Ashley L. Barba, DNP, ANP Acute Care Nurse Practitioner Duke University Medical Center Durham, North Carolina Mark E. Baus, MSN, CRNP, RNFA Lead Orthopaedic Nurse Practitioner Thomas Jefferson University Hospital Philadelphia, Pennsylvania Brennan Bowker, MHS, PA-C, CPAAPA Physician Assistant; Part-Time Clinical Assistant Professor of Physician Assistant Studies Yale New Haven Hospital Department of Surgery; Quinnipiac University Department of Physician Assistant Studies New Haven, Connecticut Theresa M. Campo, DNP, FNP-C, ENP-C, FAANP, FAAN Director of the Emergency Nurse Practitioner and Co-Director of the Family Nurse Practitioner Tracks, Associate Clinical Professor for the College of Nursing and Health Professions Drexel University College of Nursing and Health Professions Philadelphia, Pennsylvania Shawnna Cannaday, MSN, AGACNP, FNP-BC Acute Care Nurse Practitioner Department of Surgery, Surgical Oncology Jefferson University Physicians Department of Surgery, Hepato-Biliary-Pancreatic Surgery Philadelphia, Pennsylvania Dawn Carpenter, DNP, ACNP-BC, CCRN Coordinator, Adult-Gerontology Acute Care Nurse Practitioner Program University of Massachusetts Medical School Worcester, Massachusetts Nicole Cavaliere, MSN, AGACNP-BC Acute Care Nurse Practitioner Department of Surgery, Cardiothoracic Surgery Thomas Jefferson University Hospital Philadelphia, Pennsylvania Kathleen O. Chennell, MS, CNS, ACNP-BC, CCRN Adult-Gerontology Acute Care Nurse Practitioner Division of Nephrology, University of Cincinnati Cincinnati, Ohio Carolina Dimsdale Tennyson, DNP, ACNP-BC, AACC Nurse Practitioner, Clinical Associate Faculty Duke University School of Nursing Durham, North Carolina Patricia Galanis, MSN, CRNP Oncology Nurse Practitioner Thomas Jefferson University Philadelphia, Pennsylvania Carey Heck, Ph D, CRNP, AGACNP-BC, CCRN, CNRN Assistant Professor, Director, AGACNP Program Thomas Jefferson University, College of Nursing Philadelphia, Pennsylvania Heather Hobbs, MSN, CRNP, AGACNP-BC Adult-Gerontology Acute Care Nurse Practitoner Department of Otolaryngology/Head & Neck Surgery, Thomas Jefferson University Hospital Philadelphia, Pennsylvania Robert Kirk, MSN, PMHNP-BC Psychiatric Nurse Practitioner University of Pennsylvania School of Nursing Philadelphia, Pennsylvania Stefanie La Manna, Ph D, MPH, APRN, FNP-C, AGACNP-BC Program Director for the Ph D/DNP/AGACNP Programs Nova Southeastern University Palm Beach Gardens, Florida Johannah Lebow, MSN, CRNP Oncology Nurse Practitioner University of Pennsylvania Health System Philadelphia, Pennsylvania Gail Ann Lis, DNP, ACNP-BC Professor, Graduate Chair Madonna University Livonia, Michigan Karen Bradley Lodge, MSN, CRNP Nurse Practitioner Reviewers

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

xvi Northwest Internal Medicine Wydnmoor, Pennsylvania Mary Anne Mc Coy, Ph D, RN, ACNS, ACNP-BC Assistant Professor; Graduate Coordinator, AGACNP Specialty Wayne State University College of Nursing Detroit, Michigan Anne Bradley Mitchell, Ph D, MN, ANP-BC Assistant Professor of Nursing Jefferson University College of Nursing Philadelphia, Pennsylvania Dominick Osipowicz, MSN, CRNP, AGACNP-BC Nurse Practitioner Christiana Care Health System Newark, Delaware Jennifer W. Parker, Ph D, MSN, BSN Acute Care Nurse Practitioner University of Pennsylvania Health System West Chester, Pennsylvania Belbina Pereira, MSN Nephrology Nurse Practitioner Brooklyn Hospital Brooklyn, New York Marilyn Riley, Ph D, MSN, RN, APRN-BC, FNP NP Intensivist, Chief Nursing Officer Indiana University Health Indianapolis, Indiana Fred Rincon, MD, FACP Associate Professor of Medicine Thomas Jefferson University Philadelphia, Pennsylvania Tracy Setji, MD Associate Professor of Medicine Duke University Durham, North Carolina Jennifer Sheehan, MSN, CRNP, RNFA Nurse Practitioner Philadelphia VA Medical Center Philadelphia, Pennsylvania Benjamin Smallheer, Ph D, RN, ACNP-BC, FNP-BC, CCRN, CNE Assistant Professor of Nursing; Lead Faculty, Adult-Gerontology Acute Care NP Program Duke University School of Nursing Durham, North Carolina R. Shane Smith, MS, PA-C, EMT-P(NREMT), SFC (RET), US Army Trauma Surgery, Critical Care Ballad Health Systems, Milligan College Adjunct Faculty Johnson City, Tennessee Frances Stokes, DNP, RN, ACNP-BC, CMNL NP Intensivist St. Davids Medical Center Austin, Texas Kevin Tipton, MSN, CRNP Nurse Practitioner Lehigh Valley Hospital East Stroudsburg, Pennsylvania Mark Ubbens, MSN, CRNP, AG-ACNP-BC, PHRN Advanced Practice Chief, Trauma Surgery; Aquarium Medical Advisor, Ski Patroller Geisinger Medical Center, National Aquarium, Big Boulder Ski Patrol Danville, Pennsylvania; Baltimore, Maryland; Lake Harmony, Pennsylvania Karen L. Visich, MSN, RN, ANP-BC, AOCNP Nurse Practitioner, Genitourinary Oncology; Acting Associate Director of Nursing and Patient Education Rutgers Cancer Institute of New Jersey New Brunswick, New Jersey Michael Zychowicz, DNP, ANP, ONP, FAAN, FAANP MSN Program Director Duke University School of Nursing Durham, North Carolina Reviewers

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

xvii Foreword There is no blueprint for acute care. The term itself is as broad and nebulous as the field it describes. Our patients reserve the right to present with any configuration of symptoms, to respond to our treat-ments when—and if—their bodies deem appropriate, and to decompensate without warning. Unlike the neat black and white lines of our textbooks, the reality of acute medicine is a messy gray. Of course, the geriatric population adds yet another wrin-kle to that hazy clinical landscape. The aging body owes no guarantees. Every tent pole of our didactic education—the classic triads and notorious eponyms—fades with the march of time. As a young clinician thrust into the halls of famous hospitals, surrounded by brilliant clinicians and the sickest patients, these lessons often landed with a painful thud. But over time I began to appreciate the subconscious calculations that registered as subtle sensations. The flutter in my chest that told me to double-check a detail, the tickle deep in my skull that said to investigate further, the lead weight in my gut that meant something was wrong. Of course, you cannot buy those instincts in any store. They are earned over the course of a career. In the meantime, you can insulate yourself with as much raw knowledge as pos-sible. And the book you are holding is a great start. The following pages provide a skeleton on which to build that knowledge. They are not a replacement for clinical acumen but a guide to help you find a deeper understanding of acute care. They are the concepts that should flash through your mind when your patients are at their most vulnerable, when time is precious, and when mistakes are costly. This book is authored by a coalition of talented physician assistants and nurse practitioners who have collaborated as we so often do in the clinical setting. They bring decades of col-lective experience and use it to distill the cloudy concoction of acute care into clear, manageable parts. They have fortified the material with threads of relevant wisdom for the geriatric patient. This is not the dense tome that will collect dust on your bookshelf. It is designed for utility, sleek and practical. It is the book I wish I would have had as a new clinician. So, while there is no blueprint for acute care, do not worry. You may have found the next best thing. Harrison Reed, MMS, PA-C Assistant Professor School of Medicine and Health Sciences George Washington University Washington, DC Foreword

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

xix Preface The need for an acute care textbook has been growing. Although outpatient practices have long seen the value of uti-lizing advanced practice providers (APPs), the surge in acute care providers has been relatively recent. I remember when I was a registered nurse back in the 1990s, I had no idea there was such a role as a nurse practitioner or a physician assistant in the hospital, despite the fact they have been around since the 1960s! I was immediately fascinated and intrigued by the role of APPs. It was not long before I found myself enrolled in a nurse practitioner program. When I graduated, I was one of the first nurse practitioners on the neurosurgery service in the facility where I practiced. The service appreciated the help, but they did not really know what to do with me. It took many months for me to garner the trust of the surgeons, and to show them the true capacity of what APPs could do and how we could really become essential parts of the team. APPs have come a long way over the years. I have seen the role of nurse practitioners and physician assistants expand tremendously since I first began practicing in this role. I have seen the negative terms to describe us, such as midlevels, physician extenders, and helpers, evolve into advance prac-tice providers. I have also seen collaborative growth and mutual respect grow between nurse practitioners and physician assistants, arelationship that was previously more isolated. I respect my physician assistant colleagues, and, as a nurse practitioner, I have learned quite a bit from their struggles with role and identity. I find that I personally relate to these struggles in how I practice and how I see my own role on the healthcare team. I have also learned the value of combining resources and focusing on how we are similar, rather than different. It was important to write this textbook with physician assistants and nurse practitioners together. Both groups have immense value to provide each other in terms of knowledge, resources, and experience. Finally, it was essential to write this textbook because it fills a void in the marketplace. Countless times my students have asked if there were an acute care textbook that they could use. I have tried many different textbooks, but either I found them to be too cumbersome or the information provided was just too scant. This final iteration of the textbook came about as a result of those experiences and discussions with students about what they needed and they wanted. We all suffer from information overload and overwhelm, so the focus of this textbook was to provide the minimum of what new graduate students need to know in order to be competent when they start practice. Catherine Harris Preface

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

xxi Organization This book is organized into four major sections. Part I: Acute Care Guidelines by System—In Part I, the advanced practice provider (APP) is exposed to the most common medical conditions organized by system. Although it is by no means comprehensive or inclusive of every medical condition, the section is meant to provide APP students with an overview of very common medical conditions that they should focus on during their studies. In my teachings, I have found students tend to gravitate toward understanding the “zebras” in medicine, or those conditions that are unusual, instead of diagnosing common problems or unusual variants of common problems. This phenomenon might have to do with the common practice of testing on zebras or the student perception that we (as academic institutions) are out to trick them on a test. By not introducing zebras into the context of this book, the students can maintain focus on the most common disease states. Part II: Perioperative Considerations—Part II contains an operative overview. Again, this section is not a compre-hensive review of the operating room, but it does provide APP students an overview of what they should know regard-less of where they work. In the acute care setting, operativeprocedures are very common. It does not matter if acute care practitioners work directly or indirectly with patients in the perioperative period. A review of the common issues is mandatory. Part III: Procedures—Not all APPs will perform proce-dures, but students frequently feel a sense of accomplish-ment in being able to do something tangible. It is difficult to measure the progress of one's own critical thinking, but if a student can perform a procedure, his or her confidence level goes up quickly. In this section, some of the more common procedures are listed. Part IV: Special Topics—There are many issues that we will deal with as APPs; however, these issues do not all fall neatly into predefined categories. This section was created for select topics that could not be defined by systems but were equally important to address. These topics include end-of-life issues, health promotion, hemodynamic monitoring devices, telemedicine, and transitions of care. All APPs will deal with these issues during the course of their careers. These top-ics will also continue to evolve as we conduct more research and clinical studies and as technology improves. Organization

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

xxiii What Is Different About This Book This book was created for advanced practice provider (APP) students in the acute care setting. In talking to students about their wants and needs in a textbook, I found students were not able to absorb and assimilate information in heavy, dense textbooks that we had been using. I also found myself telling my students not to bother with a large portion of the text-book because it was not immediately relevant to their basic knowledge. Students struggled to understand what to focuson and what they needed to know versus what was nice to know. No one can memorize everything they need to know about medicine. As students specialize in various fields, they will learn in-depth information about their specialties that is beyond the scope of this book. However, there is a body of knowledge that every APP should know, and I have done my best to include those topics in this book. What Is Different About This Book

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

xxv Acknowledgments I have so many people to acknowledge in the creation of this textbook, particularly Dr. Ksenia Zukowsky, Dr. Carey Heck, and Dr. Jack Jallo. Dr. Zukowsky saw so much poten-tial in my plans. She pushed me to do things I was scared to do, and she made them seem possible. Her incredible stories have inspired me over the years, and she remains a powerful influence in my life. Dr. Heck has been an incredible colleague. As the direc-tor of the Acute Care Nurse Practitioner Program at Thomas Jefferson University, she has entertained my “big” ideas and helped me implement them. She has been a rock of support and has contributed massively to the publication of this book as well as the profession. Dr. Jallo has been my main physician support over the years in neurocritical care and neurosurgery. He never told me something could not be done, and he has made me believe that more was always possible. I want to acknowledge all the people who contributed to my growth as a nurse and an academic, especially Dr. Bob Hess. Dr. Hess knew me as a little girl. He was my neighboracross the street. Then, he was my teacher when I went to undergraduate nursing school at the University of Pennsyl-vania. Then he became my employer when I picked up extra time doing some editing work at the nursing magazine that he edited. Finally, he became my colleague and friend who encouraged me to keep rising through the ranks. Of course, I would not be the clinician, academic, and nurse I am today without my students, fellow faculty, friends, and family. I want to express my gratitude to so many peo-ple, but it is not possible to list them all here. From my first nursing job to where I am today, I am thankful for everyone in my life who has taught me so much. It has been an absolute pleasure to work with Springer Publishing Company. I worked most closely with Suzanne Toppy. Her talent, expertise, and encouragement were the guiding light for me through this entire process. I need to acknowledge all the work done by the edit-ing team. What you produced is absolutely amazing. I really appreciate everything you have done in the editorial process. Acknowledgments

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

xxvii Introduction Information Overload No book can serve all the needs of students, nor should that be the goal. This book was specifically designed to provide a foundation of basic information about acute care that stu-dents or any advanced practice provider (APP) should know about a body system. Acute care is defined as treatment that is received in the short term for an injury, emergency, or episode of illness. Acute care can be delivered in the hos-pital setting, EDs, or even outpatient clinics and includes a vast array of conditions and issues. However, patients come to the acute care setting with chronic problems as well that APPs need to address, and the table of contents was developed with this in mind. The table of contents is divided into four parts to accommodate the large scope of acute care. In Part I, the contents are arranged by body system and include the most commonly encountered diseases and conditions that are seen in acute care. In Part II, perioperative considerations are included because surgery is often the main reason for hos-pitalization in the acute care setting. In Part III, procedures that are commonly performed by APPs are included, as well as videos for certain procedures when a visual demonstration can be particularly helpful. Part IV is designed to address special issues that are unique to the acute care setting. The topics addressed are transi-tional care, end-of-life issues, health promotion, hemody-namic monitoring devices, and telemedicine. When a patient comes into the acute care setting, it is an opportunity for all healthcare providers to address health promotion. Not every-one sees healthcare providers on a regular basis or gets eval-uated for routine screening. Therefore, it is essential for all acute care providers to be well versed on the types of health promotion that are necessary based on a patient's age and other demographic factors. Telemedicine is also addressed because it is becoming increasingly prevalent. The ICUs in rural areas can now be monitored by intensivists and APPs in central regions. There is a burgeoning role for APPs in this area. Transitional care is the point where a patient either comes into the acute care setting or returns to the outpatient community. This period of transition is the most vulnerable time for patients. Care-ful attention must be devoted to updating and informing the accepting provider on patient status and the management plan. Finally, end-of-life issues often are addressed in the hos-pital system after an acute episode. Knowledge of these issues is essential to practice. The appendix provides normal lab values as a refer-ence tool for APPs. There may be slight variations frominstitution to institution that may be attributed to different vendors. Please use these values as guides for quick reference, but defer to your institutional normal reference range. Medicine is clearly and overwhelmingly a vast body of knowledge. Students who try to take it all on at once make learning seem like an unsurmountable task. The brain can only absorb so much information at once. When students pick up a dense textbook and see there are hundreds of con-ditions that could exist with just one body system, it makes it difficult for them to focus on the relatively few conditions that we treat commonly. The goal of this book is to decon-struct large topics into focused, core conditions. Students will not learn everything they need to know about a topic by using this book, but they will get what they need to know as a new graduate. Practicing APPs can refer to this resource as a quick review of what they need to know. Continuing to strive for more learning is a lifelong duty as an APP. Furthering the learning process far beyond graduate school and continuing to search out information that is unfamiliar is essential. In this day and age, the Internet is a quick and easy resource to utilize. Patients will be using it as well. While no one expects any one person to know everything at all times, there is an expectation that the providers are resourceful and will know how to find the information. Imposter Syndrome At the end of the day, students will never feel like they know enough to get started, and much of this anxiety can be attributed to what we know about imposter syndrome. Going from the role of an expert in one area to a novice is extremely challenging and creates feelings of uneasiness. This is a com-pletely natural transition mode. In fact, I would be more concerned about a student who thinks he or she knows everything than a student who feels like his or her peers just have not “figured out” that they do not belong. This unease and uncertainty of feeling like an imposter will help students be cautious and humble when they enter the healthcare system as an acute care provider. Developing clin-ical judgment is an art that is guided by science and occurs over time and through experiential learning. Being unsure will motivate new graduates to consult evidence-based mate-rials to search for answers. Frequently textbooks, articles, and case studies provide classic presentations that are useful for learning a concept. However, in practice, the APP quickly discovers that didac-tic content in a lecture or a book does not account for the number of variables that are present in real clinical situations. Introduction

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

xxviii Hence, textbook learning has limitations that can only be remedied with practice. A student in the novice stage of a new role would be best advised to spend as much time as possible with patients, practicing active, focused listening and asking questions. This practice will help the new graduate APP gain confidence quickly. Role of APPs The role of APPs continues to evolve and expand in the healthcare system. New opportunities open up as the health-care system begins to depend heavily on the utilization of APPs, particularly in the acute care system. It was not too long ago that most nurse practitioners (NPs) and physician assis-tants (PAs) worked primarily in primary care settings. Now, NPs and PAs work in primary care, all aspects of the acute care system, and beyond. More and more collaborative efforts are being established between NPs and PAs as we move away from contrasting how we are different and focus on achieving the same goals. Both NPs and PAs struggle with practice issues, prescrib-ing issues, and levels of autonomy. However, many legislative advancements have been achieved over the past 10 years that have created a growing demand for APPs. As the roles and responsibilities of APPs continue to expand, the stronger the collaboration between them needs to be. This book is one step forward in developing and creating these collaborative efforts for NPs and PAs. Future Opportunities There are many opportunities for APPs. One of the major next steps I see for APPs is acute care billing. Billing pro-vides visibility of the extent of work that is truly being done by APPs. Billing can also be leveraged for improved working conditions and better pay. In the current system where APP billing is absorbed by physician groups, APPs are left withbasically nothing to show for their efforts. How can a hospi-tal administration effectively determine if more or fewer APPs are needed in a particular department? How can a practice group determine if an APP is exceeding expectations in his or her work or even underperforming? How can an APP justify a raise for himself or herself when there is nothing quantifiable to show the value of what has been done? Billing is more than just sending off charges to insurance companies to get paid. Billing provides visibility, which in turn comes with responsibilities and challenges. At the time of the writing of this book, there were no models (or too few to use) of acute care billing for APPs to devote an entire section to the issue; however, it is definitely coming. Insur-ance companies and compliance programs are taking steps to implement a structure that recognizes the contribution of the APP to the patient's care. Acute care billing is going to be a controversial issue in the years to come, and APPs would be well advised to keep on top of how it is implemented and to participate in any committees that are designated to discuss such planning. Final Note Being an APP is an exciting and excellent career choice that has countless opportunities. Learning about disease states and management of patients is one aspect of the role of the APP. There is so much to learn, and it can be incredibly over-whelming. My advice to students, new graduates, and even seasoned APPs would be this: Acknowledge that there is a massive amount of information to be learned... over time. Accept that you have roles and responsibilities to the health-care system and your community that extend beyond treat-ing disease states. And accelerate your learning curve by being present with your patients, collaborating with your team, and staying involved in your profession. Best of luck in this amazing profession as an APP. Introduction

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Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

I Acute Care Guidelines by System 1. ENT Guidelines 2. Pulmonary Guidelines 3. Cardiac Guidelines 4. Gastrointestinal Guidelines 5. Nephrology Guidelines 6. Neurology Guidelines 7. Targeted Temperature Management Guidelines 8. Endocrine Guidelines 9. Psychiatric Guidelines10. Infection Guidelines 11. Peripheral Vascular Guidelines 12. Hematology Guidelines 13. Oncology Guidelines 14. Immune System, Connective Tissue, and Joints Guidelines 15. Dermatology Guidelines 16. Geriatric Guidelines 17. Trauma Guidelines

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

3 1 ENT Guidelines Carey Heck Conjunctivitis Carey Heck Definition A. Inflammation of the conjunctiva, a thin transparent membrane that lines the inside of the eyelids and covers the sclera. B. Commonly called “pink eye. ” Incidence A. Allergic conjunctivitis. 1. Most common cause of conjunctivitis (15%-40% of population). 2. Most frequently occurs in spring and summer. B. Viral conjunctivitis. 1. Most common cause of infectious conjunctivitis. 2. Most common type in adults. 3. More frequently occurs in the summer months. C. Bacterial conjunctivitis. 1. Most common cause of infectious conjunctivitis in children. 2. Most frequently occurs in the winter and early spring months. Pathogenesis A. Allergic. 1. Not contagious. 2. Common in individuals with other signs of allergic disease. 3. Reaction to allergic triggers. B. Infectious. 1. Bacterial. a. Highly contagious. b. Most common causative agents. i. Staphylococcus aureus. ii. Haemophilus influenzae. iii. Streptococcus pneumoniae. iv. Moraxella catarrhalis. 2. Viral. a. Highly contagious. b. Most common causative agent. i. Adenoviruses. ii. Rubella virus. iii. Rubeola virus. iv. Herpes viruses. C. Noninfectious. D. Other causes. 1. Environmental irritants. 2. Medications. 3. Toxins. 4. Chemicals. Predisposing Factors A. Exposure to allergens. B. Exposure to environmental irritants. C. Contact lens wearers. D. Use of ophthalmic drops. E. Old makeup products. F. Occupational exposure to chemicals. Subjective Data A. Common complaints/symptoms. 1. Redness. 2. Discharge. a. From the eye. b. Crusts over the eyelid, especially after sleep. 3. Itching, burning. 4. Increased tearing. 5. Blurred vision. 6. Painless. 7. Feeling of foreign body in the eye. B. Common/typical scenario. 1. Specific presentation varies dependent on type of con-junctivitis. 2. Symptoms of eye redness and discharge are common regardless of specific cause. 3. Contributing history and appearance of discharge often determines diagnosis. C. Family and social history. 1. Review of symptoms. a. Elicit the onset and duration of symptoms. b. Determine if the patient or close contacts have any systemic illnesses. c. Assess the patient for any risk factors. d. Associated symptoms. i. Rhinorrhea. ii. Earache. iii. Sore throat. iv. Rash. e. Single or both eyes. 2. Past medical history. a. Recent illnesses. b. Sick contacts. c. Allergies. d. Possible occupational exposure history. e. Sexual history. f. Contact lens use. Conjunctivitis

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

4 D. Review of systems. 1. Recent illnesses. Determine the onset and duration of symptoms. a. Abrupt or gradual onset. b. Determine if the patient or close contacts have any systemic illnesses. 2. Allergies. 3. Possible occupational exposure history. 4. Sexual history. 5. Pertinent systems review. a. Head, ear, eyes, nose, and throat (HEENT). i. Headache. ii. Vision loss. iii. Eye pain. iv. Eye discharge. v. Ear pain. vi. Rhinorrhea. vii. Nasal congestion. viii. Cough. b. Integumentary. i. Rash. ii. Lesions. Physical Examination A. Perform an eye examination, assessing for vision loss and eye discharge. 1. Appearance of eyes. a. Allergic: Typically both eyes are infected. b. Bacterial: Typically one eye is infected but may spread to other eye. c. Viral: Typically both eyes are infected. 2. Discharge. a. Allergic: Stringy. b. Bacterial: Mucopurulent. i. Copious yellow-green discharge is consistent with gonorrheal infection. c. Viral: Watery. 3. Visual acuity. 4. Corneal opacity. 5. Pupil size and shape. 6. Eyelid swelling. 7. Presence of proptosis. B. Red flags. 1. Reduction of visual acuity. 2. Ciliary flush. 3. Photophobia. 4. Severe foreign body sensation. 5. Corneal opacity. 6. Fixed pupil. 7. Severe headache with nausea. 8. Dendriform lesion indicative of herpes simplex virus (HSV). Diagnostic Tests A. Diagnosis is made with history and physical examination. B. Imaging studies are not indicated unless underlying con-dition is suspected. C. Culture should be considered. 1. In severe cases. 2. In patients who wear contact lenses. 3. In patient unresponsive to initial treatment. 4. If sexually transmitted disease (STD) is suspected. Differential Diagnosis A. Conjunctivitis. 1. Allergic: Likely with accompanying allergic symptoms and contributing history. 2. Bacterial: Likely with thick, yellow-green discharge. 3. Viral: Likely with accompanying cold or respiratory symptoms and watery discharge from the eye. B. Corneal abrasion. 1. Different from conjunctivitis in that there is a subjec-tive complaint of severe pain that worsens over time. C. Foreign body in the eye. D. Keratitis. E. Varicella zoster ophthalmicus. F. Glaucoma. Evaluation and Management Plan A. General plan. 1. Symptomatic relief is adequate for all forms of con-junctivitis. a. Most symptoms: Resolve without treatment. b. Supportive care. i. Over-the-counter (OTC) products. 1)Topical OTC medications are of limited efficacy for allergic conjunctivitis. 2)Systemic antihistamines may be useful for allergic conjunctivitis. ii. Moist cold compresses to eyes. iii. Avoidance of allergic triggers. 2. Antibiotics are not indicated in most cases of bacterial conjunctivitis. a. Return to work or school requirements. These may necessitate initiation of antibiotic for confirmed cases of bacterial conjunctivitis. i. Antibiotics initiated within the first 2 to 5 days can hasten the resolution of symptoms. ii. Initiation of antibiotics after 5 days of the start of symptoms has a minimal effect, and use is not recommended. b. Indications for antibiotic therapy. i. Cases caused by gonorrhea infection. ii. Cases caused by chlamydia infection. iii. Contact lens wearers. 1)Consider pseudomonas infection. B. Patient/family teaching points. 1. Use handwashing to prevent spread. 2. Avoid touching eyes. 3. Instruct patients to dispose of current contact lenses and to avoid wearing contact lenses until irritation/infec-tion is cleared. 4. Instruct patients to dispose of all eye makeup. C. Pharmacotherapy. 1. Allergic. a. Artificial tears. b. Antihistamine/decongestant drops (OTC). c. Mast cell stabilizer/antihistamine drops (OTC). 2. Viral. a. Antibiotics not indicated. b. Antihistamine/decongestant drops (OTC). c. Artificial tears (OTC). d. Viral therapy for HSV infection. 3. Bacterial conjunctivitis. a. Topical (eye drops or ointment) antibiotic therapy. i. Erythromycin 5 mg/g ophthalmic ointment: One-half inch (1. 25 cm) four times daily for 5 to 7 days. ii. Ciprofloxacin 0. 3% ophthalmic drops (pre-ferred agent in contact lens wearer): 1 to 2 drops four times daily for 5 to 7 days. b. Systemic antibiotics indicated for gonorrhea and chlamydia infections. i. 1 gm ceftriaxone IM plus azithromycin 1 gm PO for one dose. 1. ENT Guidelines

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5 D. Discharge instructions. 1. Symptoms should resolve in 5 to 7 days. 2. If symptoms continue or different symptoms appear, then follow-up is recommended. Follow-Up A. Instruct patients with acute bacterial conjunctivitis to follow-up in 1 to 2 days if symptoms worsen or do not improve. B. Instruct patients with other forms of conjunctivitis to follow-up within 2 weeks if symptoms worsen or do not improve. Consultation/Referral A. Consider referral to allergy specialist for allergen testing in severe cases of allergic conjunctivitis. B. Referral to ophthalmologist for cases that are resistant to initial treatment. C. Urgent referral to ophthalmologist due to increased risk of vision loss. 1. Hyperacute bacterial conjunctivitis. 2. Keratitis. 3. Varicella zoster ophthalmicus. Special/Geriatric Considerations A. Infants (highly susceptible to conjunctivitis). 1. At risk for more serious complications. 2. Prophylactically treated with optic antibiotics at birth. B. Contact lens wearers. 1. Higher risk for keratitis: Careful evaluation to rule out keratitis is essential before diagnosis of conjunctivitis is made. 2. Discontinue use until eye has healed. Use can begin again when eye is white and patient has no discharge for 24 hours after completion of antibiotics. C. Returning to school or work. This is appropriate 24 hours after antibiotics have been initiated or there is no discharge. D. Awareness of local board of health reporting laws for STDs. This is essential when the diagnosis of conjunctivitis is made in the setting of gonorrhea and chlamydia. Bibliography Alfonso, S. A., Fawley, J. D., & Lu, X. A. (2015). Conjunc-tivitis. Primary Care: Clinics in Office Practice, 42 (3), 325-345. doi:10. 1016/j. pop. 2015. 05. 001 Azari, A., & Barney, N. (2013). Conjunctivitis: A systematic review of diagnosis and treatment. Journal of the American Medical Association, 310(16), 1721-1729. doi:10. 1001/jama. 2013. 280318 Bielory, B. P., O'Brien, T. P., & Bielory, L. (2012). Management of seasonal allergic conjunctivitis: Guide to therapy. Acta Ophthalmologica, 90 (5), 399-407. doi:10. 1111/j. 1755-3768. 2011. 02272. x Gore, J. (2013). Conjunctivitis. Journal of the American Academy of Physician Assistants, 26 (3), 60. Mc Anena, L., Knowles, S. J., Curry, A. S., & Cassidy, L. (2015). Prevalence of gonococcal conjunctivitis in adults and neonates. Eye, 29 (7), 875-880. doi:10. 1038/eye. 2015. 57 Segal, K., Lai, L., & Starr, E. (2014). Management of acute conjunctivitis. Current Ophthalmology Reports, 2 (3), 116-123. doi:10. 1007/s40135-014-0046-4 Pharyngitis Carey Heck Definition A. Inflammation of the pharynx. B. Commonly referred to as a “sore throat. ”Incidence A. Acute pharyngitis accounts for more than 12 million office and emergency/urgent care visits in the United States annually. B. Viral pharyngitis occurs most frequently; increased inci-dence in adult population. C. Bacterial pharyngitis occurs more frequently in children and adolescents. 1. Particularly the Group A beta-hemolytic streptococci (GAS). a. Peak incidence occurs in 5 to 15 year age group. b. Only 5% to 15% of adults present with GAS. 2. Bacterial pharyngitis occurs most frequently in winter and early spring months. Pathogenesis A. Infectious. 1. Viral. a. Adenoviruses and rhinoviruses responsible for most cases of viral pharyngitis. b. Other causes include. i. Herpes simplex virus (HSV) 1 and 2. ii. Coxsackievirus. iii. Human herpes virus 4 (Epstein-Barr virus [EBV]). iv. Human herpes virus 5 (cytomegalovirus). v. HIV. 2. Bacterial. a. The most important causative agent is the GAS. i. Severe complications of GAS warrant prompt identification and treatment. b. Other causes include. i. Group C streptococci. ii. Neisseria gonorrhoeae. iii. Corynebacterium diphtheriae. iv. Treponema pallidum. v. Mixed anaerobes. B. Noninfectious. 1. Allergy. 2. Irritants. 3. Gastrointestinal reflux. Predisposing Factors A. Exposure to infectious agents. 1. Bacteria. 2. Viruses. B. Exposure to allergens. C. Exposure to environmental irritants. D. History of gastrointestinal reflux. E. History of immunosuppression. Subjective Data A. Common complaints/symptoms. 1. “Sore throat. ” 2. Difficulty swallowing. 3. Nasal congestion. 4. Sinus tenderness. 5. Cough. 6. Malaise. 7. Headache. 8. Distinguishing features of pharyngitis associated with GAS. a. Absent cough. b. Fever. Pharyngitis

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

6 c. Tonsillar exudates. d. Anterior cervical lymphadenopathy. B. Common/typical scenario. 1. Patients typically complain of sore or scratchy throat, fever, and general malaise. C. Review of systems. 1. Past medical history. a. Recent illnesses. Determine the onset and duration of symptoms. i. Abrupt or gradual onset. ii. Duration longer than 3 weeks unlikely to be pharyngitis. b. Sick contacts. Determine if the patient or close contacts have any systemic illnesses. c. Assess the patient for any risk factors. 2. Allergies. 3. Possible occupational exposure history. 4. Travel history. 5. Sexual history. 6. Pertinent systems review. a. Constitutional. i. Fever. ii. Malaise. b. Head, ear, eyes, nose, and throat (HEENT). i. Sore throat. ii. Cough. iii. Rhinorrhea. iv. Nasal congestion. v. Headache. vi. Sinus tenderness/pain. c. Integumentary. i. Rash. ii. Lesions. Physical Examination A. Appearance of pharynx. 1. Pale to red. 2. Mild erythema to profound edema. 3. Vesicular lesions. a. HSV. b. Coxsackievirus. B. Appearance of tonsils. 1. Redness. 2. Edema. 3. Exudates. a. White (oropharyngeal candidiasis, GAS). b. Grayish membrane (diphtheria). C. Lymph nodes. 1. Cervical lymphadenopathy. 2. Tonsillar lymphadenopathy. D. Integumentary. 1. Scarlatiniform rash may be present in GAS infections. 2. Palatine petechiae may be present in GAS infection. E. Red flags. 1. “Hot potato” voice. a. Garbled speech due to pharyngeal edema. b. Suggestive of peritonsillar abscess. 2. Unilateral neck swelling. 3. Difficulties with secretion management. a. Drooling. b. Compromised airway. i. Tonsillar pillars touching. ii. “Kissing tonsils. ” 4. Uvula deviation. a. Indicative of peritonsillar abscess. TABLE 1. 1 Modified Centor Criteria Clinical Finding Score Fever +1 Absence of cough +1 Anterior cervical lymphadenopathy +1 Tonsillarexudates +1 Age (years) 2-14 +1 15-44 0 45+-1 Source:Fine,A. M.,Nizet,V.,&Mandl,K. D. (2012,June11). Large-scale validation of the Centor and Mc Isaac scoresto predictgroup A streptococcalpharyngitis. Archives of Internal Medicine, 172 (11), 847-852. Diagnostic Tests A. Clinical examination: Modified Centor criteria. 1. Scoring system developed to quickly diagnose the like-lihood of GAS. 2. One point assigned for each of the following clin-ical findings: History of fever, tonsillar exudates, ante-rior cervical lymphadenopathy, and absence of cough (see Table 1. 1). 3. Empiric treatment based on symptoms and higher Centor score is no longer recommended by the Infectious Disease Society of America. B. Rapid antigen detection testing (RADT). 1. Indicated because clinical examination alone cannot differentiate between viral and bacterial pharyngitis. Modified Centor Score Guidelines for Treatment 0-1 No further evaluation necessary Providesupportive care Antibiotics not recommended 2-3 Assess for GAS pharyngitis Consider throatculturesand RADT Treatif culturespositive >4 Assess for GAS pharyngitis Throatculturesand RADT indicated Empiric treatmentcontroversial IDSA does not recommendempiric treatment Treatif culturespositive GAS, group A beta-hemolytic streptococci; IDSA, Infectious Disease Society of America; RADT,rapid antigen detection testing. 2. May not be necessary if overt viral symptoms are present (i. e., cough, rhinorrhea). a. Throat culture. 3. Pediatric: Indicated in children with negative RADT and clinical symptoms supportive of bacterial pharyngitis. 4. Adults. a. Not necessary in adults with negative RADT due to low incidence of GAS in adults. 1. ENT Guidelines

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7 b. Possibly indicated. i. In adults with negative RADT if high suspi-cion of GAS. ii. In adults at high risk for infection (immuno-compromised or other comorbidities). iii. Those who are in close contact with high risk populations. Differential Diagnosis A. Viral pharyngitis. B. Bacterial pharyngitis. C. Oropharyngeal candidiasis (thrush). 1. Immunocompromised patients. 2. Patients receiving broad spectrum antibiotics or cor-ticosteroids. D. Gonococci. Possible in patients engaging in orogenital sex. E. Diphtheria. F. Mononucleosis. Evaluation and Management Plan A. General plan. 1. Pain relief. a. Over-the-counter (OTC) oral analgesics. i. Nonsteroidal anti-inflammatory drugs. ii. Acetaminophen. iii. Aspirin. b. Topical therapies. i. Lozenges. ii. Sprays. iii. Fluids (i. e., tea, honey). c. Environmental measures. i. Humidified air. ii. Avoidance of irritants. d. Glucocorticoid. i. Not recommended for routine use. ii. Limited role in the patient with extreme sore throat and inability to swallow. 2. Antibiotics for confirmed bacterial infection. B. Patient/family teaching points. 1. Handwashing to prevent spread. C. Pharmacotherapy. 1. Avoidance of empiric antibiotics. a. Overprescribing contributes to antibiotic resis-tance. b. Antimicrobial therapy generally does not benefit bacterial pharyngitis caused by infection other than streptococcal bacteria. c. Infections due to other organisms are possible but tend to be the exception. i. N. gonorrhoeae. ii. C. diphtheriae. 2. Bacterial pharyngitis. a. Penicillin is antibiotic of choice for GAS pharyn-gitis. i. 10-day course recommended. b. First generation cephalosporin for penicillin aller-gies. c. Alternatively 5-day course of azithromycin is acceptable. i. Local and regional resistance has been reported. 3. Viral pharyngitis. a. Supportive care. D. Discharge instructions. 1. Follow-up is recommended if symptoms do not improve in 3 to 4 days. Follow-Up A. Instruct patients to follow-up if pharyngitis does not improve in 5 to 7 days. B. Further evaluation indicated if no improvement or wors-ening of symptoms. 1. Possible suppurative complication. 2. Alternative diagnosis. Consultation/Referral A. Urgent referral to otolaryngologist for suppurative com-plications. 1. Peritonsillar abscess. 2. Retropharyngeal abscess. 3. Epiglottitis. Special/Geriatric Considerations A. Suppurative complications. 1. Rare but potentially life threatening complications of GAS pharyngitis. 2. Early recognition and appropriate treatment essential to avoid associated morbidity and mortality. 3. Complications include: a. Peritonsillar abscess. b. Retropharyngeal abscess. c. Streptococcal bacteremia. d. Epiglottitis. B. Nonsuppurative complications. 1. Rheumatic fever. a. Rare in developed countries. 2. Poststreptococcal glomerulonephritis. C. Other considerations. 1. Morbilliform rash may develop in patients with pharyngitis caused by EBV who have been treated with penicillin or amoxicillin. Bibliography Fine, A. M., Nizet, V., & Mandl, K. D. (2012, june 11). Large-scale valida-tion of the Centor and Mc Isaac scores to predict group a streptococcal pharyngitis. Archives of Internal Medicine, 172 (11), 847-852. Gore, J. (2013). Acute pharyngitis. Official Journal of the American Academy of Physician Assistants, 26 (2), 57-58. doi:10. 1097/01720610-201302000-00012 Mc Isaac, W. J., White, D., Tannenbaum, D., & Low, D. E. (1998). A clinical score to reduce unnecessary antibiotic use in patients with sore throat. Canadian Medical Association Journal, 158 (1), 75-83. Nicoteri, J. (2013). Adolescent pharyngitis: A common complaint with potentially lethal complications. Journal for Nurse Practitioners, 9 (5), 295-300. doi:10. 1016/j. nurpra. 2013. 02. 023 Shapiro, D., Lindgren, C., Neuman, M., & Fine, A. (2017). Viral features and testing for streptococcal pharyngitis. Pediatrics, 139 (5), e20163403. doi:10. 1542/peds. 2016-3403 Shulman, S., Bisno, A., Clegg, H., Gerber, M., Kaplan, E., Lee, G., & Van Beneden, C. (2012). Executive summary: Clinical practice guideline for the diagnosis and management of group A streptococcal pharyngi-tis: 2012 update by the Infectious Diseases Society of America. Clinical Infectious Diseases, 55 (10), 1279-1282. doi:10. 1093/cid/cis847 Weber, R. (2014). Pharyngitis. Primary Care: Clinics in Office Practice, 41, 91-98. doi:10. 1016/j. pop. 2013. 10. 010 Pharyngitis

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8Rhinosinusitis Carey Heck Definition A. Inflammation of the nasal cavity and paranasal sinuses. B. Preferred terminology: “Rhinosinusitis” rather than “sinusitis” since inflammation of the sinuses rarely occurs without inflammation of the nasal mucosa as well. C. Classification. 1. Acute rhinosinusitis (ARS): Symptoms lasting less than 4 weeks. 2. Acute bacterial rhinosinusitis (ABRS): ARS with bac-terial etiology. 3. Chronic rhinosinusitis (CRS): Symptoms lasting greater than 12 weeks. Incidence A. Viral infection due to rhinopharyngitis (common cold) is the most common cause of ARS. B. Annually, 1 in 7-8 persons in the United States will expe-rience an episode of ARS. C. More frequent in women. D. Higher in 45-to 64-year-ld age group. E. ABRS accounts for less than 2% of the cases of ARS. Pathogenesis A. Viral. 1. Rhinovirus. 2. Influenza virus. 3. Parainfluenza virus. B. Bacterial. a. Streptococcus pneumoniae. b. Haemophilus influenzae. c. Moraxella catarrhalis. Predisposing Factors A. Older age. B. Smoking. C. Air travel. D. Exposure to changes in atmospheric pressure. E. Asthma and allergies. F. Swimming. G. Dental disease. H. Immunodeficiency. Subjective Data A. Common complaints/symptoms. 1. Nasal congestion. 2. Nasal discharge. 3. Facial pressure or feeling of fullness. 4. Reduced sense of smell. B. Other complaints. 1. Fatigue. 2. Headache. 3. Difficulty sleeping. 4. Toothache. 5. Ear pain or fullness. C. Family and social history. 1. Family and social history is noncontributory. D. Common/typical scenario. 1. Common complaints are: a. Fever. b. Sore throat. c. Nasal discharge. d. Facial pain. e. Frontal pain or pressure that worsens when patient bends forward. 2. Patients frequently complain of headaches. E. Review of systems. 1. Past medical history. a. Recent illnesses. Elicit onset and duration of symp-toms. b. Sick contacts. Determine if patient or close con-tacts have any systemic illnesses. c. Asthma. 2. Allergies. 3. Possible occupational exposure history. 4. Travel history. 5. Pertinent systems review. a. Constitutional. i. Fever. ii. Malaise. b. Head, ear, eyes, nose, and throat (HEENT). i. Sinus pain/tenderness. ii. Headache. iii. Nasal congestion. iv. Cough. v. Rhinorrhea. vi. Purulent discharge with bacterial infection. Physical Examination A. Appearance. 1. Erythema and/or edema of involved cheek. 2. Erythema and/or edema of periorbital area. B. Drainage. 1. Mucopurulent more likely ABRS. 2. Clear more likely viral ARS. C. Percussion. 1. Increased pain or tenderness of sinuses. 2. Not specific or sensitive test for diagnosis of rhinosi-nusitis. D. Transillumination of frontal and maxillary sinuses. 1. Limited diagnostic value. 2. Not specific or sensitive test for diagnosis of rhinosi-nusitis. E. Nasal examination. 1. Diffuse mucosal edema. 2. Narrowing of middle meatus. 3. Inferior turbinate hypertrophy. 4. Presence or absence of polyps. a. Presence may indicate anatomic risk for develop-ment of ABRS. Diagnostic Tests A. Generally not indicated for uncomplicated cases of rhi-nosinusitis. B. Nasal cultures are not useful in the diagnosis of ABRS. C. Gold standard for culture identification: Sinus aspiration. 1. Reserved for complicated cases. 2. Referral to otolaryngologist. D. CT. 1. Persistent symptoms. 2. Recurrent symptoms. 3. Complicated ABRS. 4. Planning for sinus surgery. Differential Diagnosis A. Rhinosinusitis. B. Allergic rhinitis. 1. ENT Guidelines

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9 C. Rhinopharyngitis. D. Headache. Evaluation and Management Plan A. General plan. 1. Use pain relief: Over-the-counter (OTC) analgesics and antipyretics. 2. Reduce mucosal inflammation: Topical nasal corticos-teroids. 3. Enhance sinus drainage: Saline irrigation. 4. Modulate environmental triggers. a. Treat concurrent allergic rhinitis symptoms if present with OTC antihistamines and allergy therapy as needed. 5. Eradicate infection indicated for ABRS. B. Patient/family teaching points. 1. Use handwashing to prevent spread. C. Pharmacotherapy. 1. Acute sinusitis. a. Most cases of acute sinusitis are viral and pharma-cotherapy is targeted to symptomatic relief. i. OTC analgesics and antipyretics. ii. Saline nasal irrigation. iii. Possibly topical corticosteroids. 1)Literature suggests that high-volume cor-ticosteroid irrigations are more effective than low-volume corticosteroid sprays. iv. Topical decongestants. 1)Use not to exceed 3 to 5 days to avoid rebound congestion. v. Antihistamines. 1)No clinical studies support use in viral sinusitis. vi. Expectorants and cough suppressants. 1)Clinical studies do not support efficacy in use for viral sinusitis. b. Suspected bacterial sinusitis. i. Classic progression is mild symptoms that begin to resolve and then suddenly become worse. ii. Watchful waiting: Plan to follow-up if symp-toms worsen or do not improve in 7 days. iii. Nonmacrolide therapy. 1)Amoxicillin/clavulanate 875/125 mg orally twice daily ×5 to 7 days. 2)Doxycycline 200 mg orally daily ×5 to 7 days for PCN allergies. iv. OTC analgesics and antipyretics. v. Saline irrigation. 1)Use as adjuvant to corticosteroids in chronic sinusitis. vi. Topical corticosteroids. 1)Literature suggests that high-volume cor-ticosteroid irrigations are more effective than low-volume corticosteroid sprays. 2. Chronic sinusitis. a. Initial management is high-volume saline irriga-tion with topical corticosteroid therapy. b. Consider short course of nonmacrolide therapy if active mucopurulence is present on examination. c. For patients with persistent symptoms. i. Consider systemic corticosteroids. ii. Use long-term macrolide therapy for patients without nasal polyps. d. Topical antibiotics and antifungals are not recom-mended in the treatment of chronic sinusitis. D. Discharge instructions. 1. Follow-up is recommended in 3 to 4 days if no improvement in symptoms. Follow-Up A. Patients should be instructed to follow-up if symptoms do not improve in 7 days. B. Further evaluation is indicated if no improvement or worsening of symptoms. Consultation/Referral A. Persistent cases should be referred to otolaryngology. 1. Endoscopic nasal evaluation. 2. Endoscopic nasal surgery. Special/Geriatric Considerations A. Long-term use of nasogastric tubes can put patients at risk for developing sinusitis. Bibliography Bird, J., Biggs, T., Thomas, M., & Salib, R. (2013). Adult acute rhinosinusi-tis. British Medical Journal, 346, f2687. doi:10. 1136/bmj. f2687 Cevc, G. (2017). Differential diagnosis and proper treatment of acute rhi-nosinusitis: Guidance based on historical data analysis. Allergy & Rhinol-ogy, 8(2), e45-e52. Advance online publication. doi:10. 2500/ar. 2017. 8. 0206 Cho, S. H., Kim, D. W., & Gevaert, P. (2016). Chronic rhinosinusitis with-out nasal polyps. Journal of Allergy and Clinical Immunology: In Practice, 4(4), 575-582. doi:10. 1016/j. jaip. 2016. 04. 015 Rosenfeld, R., Piccirillo, J., Chandrasekhar, S., Brook, I., Kumar, K., Kram-per, M.,... Corrigan, M. (2015). Clinical practice guideline (Update): Adult sinusitis. Otolaryngology-Head and Neck Surgery, 152 (2 Suppl. ), S1-S39. doi:10. 1177/0194599815572097 Rudmik, L., & Soler, Z. (2015). Medical therapies for adult chronic sinusitis: A systematic review. Journal of the American Medical Association, 314 (9), 926-939. doi:10. 1001/jama. 2015. 7544 Rhinosinusitis

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11 2 Pulmonary Guidelines Acute Respiratory Distress Syndrome E. Mone ́e Carter-Griffin Definition A. Acute respiratory distress syndrome (ARDS) is defined by three variables. 1. Bilateral opacities on imaging. 2. Onset within 7 days of a clinical event or worsening respiratory symptoms. 3. Origin of pulmonary edema not fully explained by cardiac failure or volume overload. B. ARDS is identified as mild, moderate, or severe based on the PF ratio (Pa O2/Fi O2). C. Acute lung injury does not exist in the new definition of ARDS. D. Exclusion of heart failure is not required in the new defi-nition of ARDS. Incidence A. It is difficult to obtain an accurate incidence due to vari-ations in the definition used to identify or describe ARDS. B. An estimated 200,000 cases of ARDS occur each year in the United States. C. The incidence increases with advancing age. D. ARDS has not been shown to occur more in one sex than the other. E. Mortality and morbidity are associated with worsening of the PF ratio. Pathogenesis A. An indirect or direct insult causes an inflammatory response and accumulation of pro-inflammatory mediators in the lung microcirculation. Injury occurs to the microvascu-lar endothelium and alveolar epithelium. Endothelium injury leads to capillary permeability and migration of protein-rich fluid into the alveolar space. Due to injury of the alveolar epithelium, pulmonary edema forms and damage occurs to the cells lining the alveoli. B. Damage to type I and II cells leads to decreased clear-ance of fluid in the pleural space, increased fluid entry into the alveoli, and decreased surfactant production resulting in decreased alveolar compliance and alveoli collapse. C. An influx of fibroblasts leads to collagen deposition and possibly fibrosis. Predisposing Factors A. Aspiration, including gastric content and drowning. B. Sepsis. C. Pneumonia. D. Massive transfusions. E. Pancreatitis. F. Burns. G. T rauma, including cases with and without pulmonary injury. H. Underlying interstitial lung disease. Subjective Data A. Common complaints/symptoms. 1. Severe dyspnea. 2. Chest discomfort. 3. Tachypnea. B. Common/typical scenario. 1. Onset is typically 12 to 48 hours after the insult. 2. History shows progressive worsening symptoms. 3. Extrapulmonary complaints may have led to the development of ARDS. Physical Examination A. Dyspnea (see Figure 2. 1). B. Tachypnea. C. Abdominal retractions; obvious respiratory distress. D. Hypoxia and possibly cyanosis. E. Tachycardia. F. Altered mental status, agitation, or confusion. G. Rales during auscultation. H. Additional findings that may relate to the underlying eti-ology of ARDS (e. g., febrile, hypotension, an acute abdomen, or nausea and vomiting seen in pancreatitis). Diagnostic Tests A. Chest x-ray (CXR). 1. Patchy infiltrates rapidly evolve and progress to dif-fuse, bilateral infiltrates. 2. Daily CXRs may be required, especially for patients on mechanical ventilation. B. Arterial blood gas (ABG). 1. Regular ABGs are required to evaluate management. 2. Development of respiratory acidosis (decreased p H and rising CO2). 3. Hypoxemia is defined by the PF ratio. a. Less than 300: As mild ARDS. b. Less than 200: Moderate ARDS. c. Less than 100: Severe ARDS. C. Complete blood count (CBC). 1. Evaluate the white blood cell count and platelets. D. Comprehensive metabolic panel. 1. Evaluate renal and liver function. Acute Respiratory Distress Syndrome E. Mone ́e Carter-Griffin

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12 Respirat ory ABG: Assess for hypercapnia or hypoxemia D-dimer, ag e-adj usted : Can aid in ru ling out a pulm onary embolus. Chest CT/A ngiogr aphy: Assess for pne umonia, emph ysematous c hange s, /f_luid, honeycombing sugge stive of /f_ibrosis, pulmo nary embo lus. Pulmona ry function t esti ng: Assess for obstr uctiveorrestric tive dise ase. Addit ional Testin g Thyroid studies: Assess for hyperthyroidism (high card iac output sta te). Hemogl obin/Hematocrit: Assess for anemia. Cardiopulmonary exercis e test: Can help di stinguish between the two by indicating ischemic changeson ECG (cardiac),bronchospasmduringexercise(respiratory), and so forth. Obtain the History Quality/sensation, timing, precipitating factors, allev iating factors, a ny associated factors. Gradual or sudden onset? Continuous or episod ic? Occur with exertion or at rest? Positional? Physical Ex amin ation General: Positioning? Accessor y muscle use? Paradoxical abdominal movement? O vert distress ? Able to speak in full sentences? Audible stridor? Vital Signs: Tachycardia? Tachypnea? Pulsus para doxus? Oxygen desat urations? Cardiac: Elevated JVD? Murmur? S3 or S4 gallop? Edema? Resp iratory: Adventitious b reath sounds such as cra ckles/rales, wheezes, or diminished? Chest shape? Dullness or h yperre sonance on percussio n? R espiratory pattern? Symmetrical chest movement? Extremities: Cyanosis? Edema? Clubbing? *The physical exam shoul d always focus on airway, breathing, circulation /f_irst. Proceed with a full exam in the stab le patient* Initial Diagn ostics Chest x-ray: Evidence of pulmonary edema? Pneumonia? Pleural effusion ? Hyperin/f_lation of the lungs suggestive of obstru ctive disease? Heart size? L ung volumes? Elevation of hemidiaphragm? ECG: Toassess for myocardial injury or ischemia. Cardiovasc ular Echoc ardio gram :Assess heart siz e, func tion, valves, pulmonary pressures, pericardial effusion, and so forth. NT-pro BN P: Can a id in the diagnosis of heart failure in the appro priate clinical context. FIGURE 2. 1 Algorithm for the evaluation of dyspnea. JVD, jugular venous distention; NT-pro BNP, N-Terminal pro brain natriuretic peptide. 2. Magnesium and phosphorus. Strict electrolyte reple-tion is necessary for cardiac stability and prevention of arrhythmias, especially in the setting of profound tissue hypoxia and/or septic shock, which is often concomitant. E. Coagulation studies. 1. Prothrombin time and international normalized ratio. 2. Fibrinogen level. 3. Fibrin degradation products. F. N-Terminal pro brain natriuretic peptide level. 1. This is used to assess for heart failure causing or con-tributing to the bilateral infiltrates and hypoxemia. 2. It is important for the clinician to note that this value may be elevated secondary to etiologies other than heart failure, such as sepsis and renal failure. G. Blood cultures. 1. Evaluate infective etiology as a source for ARDS devel-opment. H. Systemic infection markers. 1. Lactic acid. Measure level of end-organ tissue hypoxia and consider trend. 2. Procalcitonin. Consider trend every 24 hours and monitor for effectiveness of treatment of the primarily offending process. I. Urinalysis and urine culture. 1. Evaluate infective etiology as source for ARDS devel-opment. J. Sputum culture. 1. Evaluate infective etiology as source for ARDS devel-opment. Differential Diagnosis A. Asthma. B. Chronic obstructive pulmonary disease (COPD). C. Congestive heart failure (CHF). D. Acute lung injury. E. Pleural effusions. F. Pneumonia. 2. Pulmonary Guidelines

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13 Evaluation and Management Plan A. T reatment is dependent on the severity of ARDS. 1. Oxygen therapy (e. g., high flow nasal cannula, non-invasive positive pressure ventilation, invasive mechanical ventilation). a. In acute hypoxemic respiratory failure, high flow nasal cannula may be necessary. It resulted in improved mortality at 90 days compared to nonin-vasive and invasive mechanical ventilation. b. Invasive mechanical ventilation: Recommended tidal volume of 6 to 8 m L/kg and maintaining plateau pressures less than 30 cm H2O. i. It may be necessary to reduce the tidal volume to 4 to 5 m L/kg if one is unable to obtain a plateau pressure less than 30 cm H2O. ii. Plateau pressures less than 30 cm H2O may not be attainable in obese patients. iii. Low tidal volumes usually result in hypoven-tilation. Permissive hypercapnia is typically accepted to a p H of 7. 20. c. The use of lung recruitment measures and titrated positive end-expiratory pressure (PEEP) is contro-versial in patients with moderate to severe forms of ARDS due to recent studies indicating negative con-sequences. Recent recommendations are conditional for use of higher levels of PEEP. d. Weaning from mechanical ventilation is typically initiated once the patient requires 50% or less Fi O2, physiologic levels of PEEP, hemodynamically stable, assessed neurological status, and so forth. 2. Positioning. a. Studies have shown that prone positioning results in decreased mortality. i. Recommended to start in early and severe ARDS. b. Prone positioning requires the patient to be hemo-dynamically stable while proning, adequate seda-tion and paralytics, well-trained staff to care for the patient, and adequate space for the equipment. 3. Conservative fluid management. a. Increased ventilator-free days but no difference in mortality. b. Initial fluid resuscitation depends on the under-lying etiology for the development of ARDS. Con-ditions such as hemorrhagic shock and pancreatitis initially require more aggressive fluid management. c. Guidelines for fluid resuscitation should be fol-lowed for certain diagnoses such as sepsis, pancreatitis, and so forth. B. Pharmacotherapy. 1. Paralytics and sedatives. a. Paralytics should be administered in combination with sedatives. i. Minimal sedation to achieve compliance with ventilation and early mobilization show improved outcomes in the ICU setting when clinically appropriate in mild-moderate ARDS. ii. Daily sedation vacation and ventilator libera-tion procedures should be initiated when oxygen requirements are compatible with extubation. b. Paralytics should be considered with ventilatory dyssynchrony and difficulty with ventilation such as poor airway compliance. c. Early administration in severe ARDS has not been associated with increased muscle weakness. d. A commonly used paralytic is cisatracurium. 2. Corticosteroids: Evidence is lacking to recommend for or against steroid use in ARDS. 3. Antibiotics are indicated in patients with an infective etiology. 4. Nitric oxide has not shown to improve outcomes. 5. Deep vein thrombosis (DVT) and stress ulcer prophy-laxis is required. a. DVT prophylaxis is held in patients with signif-icant coagulopathies using subcutaneous heparin or lovenox. b. Proton pump inhibitors and fluoroquinolones are used with caution due to increasing incidence of renal complications and Clostridium difficile colitis with concurrent use. C. Other treatment methods. 1. High frequency ventilation: Has not shown to improve outcomes and some evidence suggests it may increase mortality. 2. Extracorporeal membrane oxygenation. a. Limited evidence to support regular use and no guidelines for widespread use. b. Limited to certain institutions. Follow-Up A. This is dependent on the patient's clinical course, out-comes, and length of hospital stay. Consultation/Referral A. Consultation with a pulmonologist and/or intensivist would be required for management of mechanical ventilation and critical care needs. B. Additional consultation may be required depending on the underlying etiology for ARDS (e. g., trauma, infectious disease). Special/Geriatric Considerations A. Open communication with the family is required. B. Nutritional support is recommended. The preferred route is enteral. C. Patients with prolonged mechanical ventilation— typically greater than 14 days—should undergo tra-cheostomy placement. Bibliography Adhikari, N. K., Dellinger, R. P., Lundin, S., Payen, D., Vallet, B., Gerlack, H.,... Friedrich, J. O. (2014). Inhaled nitric oxide does not reduce mortality in patients with acute respiratory distress syndrome regardless of severity: Systematic review and meta-analysis. Critical Care Medicine, 42, 404-412. doi:10. 1097/CCM. 0b013e3182a27909 Cavalcanti, A. B., Suzumura, R. A., Laranjeira, L. N., de Mores Paisani, D., Damiani, L. P., Guimaraes, H. P.,... Ribeiro de Carvalho, C. R. (2017). Effect of lung recruitment and titrated positive end-expiratory-pressure (peep) vs low peep on mortality in patients with acute respiratory dis-tress syndrome: A randomized clinical trial. Journal of American Medical Association, 318, 1335-1345. doi:10. 1001/jama. 2017. 14171 Fan, E., Del Sorbo, L., Goligher, E. C., Hodgson, C. L., Munshi, L., Walkey, A. J.,... Brochard, L. J. (2017). An official American Tho-racic Society/European Society of Intensive Care Medicine/Society of Critical Care Medicine clinical practice guideline: Mechanical ventila-tion in adult patients with acute respiratory distress syndrome. Ameri-can Journal of Respiratory and Critical Care Medicine, 195, 1253-1263. doi:10. 1164/rccm. 201703-0548ST Ferguson, N. D., Fan, E., Camporota, L., Antonelli, M., Anzueto, A., Beale, R., & Ranieri, V. M. (2012). The Berlin definition of ARDS: An expanded rationale, justification, and supplementary material. Intensive Care Medicine, 38, 1573-1582. doi:10. 1007/s00134-012-2682-1 Frat, J. P., Thille, A. W., Mercat, A., Girault, C., Ragot, S., Perbet, S., & Robert, R. (2015). High-flow oxygen through nasal cannula in acute hypoxemic respiratory failure. New England Journal of Medicine, 372, 2185-2196. doi:10. 1056/NEJMoa1503326 Acute Respiratory Distress Syndrome

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14 Guerin, C., Reignier, J., Richard, J. C., Beuret, P., Gacouin, A., Boulain, T.,... Ayzac, L. (2013). Prone positioning in severe acute respiratory distress syndrome. New England Journal of Medicine, 368, 2159-2168. doi:10. 1056/NEJMoa1214103 Papazian, L., Forel, J.-M., Gacouin, A., Penot-Ragon, C., Perrin, G., Loun-dou, A.,... Roch, A. (2010). Neuromuscular blockers in early acute respiratory distress syndrome. New England Journal of Medicine, 363, 1107-1116. doi:10. 1056/NEJMoa1005372 Rhodes, A., Evans, L. E., Alhazzani, W., Levy, M. M., Antonelli, M., Ferrer, R.,... Dellinger, R. (2017). Surviving sepsis campaign: International guidelines for management of sepsis and septic shock: 2016. Critical Care Medicine, 45, 486-552. doi:10. 1097/CCM. 0000000000002255 Tenner, S., Baillie, J., De Witt, J., & Vege, S. S. (2013). American College of Gastroenterology Guideline: Management of acute pancreatitis. Ameri-can Journal of Gastroenterology, 108, 1400-1415. doi:10. 1038/ajg. 2013. 218 Asthma E. Mone ́e Carter-Griffin Definition A. A chronic airway inflammatory disease defined by a vari-ation of expiratory airflow limitation and history of respi-ratory symptoms that vary in intensity over time. There are various asthma phenotypes, such as allergic asthma and late-onset asthma. Incidence A. Approximately 39. 5 million people in the United States have been diagnosed with asthma in their lifetime. B. It is estimated that 18. 9 million adults still have asthma. C. Asthma accounts for greater than 400,000 hospitaliza-tions, 1. 8 million ED visits, and 14. 2 million office visits. D. The prevalence in adults is highest in women and African Americans. Pathogenesis A. Interplay among host factors and environmental expo-sures, resulting in airway inflammation, airflow obstruction, and bronchial hyperresponsiveness. 1. Immune response to antigen, causing activation of T-lymphocytes. 2. Release of cytokines and interleukins, leading to a release of mast cells, eosinophils, and basophils. 3. Subsequent release of inflammatory mediators (e. g., histamine, prostaglandins) that cause airway inflamma-tion and mucus secretion. B. Resulting development of airway hyperplasia, airway obstruction, and bronchial hyperresponsiveness. Predisposing Factors A. Direct and indirect exposure to tobacco smoke. B. Allergens (e. g., animals such as cats and dogs, dust mites, pollen). C. Occupational exposures or irritants (e. g., paint, sprays). D. Pollution. E. Respiratory infections. F. Exercise. G. Stress. H. Gastroesophageal reflux disease. I. Obesity. J. Sex (more likely in female adults). K. Viral infections. Subjective Data A. Common complaints/symptoms. 1. Respiratory symptoms (e. g., wheezing, dyspnea, chest tightness, and cough). 2. Possible extrapulmonary manifestations (e. g., allergic skin conditions or conjunctival irritation). B. History of the present illness. 1. Onset of asthma and/or symptoms. 2. Precipitating factors. 3. Asthma severity such as frequency of rescue inhaler use. 4. Comorbid conditions that may predispose the patient to developing asthma. 5. Number of exacerbations in the past year. 6. History of ED visits, hospitalizations, and intubations related to asthma. C. Family and social history. 1. Family history of asthma. 2. Social history such as smoking and inhaled illicit drug use. 3. Employment/environmental factors (e. g., working outside, mining operations, military service). Physical Examination A. The physical examination may vary depending on the severity of the asthma and if the patient is having an exac-erbation. B. Expiratory wheezing on auscultation may be audible (see Figure 2. 2). C. Dyspnea may be evident (see Figure 2. 1). D. Changes in mentation (e. g., confusion, lethargy) may be apparent. E. Patients with moderate to severe asthma exacerbations may be in a tripod position and have tachypnea, absent breath sounds (silent chest) on auscultation, accessory muscle use (e. g., intercostal), and tachycardia. F. As previously stated, some patients may have extrapul-monary symptoms such as dermatitis, conjunctival irritation, and a swollen nasal mucosa. Diagnostic Tests A. Lung function. Initial diagnosis is based on a history of variable symptoms and confirmed variation in expiratory air-flow limitation. Lung function is typically normal between symptoms. 1. Evidence of obstruction with reduction in the forced expiratory volume in 1 second/forced vital capacity (FEV1/FVC) and at least one low FEV1. 2. One or more tests documented with excessive variabil-ity in lung function. a. Positive bronchodilator reversibility test with a greater than 12% and 200 m L increase from baseline in the FEV1. b. Excessive variability of greater than 10% in twice-daily peak expiratory flow (PEF) over 2 weeks. c. Positive exercise challenge test with decrease in FEV1of greater than 10% and 200 m L from base-line. d. Positive bronchial challenge test. e. Increase in the FEV1by greater than 12% and 200 m L OR a greater than 20% increase in the PEF from baseline after 4 weeks of treatment. f. Variation of lung function between office visits. B. PEF. 1. Can be routinely monitored in the outpatient setting. 2. Repeat values compared with personal best or pre-dicted value by patients. 3. Typically, severe symptoms: At or less than 50% predicted. 2. Pulmonary Guidelines

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15 Physical Ex amin ation General: Accessory muscle use? Diaphoresis? Flushing? Vital Signs: Febrile? Tachypnea? Tachycardia? Oxygen desaturations? HEENT: Facial or lip/oropharynx swelling? Central cyanosis? Rhinorrhea? Redness and/or watery eyes? Assessment of voice quality? Neck: Surgical scars? Old tracheostomy sites? Swelling? Goiter? Tracheal deviation? High pitched noises or stridor on auscultation? Cardiac: Elevated JVD? Murmur? S3 or S4 gallop? Edema? Respiratory: Inspiratory or expiratory wheezing? Other adventitious breath sounds such as crackles? Diminished breath sounds? Chest shape? Respiratory pattern? Retractions? Dullness or hyperresonance on percussion? Extremities: Cyanosis? Edema? Clubbing? Skin: Rash? Hives? Noted insect stings or bites? Diagnostics Pulse oximetry: Assess oxygen saturations ABG: Assess oxygenation and ventilation Chest x-ray: Assess for lung mass, consolidation/infiltrate, pulmonary edema, or hyperinfiation Pulmonary function testing: Assess for obstructive or restrictive disease Chest CT/Angiography: Assess for pneumonia, changes associated with obstructive disease, fluid, fibrosis, pulmonary embolus, mass, tracheal narrowing/stenosis, and so forth Allergy testing Respiratory viral testing: Such as RSV Bronchoscopy: Assess for tracheomalacia, tracheal narrowing/stenosis, foreign objects, masses/tumors Echocardiogram: To evaluate for heart failure Esophagram/barium swallow: Assess for reflux disease or aspiration Obtain the hist ory. Onset, quality, precipitating factors, alleviating factors, any associated f actors. Acute or gradual onset ? Associated with other sym ptoms such as dyspnea, cou gh, hoarsen ess, ushing, pruritus, chest discomfort/tightness, and so forth? Triggers such as exerc ise, fumes/smoke, allergens, and so forth? Medicati on or food allergies? Initiation of new medications? Com orbid conditions such as asthm a, COPD, heart failure, myocard ial infarction, GERD, and so forth? Recent respiratory infections? Curre nt or history of smoking? Prior intubations? History of throat or neck cancer, surgeries, and so forth? Aspiration? **Completed in the stab le patient with wheezing** FIGURE 2. 2 Algorithm for the evaluation of wheezing. ABG, arterial blood gas; COPD, chronic obstructive pulmonary disease. GERD, gastroesophageal reflux disease; JVD, jugular venous distention; RSV, respiratory syncytial virus C. Allergy skin testing. 1. Positive allergen test: Allergen not necessarily causing asthma symptoms. 2. Essential to account for the timing of symptoms in relation to allergen exposure and the patient's history. D. Chest x-ray. 1. Usually normal in patients with asthma but may reveal hyperinflation. 2. If a patient has a fever in conjunction with respiratory symptoms: May be diagnostic for pneumonia. E. Pulse oximetry and arterial blood gas (ABG). 1. Used to evaluate for hypoxemia. 2. ABG: Can also be used to evaluate for hypercapnia and respiratory acidosis, especially in those patients pre-senting with an acute exacerbation. Differential Diagnosis A. Chronic obstructive pulmonary disease (COPD). B. Pulmonary embolism. C. Congestive heart failure (CHF). D. Chronic rhinosinusitis. E. Alpha-1 antitrypsin deficiency. Evaluation and Management Plan A. General plan. 1. The goal is to control symptoms and minimize the risk of asthma exacerbations. 2. T reatment includes assessment, adjustment of medi-cations, and response review. 3. Emergency treatment: Patients with progressively worsening symptoms may present to the ED. a. Evaluation of ABCs, physical assessment, and PEF is necessary. b. Medication management consists of a short-acting beta2agonist (SABA) via continuous nebulizer or a metered-dose inhaler, corticosteroids, oxygen therapy, and ipratropium bromide. c. Patients with a more severe exacerbation as demonstrated by a PEF less than 50% will receive Asthma

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16 intravenous instead of oral corticosteroids (OCS) and possibly intravenous magnesium sulfate. d. Posttreatment, the PEF should be reassessed. e. Patients with an alteration in mental status (e. g., somnolence, confusion), absent breath sounds, worsening hypoxemia or hypercapnia, and hemo-dynamic instability should be placed on invasive mechanical ventilation and admitted to the ICU. B. Patient/family teaching points. 1. Nonpharmacological interventions should be addressed such as smoking cessation, engagement in regular physical activity, and avoidance of known occu-pational exposures and allergen triggers. 2. Patients should be provided with self-management education to reduce morbidity. Essential components included in self-management are: a. Self-monitoring of symptoms and/or PEF. b. A written action plan that includes recognition and response to worsening asthma symptoms. c. Regular review of asthma control and treatment by a healthcare provider. C. Pharmacotherapy. 1. A daily controller treatment is recommended once an asthma diagnosis has been confirmed. 2. Early treatment with an inhaled corticosteroid (ICS) has been shown to improve lung function. a. A controller treatment is not indicated in patients with rare asthma symptoms, no night awakenings, no exacerbations in the past year, and a normal FEV1. b. An ICS (controller treatment) is recommended in patients with two or more asthma symptoms monthly, waking from asthma more than one night per month, and asthma symptoms plus risk factors for exacerbations. 3. A stepwise approach is used for treatment adjustment. See Table 2. 1 for commonly used medications in asthma management. a. Step 1: SABA as needed with consideration of a controller treatment with an ICS. b. Step 2: Low dose ICS plus a SABA as needed. i. The provider can consider a leukotriene recep-tor antagonist (LTRA) but research has shown it to be less effective. ii. An ICS and long-acting beta2agonist (LABA) combination leads to improvement in symptoms but is more expensive and has similar exacerbation rates compared to an ICS alone. c. Step 3: Low dose ICS/LABA plus a SABA as needed ORICS/formoterol and reliever therapy. d. Step 4: Low dose ICS/formoterol plus a reliever therapy ORmedium dose ICS/LABA plus a SABA as needed. The provider can add on tiotropium in patients with a history of exacerbations. e. Step 5: Patients should be referred to an expert. Additional medication management includes chang-ing the patient to a high dose ICS/LABA plus oral corticosteroids OCS. 4. With the stepwise approach, the treatment regimen can be adjusted up or down by the provider based on fre-quency and severity of asthma symptoms. 5. Asthma exacerbations are characterized by an increase or worsening in respiratory symptoms and lung function compared to the patient's baseline. 6. Patients with acute exacerbations and an asthma action plan in place can increase their SABA or usual reliever, as well as maintenance controller. OCS can be TABLE 2. 1 Asthma Medications Beta2agonists SABA Levalbuterol Salbutamol (albuterol) Terbutaline Anticholinergics/Antimuscarinics SAMA Ipratropium bromide (reduces risk of admissions in acute asthma; less effective in the long term) LAMA Tiotropium (add-on option in patients with history of exacerbations on controller medications) ICSs Beclometasone Budesonide Fluticasone furoate Fluticasone propionate Mometasone Triamcinolone acetonide Combination ICS plus LABA ICS/LABA Beclometasone/formoterol Budesonide/formoterol Fluticasone furoate/vilanterol Fluticasone propionate/formoterol Fluticasone propionate/salmeterol Mometasone/formoterol Systemic corticosteroids Prednisone (oral) Methylprednisolone (intravenous) LTRA Montelukast Pranlukast Zafirlukast Zileuton ICS, inhaled corticosteroid; LABA, long-acting beta2agonist; LAMA, long-acting muscarinic antagonist; LTRA, leukotriene receptor antagonist; SABA, short-acting beta2agonist; SAMA, short-acting muscarinic antagonist. added for patients who fail to respond to treatment or severe exacerbations with a PEF or FEV1less than 60% predicted or their personal best (see Exhibit 2. 1). D. Discharge instructions. 1. Discharge criteria. Patients should a. Show improvement in symptoms such as resolu-tion of accessory muscle use and dyspnea, improved respiratory rate, and O2saturation greater than 94% on room air. b. Improved PEF of greater than 60% predicted or personal best. c. Have adequate home resources. 2. Pulmonary Guidelines

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17 2. Diet. a. Restrictions: Specific diet based on whether the patient has underlying comorbid conditions such as diabetes or renal disease. b. No restrictions: Patient can resume a regular diet. 3. Medications. a. OCS: Usually prescribed for 5 to 7 days. b. Reliever medications such as SABA: Can be resumed on an as-needed basis. c. ICS prior to discharge. i. ICS/LABA ORICS/formoterol. ii. If the patient is already on an ICS: Increase the dose for 2 to 4 weeks. d. Medication reconciliation and continuation of appropriate medications for comorbid conditions. 4. T reatment plan. a. Identification of risk factors that contribute to exacerbations. b. Individualized written asthma action plan. c. Evaluation of maintenance therapy understand-ing. d. Assessment of inhaler technique. e. Assessment of PEF meter technique if applicable outside of an acute exacerbation. f. Smoking cessation counseling. g. Immunizations such as influenza. Influenza can trigger acute and severe asthma exacerbations that could potentially result in necessitating ventilatory support. h. Management of comorbid conditions. 5. Discuss with patient. a. Importance of medication compliance and proper inhaler technique to reduce symptoms and exacerba-tions. b. As previously stated, avoidance of known risk fac-tors that worsen asthma symptoms or lead to exacer-bations such as smoking or other known allergens. c. Signs and symptoms of an impending exacerbation such as increasing reliever inhaler use, frequent awak-ening at night with coughing or dyspnea, and PEF less than 60% of predicted or personal best. Follow-Up A. Regular follow-up is dependent on symptom control and exacerbation risk but should last for 1 to 3 months after treat-ment initiation and every 3 to 12 months once stabilized. B. Patients should see their primary care provider or pulmo-nologist 1 to 2 weeks after self-management of an exacerba-tion. C. Patients should see their primary care provider or asthma specialist/pulmonologist within 2 to 7 days of discharge from the ED or hospital. Consultation/Referral A. Patients with progressively worsening asthma despite increasing treatment may require a referral to a pulmonolo-gist or allergist. B. A pulmonologist and/or intensivist consultation is indi-cated for patients with a moderate to severe exacerbation necessitating ICU admission and/or noninvasive and inva-sive mechanical ventilation. Special/Geriatric Considerations A. Poor inhaler technique needs to be considered in patients with persistent symptoms. B. Comorbid conditions may contribute and complicate asthma management. C. Routine chest x-rays and antibiotic therapy are not indi-cated in asthma management. D. In the elderly population, asthma can be underdiagnosed or overdiagnosed due to varying assumptions and perceptions over dyspnea. Bibliography Centers for Disease Control and Prevention. (2013). Asthma facts: CDC's National Asthma Control Program Grantees. Atlanta, GA: U. S. Depart-ment of Health and Human Services. Retrieved from https://www. cdc. gov/asthma/pdfs/asthma_facts_program_grantees. pdf Global Initiative for Asthma. (2017). Global strategy for asthma man-agement and prevention. Retrieved from https://ginasthma. org/wp-content/uploads/2016/01/wms-GINA-2017-main-report-tracked-changes-for-archive. pdf Chronic Obstructive Pulmonary Disease E. Mone ́e Carter-Griffin Definition A. A chronic and progressive respiratory disease character-ized by expiratory airflow limitation. Incidence A. Chronic obstructive pulmonary disease (COPD) is the third leading cause of death in the United States and fourth leading cause of death worldwide. B. The incidence is much higher in smokers and ex-smokers compared to nonsmokers. C. It is more prevalent in individuals greater than 40 years with the greatest prevalence in those greater than 65 years. D. T raditionally, prevalence has been higher in men but recent literature suggests the occurrence may be rising in women, and women may be more susceptible to poorer out-comes. Pathogenesis A. The lungs are exposed to a stimulus (e. g., smoking, fumes) that causes inflammation of the airways. Neutrophils and var-ious other immune cells are recruited to the airways lead-ing to breakdown of elastin fibers and increasing oxidative stress. B. Ultimately, there is destruction of alveolar walls, decreased repair of the alveoli, fibrosis, and bronchiolar wall thickening leading to narrowed airways, impaired gas exchange, and enlarged air spaces. Predisposing Factors A. Tobacco smoke: Leading environmental risk factor. B. Individuals greater than 40 years. C. Occupational exposures to lung irritants (e. g., dust, chemical agents, fumes). D. Alpha-1 antitrypsin is a genetic condition leading to COPD that should be tested in a new diagnosis of COPD. E. Airway hyperresponsiveness (e. g., asthma). F. Allergies. G. Recurrent respiratory infections. Subjective Data A. Common complaints/symptoms. 1. Dyspnea (see Figure 2. 1): Chronic and progressive. This is a cardinal symptom. Chronic Obstructive Pulmonary Disease

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18 2. Pulmonary Guidelines FIGURE 2. 3 Algorithm for the evaluation of cough. ACE, angiotensin-converting enzyme; COPD, chronic obstructive pulmonary disease; GERD, gastroesophageal reflux disease; HEENT, head, ear, eyes, nose, and throat. 2. Cough (see Figure 2. 3) with or without sputum pro-duction. a. Not uncommon for individuals to produce small amounts of sputum. b. Increasing sputum production, especially with change in color: May indicate bacterial infection. 3. Wheezing (see Figure 2. 2) and/or chest tightness. 4. Severe COPD: Possible fatigue, weight loss, and anorexia. B. Family and social history. 1. Inquire about environmental risk factors and family history. 2. Inquire about smoking because it can accelerate or exacerbate COPD symptoms. C. Review of symptoms. 1. Evaluate for symptom onset, duration, severity, asso-ciated symptoms (e. g., increased wheezing or sputum), and aggravating and alleviating factors. 2. Inquire about early onset of COPD. 3. Assess for risk factors such as a history of allergies, asthma, or recurrent respiratory infections. Physical Examination A. The physical examination for COPD is rarely diagnostic. Physical signs of COPD may or may not be present, depend-ing on the severity of disease. However, it is still important to assess for the respiratory and systemic symptoms that may be associated with COPD. B. General examination. 1. Assess the respiratory rate. It may be normal or increased. 2. Assess the patient's posture. Leaning forward with out-stretched palms is associated with an attempt to relieve dyspnea. 3. Check breathing. In advanced disease or severe dysp-nea, pursed-lip breathing is possible. Obtain the hist ory. Onset, timing, description of cough, alleviating factors, any assoc iated f actors. Acute (<3 wee ks), subacute (3-8 weeks), or chronic (>8 wee ks)? Associated with other sym ptoms such as dyspnea, wheezing, chest tightne ss, or hemoptysis? Recent respiratory infection? Occupational or environmental exposures? Medicati ons such as ACE inhibitors? Known comorbid conditions such as asthma, COPD, GERD, and so forth Curre nt or history of smoking? Occurrence of cough? Upon awaken ing? Lying down? During exercise? Initial Diagnostic Chest x-ray: All individuals with a chronic cough. All individuals with an acu te cough AND dyspnea, chest pa in, fever, hemoptysis, or weight loss Physic al Ex amination The initial physical exam focuses on clues suggestive of cardiopulmonary disease. A thorough full exam should follow because a cough may be a manifestation of a more systemic disease process. General: Weight loss? Fatigue? Vital Signs: Usually normal unless associated with another disease process. May have tachypnea, tachycardia, oxygen desaturations, and/or fever. HEENT: Red and/or watery eyes? Fluid behind eardrum? Boggy, swollen, and/or pale mucus membranes? Nasal polyps? Thin, watery, or purulent secretions? Congestion? Throat redness? Hoarseness? Respiratory: Adventitious breath sounds such as crackles or wheezing? Chest shape? Respiratory pattern? Dullness or hyperresonance on percussion? Extremities: Clubbing? Edema? Acute/Subacute Usually does not req uire further testing. Additional testing focuses on a susp ected etiology. Allergy testing Chest CT/Angiography: Assess f or pneumonia, changes a ssociated w ith obstructive disea se, fluid, fibrosis, pulmonary embolus Pulmon ary function testing: Assess for obstructive or restrictive disea se Tuberculosis skin tes ting Pertus sis testing Chron ic Pulmona ry funct ion testi ng: Assess for obstructive or restrictive disease Additional work-up may follow after empirical treat ment for disorders suc h as GERD. Bronchoscopy: To evaluate for chronic infla mmation Sinus Imaging High-resolution Chest CT: Used in cough with atypical presentations a nd concern for chronic pulmonary disea se Eso phagram or swallow evaluation: Assess for reflu x disease or aspiration Echocardigram: To evaluate for heart failure or elevated p ulmonary pressures ?

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19 4. Inspect for clubbing. 5. In more severe disease, cyanosis, elevated jugular venous pressure, and peripheral edema may be present. C. Respiratory examination. 1. Inspect the chest. a. Check for an increased anteroposterior chest diameter due to hyperinflation of the lungs, giving a barrel chest shape. b. Assess for use of accessory muscles (e. g., sternoclei-domastoids, scalenes, intercostals). 2. Percuss the chest wall. a. Observe for hyperresonance due to overinflation of the lungs. 3. Auscultate bilaterally. a. Diminished breath sounds throughout. b. Occasional expiratory wheezing. c. Prolonged expiratory phase. d. Coarse rhonchi throughout the respiratory phase, especially during times of increased sputum pro-duction. Diagnostic Tests A. Pulmonary function test: Spirometry. 1. Objective measurement of airflow limitation. 2. Ratio between the volume of air forcibly exhaled after maximal inspiration (forced vital capacity [FVC]) and the volume of air forcibly exhaled during the first second (forced expiratory volume [FEV1]). A ratio less than 0. 7 after bronchodilator testing indicates obstruction. 3. Reduced FEV1(reduction in expiratory flow rates). 4. Possibly reduced FVC, usually to a lesser extent than the FEV1. B. Chest x-ray (see Figure 2. 3). 1. Hyperinflation, as evidenced by a flattened diaphragm and increased retrosternal air space. 2. Hyperlucency of the lungs. 3. Rapid tapering of the vascular markings. C. Arterial blood gas (ABG). 1. May reveal hypercapnia and/or hypoxemia. a. Early or mild COPD: Typically normal. b. Worsening as COPD progresses. Individuals with moderate to severe disease may have a chronic respi-ratory acidosis often with metabolic compensation as evidenced by increased serum bicarbonate. 2. Can provide clues to the acuteness and severity of COPD in those individuals with an exacerbation. D. Pulse oximetry. 1. Used to assess arterial oxygen saturation. If the pulse oximetry is less than 92%, then an ABG is warranted. E. Exercise testing (e. g., 6-minute walking distance). 1. Objectively measures functional capacity by evaluat-ing whether the individual has a reduction in walking dis-tance. 2. Useful for disability assessment, risk of mortality, and indicator of impairment of health status. F. Laboratory evaluation. 1. Alpha-1 antitrypsin screening: This should be assessed in those individuals with a family history of COPD at an early age and less than 45 years. Differential Diagnosis A. Bronchitis. B. Chronic cough. C. Congestive heart failure (CHF). D. Emphysema. E. Asthma. Evaluation and Management Plan A. General plan. 1. The interventions listed in the following are part of the general plan for a COPD patient. We should incorpo-rate these interventions in all COPD patients who meet criteria. 2. Specific interventions. a. Smoking cessation. i. Literature has indicated that counseling from healthcare professionals increases cessation rates compared to self-initiated strategies. ii. A five-step program initiated by healthcare providers offers a helpful framework for cessation. iii. Nicotine replacement (e. g., gum, lozenge, transdermal patch) can increase long-term cessa-tion rates. iv. Pharmacologic agents, such as varenicline and bupropion, can increase long-term cessation rates but should be used as an adjunct to an interven-tion program. b. Individuals should receive the influenza and pneu-mococcal. c. Reduction of risk factors such as avoidance of occupational irritants can help. d. Pulmonary rehabilitation lasting from 6 to 8 weeks has been shown to improve dyspnea, health status, exercise intolerance, and hospitalizations in patients with a recent exacerbation. This requires collaboration among multiple healthcare professionals. e. T reatment recommendations should consider the symptomatic assessment (ABCD group) and the indi-vidual's spirometric classification (GOLD 1-4). In addition, they should consider comorbid conditions and other medications. f. The GOLD categories one through four (spiro-metric grade) are used to classify the degree or severity of airflow limitation, which is identified using: i. GOLD 1: Mild, FEV180% or greater than the predicted. ii. GOLD 2: Moderate, FEV1greater than or equal to 50% predicted but less than 80% predicted. iii. GOLD 3: Severe, FEV1greater than or equal to 30% predicted but less than 50% predicted. iv. GOLD 4: Very severe, FEV1is less than 30% predicted. g. Symptom assessment can be evaluated using the COPD Assessment Test (CAT) or the COPD Control Questionnaire (CCQ). The CAT is commonly used in the clinical setting and a score greater than t10 is associated with symptoms. h. The ABCD Assessment Tool (Groups A-D) is a measure of the individual's symptoms and history of exacerbations. i. Groups A and B indicate the individual has no more than one exacerbation with no hospitaliza-tions and a CAT score less than 10 or greater than 10, respectively. ii. Groups C and D indicate the individual has more than two exacerbations or more than one exacerbation leading to hospitalization and a CAT score less than 10 or greater than 10, respectively. 3. Management of stable COPD. a. T reatment should be individualized based on symptoms and risk for exacerbations. 4. Goals of treatment. a. Symptom relief. Chronic Obstructive Pulmonary Disease

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20 b. Increased exercise tolerance. c. Improved health status. d. Reduction of mortality. e. Prevention of disease progression and exacerba-tions. f. Management should include pharmacological and nonpharmacological interventions. g. Smoking cessation and avoidance of occupational irritants are important. h. The GOLD guidelines suggest treatment escala-tion or de-escalation in those with persistent symp-toms or resolution of symptoms, respectively. T rials are needed to investigate treatment escalation and de-escalation. 5. Management of exacerbations. a. Acute worsening in symptoms from baseline occurs. i. Increased sputum, including purulence, increased dyspnea, and increased cough and/or wheezing. b. Can be classified as: i. Mild: T reatment with short-acting bron-chodilators. ii. Moderate: T reatment with short-acting bron-chodilators plus antibiotics and/or oral steroids. iii. Severe: Requires hospitalization or ED visits. c. Symptoms can last 7 to 10 days and contribute to disease progression. d. Severity of exacerbation is based on the individ-ual's symptoms and whether respiratory failure is present. i. No respiratory failure to respiratory rate 20 to 30/minute; no accessory muscle use, mental status change, or elevation in Pa CO2; hypoxemia improved with less than 35% of inspired oxygen. ii. Respiratory failure, nonlife threatening to res-piratory rate greater than 30/minute; use of acces-sory muscles, no change in mental status, Pa CO2 above baseline or 50 to 60 mm Hg; hypoxemia improved with less than 30% of inspired oxygen. iii. Respiratory failure, life threatening to res-piratory rate greater than 30/minute; accessory muscle use, mental status changes, Pa CO2above baseline or greater than 60 mm Hg or presence of a respiratory acidosis with a p H less than 7. 25; hypoxemia requiring greater than 40% of inspired oxygen or not improving with supplemental oxygen. B. Pharmacotherapy. 1. See Table 2. 2. 2. Adequate pharmacotherapy can reduce symptoms and severity of exacerbations, and improve overall health status. 3. Most medications are inhaled. It is essential that indi-viduals receive education on proper technique. 4. Bronchodilators. a. Often prescribed in COPD to prevent or reduce symptoms. b. Central to symptom management. c. Inhaled beta2agonists. i. Functional antagonism to bronchoconstric-tion by relaxing airway smooth muscle. ii. Short-acting (SABA) and long-acting (LABA) beta2agonists. iii. SABAs: Typically last 4 to 6 hours; shown with regular use to improve symptoms and FEV1in COPD. TABLE 2. 2 COPD Medications Beta2agonists (inhaled) SABA Fenoterol Levalbuterol Salbutamol (albuterol) Terbutaline LABA Arformoterol Formoterol Salmeterol Anticholinergics/Antimuscarinics (inhaled) SAMA Ipratropium bromide Oxitropium bromide LAMA Aclidinium bromide Glycopyrronium bromide Tiotropium Combination SABA plus short-acting anticholinergic (inhaled) SABA/SAMA Fenoterol/ipratropium Salbutamol/ipratropium Combination LABA plus long-acting anticholinergic (inhaled) LABA/LAMA Formoterol/aclidinium Formoterol/glycopyrronium Combination LABA plus ICS (inhaled) LABA/ICS Formoterol/budesonide Formoterol/mometasone Salmeterol/fluticasone Vilanterol/fluticasone furoate Methylxanthines (oral and intravenous) Theophylline (SR) Systemic Corticosteroids Prednisone (oral) Methylprednisolone (intravenous) Phosphodiesterase-4 inhibitors (oral) Roflumilast Antibiotics (oral) Azithromycin Erythromycin COPD, chronic obstructive pulmonary disease; ICS, inhaled corticosteroid; LABA, long-acting beta2agonist; LAMA, long-acting antimuscarinics; SABA, short-acting beta2agonist; SAMA, short-acting antimuscarinics. 2. Pulmonary Guidelines

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21 iv. LABAs: Duration of 12 hours or more; shown to improve lung function, dyspnea, and reduce exacerbations. d. Anticholinergics/antimuscarinics. i. Blockage of acetylcholine on muscarinic receptors leading to relaxation of airway smooth muscle. ii. Short-acting (SAMA) and long-acting (LAMA) antimuscarinics. iii. SAMAs: Shown to improve symptoms and FEV1with regular or as needed use. iv. LAMAs: Shown to improve lung function, dyspnea, and health status. Literature has shown that LAMAs compared to LABAs reduce exacer-bations and decrease hospitalizations. e. Methylxanthines. i. Need to monitor therapeutic drug levels and for signs and symptoms of toxicity. f. Inhaled corticosteroids (ICS). i. No mortality benefit or modification in the long-term decline of the FEV1with ICS monotherapy. ii. Severe COPD and regular use of ICS: Increased risk for pneumonia. g. Combination inhaled therapy. i. Combination of a SABA and SAMA: Superior in improving symptoms compared to either med-ication used alone. ii. Combination of an LABA and LAMA: Improves FEV1and reduces symptoms and exac-erbations compared to either medication used alone or compared to those individuals treated with a combination of ICS and LABA. iii. Combination therapy with an ICS and LABA compared to monotherapy with either medica-tion: Improves lung function and health status as well as reduces exacerbations. h. Oral glucocorticoids. i. Long-term risks: Preclude use in stable COPD. ii. In acute exacerbations in hospitalized patients: Decreased treatment failure and relapse as well as improved lung function. i. Phosphodiesterase4inhibitors. i. Only one approved drug, roflumilast: Used for patients with a history of exacerbations and severe to very severe COPD. ii. Has been shown to improve lung function and decrease moderate to severe exacerbations. iii. Requires caution in those with depression and those who are underweight. j. Antibiotics. i. Reduced exacerbations: Azithromycin 250 mg daily or 500 mg three times a week OR ery-thromycin 500 mg twice daily for 1 year. 1)Use of azithromycin: Association with increased antibiotic resistance. ii. No data indicating efficacy of chronic antibi-otic therapy beyond 1 year. k. Mucolytics. i. Reduced risk of exacerbation in select popula-tions. 5. Pharmacologic treatment using the ABCD Assess-ment Tool. a. Utilization of an algorithm based on the ABCD Assessment Tool Groups A-D. b. Group A. i. Should be placed on a bronchodilator. ii. The provider should evaluate drug effective-ness and decide to continue, stop, or try an alter-native bronchodilator class. c. Group B. i. Should be initiated on a long-acting bron-chodilator. Choice of long-acting bronchodilator should be based on symptom relief. ii. T wo bronchodilators: Recommended for indi-viduals with persistent dyspnea. d. Group C. i. Should be initiated on a bronchodilator; pre-ferred choice is a LAMA secondary to superior exacerbation prevention. ii. Individuals with persistent dyspnea: T wo long-acting bronchodilators (LABA/LAMA) OR combination of long-acting bronchodila-tor and ICS (LABA/ICS). The primary choice is LABA/LAMA secondary to the increased risk of pneumonia in certain individuals on ICS. e. Group D. i. LABA/LAMA combination for certain patients. In individuals with findings suggestive of asthma-COPD overlap, initiation of LABA/ICS may be the first choice. ii. Individuals with persistent exacerbations despite being on LABA/LAMA triple inhaled therapy with a LABA/LAMA/ICS OR switch to a LABA/ICS. However, there is no clinical evidence that switching to a LABA/ICS from LABA/LAMA will improve symptoms. iii. For continued exacerbations despite triple inhaled therapy, possible: 1)Addition of roflumilast. 2)Addition of a macrolide, specifically azithromycin. 3)Stopping the ICS. 6. Hospital medication management and medical ther-apy of COPD exacerbations. a. Combination of SABA and anticholinergics. b. Possible systemic steroids. i. Have been shown to shorten recovery time, improve oxygenation, and improve the risk of early relapse and treatment failure. ii. Oral prednisone recommended at 40 mg daily for 5 days. c. Consideration of oral antibiotics when signs of bacterial infection are present. d. Possible O2therapy and noninvasive ventilation. i. Noninvasive ventilation: Shown to reduce intubation rates, mortality, and hospital length of stay. 7. Invasive mechanical ventilation: Warranted in patients who are unable to undergo or fail noninva-sive ventilation, are hemodynamically unstable, have status postarrest, have profound hypoxemia in patients not able to tolerate noninvasive ventilation, massive aspi-ration, and encounter significant changes in levels of consciousness. C. Discharge instructions. 1. Be aware that these vary based on the severity of the underlying COPD and exacerbation. 2. Review all clinical (e. g., improved dyspnea, sputum production, cognition) and laboratory data. Chronic Obstructive Pulmonary Disease

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22 3. Assess continual need for oxygen therapy. Patients on chronic home O2should resume their baseline O2 requirements. 4. Check functional status. 5. Ensure adequate home resources. 6. Activity. a. Pulmonary rehabilitation. i. Shown to reduce hospitalizations, as well as improve dyspnea and health status. ii. Indicated in all patients with symptoms and/or high risk for exacerbation. iii. Early rehabilitation has been associated with improved mortality. b. Regular physical activity. i. Combination interval training with strength training. ii. Strong predictor of mortality. 7. Diet. a. May vary depending on underlying comorbid conditions such as diabetes, heart failure, or renal disease. b. Nutritional supplementation: Recommended; should be considered in malnourished COPD patients. 8. Medications (see section “Pharmacotherapy”). a. Bronchodilators. i. Most patients are likely to receive two long-acting bronchodilators (LABA/LAMA) or a long-acting bronchodilator and ICS (LABA/ICS). b. Additional agent: The provider may choose to ini-tiate a long-term macrolide or roflumilast in patients who meet criteria and continue to have exacerba-tions despite multimedication inhaled therapy. c. Other drugs: Medication reconciliation and con-tinuation of medications for comorbid conditions are necessary. 9. T reatment plan. a. Evaluation of psychosocial needs and home resources such as availability of home O2. b. Inclusion of family in the treatment and educa-tion plan. c. Evaluation maintenance therapy understanding. d. Ensuring of understanding of withdrawal medi-cations prescribed for an acute exacerbation such as steroids. e. Assessment of inhaler technique. f. Pulmonary hygiene (e. g., deep breathing). g. Smoking cessation counseling. h. Encouragement of pneumococcal and influenza vaccinations. i. Setting up of pulmonary rehabilitation. j. Management of comorbid conditions such as gastroesophageal reflux disease (GERD) and heart failure. 10. Discuss with patient. a. Discuss signs and symptoms associated with infection and/or exacerbations such as fever, chills, increased dyspnea, and increasing sputum produc-tion or change in sputum color. b. Instruct patients on the importance of medica-tion compliance and physical activity to reduce the occurrence of exacerbations, reduce symptoms, and improve quality of life. Follow-Up A. Follow-up with a primary care physician or pulmonolo-gist, ideally within 1 to 4 weeks of discharge. 1. Especially during initiation, escalation, and de-escalation in therapy. 2. With new or worsening symptoms. 3. Posthospitalization. B. Association of early follow-up with fewer readmissions. Consultation/Referral A. Consultation with a pulmonologist: In patients with pro-gressively worsening symptoms, severe or very severe COPD, frequent exacerbations, and respiratory failure. Special/Geriatric Considerations A. Chronic use of oxygen is indicated for patients with severe hypoxemia at rest and chronic respiratory failure. B. Patients should be evaluated and treated for comorbid conditions such as heart failure, obstructive sleep apnea, obe-sity, hypoventilation syndrome, and so forth. C. Education alone has not been shown to change behaviors; however, education and self-management with a case man-ager may prevent exacerbation complications. D. Physical activity is highly encouraged given its strong mortality prediction. E. Nutritional supplements may be indicated in malnour-ished patients. F. Patients should be considered for lung volume reduction surgery if they have upper-lobe predominance emphysema. G. Patients with very severe COPD and advanced systemic symptoms may be considered for lung transplantation. H. Discussions with patients and families regarding palliative and end-of-life care should take place in the event the patient becomes critically ill. Bibliography American Lung Association. (2013). T aking her breath away: The rise of COPD in women. Chicago, IL: Author. Retrieved from https://www. lung. org/assets/documents/research/rise-of-copd-in-women-full. pdf Decramer, M. L., Chapman, K. R., Dahl, R., Frith, P., Devouassoux, G., Fritscher, C., & Mc Bryan, D. (2013). Once-daily indacaterol versus tiotropium for patients with severe chronic obstructive pulmonary dis-ease (INVIGORATE): A randomized, blinded, parallel-group study. The Lancet Respiratory Medicine, 1, 524-533. doi:10. 1016/S2213-2600(13) 70158-9 Global Initiative for Chronic Obstructive Lung Disease. (2017). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. Retrieved from https://www. goldcopd. org Karner, C., Chong, J., & Poole, P. (2012). Tiotropium versus placebo for chronic obstructive pulmonary disease. Cochrane Database of System-atic Reviews, 2014 (7), CD009285. doi:10. 1002/14651858. CD009285. pub3 Vogelmeier, C., Hederer, B., Glaab, T., Schmidt, H., Rutten-van Molken, M., Beeh, K.,... Fabbri, L. M. (2011). Tiotropium versus salmeterol for the prevention of exacerbations of COPD. New England Journal of Medicine, 364, 1093-1103. doi:10. 1056/NEJMoa1008378 Pleural Effusions E. Mone ́e Carter-Griffin Definition A. Result of excess fluid production or decreased absorption of fluid in the pleural space. 2. Pulmonary Guidelines

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23 Incidence A. There are an estimated 1 to 1. 5 million cases annually. B. In general, the incidence is similar in both males and females. However, certain causes are more likely in males or females. Pathogenesis A. Pleural effusions are a manifestation of an underlying dis-ease process. B. Effusions can be transudative or exudative. 1. T ransudative effusions are typically due to imbalance that occurs between the hydrostatic pressure and oncotic pressure. 2. Exudative effusions are the result of an alteration of the pleural surface such as pleural or lung inflammation, impairment of lymphatic drainage, and so forth. Predisposing Factors A. Any disease that may lead to accumulation of pleural fluid. The most common causes of pleural effusions are heart failure, malignancy, and pneumonia. B. Diseases that can predispose a patient to a transudative effusion. 1. Heart failure. 2. Cirrhosis. 3. Nephrotic syndrome. C. Diseases that can predispose a patient to an exudative effusion. 1. Pneumonia (parapneumonic effusion or empyema). 2. Malignancy. 3. Pancreatitis/pancreatic disease. 4. T rauma. Subjective Data A. Common complaints/symptoms. 1. Patients may have complaints of cough, pleuritic chest pain, and dyspnea. 2. Patients may have additional symptoms or clinical manifestations secondary to the underlying etiology for the pleural effusion. B. Review of systems. 1. Depending on the suspected etiology of the effusion, the provider may want to inquire about heart failure, known liver disease or chronic alcoholism, recent trauma, history of cancer, occupational exposures, recent signs and symptoms of respiratory infection, and so on. Physical Examination A. Typically, no physical findings when the pleural effusion is less than 300 m L. B. Other findings. 1. Diminished breath sounds. 2. Dullness on percussion. 3. Pleural friction rub. 4. Decreased tactile fremitus. C. Possible other findings such as fever and edema, depend-ing on the etiology. Diagnostic Tests A. Chest x-ray (see Figure 2. 4). 1. Blunting of costophrenic angle in upright posteroan-terior x-ray when 175 m L or more is present. B. Smaller pleural effusions observed in lateral decubitus x-rays. C. Failure of a pleural effusion to layer on a lateral decubitus x-ray. This may indicate a loculated pleural effusion. D. Chest CT: Possible for evaluation of a loculated pleural effusion. E. Ultrasonography: Can be used to evaluate the size of the pleural effusion and location. F. Diagnostic thoracentesis. 1. Should be performed in patients whose etiology is unclear and who fail to respond to therapy. 2. Pleural fluid for diagnosis. Send for glucose, lactate dehydrogenase (LDH), p H, cell count, protein, and cul-ture to aid with a possible diagnosis. Serum blood levels of LDH, total protein, and glucose are needed for com-parison. 3. Light's criteria: Used to differentiate between tran-sudative and exudative pleural effusions. a. Exudative if one of the following is present. i. Ratio of pleural fluid to serum protein is greater than 0. 5. ii. Ratio of pleural fluid to serum LDH is greater than 0. 6. iii. Pleural fluid LDH is greater than two-thirds the normal serum LDH. 4. Additional testing may be indicated when trying to identify the etiology. Differential Diagnosis A. First, it is important to determine if the pleural effusion is transudate or exudate using Light's criteria in order to estab-lish a differential diagnosis. B. T ransudate pleural effusion. C. Congestive heart failure (CHF). D. Cirrhosis. E. Exudate pleural effusion. F. Pneumonia. G. Cancer. H. T uberculosis. I. Pulmonary embolism. Evaluation and Management Plan A. General plan. 1. For transudative effusions, manage the underlying dis-ease process such as diuretics for patients with effusions due to heart failure. 2. Specific interventions. a. Monitoring of chest x-rays: As needed pending the size, symptoms associated with the effusion, and fol-lowing treatment to evaluate for reaccumulating fluid. b. Therapeutic thoracentesis: Used for patients with refractory, large pleural effusions and/or severe respi-ratory compromise to relieve symptoms. Diagnostic evaluation may be required if concerned for malig-nancy, infectious process, and so forth. i. Patients with malignant pleural effusions may require more than one thoracentesis due to reac-cumulating fluid. ii. Patients who need frequent thoracentesis may require a pleurodesis or indwelling tunneled pleu-ral catheter for home drainage. The patient and family will require teaching about home use of the tunneled pleural catheter. c. Chest tube. i. Required for a parapneumonic effusion or an empyema, but ultimately the patient will need to be treated with antibiotics and possible surgical intervention. Pleural Effusions

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24 FIGURE 2. 4 Chest x-ray of left pleural effusion. Source: By Tomatheart/Shutterstock. ii. Required for patients with a hemothorax (bloody pleural effusion). B. Patient/family teaching points. 1. Teach patients that it may help to cough or take a deep breath by holding a pillow against your chest to prevent pain. 2. Practice smoking cessation and avoid secondhand smoke. 3. Keep hydrated. 4. Use an incentive spirometer for frequent deep breath-ing and coughing exercises. C. Pharmacotherapy—depends on the etiology of pleural effusion. 1. Antibiotics. a. For use in parapneumonic effusions, empyemas, and abscesses. b. Use empiric coverage and consider the patient's age, comorbidities, and clinical picture before tailor-ing the final selection of antibiotics. c. In general, the antimicrobial coverage should cover anaerobic organisms. 2. Vasodilators and diuretics: For use in pleural effusions related to CHF and pulmonary edema. 3. Anticoagulants: For use in pleural effusions due to pulmonary emboli. D. Discharge instructions. 1. Instruct patients to report any increased work in breathing, fevers, and pain that does not go away or gets worse. Take medications as prescribed. Follow-Up A. Patients in the hospital: Monitor with serial chest x-rays and/or based on their symptoms. B. Etiology of the effusion: Determines the course and fre-quency of outpatient follow-up. Consultation/Referral A. Thoracentesis: This can be completed by a hospitalist, pulmonologist, or interventional radiologist. If a more inva-sive procedure such as a surgical intervention is indicated, then a cardiothoracic surgeon will need to be consulted. B. Further referrals may be indicated depending on the eti-ology of the effusion. If the effusion is malignant, then oncol-ogy will need to be consulted. Bibliography Bhatnagar, R., & Maskell, N. (2015). The modern diagnosis and manage-ment of pleural effusions. British Medical Journal, 351, 26-30. doi:10. 1136/bmj. h4520 Kummerfeldt, C. E., Pastis, N. J., & Huggins, J. T. (2017). Pleural diseases. In S. C. Mc Kean, J. J. Ross, D. D. Dressler, & D. B. Scheurer (Eds. ), Principles and practice of hospital medicine (2nd ed., pp. 1923-1932). New York, NY: Mc Graw-Hill. Saguil, A., Wyrick, K., & Hallgren, J. (2014). Diagnostic approach to pleu-ral effusion. American Family Physician, 90, 99-104. Retrieved from https://www. aafp. org/afp/2014/0715/p99. html Pneumonia E. Mone ́e Carter-Griffin Definition A. An infection of the lungs that can have varying degrees of severity. B. Caused by bacteria, viruses, or fungi. C. Can be further divided into four types: Community, hospital, ventilator acquired, and aspiration. Incidence A. Pneumonia (combined with influenza) is the eighth lead-ing cause of mortality in the United States, accounting for approximately 50,000 deaths annually. B. Thirty-day mortality is higher in elderly patients treated for hospital-acquired pneumonia (HAP) compared to community-acquired pneumonia (CAP). C. Pneumonia is the third leading cause of ED visits that led to a hospitalization, with the highest prevalence in patients 65 to 84 years. D. It is the most common cause of readmissions for the elderly population. E. It accounts for the top 10 most costly hospitalizations in the United States, with approximately $10. 6 billion spent for 1. 1 million hospital stays. F. Most common cause of sepsis and septic shock. 2. Pulmonary Guidelines

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25 Pathogenesis A. A pathogenic microorganism invades the lung parenchyma. Neutrophils aggregate to the site of invasion and begin to phagocytize the microorganisms and release an extracellular trap. B. The immune response is activated. Inflammatory media-tors are released, causing the capillaries to become permeable and an exudative fluid to be formed. The protein rich fluid containing neutrophils, bacteria, fibrin, and so forth, fills the alveoli, leading to a lung consolidation. Predisposing Factors A. An impaired immune response and/or dysfunction of the body's defense mechanism, HIV. B. Advanced age. C. Smoking. D. Chronic lung disease (e. g., chronic obstructive pul-monary disease [COPD] and asthma). E. Other chronic comorbid conditions (e. g., heart failure, diabetes). F. Recent respiratory viral infection. G. Excessive alcohol consumption. Subjective Data A. Common complaints/symptoms. 1. Cough with sputum production (see Figure 2. 3). 2. Fever. 3. Chills. 4. Altered mental status or confusion, especially in the elderly. 5. Pleuritic chest pain. B. Common/typical scenario. 1. Patients typically present with sudden onset of symp-toms such as shortness of breath, productive cough, and fever. They may also complain of chills and malaise. C. Family and social history. May be more prevalent in smokers, among the elderly, and in the chronically ill. D. Review of symptoms. 1. Symptoms may vary depending on the age, activity level, and underlying comorbid conditions. Elderly peo-ple typically present differently than younger adults. 2. The provider should inquire about onset, severity, and associated symptoms. 3. Assessment of recent respiratory viral illnesses is important, especially given the correlation of pneumonia following influenza. 4. It may help to enquire about recent sick contacts. Physical Examination A. General: Vital signs. 1. Fever, which may occur. Note that approximately 30% of patients are afebrile on presentation. 2. Tachycardia, which may or may not be present. 3. Possibly high respiratory rate; this may be normal or increased. B. Neurological. 1. More likely to see changes in the elderly. Patients can be described as having confusion, decreased interactions, and/or “acting differently. ” C. Respiratory. 1. Rales/crackles on auscultation in the affected area. Patients may also have rhonchi. 2. Dullness on percussion in the affected area. 3. Increased tactile fremitus in the affected area. 4. Possible pleural friction rub. 5. Decreased breath sounds. D. Possible other findings. 1. Cyanosis, respiratory failure, and septic shock in patients with a more virulent type of pneumonia, mul-tilobar pneumonia, age, and/or comorbid conditions. Diagnostic Tests A. Chest x-ray. 1. Evidence of an infiltrate, which can be patchy or a dense consolidation of a lobe(s) or segment. B. Sputum culture and gram stain. 1. Used to identify the microorganism responsible for the pneumonia. 2. Most sensitive if the patient can provide an adequate specimen and has not recently been treated or is not cur-rently receiving treatment with antibiotics. 3. Intubated patient: Obtain an endotracheal aspirate. C. Blood cultures. 1. Usually indicated for patients with more severe forms of pneumonia, specifically CAP. 2. Most common pathogen isolated in patients with CAP: Streptococcus pneumoniae. However, in more severe infections, other microorganisms may be present. D. Urinary antigen testing. 1. Used to assess for pneumococcal pneumonia, mycoplasma pneumonia, and Legionnaire's disease. 2. Rapid and simple; however, do not provide informa-tion for narrowing of antibiotics. E. Serum procalcitonin. 1. Can assist the provider with antibiotic duration in conjunction with the patient's clinical presentation. 2. No recommended use of procalcitonin in patients with hospital or ventilator-acquired pneumonia accord-ing to Infectious Diseases Society of America and the American Thoracic Society guidelines. F. Comprehensive metabolic panel. 1. Can assist with risk stratification and sequela of pneu-monia. G. Complete blood count. 1. Assessment of a leukocytosis or leukopenia. H. Arterial blood gas (ABG). 1. May be indicated in more severe presentations such as cyanosis or respiratory failure to evaluate for hypoxemia and/or hypercapnia. I. Chest CT scan. 1. Not typically indicated, especially if one is able to obtain a good-quality chest x-ray. Differential Diagnosis A. COPD. B. Asthma. C. Pulmonary edema. D. Bronchiectasis. E. Lung cancer. F. Pulmonary embolism. G. Bronchitis. H. Viral or bacterial pneumonia. I. Pneumocystis pneumonia (PCP). Evaluation and Management Plan A. General plan. 1. Management of pneumonia: Dependent on the sever-ity of the disease, classification or type of pneumonia (e. g., community vs. hospital acquired), and pathogens involved. 2. Supportive care, such as oxygen therapy or other methods of respiratory support (e. g., noninvasive Pneumonia

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26 ventilation, invasive mechanical ventilation); this should be considered in those patients with hypoxemia and/or respiratory failure. 3. Patients presenting with sepsis due to pneumonia. These patients should receive care in accordance with the sepsis guidelines. 4. Guidelines suggest that antimicrobial therapy be de-escalated rather than fixed therapy. 5. T ransitioning to oral therapy. Oral therapy is appro-priate once patients' clinical status has improved, and they are hemodynamically stable. 6. Patients with coexisting Influenza A. Early treatment with oseltamivir or zanamivir is appropriate. 7. Systematic corticosteroids: May be appropriate in cer-tain patient populations who present with severe CAP. B. CAP. 1. Evaluation of patients for hospital admission. Use the CURB-65 criteria, which evaluates/looks at confu-sion, uremia, respiratory rate, low blood pressure, and age 65 years or greater, or pneumonia severity index (PSI) to identify patients who can be treated as outpatient versus inpatient. 2. Duration of treatment. Patients should receive a min-imum of 5 days of treatment and literature suggests that more than 7 days is typically not needed. 3. Antibiotic therapy, which focuses on the likely pathogen and severity. a. The most common outpatient pathogens are S. pneumoniae, Haemophilus influenzae, Mycoplasma pneumoniae, Chlamydia pneumoniae, Legionella, and respiratory viruses. i. Previously healthy patients with no exposure to antibiotics within the past 3 months should be started on a macrolide. If they are unable to toler-ate a macrolide, then doxycycline may be used. ii. Patients with chronic comorbid conditions (e. g., heart failure, liver or renal disease, diabetes) or antibiotic therapy within the past 3 months should be started on a respiratory fluoroquinolone (e. g., moxifloxacin, levofloxacin, or gemifloxacin) ORbeta-lactam plus a macrolide. Remember, a beta-lactam alone will not work for atypical pneu-monia because of the lack of a beta-lactam ring. b. The most common inpatient, non-ICU pathogens are S. pneumoniae, M. pneumoniae, C. pneumoniae, H. influenzae, Legionella species, aspiration, and respira-tory viruses. i. Patients should be treated with a respira-tory fluoroquinolone OR a beta-lactam plus a macrolide. c. The most common inpatient, ICU pathogens are S. pneumoniae, Staphylococcus aureus, Legionella species, gram-negative bacilli, and H. influenzae. i. Patients should be started on a beta-lactam (e. g., cefotaxime, ceftriaxone, or ampicillin-sulbactam) plus either azithromycin or a respira-tory fluoroquinolone. ii. If the patient has a penicillin allergy, then a res-piratory fluoroquinolone and aztreonam are rec-ommended. iii. Gram-negative organisms are selectively responsive to aztreonam treatment. d. If a pseudomonal infection is suspected, then providers should prescribe one of the following. i. Antipneumococcal, antipseudomonal beta-lactam plus levofloxacin OR,ii. Beta-lactam plus an aminoglycoside and azithromycin OR, iii. Beta-lactam plus an aminoglycoside and antipneumococcal fluoroquinolone. e. If methicillin-resistant Staphylococcus aureus ( MRSA) is suspected, then intravenous vancomycin or linezolid is indicated. C. HAP. 1. Develops 2 or more days after admission to the hospital. 2. Use of a local antibiogram tailored to HAP pathogens and susceptibilities for empiric coverage as recommended by guidelines. 3. Antibiotic treatment: Recommended 7-day course. a. Empiric coverage depends on the patient's mortal-ity risk and suspicion for multidrug resistant (MDR) pathogens. b. Patients not at high risk for mortality or likelihood of MDR pathogens can be placed on piperacillin-tazobactam (Zosyn) ORcefepime ORlevofloxacin. c. Patients not at high risk for mortality but who have factors that may increase their likelihood of MRSA should be placed on cefepime ORlevofloxacin OR meropenem ORaztreonam plus vancomycin or line-zolid (second line due to toxic effects if vancomycin cannot be used). d. Patients with a high mortality risk, coverage for pseudomonas, or who have received intravenous antibiotics in 3 months should be started on: i. Piperacillin-tazobactam (Zosyn) OR cefepime ORlevofloxacin ORmeropenem OR amikacin/gentamicin/tobramycin ORaztreonam plus vancomycin or linezolid. ii. Providers should cover for MRSA and pick two additional medications while avoiding pre-scribing two beta-lactams. D. Ventilator-acquired pneumonia (VAP). 1. A pneumonia that develops more than 2 days after intubation and mechanical ventilation. 2. Use of a local antibiogram tailored to the ICU popu-lation, VAP pathogens, and susceptibilities for adequate coverage as recommended per guidelines. 3. Antibiotic treatment: Recommended 7-day course. a. S. aureus, Pseudomonas, and other gram-negative bacilli coverage should be included in all empiric reg-imens. b. Patients with risk factors for MRSA should receive empiric coverage with vancomycin or linezolid. c. Patients with no known risk factors for MRSA and suspected of methicillin-susceptible Staphylococcus aureus (MSSA), then the suggested regimen includes piperacillin-tazobactam, cefepime, levofloxacin, or meropenem. If the patient has proven MSSA, then the preferred agents are cefazolin or nafcillin. d. Patients with risk factors for gram-negative infection, including pseudomonas and resistant microorganisms, should receive treatment with two antipseudomonal drugs. i. Piperacillin-tazobactam OR, ii. Cefepime OR, iii. Meropenem OR, iv. Aztreonam OR, v. Ciprofloxacin. e. Guidelines recommend against the routine use of aminoglycosides and colistin if adequate coverage is available with alternative antibiotics. 2. Pulmonary Guidelines

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27 E. Discharge instructions. 1. Discharge criteria. These primarily focus on improve-ment in the clinical status/condition. a. Resolution of fever (e. g., <38∘C). b. Improving symptoms (e. g., dyspnea, cough, spu-tum production). c. Heart rate less than 100 bpm. d. Respiratory rate less than 24/minute. e. Oxygen saturations greater than 90%. f. Diminishing leukocytosis. g. Maintaining oral intake. h. Systolic blood pressure greater than 90 mm Hg. i. Return to baseline mentation. 2. Activity. a. Regular or baseline activity as tolerated. 3. Diet. a. Comorbid conditions such as diabetes, heart fail-ure, or renal disease: May vary. b. No underlying comorbid conditions: Resumption of regular diet. 4. Medications. a. Antibiotics: Duration of 7 days. This includes the days the patient received antibiotics while hospital-ized. b. Other drugs. Medication reconciliation and con-tinuation of medications for comorbid conditions. 5. T reatment plan. a. Important for patient to complete the full course of antibiotics even if feeling better. b. Coughing with sputum production: Normal. This should improve over time. c. Vaccinations such as influenza annually and pneu-mococcal disease necessary for those at risk. d. Pulmonary hygiene (e. g., deep breathing). e. Smoking cessation counseling. f. Remaining hydrated. g. Managing comorbid conditions. 6. Discuss with patient. a. Stress that patients should contact their provider if they develop fever or worsening symptoms such as increased cough and dyspnea despite antibiotic therapy, decreased appetite, nausea, and mentation changes. b. Reemphasize the importance of completing antibiotic therapy to reduce reoccurrence and avoid resistance emergence. Follow-Up A. Follow-up is highly dependent on the type and severity of pneumonia as well as functional status and comorbid con-ditions. B. Patients in the outpatient setting typically see improve-ment in symptoms within 3 to 7 days, so failure to see improvement or clinical deterioration should be dealt with immediately. C. Patients discharged from the hospital should be seen 1 to 2 weeks after discharge. Consultation/Referral A. Outpatient management typically does not require a referral unless the patient's clinical status worsens, in which case the patient should be sent to the hospital. B. Inpatient management may include a pulmonologist and infectious disease pending the severity of the pneumonia and the patient's condition. Special/Geriatric Considerations A. The elderly should be instructed to receive pneumococcal and influenza vaccinations. B. All patients should be counseled regarding smoking cessation. Bibliography American Thoracic Society. (2018). Top 20 pneumonia facts. Retrieved from https://www. thoracic. org/patients/patient-resources/resources/ top-pneumonia-facts. pdf Hines, A. L., Barrett, M. L., Jiang, J., & Steiner, C. A. (2014). Con-ditions with the largest number of adult hospital readmissions by payer, 2011. Retrieved from https://www. hcup-us. ahrq. gov/reports/statbriefs/ sb172-Conditions-Readmissions-Payer. pdf Kalil, A. C., Metersky, M. L., Klompas, M., Muscedere, J., Sweeney, D. A., Palmer, L. B., & Brozek, J. L. (2016). Management of adults with hospital-acquired and ventilator-associated pneumonia: 2016 clinical practice guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clinical Infectious Diseases, 63, e61-e111. doi:10. 1093/cid/ciw353 Klompas, M. (2017). Health care and hospital-acquired pneumonia. In S. C. Mc Kean, J. J. Ross, D. D. Dressler, & D. B. Scheurer (Eds. ), Principles and practice of hospital medicine (2nd ed., pp. 1514-1518). New York, NY: Mc Graw-Hill. Kochanek, K. D., Murphy, S. L., Xu, J., & Tejada-Vera, B. (2016). Deaths: Final data for 2014. National Vital Statistics Reports, 65, 1-122. Retrieved from https://www. cdc. gov/nchs/data/nvsr/nvsr65/ nvsr65_04. pdf Mandell, L. A., Wunderlink, R. G., Anzueto, A., Bartlett, J. G., Campbell, G. D., Dean, N. C., & Whitney, C. G. (2007). Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clinical Infectious Diseases, 44, S27-S72. doi:10. 1086/511159 Musher, D. M. (2017). Community-acquired pneumonia. In S. C. Mc Kean, J. J. Ross, D. D. Dressler, & D. B. Scheurer (Eds. ), Principles and practice of hospital medicine (2nd ed., pp. 1503-1513). New York, NY: Mc Graw-Hill. Musher, D. M., & Thorner, A. R. (2014). Community-acquired pneumo-nia. New England Journal of Medicine, 371, 1619-1628. doi:10. 1056/ NEJMra1312885 Wunderlink, R. G., & Waterer, G. W. (2014). Community-acquired pneu-monia. New England Journal of Medicine, 370, 543-541. doi:10. 1056/ NEJMcp1214869 Pulmonary Embolism E. Mone ́e Carter-Griffin Definition A. A blockage of a pulmonary artery or one of the smaller branches. Most commonly, pulmonary embolism (PE) is the result of an embolic thrombus formation elsewhere in the body (e. g., lower extremity). Incidence A. PE is more common in patients with deep vein thrombo-sis (DVT). B. It affects more than 600,000 people annually. C. An estimated 60,000 to 100,000 people die annually. D. Approximately one-third of patients will have a recur-rence within 10 years. Pathogenesis A. A thrombus forms secondary to a hypercoagulable state, injury to the vascular endothelium, and venostasis, which concentrates blood clotting factors at the site of vessel injury. Clot formation occurs as a result of blood pooling. B. The clot can dislodge from the extremity, travel through the venous system, move through the right side of the heart, and obstruct a pulmonary artery or the smaller branches. Pulmonary Embolism

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28 Large enough obstructions can prevent blood flow to the affected area, creating a ventilation/perfusion mismatch lead-ing to respiratory failure and/or increase the pulmonary artery pressure, resulting in right-sided heart failure. Predisposing Factors A. Factor V mutation. B. Protein C or S deficiency. C. Malignancy. D. Immobility. E. T rauma. F. Surgery. G. Smoking. H. Obesity. I. Prior PE. J. Chronic diseases such as heart failure and chronic obstructive pulmonary disease (COPD). K. Prolonged travel. Subjective Data A. Common complaints/symptoms. 1. These can vary depending on the degree of clot burden. 2. Patients may be asymptomatic, especially in the setting of a small segmental branch PE. The condition is usually found incidentally in these cases. 3. Symptoms may include: a. Pleuritic chest pain. b. Dyspnea/Tachypnea. c. Hypoxia. d. Cough with possible blood-tinged sputum pro-duction. e. Tachycardia. f. Dizziness or syncope. g. Hypotension/shock with a massive PE. h. Recent symptoms associated with a DVT (e. g., extremity pain, warmth, erythema, edema). B. Family and social history. C. The provider should assess symptom onset and any asso-ciated risk factors for PE development such as history or cur-rent malignancy, decreased mobility, travel, recent surgeries, and so forth. D. It is important for the provider to assess for family history of clot formation or known factor deficiencies. Physical Examination A. Findings depend on the degree of clot burden. B. Perform a general examination, which may reveal diaphoresis, fever, and tachycardia. On presentation, most patients are hemodynamically stable. C. Assess neurological status. Patients may present with syn-cope, altered mentation, or agitation. D. Assess the respiratory rate. In more significant PEs, the rate will be increased. Auscultation of breath sounds may reveal rales or crackles. E. Perform a cardiac examination. Patients may have a murmur, accentuated second heart sound, or S3/S4 gallop. F. Extremities may reveal signs of a deep vein thrombosis such as pain, edema, or erythema. Diagnostic Tests A. D-dimer (age adjusted). 1. High sensitivity: With negative results and a low prob-ability of a PE. 2. Most reliable in young patients with no comorbid conditions and short symptom onset. 3. Can have nonspecific elevations in the elderly and those with other acute illnesses requiring hospitalization. B. Chest CT Angiography (CTA). 1. Allows for direct visualization of the emboli. 2. Considered the standard of care for diagnosing patients with high probability of a PE or low/interme-diate probability but positive D-dimer. 3. Right ventricular (RV) dilation: Associated with short-term adverse outcomes. C. Ventilation/Perfusion (V/Q) Lung Scan. 1. An alternative to the chest CTA, especially in the set-ting of contraindications such as renal failure. 2. Evaluates for perfusion defects, which are nonspecific and only present in one-third of patients with PE. 3. Increased likelihood of nonconclusive results in patients older than 75 years. D. Echocardiography. 1. Often indirectly helps diagnose PE in conjunction with the patient's clinical presentation. 2. Can also be utilized as a prognostic factor in PE. 3. Possible findings consistent with a PE: Acute RV enlargement and in some cases dysfunction, evidence of pulmonary hypertension with elevated RV systolic pres-sures, and possible flattening of the septum. 4. May be able to visualize an intracardiac thrombi. 5. RV dilation: Associated with an increased risk for adverse outcomes. E. Ultrasonography. 1. Can assist in the diagnosis of PE. F. Additional diagnostics for acute risk stratification. 1. Pulmonary embolism severity index (PESI). a. Used to predict the 30-day outcomes/mortality in patients with acute PE. b. Score greater than 106 on the original PESI: High risk for morbidity and mortality. c. Score greater than 1 on the simplified PESI: High risk for morbidity and mortality. 2. T roponin. a. Elevated troponin levels in patients presenting or receiving treatment for PE: Associated with adverse outcomes. 3. N-Terminal pro brain natriuretic peptide (NT-pro BNP). 4. Elevated levels: Associated with adverse outcomes (in literature). Differential Diagnosis A. Pericarditis. B. Pleuritis. C. Musculoskeletal pain. Evaluation and Management Plan A. General plan. 1. Diagnosis of a PE requires the provider to account for the patient's clinical presentation as well as evaluat-ing diagnostic tests. 2. T reatment recommendations are highly dependent on the patient's clinical status including respiratory and hemodynamic stability at the time of presentation. 3. In the clinical setting and literature, PEs have been described as low risk, submassive, and massive. a. Low risk PEs: Patients with hemodynamic stabil-ity, no elevation in biomarkers, and no evidence of RV dysfunction on imaging. 2. Pulmonary Guidelines

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29 b. Submassive PEs: Patients with hemodynamic sta-bility but evidence of RV dysfunction on imaging and/or biomarker elevation. c. Massive PEs: Patient with hemodynamic instabil-ity, elevation in biomarkers, and evidence of RV dys-function. 4. Ideally, patients should have pretest clinical assess-ment, diagnostics with consideration of risk stratification, and initiation of treatment. 5. Low to intermediate probability of PE. a. Pretest clinical assessment. i. Wells Clinical Prediction Rule for PE. Patients are evaluated using seven variables in which they can receive 1 to 3 points. A score of 2 to 6 points indicates a moderate risk and a score greater than 6 indicates high risk. ii. Revised Geneva Score. Patients are evaluated using eight variables in which they can receive 1 to 5 points. A score of 4 to 10 points indi-cates an intermediate risk and a score greater than 11 indicates high risk. iii. Appropriate for patients who are hemody-namically stable. Patients with a high probability of PE should proceed immediately to diagnostic testing. b. Age-adjusted D-dimer. i. If negative: No further imaging needed. ii. If positive: Further imaging needed. iii. It is important that the provider use an age-adjusted scale due to decreased specificity in the elderly population. Using the appropriate scale can reduce the number of false-positive results. c. Chest CTA versus V/Q Lung Scan. i. If no contraindications to CTA: Chest CTA is preferred. d. T reatment: Anticoagulation therapy. 6. High probability of PE. a. Patients likely to be hemodynamically unstable; pretest clinical assessment not appropriate. b. Immediate chest CTA. If unable to obtain a chest CTA due to hemodynamic instability/uncontrolled hypotension, then findings consistent with a PE on echocardiography may be a suitable alternative. B. Pharmacotherapy. 1. Decision about medication management should consider whether the PE was provoked (caused by an identifiable risk factor such as cancer) and duration of therapy. 2. Patients should be routinely reevaluated for antico-agulation needs if receiving extended therapy. 3. T reatment with dabigatran, rivaroxaban, apixaban, or edoxaban is recommended over a vitamin K antagonist in patients with a PE. 4. A vitamin K antagonist is recommended for patients with an unprovoked PE if not receiving treatment with dabigatran, rivaroxaban, apixaban, or edoxaban. 5. It is suggested that a provider treating a patient with a PE and cancer use a low molecular weight heparin (LMWH). It is also recommended that patients receive extended therapy (e. g., no stop date) depending on their bleeding risk. 6. Anticoagulation is recommended for 3 months in patients with a PE provoked by surgery or transient risk factors. 7. For patients with an unprovoked PE at a low or mod-erate bleeding risk, initiation of extended anticoagulationtherapy (e. g., no stop date) is suggested. For patients with a high bleeding risk, it is recommended to initiate anti-coagulation for 3 months. 8. Surveillance is suggested in patients with a distal (subsegmental) PE who have no proximal DVTs and a low risk for recurrent venous thromboembolism (VTE). 9. Systemic thrombolytic therapy is suggested for hemodynamically unstable patients. 10. Additional management: Catheter-directed throm-bolysis. C. Patient/family teaching. 1. Prevent more blood clots from forming by taking the medication as prescribed. 2. Be sure to follow-up with lab tests as directed. 3. Encourage patients to get up and be active. 4. Smoking cessation. 5. On long trips, make frequent stops to get out and move about. 6. On airplane rides, perform exercises that keep your legs, feet, and toes moving. D. Discharge. 1. Call your healthcare provider if there is any increase in symptoms. Follow-Up A. Patient follow-up is variable in the literature primarily due to the type of medication, cause of PE, and severity of illness due to the PE. B. A vitamin K antagonist requires that the patient follow-up 2 to 3 days postdischarge for international normalized ratio (INR) evaluation. Consultation/Referral A. Pulmonologist may be consulted due to the pulmonary symptoms associated with a PE. B. Hematologist may be warranted especially if concerned for a procoagulant defect. C. An interventional radiologist or interventional cardiolo-gist may be consulted for catheter-directed thrombolysis. D. Critical care may be needed if the patient is admitted to the ICU or becomes hemodynamically unstable. Special/Geriatric Considerations A. Inferior vena cava (IVC) filters are not recommended for patients treated with anticoagulation. B. IV anticoagulation therapy should be started prior to administering dabigatran and edoxaban. Bibliography Beckman, M. G., Hooper, W. C., Critchley, S. E., & Ortel, T. L. (2010). Venous thromboembolism: A public health concern. American Journal of Preventive Medicine, 38, S495-S501. doi:10. 1016/j. amepre. 2009. 12 017 Jaff, M. R., Mc Murtry, S., Archer, S. L., Cushman, M., Goldenberg, N., Goldhaber, S. Z., & Zierler, B. K. (2011). Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombo-sis, and chronic thromboembolic pulmonary hypertension. Circulation, 123, 1788-1830. doi:10. 1161/CIR. 0b013e318214914f Kearon, C., Akl, E. A., Ornelas, J., Blaivas, A., Jimenez, D., Bounameaux, H., Huisman, M., & Moores, C. L. (2016). Antithrombotic therapy for VTE disease: CHEST guideline and expert panel report. Chest, 149, 315-352. doi:10. 1016/j. chest. 2015. 11. 026 Konstantinides, S. V., Barco, S., Lankeit, M., & Meyer, G. (2016). Man-agement of pulmonary embolism: An update. Journal of the American College of Cardiology, 67, 976-990. doi:10. 1016/j. jacc. 2015. 11. 061 Meyer, N. J., & Schmidt, G. A. (2015). Pulmonary embolic disorders: Thrombus, air, and fat. In J. B. Hall, G. A. Schmidt, & J. P. Kress Pulmonary Embolism

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30 (Eds. ), Hall, Schmidt, and Wood's principles of critical care (4th ed., pp. 318-336). New York, NY: Mc Graw-Hill. Raja, A. S., Greenberg, J. O., Qaseem, A., Denberg, T. D., Fitterman, N., & Schuur, J. D. (2015). Evaluation of patients with suspected acute pulmonary embolism: Best practice advice from the clinical guidelines committee of the American College of Physicians. Annals of Internal Medicine, 163, 701-711. doi:10. 7326/M14-1772 Restrictive Lung Disease E. Mone ́e Carter-Griffin Definition A. A reduction in the total lung capacity secondary to a decrease in lung elasticity or disease of the chest wall, pleura, or neuromuscular etiology. Disorders can be classified as intrinsic or extrinsic. Incidence A. The incidence is highly variable and dependent on the etiology of restriction. B. The incidence of some disorders is not well known. C. Interstitial lung diseases (ILDs), although rare, are a cause of restrictive lung disease affecting approximately 500,000 individuals each year and resulting in 40,000 deaths. D. Nonidiopathic and idiopathic pulmonary fibrosis (type of ILD) are a common cause of restrictive lung disease. E. Approximately 30 cases per 100,000 of restrictive lung disease are due to idiopathic pulmonary fibrosis. F. The prevalence of disease increases with age. G. Frequency of occurrence is typically higher in men. Pathogenesis A. An exogenous or endogenous stimulus causes repetitive injury to the lung parenchyma, leading to epithelial and endothelial damage. Activation of local and systemic factors (e. g., fibroblasts, growth factors, clotting, factors, cytokines) occurs. B. A provisional matrix is formed. There is a dysregulation of the intricate network and lack of matrix degradation, leading to aberrant wound healing and progressive lung remodeling, ultimately causing pulmonary fibrosis. Predisposing Factors A. Predisposing factors depend on the etiology of the restric-tive lung disease. B. Risk factors include: 1. Obesity. 2. Kyphoscoliosis. 3. Myasthenia gravis. 4. Chronic pleural disease (e. g., trapped lung). 5. Autoimmune disease (e. g., scleroderma, systemic lupus erythematosus). 6. Occupational exposures. 7. Medications such as amiodarone, bleomycin, and methotrexate. 8. Idiopathic lung disease such as pulmonary fibrosis, more common in the elderly and men. 9. Sarcoidosis. Subjective Data A. Common complaints/symptoms. 1. Symptoms and complaints may vary depending on the underlying cause of the restrictive lung disease. 2. Dyspnea (see Figure 2. 1): Most common complaint. It can be present with exercise or at rest as the disease progresses. 3. Possible chronic cough (see Figure 2. 3), wheezing (see Figure 2. 2), or chest discomfort. 4. Possible hemoptysis. 5. Fatigue. B. Common/typical scenario. 1. Duration of illness (e. g., acute onset, chronic). C. Family and social history. 1. Smoking history. 2. Occupational history or exposures. 3. Family history of fibrotic lung disease. D. Review of symptoms. 1. Neurologic—any confusion, fatigue, muscle weak-ness. 2. Respiratory—shortness of breath at rest, upon exer-tion, or that is progressive; dry cough; bloody spu-tum; pain on inspiration; recent or frequent colds. 3. Use of medications such as nitrofurantoin, amio-darone, or others that have the potential to cause lung disease. Physical Examination A. Dyspnea, which may be more evident with activity. B. Tachypnea. C. Cyanosis or oxygen desaturation with activity. D. Possible bibasilar inspiratory crackles, scattered inspira-tory rhonchi, or wheezing. E. Digital clubbing. F. Obese. G. Other disease-specific signs and symptoms (e. g., rash, Raynaud's, muscle weakness), depending on the underlying etiology. Diagnostic Tests A. Laboratory studies. 1. Usually nonspecific. 2. Serologic testing. This may be appropriate in patients suspected of having an underlying disorder causing restrictive disease such as rheumatoid arthritis. B. Chest x-ray. 1. Typically nonspecific findings, which may vary with the type of restrictive disease. 2. Possible evidence of increased interstitial markings, bibasilar reticular pattern, or a nodular pattern. 3. Honeycombing, which is typically noted as a late or advanced finding. 4. If an extrinsic factor is suspected, then imaging may reveal a trapped lung, pleural effusion, etc. C. Chest CT 1. More sensitive and better assessment of the extent of disease compared to a chest x-ray. 2. May reveal findings characteristic of specific restric-tive diseases. Some restrictive diseases such as idiopathic pulmonary fibrosis can be diagnosed solely with a chest CT. 3. If an extrinsic factor is suspected, then imaging may reveal a trapped lung, pleural effusion, etc. D. Pulmonary Function Testing 1. Valuable for assessing the response to therapy and monitoring disease progression. 2. Does not diagnosis a specific disease. 3. Characteristic findings include a reduced total lung capacity (TLC), functional residual capacity (FRC), and residual volume (RV). 2. Pulmonary Guidelines

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31 4. The forced expiratory volume in one second (FEV1) and forced vital capacity ratio is usually normal or increased. 5. The diffusing capacity of carbon monoxide is reduced in patients with an intrinsic etiology of restrictive disease. If the diffusing capacity is normal, then the etiology of restrictive disease is an extrinsic factor such as neuromus-cular disease. E. Arterial blood gas 1. May be normal or indicate hypoxemia and a respira-tory alkalosis. 2. May reveal an increased alveolar-arterial gradient. F. Bronchoscopy and/or lung biopsy 1. Beneficial for identifying diseases associated with intrinsic factors or the lung parenchyma. 2. A bronchoalveolar lavage (BAL) may be useful in nar-rowing the differential diagnoses. a. The clinical usefulness of the BAL has not been well established. 3. A lung biopsy can confirm the diagnosis, evaluate dis-ease activity, and exclude other diagnoses. a. Open thoracotomy b. Video-assisted thoracoscopic lung biopsy c. T ransbronchial lung biopsy via bronchoscopy G. Additional imaging or testing may be warranted to assess for complications resulting from restrictive diseases such as an echocardiogram to evaluate for pulmonary hypertension or right-sided heart failure. Evaluation and Management Plan A. T reatment may vary depending on the underlying etiol-ogy for restrictive disease. B. Intrinsic etiologies are defined as diseases of the lung parenchyma. Extrinsic etiologies are extra-pulmonary causes including neuromuscular disorders, the chest wall, etc. C. Patients should receive smoking cessation counseling. D. Avoidance of environmental and/or occupational expo-sures. E. Medications suspected of causing restrictive disease should be stopped immediately. F. Supplemental oxygen therapy should be administered for all patients with oxygen saturations less than 88% on room air at rest or upon exertion. G. Pulmonary rehabilitation or regular activity/exercise should be encouraged because it has been shown to improve endurance and quality of life. H. Patients should receive vaccinations for influenza and pneumococcal. I. T reatment regimens for intrinsic causes usually includes: 1. Corticosteroid therapy a. Use of corticosteroids is generally accepted; however, timing, dosing, and continuation versus discontinuation of treatment is highly variable and dependent on the intrinsic cause for restrictive disease as well as patient responsiveness. b. The long-term effects of corticosteroid therapy must be considered. c. Pulse high dose corticosteroids are typically used for acute exacerbations. 2. Immunosuppressive agents (e. g. cyclosporine, aza-thioprine) may be used in certain diagnoses. These medi-cations should not be routinely or empirically used with-out a definitive diagnosis. 3. If worsening respiratory symptoms, patients may require invasive mechanical ventilation. 4. Patients with refractory disease to treatment and pro-gressive worsening, may be a candidate for lung trans-plantation and should be referred to lung transplant spe-cialist and center. J. T reatment for extrinsic causes include: 1. Weight loss counseling and plan for obese patients 2. Non-invasive positive pressure ventilation for patients who have impaired gas exchange 3. Identification of the extrinsic disorder and treatment accordingly. 4. For patients with a trapped lung, chronic effusion, or empyema, a decortication may be required. Follow Up A. Follow-up is variable and dependent on the patient's symptoms and medical management. It should be individ-ualized. B. Post-hospital discharge, patients will follow-up with their provider in one week. Consultation/Referral A. Patients with restrictive lung disease should be referred to a pulmonologist for diagnosis and management. B. Patients with an extrinsic etiology for restrictive disease such as myasthenia gravis should be referred to a neurologist or the appropriate consultant for the disorder. Individual/Special/Geriatric Considerations A. To adequately assess responsiveness to immunosuppres-sive medications, the provider should note it may not be evi-dent until eight to twelve weeks after therapy initiation. B. Patients with parenchymal restrictive disease (e. g. idio-pathic or non-idiopathic pulmonary fibrosis) receiving treat-ment with high dose steroids should receive prophylactic treatment for pneumocystis jiroveci pneumonia (PJP). C. Patients with progressive disease are typically discharged on home oxygen therapy. Increased oxygen requirements may be necessary to maintain a goal saturation greater than 88%. The patient and family is instructed that oxygen ther-apy may be tailored to maintain oxygen saturations at rest and with exertion. If the patient is requiring increased oxygen therapy from baseline, then an immediate follow-up appoint-ment with their pulmonologist or hospital admission may be warranted. Restrictive Lung Disease

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32 EXHIBIT 2. 1 Stepwise Approach for Managing Asthma Long Term The stepwise approach tailors the selection of medication to the level of asthma severity or asthma control. The stepwise approach is meant to help, not replace, the clinical decision making needed to meet individual patient needs. ASSESS CONTROL:STEP UP IF NEEDED (first, check me dication adherence, inhaler technique, environmenta l control, and comorbiditie s) STEP DO WN IF POSSIBLE (and a sthma is well controlled for at le ast 3 month s) STEP 1 STEP 6 STEP 5 STEP 4 STEP 3 Ateach step: Patient education, envir onmental contr ol,and management ofcomorbidities0-4 years of age 5-11 years of age Intermittent Asthma Persistent Asthma: Daily Medication. Consult with asthma spec ialist ifstep3car eorhigher isrequir ed. Consider consul-tation atstep 2. Preferred Treatmentb SABAaas needed Low-dose ICSa Medium-dose ICSa Medium-dose ICSa+ either LABAaor montelukast High-dose ICSa+either LABAaor montelukast High-dose ICS a+either LABA or montelukast+ oralcorticoster oids Alternative Treatmentb,c Cromolyn or montelukast If clear bene/f_it is not observed in 4-6 weeks, and medication technique and adherence are satisfactory,consider adjusting therapy or alternate diagnoses. Quick-Relief Medication/uni25A0SABAaasneeded forsymptoms; intensity oftreatment depends onseverity ofsymptoms. /uni25A0With viral respiratory symptoms: SABA every 4-6hours upto24hours (longer with physician consult). Consider short course oforalsystemic corticoster oids ifasthma exacerbation issever e orpatient hashistory ofsever eexacerbations. /uni25A0Caution: Frequent useof SABA may indicate theneedtostep uptreatment. Intermittent Asthma Persistent Asthma: Daily Medication. Consult with asthma spec ialist ifstep4car eorhigher isrequir ed. Consider consul-tation atstep 3. Preferred Treatmentb SABAaas needed Low-dose ICS a Low-dose ICSa +either LABA, LABA ,a theophyllinebor Medium-dose ICS a + LABAa High-dose ICS a+LABAa High-dose ICSa +LABAa+ OCS Alternative Treatmentb,c Cromolyn, LTRAa,or theophyllined Medium-dose ICSa+ either LTRAa or theophyllined High-dose ICSa+either LTRAaor theophyllined High-dose ICSa +either LTRAa ortheophyllined +OCS Consider subcutaneous allergenimmunotherapy for patients who have persistent, allergicasthma. e Quick-Relief Medication/uni25A0SABAaasneeded forsymptoms. Theintensity oftreatment depends onseverity ofsymptoms: Uptothreetreatments every 20minutes asneeded. Short course oforalsystemic corticoster oids may beneeded. /uni25A0Caution: Increasing useof SABA oruse >2days/week forsymptom relief (nottoprevent EIB) generally indicates inadequate contr olandtheneed tostep uptreatment. (continued )STEP 2 medium-dose ICSa2. Pulmonary Guidelines

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33 Restrictive Lung Disease EXHIBIT 2. 1 Step wise Approach for Managing Asthma Long Term (continued ) Ateach step: Patient education, envir onmental contr ol,and management ofcomorbid Ities Preferred Treatmentb SABAaas needed Low-dose ICSa Low-dose ICSa +LABAa OR medium-dose ICSa Medium-dose ICSa+ LABAa High-dose ICSa+LABAa AND consider omalizumab forpatients who have allergiesf High-dose ICSa +LABAa+ OCSh AND consider omalizumab for patients who have allergiesf Alternative Treatmentb,c Cromolyn, LTRAa,or theophyllined Low-dose ICSa +either theophylline , or zileutong Medium-dose ICSa+either theophylline , orzileutong Consider subcutaneous allergenimmunotherapy forpatients who have persistent, allergicasthma. e Quick-Relief Medication/uni25A0SABAaasneeded forsymptoms. Theintensity oftreatment depends onseverity ofsymptoms: Up tothreetreatments every 20minutes asneeded. Short course oforalsystemic corticoster oids may beneeded. /uni25A0Caution: Use of SABA >2days/week forsymptom relief (nottoprevent EIBa)generally indicates inadequate contr olandtheneed tostep uptreatment. ASSESS CONTROL:STEP UP IF NEEDED (first, check medication adherence, inhaler technique, environment al control, and comorbiditi es) STEP DO WN IF POSSIBLE (and asthma is well controlled for at least 3 mont hs) STEP 1 STEP 6 STEP 5 STEP 4 STEP 3 STEP 2 a EIB, exercise-induced bronchospasm; ICS, inhaled corticosteroid; LABA, long-acting beta 2agonist; LTRA, leukotriene receptor antagonist; OCS, oral corticosteroids ;SABA, short-a cting beta 2agonist. b Treatment option sarelisted inalphabetical order,ifmorethan one. c Ifalternative treatment isused andresponse isinadequate, discontinue andusepreferredtreatment befor estepping up. d Theophylline isalessdesirable alternative because oftheneed tomonitor serum concentration levels. e Based onevidence fordust mites, animal dander,andpollen; evidence isweak orlacking formolds andcockr oaches. Evidence isstrongest for immunotherap ywith single allergens. Theroleofallergyinasthma isgreater inchildr enthan inadults. f Clinicians who administer immunotherapy oromalizumab should bepreparedtotreatanaphylaxis thatmay occur. h Befor eoralcorticoster oids areintroduced, atrialofhigh-dose ICS + LABA + either LTRA, theophylline, orzileuton, may beconsider ed,although this approach hasnotbeen studied inclinical trials. SABA,short-act ingbeta Source: U. S. Department of Health and Human Services. (2012). Asthma carequick reference: Diagnosing and man aging asthma. Retrieved from https://www. nhlbi. nih. gov//f_iles/docs/guidelines/asthma_qrg. pdf /uni2265 12 years of age Intermittent asthma Persistent asthma: Daily medication. Consult with asthma spec ialist ifstep4careorhigher isrequir ed. Consider consul-tation atstep 3. LTRAa, LTRAa d,d g Zileuton islessdesirable because oflimited studies asadjunctive therapy andtheneed tomonitor liver function.

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

35 3 Cardiac Guidelines Allison Rusgo Acute Coronary Syndromes Allison Rusgo Definition A. Umbrella term encompassing unstable angina (UA), non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI). B. UA: No cardiac damage, no elevation in cardiac labora-tory biomarkers, and no ST-segment elevation on ECG, but may show ST-segment depression. 1. Indicates narrowing of coronary arteries secondary to thrombosis, hemorrhage, or plaque rupture. In variant angina (Prinzmetal) cause is vasospasms. 2. Myocardial oxygen demand: Unchanged but available blood supply is decreased because of overall reduced coro-nary blood flow. C. NSTEMI: Evidence of cardiac damage, evidence of ele-vation in cardiac laboratory biomarkers, and no ST-segment elevation on ECG (but may show ST-segment depression and other ECG abnormalities; T wave inversion, or peaked T waves). 1. Indicates partial blockage of coronary artery sec-ondary to atherosclerotic narrowing. 2. Cardiac damage at the area of the heart supplied by the partially blocked artery. D. STEMI: Evidence of cardiac damage, evidence of eleva-tion in cardiac biomarkers, and positive ST-segment elevation on ECG. Infarction may produce Q waves (pathologic). 1. Indicates complete blockage of an artery, damaging the area of the heart supplied by the completely occluded vessel. E. Important note: Patients with stable coronary artery dis-ease (CAD) can have acute coronary syndrome (ACS) with-out atherosclerotic plaque rupture where physiologic stress (i. e., trauma, anemia, infection, acute blood loss) increases the myocardial oxygen demand of the heart. Incidence A. Ischemic heart disease is the leading cause of death among U. S. adults, estimated to be 405,000/annually. B. Approximately 1. 4 million individuals are hospitalized for ACS; of these, 810,000 experience an myocardial infarction (MI). C. STEMI is more common in middle-aged patients, and NSTEMI is more common in elderly patients. Pathogenesis A. Mismatch between myocardial oxygen supply and demand, where supply is affected by coronary blood flow and oxygen-carrying capacity of the blood. B. Overall oxygen-carrying capacity determined by hemoglobin level and oxygen saturation. C. Coronary artery blood flow: Interplay between periph-eral vascular resistance and ability of the heart to relax during diastole. D. Primary cardiac ischemia caused by atherosclerotic nar-rowing of the coronary vasculature. E. Secondary cardiac ischemia (less common) secondary to causes unrelated to atherosclerotic narrowing of the coronary vasculature. 1. Increased myocardial oxygen demand (i. e., infection, tachyarrhythmias, thyrotoxicosis). 2. Decreased blood flow (i. e., hypotension). 3. Decreased oxygen availability (i. e., anemia). F. Atherosclerotic-related ACS: Coronary arteries undergo a cascade of reactions leading to increased plaque accu-mulation, resulting in plaque rupture, and finally artery blockage. 1. Vascular injury: T riggered by factors such as tobacco by-products, elevated blood pressure (BP), elevated glu-cose, and oxidized low-density lipoproteins. 2. Results in increased vascular permeability and inflammation. 3. Inflammatory mediators (macrophages and smooth muscle cells) activated: Create “fatty streaks” in vasculature. 4. “Fatty streaks”: T ransformed into foam cells (i. e., plaque), which form fibrous caps. 5. When the top layer of the fibrous cap ruptures, platelets are activated. 6. Platelet response: Consists of adhesion, aggrega-tion, and activation; potentiates further damage to affected artery via platelet-laden thrombi, hemorrhage, and inflammation (overall blood flow decreased). 7. Immediate onset of the artery blockage created by ischemia secondary to rapid decrease in blood flow. 8. Amount and duration of the myocardial oxygen sup-ply and demand mismatch related to whether person experiences reversible ischemia (UA) or irreversible dam-age with cell death (STEMI or NSTEMI). Predisposing Factors A. Hypertension (HTN). B. Hyperlipidemia. C. Diabetes mellitus (DM). D. Metabolic syndrome. E. Obesity and sedentary lifestyle. F. Tobacco use. G. Family history of cardiovascular disease. H. Medications/toxins (cocaine, ergonovine, serotonin). Acute Coronary Syndromes

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

36 Subjective Data A. Common complaints/symptoms. 1. Chest discomfort (vise-like or crushing, aching, pres-sure, tightness, or burning); less likely sharp/stabbing or knife-like. a. Reproducible chest tenderness in some cases. b. Classic: Left-sided or substernal chest discomfort that radiates to the jaw or left arm. c. Can also radiate to the upper abdomen, back, or shoulders. 2. Nausea/vomiting. 3. Diaphoresis. 4. Palpitations. 5. Dyspnea. 6. Lightheadedness or syncope. 7. Feelings of anxiety. 8. Women, elderly persons, and those with DM: More likely to experience atypical ACS presentations. a. Fatigue. b. Weakness. c. Generalized malaise. d. Nonspecific chest or back discomfort. e. Decreased exercise tolerance. f. Altered mental status (elders). g. Gastrointestinal symptoms radiating the back (women). h. No pain (elders and DM persons). B. History of the present illness. 1. Information regarding onset, provoking and alleviat-ing factors, duration, quality, severity, and timing of chest discomfort. a. Compared to stable angina or UA, MIs cause more severe chest discomfort that is prolonged ( >20 min-utes) and unrelieved by nitroglycerin. b. Can be potentiated by exposure to cold, physical activity, or emotional stress. c. Possible previous history of angina and any recent changes in anginal symptoms over the past several months. d. Possible recent decrease in activity level due to decreased tolerance. 2. More likely to experience associated symptoms with MIs as opposed to angina (i. e., nausea, dyspnea, fatigue, diaphoresis). C. Family and social history. 1. Family history of premature CAD or MI in first-degree relative (males <45 years and females <55 years). 2. Tobacco or illegal substance use, especially cocaine. 3. Lifestyle factors, including level of exercise and dietary habits. D. Review of systems. 1. General: Fatigue and diaphoresis. 2. Cardiovascular: Chest pain/discomfort (with radia-tion) and palpitations. 3. Pulmonary: Dyspnea on exertion and shortness of breath. 4. Abdominal: Epigastric discomfort, indigestion, nau-sea, and vomiting. 5. Neurological: Dizziness, lightheadedness, near-syncope/syncope, and mental status changes. Physical Examination A. General appearance (one of the following). 1. Unremarkable and appearing well without any signs of distress, resting calmly. 2. Insignificant clinical/respiratory distress and insta-bility. 3. Cyanotic, in respiratory distress. B. Vital signs: Assess pulse, BP, respirations, oxygen satura-tion, and temperature. 1. Pulse: Can be regular, irregular, tachycardic, or brady-cardic (bradycardia can occur with anterior or inferior wall MIs). 2. BP: Can be elevated (due to anxiety, pain, underly-ing HTN, catecholamine surge) or decreased (indicates ventricular dysfunction). C. Skin: Diaphoresis, cool/clammy skin (concern for cardio-genic shock), and peripheral edema. D. Neck: Possible jugular venous distention (JVD). E. Cardiac. 1. Inspect for lifts, heaves, and pulsations. 2. Palpate for possible chest wall tenderness. 3. Auscultate. a. Extra heart sounds. S3 is present in approximately 15% of cases and indicates acute MI with heart failure. b. A new systolic murmur. This is concerning for papillary muscle dysfunction, ventricular septal defect, or new mitral regurgitation from a flail seg-ment of the valve. F. Pulmonary: Auscultate lung sounds for evidence of rales/crackles; concern for pulmonary edema or congestive heart failure. G. Abdominal: Inspect, auscultate for bruits, and palpate for tenderness and evidence of pulsatile abdominal mass (con-cern for abdominal aortic aneurysm). Diagnostic Tests A. ECG: Should be performed within 10 minutes of presen-tation to healthcare provider. Note that a normal ECG or one unchanged from the patient's baseline does not rule out the possibility of ischemic cardiac damage. 1. Fixed ST-segment elevations (STEMI). 2. Fixed ST-segment depressions (shows ischemia). 3. T-wave changes (can indicate ischemia). 4. T ransient ST-segment elevations (consider pericardi-tis, Prinzmetal angina, left ventricular aneurysm). B. Cardiac biomarkers. 1. Serial troponins (c Tn I or c Tn T): Sensitive and spe-cific for ACS diagnosis (biomarker of choice); recom-mended as set of three drawn approximately 4 to 6 hours apart. 2. Complete blood count: Useful for baseline informa-tion and ruling out anemia as cause of ACS. C. Basic metabolic panel. 1. To assess electrolytes, especially magnesium and potassium (causes of cardiac arrhythmias). 2. To assess renal function: Important if going to use angiotensin-converting enzyme (ACE) inhibitors for future therapy and/or contrast dye during catheterization (want to avoid contrast-induced nephropathy). D. Chest radiography: To assess for pulmonary edema and cardiomegaly, and rule out other causes of chest pain such as pneumonia or thoracic aneurysm. E. Cardiac echocardiography: Can be especially helpful if diagnosis is questionable. It is used to : 1. Assess left ventricular function. 2. Evaluate for regional wall motion abnormalities. 3. Check for pericardial effusions or valvular abnormal-ities (i. e., acute mitral regurgitation). 3. Cardiac Guidelines

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

37 F. Computed tomography coronary angiography (CTCA)/CT coronary artery calcium (CAC) scoring. 1. Noninvasive diagnostic studies: Aid in early CAD diagnosis. 2. CTCA: Uses contrast dye to evaluate the integrity of coronary arteries (can also evaluate previously implanted stents and bypass grafts for patency). 3. CT CAC: Useful for low-risk ACS patients (no con-trast dye and low radiation levels; evaluation of calcium in coronary arteries, which is related to atherosclerotic burden. Differential Diagnosis A. Myocardial infarctions (STEMI, NSTEMI). B. Stable or unstable angina. C. Pericarditis. D. Myocarditis. E. Esophagitis/gastritis/ruptured peptic ulcer. F. Hypertensive emergency. G. Anxiety/panic attack. H. Ruptured thoracic or abdominal aortic aneurysm. I. Pulmonary embolus. J. Pneumonia. Evaluation and Management Plan A. General plan. 1. Management based on patient presentations, char-acteristics of symptoms, past medical history, physical examination findings, and diagnostic results. 2. Goal: To limit necrosis and overall cardiac damage. 3. Risk stratification: Imperative when designing treat-ment plan. One option is the Thrombosis in Myocardial Infarction (TIMI) Score (see Table 3. 1). a. Instrument for determining risk of all-cause mor-bidity, new or recurrent MI, or need for emergent revascularization within 14 to 30 days of presentation of NSTEMI or UA. b. Each of the seven items on the checklist is equiv-alent to 1 point; the higher the score, the higher the patient's risk. B. Management of STEMI. 1. Aspirin 324 mg in ED (or prehospital). 2. Loading dose of antiplatelet agent (i. e., clopidogrel, 300-600 mg). 3. Supplemental oxygen if hypoxemia. TABLE 3. 1 Thrombosis in Myocardial Infarction Score Age>65 y 1 point ≥CAD risk factors (HTN, hyperlipidemia, DM, tobacco use, family history of CAD)1 point Known CAD with stenosis ≥50% 1 point Acetylsalicylic use in past 7 d 1 point At least two episodes of severe angina in past 24 hr1 point ST changes on ECG 0. 5 mm above baseline 1 point Positive cardiac biomarkers 1 point CAD, coronary artery disease; DM, diabetes mellitus; HTN, hypertension. Source: Agabegi, S. S., & Agabegi, E. D. (2008). Step-up to medicine (2nd ed. ). Philadelphia, PA: Wolters Kluwer. 4. Antithrombolytic agent (unfractionated or low-molecular weight heparin). 5. Nitrates: Provide symptomatic relief; do not improve mortality. a. Strong risk of hypotension: Causes decreased coro-nary perfusion. b. Should not be given if patient has hypotension, known right ventricular infarction, large pericardial effusion, recent use of 5-phosphodiesterase inhibitor, or severe aortic stenosis. 6. Beta-blockers. a. Caution if decreased systolic BP, cardiogenic shock, severe asthma, decompensated congestive heart failure, or severe bradycardia. 7. Goal: Reperfusion therapy. a. Obtained via percutaneous coronary intervention (PCI) with or without stent placement. i. Should be achieved within 90 minutes of patient arrival at PCI-capable hospital. ii. If hospital is without PCI capabilities, goal is patient transfer to PCI center within 120 minutes of patient arrival. b. PCI options. i. Coronary angioplasty with or without stent placement. ii. Balloon angioplasty stretches inner layer of the coronary artery. iii. Drug eluting stents (DES) or bare metal stents (BMS): Wire mesh cage implanted in the blocked vessel for structure and patency. iv. BMS preferable if unable to utilize dual antiplatelet therapy (DAPT) for at least a year or upcoming invasive surgical procedure. c. If PCI is not achievable in these time parameters, fibrinolytics should be administered within 30 min-utes of patient arrival to hospital. i. Indicated if symptom onset is within 6 to 12 hours; 1 mm ST-segment elevation in more than 2 ECG leads. ii. Aims to dissolve existing clot, improve left ventricular function, and decrease mortality. iii. Examples: Tissue plasminogen factor, strep-tokinase, or tenecteplase. iv. Major risk: Bleeding such as intracranial hem-orrhage (ICH). d. At discretion of cardiothoracic surgeon and interventional cardiologist, consider coronary artery bypass grafting (CABG) if cardiac catheterization yields extensive stenosis and/or stenosis not amenable to stenting/balloon options. e. For unconscious STEMI patients with prehospi-tal cardiac arrest caused by ventricular fibrillation or pulseless ventricular tachycardia, obtain immediate cardiology consultation regarding the usage of ther-apeutic hypothermia prior to cardiac intervention. C. Management of NSTEMI and/or UA. 1. Monitoring during inpatient hospitalization for serial ECGs, biomarker elevation, and symptom evolution. 2. Early invasive therapy (PCI) in NSTEMI or UA: Rec-ommended only if refractory angina; high risk for cardiac events or hemodynamic instability. 3. American Heart Association ( AHA) and American College of Cardiology ( ACC) recommendations for early (within 48 hours) PCI intervention in NSTEMI/UA if: Refractory angina, elevated biomarkers, new ST-changes, Acute Coronary Syndromes

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

38 positive stress test results, decreased left ventricular func-tion, or hemodynamic instability. 4. NSTEMI/UA patients requiring PCI should receive similar medications to STEMI management. a. Aspirin 324 mg initially followed by daily dose of 81 mg. b. Antiplatelet agent (clopidogrel). c. Supplemental oxygen if evidence of hypoxemia. d. Nitrates. e. Antithrombolytic agent (unfractionated or low-molecular weight heparin). f. Beta-blockers if not contraindicated. 5. Patients admitted for ACS evaluations with normal serial ECGs, normal biomarkers, and complete resolution of symptoms can undergo stress testing or CTCA prior to discharge or within 72 hours of discharge if deemed appropriate by cardiologist. The following is for patients discharged prior to definitive diagnostic testing. a. Prescribe aspirin, short-acting nitroglycerin, and beta-blockers (if appropriate). b. Provide instructions regarding lifestyle modifica-tion (i. e., no physical activity until evaluated by car-diologist), tobacco cessation, and cardiac healthy diet. 6. Helpful flow chart for evaluation of patients with ACS (see Figure 3. 1). D. Patient/family teaching points. 1. Knowledge of ACS/angina symptoms: Decreases time before presenting for medical care (decreases door to PCI time, if STEMI). 2. Tobacco cessation. 3. Importance of regular physical activity. 4. Use of heart-healthy (low fat, low cholesterol, low salt) diet. 5. Compliance with all medications (especially aspirin and antiplatelet agent) and clinic follow-up visits. E. Pharmacotherapy. 1. Antiplatelet drugs. a. Aspirin: To prevent platelet aggregation. i. Immediate administration of 324 mg aspirin if STEMI, NSTEMI, or UA. ii. Daily use of aspirin to reduce cardiac mortal-ity; for patients with high risk for ICH, a lower ASA dose of 81 to 160 mg should be considered. iii. Can be combined with other antiplatelets for DAPT. iv. Consider use of proton pump inhibitor or H2 receptor block to prevent gastrointestinal irritation. b. Adenosine diphosphate receptor antagonists. i. Examples: Prasugrel, clopidogrel, or ticagrelor. ii. Overall function: Platelet inhibition via com-plex pharmacologic mechanisms. iii. Major risk: Bleeding—Food and Drug Administration issued Black Box Warning for prasugrel (not for use in those with prior cere-brovascular accident [CVA]/transient ischemic attack [TIA] or bleeding disorders). iv. Can be combined with aspirin for DAPT. v. If elective CABG planned: Recommended to hold clopidogrel for 5 days to reduce risk of bleed-ing and improve morbidity/mortality. History, physical examination, ECG ST-segment elevation AMI Aspirin Clopidogrel or ticagrelor* Nitroglycerin -Blockers in antithrombin† Emergent PCI consider glycoprotein IIB/IIIa inhibitors with PCIEarly intervention consider glycoprotein IIb/IIIa inhibitors or bivalirudin with PCI *Prasugrel should be considered at the time of PCI in patients who have not yet received either clopidogrel or ticagrelor. †Enoxaparin, unfractionated heparin, or fondaparinux. Note: See text for discussion of individual treatment options, indications, and contraindications. †Risk factors for cardiogenic shock/adverse effects: 1. Signs of heart failure; 2. evidence of a low cardiac output state; 3. increased risk for cardiogenic shock (cumulatively: Age>70-year old, systolic blood pressure <120 mm Hg, sinus tachycardia >110 beats/min orbradycardia <60 beats/min, and longer duration of ST-segment elevation myocardialinfarction symptoms before diagnosis and treatment); or 4. standard relativecontraindications to blockade (PR interval >0. 24 s, second-or third-degree heartblock, active asthma, or reactive airway disease). Medical managementconsider glycoprotein IIB/IIIa inhibitors or bivalirudin for high-risk patients Fibrinolytic therapy Nondiagnostic or ischemic ECG (without ST elevation) Aspirin Clopidogrel or ticagrelor* Nitroglycerin -Blockers in antithrombin† FIGURE 3. 1 Algorithm for evaluation of patients with ACS. ACS, acute coronary syndrome ; AMI, acute myocardial infarction; PCI, percutaneous coronary intervention; PR, progesterone. Source: Hollander, J. E., & Diercks, D. B. (2016). Acute coronary syndromes. In J. E. Tintinalli, J. Stapczynski, O. Ma, D. M. Yealy, G. D. Meckler, & D. M. Cline. Tintinalli's emergency medicine: A comprehensive study guide (8th ed., pp. 332-348). New York, NY: Mc Graw-Hill. 3. Cardiac Guidelines

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

39 vi. Specific agent chosen by cardiologist/interven-tional cardiologist and continued for at least sev-eral months post-PCI. c. Glycoprotein IIB/IIIA inhibitors. i. Examples: Abciximab and tirofiban. ii. Routine administration in ED not recom-mended due to timing of PCI and risk of bleeding. iii. During hospitalization, can be used in combi-nation with aspirin for high-risk ACS patients and those likely to undergo PCI. 2. Thrombolytics. a. Examples: Low-molecular weight (enoxaparin) or unfractionated heparin. b. Used in STEMI and NSTEMI management. c. Combining aspirin with heparin should be done in ACS. 3. Beta-blockers. a. Examples: Metoprolol, bisoprolol. b. Very useful in patients with STEMI/NSTEMI (if no known contraindications) because of anti-ischemic characteristics (decreases infarct size and mortality). c. Maintains anti-arrhythmic and antihypertensive properties. d. Reduces cardiac afterload and overall cardiac stress (helps to equalize myocardial oxygen supply and demand levels). 4. Additional medication options. a. ACE inhibitors: For those with left ventricu-lar ejection fraction less than 40% and/or HTN, DM, or stable chronic kidney disease (can consider angiotensin receptor blockers if ACE intolerant). b. High-intensity statin (if no contraindications; as tolerated) with ongoing lipid panel and side effect monitoring. c. Nondihydropyridine calcium channel blockers: Can be used if intolerance or contraindication to beta-blockers as long as there is no left ventricular dysfunction, known prolonged PR interval on ECG, or second-or third-degree heart block. F. Discharge instructions. 1. Prior to hospital discharge. a. Ensure all required prescriptions have been given based on cardiac status and interventions performed during hospitalization. b. Emphasize lifestyle modifications via teach-back method regarding tobacco cessation, cardiac rehabili-tation for exercise program, and eating heart-healthy diet. 2. Verify that patient has appropriate follow-up with cardiologist/interventional cardiologist, primary care provider, and cardiac rehabilitation. 3. For patients discharged with instructions to follow-up with cardiologist for stress testing, ensure appointment occurs within 72 hours after discharge with instructions for no physical activity prior to appointment. 4. Ensure patients understand all reasons to return to ED regarding cardiac-related symptoms. Follow-Up A. Patients should have regular monitoring by their primary care provider and/or cardiologist to address medi-cation compliance; adherence to lifestyle changes; and mon-itoring laboratory markers, including lipid and metabolic panels. B. Cardiologist may consider follow-up echocardiogram to assess left ventricular function ([EF] percentage) at40 days post-MI; this will help determine the need for fur-ther interventions such as an implantable cardiac defibrillator (ICD). Consultation/Referral A. Consult with cardiologist for all ACSs. B. Consult with interventional cardiologist for cardiac catheterization. C. Consult with cardiothoracic surgeon for CABG and/or acute valvular complications. D. Referral to cardiac rehabilitation recommended for patients with ACS. Special/Geriatric Considerations A. Chest pain following PCI or CABG. 1. Patients presenting with chest pain immediately after PCI or angioplasty warrant consideration for sudden ves-sel closure (i. e., in-stent stenosis, in-stent thrombosis, or stent failure). a. T reat aggressively for ACS and immediately con-sult cardiologist. b. Use of BMS is more likely to lead to restenosis in the short term while the use of DES is more likely to lead to restenosis within 9 to 12 months (after cessa-tion of daily antiplatelet such as clopidogrel). 2. Chest pain after CABG may indicate possible graft failure; immediate consultation with cardiologist and car-diothoracic surgeon is necessary. 3. Consider other etiologies such as post-MI pericarditis. B. Chest pain secondary to cocaine intoxication. 1. MI occurs in approximately 6% of patients after cocaine use. 2. Use of cardiac biomarkers is imperative for diagnosis. 3. T reatment involves aspirin, nitrates, and benzodi-azepines (no beta-blockers for first 24 hours). 4. For STEMI secondary to cocaine, patients typ-ically undergo PCI with antithrombolytic and antiplatelet agents per cardiologist and interventional cardiologist. C. Geriatric considerations. 1. Recognize that atypical symptoms are common (con-fusion, malaise, weakness, fatigue). 2. Considerations must be made regarding the use of the most beneficial diagnostic testing. a. Age-related cardiac changes (specifically, if unable to reach target heart rate during stress testing) can mask diagnosis. b. Elderly patients may be unable to walk on tread-mill due to orthopedic comorbidities (nuclear or pharmacologic stress testing is often preferred). c. Coronary atherosclerosis is more diffuse and more calcified combined with decreased diastolic filling. d. Risk versus benefit analysis should be done with regard to the use of multiple antiplatelet and antico-agulant agents due to increased risk of bleeding. e. Overall health status, cognitive abilities, and comorbidities should be considered before utilizing invasive clinical or surgical interventions. Bibliography Agabegi, S. S., & Agabegi, E. D. (2008). Step-up to medicine (2nd ed. ). Philadelphia, PA: Wolters Kluwer. Amsterdam, E. A., Wenger, N. K., Brindis, R. G., Casey, D. E., Jr., Ganiats, T. G., Holmes, D. R., Jr., & Zieman, S. J. (2014). 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute Acute Coronary Syndromes

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

40 coronary syndromes. Circulation, 130, e344-e426. doi:10. 1161/CIR. 0000000000000134 Coven, D., Shirani, J., & Kalyanasundaram, A. (2018, Septermber 5). Acute coronary syndrome. In E. Yang (Ed. ), Medscape. Retrieved from http: //emedicine. medscape. com/article/1910735-overview Hollander, J. E., & Diercks, D. B. (2016). Acute coronary syndromes. In J. E. Tintinalli, J. Stapczynski, O. Ma, D. M. Yealy, G. D. Meckler, & D. M. Cline. Tintinalli's emergency medicine: A comprehensive study guide (8th ed., pp. 332-348). New York, NY: Mc Graw-Hill. Angina Allison Rusgo Definition A. Most common symptom of coronary artery disease (CAD) secondary to coronary vascular obstruction from atherosclerosis. B. Three types. 1. Stable angina. a. Secondary to fixed atherosclerotic plaques that narrow coronary vasculature. b. Occurs because of an imbalance between myocar-dial blood supply and oxygen demand. 2. Unstable angina (UA). a. Progression from stable angina, leading to total vessel occlusion. b. Indication that narrowing of coronary vasculature has increased via thrombosis, hemorrhage, or plaque rupture. c. Myocardial oxygen demand unchanged, but blood supply decreased because of reduced coronary flow. 3. Prinzmetal angina: T ransient coronary vasospasms in the setting of fixed atherosclerosis (75% of cases) or healthy coronary arteries. Incidence A. Estimated 9. 8 million Americans experience angina yearly. B. Age-adjusted prevalence of angina is higher in females than males. C. Annual incidence rates are highest in African Americans as compared to other ethnicities. D. Incidence and prevalence of angina and CAD increase with age. Pathogenesis A. Coronary atherosclerosis causes narrowing of the coro-nary arteries, thereby reducing blood flow through the system. B. Myocardial ischemia (damage) results when the amount of blood flow through the coronary arteries is insufficient to meet myocardial oxygen demand. C. Sensation of angina is caused by the stimulation of the sensory nerve fibers in the coronary vessels. 1. The nerve fibers extend from the spinal nerves (via the spinal cord) to the thalamus to the cerebral cortex to con-vey pain. 2. Adenosine is thought to be the chemical mediator of angina by stimulating the afferent cardiac nerve fibers. Predisposing Factors A. Diabetes mellitus. B. Hyperlipidemia (elevated low-density lipoprotein [ LDL], low high-density lipoprotein [HDL], or elevated triglycerides [TGs]). C. Hypertension (HTN). D. Tobacco use. E. Increased age (males >45 years and females >55 years). F. Family history of premature CAD or MI in first-degree relative (males <45 years and females <55 years). G. Obesity or metabolic syndrome. H. Sedentary lifestyle. I. Underlying valvular heart disease such as aortic stenosis. Subjective Data A. Common complaints/symptoms. 1. Stable angina. a. Retrosternal chest discomfort: Described as pres-sure, heaviness, burning, squeezing. b. Can be located in central chest, epigastrium, neck, back, or shoulders (pain below mandible and below epigastrium is rarely angina). c. Can radiate to jaw, left arm, or shoulders. d. Typically preceded by exertion, eating, cold expo-sure, or emotional upset. e. Usually does not change with positions or respiration. f. Typically lasts 1 to 5 minutes and relieved by rest or use of nitroglycerin. 2. Differentiating features of UA. a. Symptoms occur at rest. b. Any new-onset angina or change in usual stable anginal symptoms. c. Angina unrelieved by rest or nitroglycerin. d. Typically lasts longer than stable angina. B. History of the present illness. 1. Obtain information regarding onset, provoking and alleviating factors, duration, quality, severity, and timing of the anginal-type discomfort. 2. Assess for associated symptoms, including: a. Fatigue. b. Diaphoresis. c. Shortness of breath. d. Decreased exercise tolerance. e. Nausea/vomiting. C. Family and social history. 1. Family history of premature CAD or MI in first-degree relative (males <45 and females <55 years). 2. Tobacco use, alcohol consumption, and illegal sub-stance use (especially cocaine). 3. Lifestyle, including exercise and dietary habits. D. Review of systems. 1. General: Fatigue or diaphoresis. 2. Cardiovascular: Chest pain or palpitations. 3. Pulmonary: Dyspnea on exertion or shortness of breath. 4. Abdominal: Epigastric discomfort, nausea, or vomiting. 5. Peripheral vascular: Claudication or skin changes related to venous stasis and HTN. Physical Examination A. Unremarkable in most patients with stable angina. B. Vital signs: Assess heart rate and rhythm, blood pressure, oxygen saturation, and respiration rate. C. General: Observe patient's level of distress. 1. Levine sign: Fist clenched over sternum is suggestive of angina. D. Skin: Diaphoresis and evidence of poor lipid metabolism (xanthoma) are possible. E. Neck: Carotid bruits and increased jugular venous pres-sure are possible. 3. Cardiac Guidelines

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

41 F. Cardiovascular: Inspect, palpate (pain on chest wall pal-pation is not usually cardiac in nature), and auscultate (par-tially audible S3, S4 due to left ventricular dysfunction and/or murmur of mitral regurgitation as sign of papillary muscle dysfunction). G. Pulmonary: Auscultate lungs for evidence of rales/crack-les (concern for congestive heart failure and pulmonary edema). H. Abdomen: Auscultate for bruits, palpate for discomfort, assess for a pulsatile abdominal mass. I. Peripheral vascular: Assess peripheral pulses, possible venous stasis changes, and peripheral edema. Diagnostic Tests A. ECG: Usually normal in patients with stable angina (if prior MI, could see Q-waves). B. Chest radiograph: Usually normal but evaluate for car-diomegaly, pulmonary edema, pericardial effusion. C. Cardiac biomarkers: Serial troponins, troponin T (c Tn T), and troponin I (c Tn I) to rule out MI. D. Lipid panel to assess for risk of atherosclerosis. E. Complete blood count to assess for underlying exacerbat-ing cardiac factors such as evidence of anemia. F. Complete metabolic panel to assess electrolytes (metabolic dysfunction can lead to arrhythmias) and kidney function (important if cardiac catheterization with contrast dye is needed). G. Stress testing. 1. For a positive stress test and when deemed appropri-ate by the cardiologist and interventional cardiologist, a cardiac catheterization with coronary angiography is performed. During this intervention, contrast dye is injected into the coronary vasculature to aid in the visualization and revascularization of the affected vessel(s). 2. Exercise stress testing. a. Stress ECG: An ECG is performed before, dur-ing, and after treadmill exercise. The test is 75% sensitive if heart rate reaches 85% of maximum pre-dicted value for age. Exercise-induced ischemia results in subendocardial ischemia (ST-segment depression on ECG); can also see hypotension or ventricular arrhythmias. b. Stress echocardiography: Cardiac echocardiogra-phy is performed before and after exercise. i. Exercise-induced ischemia is detected by car-diac wall-motion abnormalities not present at rest. ii. It is more sensitive for detecting ischemia than stress ECG and beneficial for determining left ventricular function. 3. Pharmacologic stress testing (for patients unable to walk on treadmill). a. Intravenous adenosine or dobutamine can be used to replace treadmill activity. b. These agents create cardiac stress, and they can be combined with an ECG, echocardiogram, or nuclear imaging. 4. Nuclear stress testing. a. Thallium or technetium 99m Tc sestamibi are used in patients with baseline ECG abnormalities to localize ischemia. b. Areas of damage will be ill-perfused on imaging. H. Other cardiac diagnostic testing. 1. Computed tomography coronary angiography (CTCA). a. Relatively new test. b. Utilizes electron-beam or multidetector CT imag-ing to evaluate the coronary arteries for level of cal-cium (coronary artery calcium [CAC] score). c. Useful in detecting the amount of atherosclerosis within the coronary arteries. I. The flow chart in Figure 3. 2 can help with diagnosis and risk stratification in angina. Differential Diagnosis A. MI. B. Coronary vasospasm. C. Pulmonary embolus. D. Pericarditis. E. Congestive heart failure. F. Acute gastritis. G. Cholecystitis. H. Ruptured abdominal or thoracic aortic aneurysm. I. Anxiety/panic attack disorders. J. Gastroesophageal reflux/peptic ulcer disease. K. Cocaine toxicity. L. Hypertensive urgency or emergency. M. Valvular abnormalities. N. Hiatal hernia. O. Costochondritis. Evaluation and Management Plan A. General plan. 1. Prevention of MIs and reduction of angina-type symptoms; can consider the ABCDE mnemonic. A:Aspirin and antianginal agents. B:Beta-blockers and blood pressure management. C:Cholesterol management and cigarette smoking abstinence. D:Diet and diabetic management. E:Education and exercise. 2. T reatment using risk stratification considerations. a. Mild disease (normal cardiac function and mild angina): Aspirin, nitrates, and beta-blockers (possibly calcium channel blockers). b. Moderate disease (moderate angina, normal car-diac function, two-vessel coronary disease): Use of medications for mild disease and cardiac catheteriza-tion for revascularization. c. Severe disease (decreased cardiac function, three-vessel/left main/left anterior artery disease with severe angina): Pharmacologic and consideration of coro-nary artery bypass grafting ( CABG). 3. Evaluation of patients with anginal symptoms for acute cardiac ischemia (ST-elevation MI or non-ST-segment elevation MI). 4. For patients with UA, hospitalization for monitor-ing, stabilization, and possible cardiac catheterization (or stress testing if determined safe by cardiologist). B. Patient/family teaching points. 1. Compliance with medications and primary care provider appointments. 2. HTN: Tight blood pressure (BP) control decreases CAD risk, especially in those with diabetes mellitus. 3. Diabetes mellitus: Strict control of blood sugars to reduce macrovascular (CAD) disease. 4. Hyperlipidemia: Using lifestyle modifications and the enzyme hydroxymethylglutaryl-coenzyme A ( HMG-Co A) reductase inhibitors to reduce cholesterol. 5. Obesity: Weight loss, which is imperative for cardio-vascular health. Angina

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42 Stress testing Normal Inactive or elderly patient with mild symptoms Consider alternate diagnosis Positive or nondiagnostic test Consider coronary arteriography Markedly positive test Trial of medical therapy Continue medical therapy Assess LV function (e. g., by echo)Symptoms controlled Symptomatic stable angina Refractory controlled Symptoms consistent with angina pectoris EF ≤ 40%EF > 40% FIGURE 3. 2 Diagnosis and risk stratification in angina. EF, ejection fraction Source: Kasper, D. L., Fauci, A. S., Hauser, S. L., Longo, D. L., Jameson, J. L., & Loscalzo, J. (Eds. ). (2015). Chronic stable angina. Harrison's principles of internal medicine (19th ed. ). New York, NY: Mc Graw-Hill. 6. Diet: Reducing saturated fat ( <7% of total calories) and total cholesterol ( <200 mg/d). 7. Physical activity: Imperative for cardiovascular health; recommend aerobic exercise for 30 minutes/day for 5 to 7 days/week. 8. Tobacco cessation to decrease risk of CAD. C. Pharmacotherapy. 1. Aspirin: Antiplatelet that decreases risk of MI. 2. Beta-blockers: Decrease cardiac work (decrease pulse, BP, contractility), thus lowering myocardial oxygen demand. 3. Nitrates: Work via vasodilation. a. Alleviate angina via reduction of cardiac preload and myocardial oxygen demand. b. Can be administered sublingually, orally, transder-mally, or intravenously. c. Side effects: Flushing, headache, dizziness, and/or hypotension. 4. Phosphodiesterase inhibitors: Caution necessary with medications such as sildenafil, tadalafil, and vardenafil; risk of hypotension. 5. Calcium channel blockers: Decrease cardiac afterload and cause coronary vasodilation to increase coronary blood flow. 6. Lipid lowering agents: HMG-Co A reductase inhibitors to decrease atherosclerosis and risk of MIs. Follow-Up A. Important issues during follow-up visits for patients with angina. 1. Increased or decreased exercise tolerance. 2. Any change in anginal symptoms. 3. Problems with medication compliance. 4. Any changes in modifiable risk factors (diet, activity level, tobacco cessation). 5. Monitoring of management of comorbid conditions that contribute to CAD. B. Additional recommendations. 1. Annual treadmill stress testing for patients with stable CAD. 2. Stress imaging in patients with change in CAD status or who underwent initial stress imaging due to known risk factors. 3. Use of echocardiography to evaluate left ventricular function and wall motion in CAD patients with worsen-ing congestive heart failure or recent MI. Consultation/Referral A. Consult with a cardiologist in patients with angina/CAD for proper risk stratification, diagnostic testing, treatment regimen planning, and ongoing monitoring. B. Consult with an interventional cardiologist for patients requiring cardiac catheterization. C. Consult with a cardiothoracic surgeon for patients requir-ing CABG or those with severe valvular disease requiring repair/replacement. Special/Geriatric Considerations A. Prinzmetal angina. 1. Also known as variant angina caused by coronary vasospasms. 3. Cardiac Guidelines

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43 2. Rare diagnosis: Usually occurs in patients 40 to 60 years of age. 3. Can be provoked by factors such as cold exposure, tobacco use, cocaine use, emotional stress, thyrotoxico-sis, excessive alcohol use, and medications (histamine, serotonin). 4. Underlying atherosclerosis in 75% of patients. 5. Chest pain episodes: Very painful; last approximately 15 minutes and usually occur at rest. 6. Can mimic symptoms of MIs; very difficult to dif-ferentiate on history and physical examination. 7. Hallmark: T ransient ST elevation on ECG during chest pain episodes. 8. Coronary angiography is test of choice: Will see evidence of coronary vasospasm when IV ergonovine is administered (to stimulate chest pain). 9. Can be relieved by antianginal medications. 10. Use of calcium channel blockers and nitrates can be helpful for treatment. B. Geriatric considerations. 1. Age: Not a limitation for evaluation and treatment of CAD. 2. Presentation: Possibly atypical symptoms. 3. Higher incidence of multivessel coronary disease. 4. Greater prevalence of renal impairment (concern for use of contrast dye during catheterization). 5. Higher incidence of polypharmacy: Potential drug interactions and medication compliance. 6. Possibly too risky for surgical intervention, thus requiring only conservative (medical) management. 7. Important to assess baseline cognitive status and comorbidities when discussing treatment plan and to involve family when necessary. Bibliography Agabegi, S. S., & Agabegi, E. D. (2008). Step-up to medicine (2nd ed. ). Philadelphia, PA: Wolters Kluwer. Alaeddini, J., & Shirani, J. (2018, July 19). Angina pectoris. In E. Yang (Ed. ), Medscape. Retrieved from http://emedicine. medscape. com/ article/150215-overview Kasper, D. L., Fauci, A. S., Hauser, S. L., Longo, D. L., Jameson, J., & Loscalzo, J. (Eds. ). (2015). Chronic stable angina. In Harrison's manual of medicine (19th ed. ). New York, NY: Mc Graw-Hill. Arrhythmias Allison Rusgo Definition A. Any change from the normal electrical cardiac conduc-tion: Can result in impulses that occur too quickly, too slowly or erratically. B. Divided into two categories: Ventricular and supraven-tricular. 1. Ventricular abnormalities begin in the ventricles. 2. Supraventricular disorders originate above the ventri-cles (in the atria). C. Can result in tachycardias or bradycardias. 1. With respect to bradycardia: Typically defined as a pulse less than 60 beats/minute and clinically significant when pulse is less than 45 beats/minute. 2. Possible causes of bradycardia: Sick sinus syndrome (SSS) or heart block (first-degree atrioventricular [AV] block, second-degree AV block types 1 and 2, and third-degree AV block). Incidence A. Atrial fibrillation (AF) is the most common sustained car-diac arrhythmia where prevalence increases with age. It affects 2. 7 to 6. 1 million U. S. adults. 1. Median age of AF presentation is 75 years; 84% of patients are older than 65 years of age at time of diagnosis. 2. AF affects 4% of patients younger than 60 years of age and 8% of patients younger than 80 years of age. 3. The incidence of AF is greater in males than in females and more common in Caucasians than in African Americans. B. Approximately 50% of patients experience sudden cardiac death as an initial clinical presentation of a cardiac arrhythmia. 1. The arrhythmias most likely to cause sudden car-diac death are ventricular fibrillation (VF) or ventricu-lar tachycardia (VT), with approximately 300,000 deaths per year. 2. VT is more commonly seen in males secondary to underlying CAD. C. Supraventricular tachycardias: Specifically, paroxysmal supraventricular tachycardia (PSVT) maintains a prevalence of approximately 0. 2% of U. S. population; noted to also increase with age. Pathogenesis A. The pathophysiology of arrhythmias can be complex and vary based on type of abnormality. B. Overall, there is an abnormality in the normal activation sequence of the cardiac fibers within the myocardium. There are three primary mechanisms. 1. Increased or decreased automaticity: Increased auto-maticity can result in atrial or ventricular arrhythmia. 2. T riggered activity. 3. Dysfunction in circulatory pathways: Specifically notable for reentry conduction pathways. C. The pathogenesis of AF occurs because of three underly-ing factors: Electrical, structural, and contractile dysfunction. 1. In the simplest terms, AF's irregularly irregular tachy-cardic rhythm arises because of multiple foci within the atria (principally around orifices of the pulmonary arter-ies) that send chaotic impulses through the heart's elec-trical system. 2. This causes the atria to quiver or “fibrillate” instead of contract normally. 3. Typically, the atrial rate is greater than 400 beat-s/minute, but some impulses are successfully blocked by the AV node. Thus, a ventricular (or calculated pulse) rate of 75 to 175 beats/minutes is appreciated. D. Atrial flutter is a variation of AF where there is one pri-mary automatic focus in the atria that fires between 250 and 350 beats/minute. The ventricular rate is typically one-half to one-third the atrial rate due to a refractory period of the AV node. E. PSVT occurs because of AV nodal reentry tachycardia. 1. T wo pathways within the AV node: Fast and slow. 2. Reentrant circuit revolving around the AV node. F. Ventricular arrhythmias. 1. VT originates below the bundle of His and occurs because of quick and constant firing of three or more pre-mature ventricular contractions (PVCs) at a rate of 100 to 250 beats/minute. 2. PVCs are defined as a heartbeat that fires on its own accord from a specific focus in one ventricle and proceeds to simulate the other ventricle. Arrhythmias

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44 3. VF occurs when there are multiple foci within the ventricles that are functioning on overdrive. This leads to irregular quivering of the ventricles and results in no car-diac output. G. Bradycardias. 1. SSS: Typically occurs because of spontaneous persis-tent bradycardia. 2. First-degree AV block: Noted to have a conduction delay at the AV node that results in decreased pulse. 3. Second-degree AV block. a. Type 1: Occurs because of a block within the AV node to cause bradycardia. b. Type 2: Occurs because of a block within the bun-dle of His-Purkinje fibers to cause bradycardia (this can also progress to third-degree AV block). 4. Third-degree AV block: Complete dissociation between the atria and ventricles. There is no continuation of cardiac impulses between the two structures; results in significant bradycardia, typically 25 to 40 beats/minutes. Predisposing Factors A. AF. 1. Underlying CAD/previous MI. 2. HTN. 3. Mitral valve dysfunction. 4. History of pulmonary embolus. 5. Endocrine and adrenal disorders: Hypothyroidism or hyperthyroidism, pheochromocytoma. 6. Postoperative physiologic stress. 7. SSS. 8. Systemic illnesses such as sepsis or cancers. 9. Excess alcohol consumption (known as “holiday heart syndrome”). 10. Age. B. Atrial flutter. 1. Chronic obstructive pulmonary disease (most com-mon cause). 2. Comorbid CAD. 3. Congestive heart failure (CHF). 4. Atrial septal defects or rheumatic heart disease. C. PSVT. 1. Acute cardiac ischemia. 2. Medications: Most common is digoxin toxicity (causes paroxysmal atrial tachycardia with 2:1 block). 3. Atrial flutter with rapid ventricular response. 4. Excess caffeine, stimulant, or alcohol consumption. D. VT. 1. Comorbid MI and CAD (most common causes). 2. Acute cardiac ischemia or hypotension. 3. Cardiomyopathy. 4. Congenital heart defects. 5. History of prolonged QT syndrome. E. VF. 1. Ischemic cardiac damage (most common cause). 2. Medications: Antiarrhythmic drugs that prolong the QT interval and combination of drugs, particularly antidepressive agents (SSRIs and T ricyclics). Subjective Data A. Common complaints/symptoms. 1. Fatigue. 2. Dyspnea on exertion (or at rest). 3. Chest discomfort. 4. Palpitations or “heart fluttering. ” 5. Dizziness, lightheadedness, syncope, or near-syncope. 6. Diaphoresis. B. History of the present illness. 1. Recognize that patient presentation varies based on type and degree of arrhythmia. a. For example, SSS can present with dizziness, fatigue, and change in mental status while VT can present asymptomatically as sudden cardiac death (if rate is slow enough). 2. Understand onset, provoking/palliative factors, qual-ity, severity, and timing of symptoms. 3. Obtain information regarding a patient's past med-ical history, specifically regarding the aforementioned conditions, that can predispose patients for abnormal heart rhythms. C. Family and social history. 1. Determine any family history of CAD, HTN, hyper-lipidemia, valvular heart disease (VHD), congenital heart defects, or arrhythmias. 2. Obtain information on tobacco use, alcohol/caffeine consumption, and illegal substance use (especially stimu-lants). D. Review of systems. 1. General: Fatigue, malaise, fevers, and chills. 2. Cardiac: Angina, racing heartbeat, palpitations, decreased exercise tolerance, and peripheral edema. 3. Pulmonary: Shortness of breath and dyspnea on exer-tion. 4. Neurological: Lightheadedness, dizziness, syncope, and near-syncope. Physical Examination A. Vital signs: Assess heart rate, blood pressure, respiration, temperature, and oxygen saturation. 1. Important to note temperature, as an underlying febrile illness can exacerbate underlying AF. 2. In VF, it is likely that the patient will be unconscious with no pulse and unmeasurable BP. B. Neck: Jugular venous distention (JVD; concern for CHF). C. Pulmonary: Possible rales or crackles (sign of increased fluid accumulation as related to underlying CHF). D. Cardiac: Inspection and palpation for thrills and auscul-tation. 1. Auscultation. a. Assess rate (tachycardic or bradycardic). b. Rhythm (regular, irregularly irregular, or irregu-larly regular). c. Extra heart sounds (S3and S4). d. Murmurs consistent with underlying VHD. E. Peripheral vascular: Assess peripheral pulses, possible peripheral edema (sign of fluid overload and concomitant CHF). F. Neurology: Mental status examination (if mental status changes) or complete neurological examination if concern for associated syncope/near-syncope. Diagnostic Tests A. ECG. 1. AF: Tachycardia rate (110-180 beats/minute), irreg-ularly irregular rhythm (irregularly spaced R-R intervals) with no discernable P-waves. 2. Atrial flutter: Tachycardic rate with a “saw-tooth” (F-wave) baseline pattern; best seen in leads VI, II, III and a VF where the QRS complex appears after several “saw-tooth” P-waves (number of F waves can vary depending on atrioventricular node [AVN] blockade). 3. Cardiac Guidelines

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45 3. VF: Irregular rhythm, no identifiable P-waves, or QRS complexes. 4. VT: Tachycardic rate (150-250 beats/minute) and wide QRS complexes (can have identical morphologies in monomorphic VT or different ones in polymorphic VT). 5. PSVT (most common etiology of reentry conduc-tion): Tachycardic rate, narrow QRS complexes with no discernable P-waves (P-waves are buried within the QRS complexes secondary to simultaneous rapid firing of the atria and ventricles). 6. First-degree heart block: Hallmark is a PR interval greater than 0. 20 seconds where a QRS complex follows each P-wave. 7. Second-degree heart block. a. Type 1 (Mobitz Type I or Wenckebach): Hallmark is progressive prolongation of the PR interval with a nonconducted P-wave. The longest PR interval pre-ceding the dropped QRS and the shortest immedi-ately after. b. Type 2 (Mobitz Type II): Hallmark is an inter-mittent nonconducted P-wave without progressive prolongation, but immediate PR interval to dropped QRS is prolonged. 8. Third-degree heart block: Bradycardic rate, with no discernable pattern or connection between P-waves and QRS complexes. B. Laboratory tests. 1. Complete blood count with differential: Determine if an anemia is contributing to the arrhythmia. 2. Complete metabolic panel: Determine if an elec-trolyte disturbance or renal dysfunction is contributing to the arrhythmia. 3. Thyroid panel: Hypothyroidism or hyperthyroidism can be an underlying etiology for arrhythmias (i. e., thy-rotoxicosis can trigger AF). 4. Cardiac biomarkers: These should be obtained in any patient with chest discomfort or evidence of an arrhythmia; they evaluate for the possibility of underlying myocardial infarction. 5. Digitalis level (if clinically indicated): Supratherapeu-tic levels can lead to various arrhythmias, including PSVT and AF with rapid ventricular response. 6. Toxicology screening (if clinically indicated): Illegal substances, especially stimulants, can precipitate arrhyth-mias. 7. D-dimer: This can help rule out a pulmonary embo-lus, which can occur in the setting of AF. C. Chest x-ray: Checks for underlying cardiomegaly, pul-monary edema, or pulmonary infections such as pneumo-nia, or pneumothorax, which can exacerbate or precipitate arrhythmias. D. Exercise stress testing: Helps provide an overall under-standing of one's cardiovascular health and evaluate for underlying ischemia. E. Holter monitor or loop recorder: Can be helpful for mon-itoring patients on a continuous basis when an arrhythmia is suspected but unable to be captured via ECG; can also be helpful for patients with vague or nonspecific cardiac symp-toms. F. T ransesophageal echocardiogram (TEE): Especially important for new-onset arrhythmias to evaluate overall cardiac function (ejection fraction [EF]), identify VHD, and measure atria and ventricle sizes. 1. With AF, if there is concern for a thrombus, particu-larly within the left atrial appendage, the test of choice is a TEE. Differential Diagnosis A. AF. B. Atrial flutter. C. VF. D. Ventricular flutter. E. Atrial tachycardia. F. PSVT. G. SSS. H. First-degree heart block. I. Second-degree heart block types 1 and 2. J. Third-degree heart block. Evaluation and Management Plan A. General plan. 1. Determine type of arrhythmia. 2. Stabilize heart rate and rhythm based on clinical sce-nario using pharmacologic or procedural methods such as electrocardioversion or transcutaneous/transvenous pacing. 3. Evaluate underlying cardiac status and comorbidities to guide treatment plan. 4. Determine if arrhythmia is secondary to an under-lying etiology that requires additional management (i. e., sepsis, thyrotoxicosis, myocardial infarction). 5. Consult with cardiologist (and electrophysiologist) if device implantation or ablation procedures are required. 6. For arrhythmias requiring anticoagulation (AC) for thromboembolic prophylaxis, such as AF, complete risk stratification assessment, and discuss risks and benefits of these medications with patients and families. a. Utilize the CHA2DS2-VASc score, which is a risk stratification tool to determine the chance of throm-boembolic strokes (see Table 3. 2). b. For patients with a score of 2 +, oral AC is recom-mended using a vitamin K antagonist (i. e., warfarin with international normalized ratio [INR] goal 2. 0-3. 0) or a novel anticoagulant (i. e., dabigatran, rivarox-aban, edoxaban, or apixaban). c. For patients with a score of “0” in males or “1” in females, no therapy is recommended. B. Patient/family teaching points. 1. Educate regarding specific arrhythmia and symptoms that can precipitate recurrence (if clinically relevant). 2. Educate on reasons to return to the ED, specifically those that signal worsening cardiac status or development of a life-threatening arrhythmia. 3. Educate on the importance of medication compliance and regular follow-up appointments with cardiologist/ electrophysiologist. 4. For patients utilizing warfarin for AC, it is important to discuss dietary restrictions. It is also essential to educate patients on any anticoagulant regarding risk of bleeding. 5. For implantable devices—ensure patients understand the purpose of their device, importance of device mainte-nance, who to contact if there is an equipment malfunc-tion, and how device monitoring will occur. C. Pharmacotherapy. 1. Acute AF/atrial flutter. a. Rate control: Target rate is 60 to 100 beats/ minute. Arrhythmias

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46 i. Calcium channel blockers are preferred (can use beta-blockers). ii. If there is significant left ventricular dysfunc-tion, consider digoxin or amiodarone. iii. For patients with chronic AF: Can utilize cal-cium channel blockers or beta-blockers for long-term rate control. b. Rhythm control. i. Can utilize electrical or pharmacological methods (electrical cardioversion is preferred). ii. If pharmacologic conversion, consider options such as sotalol, flecainide, amiodarone, dofetilide. c. AC: Assess need based on risk stratification tools and comorbidities. i. If a patient is hemodynamically unstable, ini-tiate immediate electrical cardioversion to convert to normal sinus rhythm regardless of AC consid-erations. ii. If a patient is hemodynamically stable and AF is under hypothermic conditions, gradual slow rewarming via a warming blanket is recom-mended. iii. AF present for greater than 48 hours (or unknown period of time), there is high risk of stroke if electrical cardioversion is performed immediately; recommend AC for 3 weeks before and at least 4 weeks after successful cardioversion (INR goal 2. 0-3. 0 if using warfarin). iv. To expedite cardioversion timing: Obtain TEE to rule out thrombus in left atrial appendage, administer IV heparin, cardiovert within 24 hours, and then utilize oral AC agent for 1 month. v. If a patient is hemodynamically stable and AF is present for less than 48 hours, electrical car-dioversion without prior AC or TEE can occur at the discretion of the cardiologist and must take into account a patient's CHA2DS2VASc Score. If the procedure is completed, postprocedure AC is also utilized for 1 month. 2. PSVT. a. If hemodynamically stable, first attempt vagal maneuvers such as Valsalva, breath holding, or immersion of head in cold water. TABLE 3. 2 CHA2DS2VASc Score for Risk Assessment in AF Criteria Score C Congestive heart failure 1 H Hypertension: Blood pressure consistently above 140/90 mm Hg (or treated hypertension on medication)1 A2 Age≥75 y 2 D Diabetes mellitus 1 S2 Prior stroke or transient ischemic attack 2 V Vascular disease (e. g., peripheral artery disease, myocardial infarction, aortic plaque)1 A Age 65-74 y 1 Sc Sex (i. e., female gender) 1 AF, atrial fibrillation. b. If nonpharmacological maneuvers are unsuccess-ful, administer intravenous adenosine (drug of choice) to reduce sinoatrial (SA) and AV node activity using a short-acting medication. c. If adenosine is unsuccessful in converting acute PSVT to normal sinus rhythm, the most common intravenous alternatives are beta-blockers (i. e., meto-prolol, propranolol, esmolol) or calcium channel blockers (i. e., verapamil, diltiazem) for patients with-out left ventricular dysfunction; for individuals with heart failure or structural heart disease, intravenous amiodarone can be used. d. If pharmacologic methods are unsuccessful or the patient is hemodynamically unstable, perform electri-cal cardioversion (almost always successful). e. For long-term rate control, beta-blockers and cal-cium channel blockers are used. Digoxin can also be used in the setting of heart failure; if symptoms are recurrent and persistent, refer to electrophysiologist for ablation. 3. VT. a. If sustained VT (lasts longer than 30 seconds, usu-ally symptomatic and with hemodynamic instability), initiate immediate electrical cardioversion and then intravenous amiodarone to maintain sinus rhythm. i. If sustained VT without hemodynamic com-promise and mild symptoms, consider intra-venous medications such as sotalol, procainamide, or lidocaine. ii. If sustained VT and abnormal EF, placement of ICD for long-term management will likely be required. b. If nonsustained VT (brief asymptomatic episodes of VT) without cardiac comorbidities, do not treat (no increased risk of morbidity). i. If nonsustained VT with underlying cardiac disease, consider ICD as first-line long-term man-agement. 4. VF. a. Medical emergency that requires immediate CPR and defibrillation. b. Imperative to follow Advanced Cardiac Life Sup-port (ACLS) algorithm for pharmacologic recom-mendations. 5. Bradycardic rhythms. a. For several types of bradycardias, including SSS, second degree heart block type 2, and third degree heart block, pacemaker implantation is the most effec-tive long-term monitoring strategy. b. Pharmacologic interventions. i. Atropine: Can utilize for acute symptomatic bradycardia (if reversible cause not identified). ii. Dopamine: Second-line drug for symptomatic bradycardia if atropine is ineffective. iii. Epinephrine: Can utilize as an infusion for symptomatic bradycardia if atropine or pacing methods are unsuccessful. D. Discharge instructions. 1. Ensure patients receive all appropriate prescriptions prior to discharge. 2. Ensure patients have prearranged follow-up appoint-ments with cardiologist/electrophysiologist. 3. For patients with newly implanted devices, ensure information is provided regarding the device, clinic follow-up, and home monitoring systems (if indicated). 3. Cardiac Guidelines

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47 a. Educate on proper wound care of incision site for a newly implanted device and reasons to return to a healthcare provider for signs of infection (i. e., ery-thema, edema, worsening pain, drainage, dehiscence, systemic symptoms). 4. Understand that it is important that patients under-stand limitations regarding physical activity, depend-ing on their type and degree of arrhythmia and cardiac status. Follow-Up A. Ensure patient compliance with all medications, particu-larly with respect to antiarrhythmic or AC therapy. 1. Patients on antiarrhythmic therapy should have close follow-up with a cardiologist or electrophysiologist to minimize adverse effects. a. Patients utilizing amiodarone should have a clear understanding of its side effects and monitor closely for amiodarone-induced liver, lung, thyroid, and other organ toxicities. 2. Patients on AC therapy with warfarin should under-stand their follow-up plan with regard to frequency of INR monitoring and how dosing adjustments will be communicated. B. Outpatient oral medication choices for arrhythmias depend on degree of ventricular dysfunction, type of arrhyth-mia, and comorbidities. C. Patients should have close monitoring of their electrolytes to reduce the risk of arrhythmias secondary to electrolyte imbalances. D. Patients with ICDs and pacemakers require regular outpatient device follow-up at electrophysiology clinics where their devices are monitored for lead integrity and battery-life. Consultation/Referral A. Consult with cardiologist to further evaluate arrhythmia and underlying cardiac status. B. Consult with electrophysiologist for in-depth electro-physiologic diagnostics and ablative procedures. Special/Geriatric Considerations A. Additional device considerations. 1. Temporary pacemakers. a. T ranscutaneous pacing. i. Used for symptomatic bradycardias if the patient fails to respond to atropine, dopamine, or epinephrine (can also be utilized in setting of tachyarrhythmias to break the conduction distur-bance). ii. Should be started immediately if patient is hemodynamically unstable, especially in those with second degree heart block type II or third degree heart block. iii. Can be painful; use analgesia and sedation for pain control. iv. Use transvenous pacing if transcutaneous pac-ing is unsuccessful (cardiologist or electrophysiol-ogist should be consulted prior to initiation). 2. Permanent pacemakers. a. Single-chamber pacemakers: Stimulate either the atria or (more commonly) the ventricle. b. Dual-chamber pacemakers: Send electrical impulses to both the atrium and the ventricle;provides synchronization that closely mimics the natural heartbeat (commonly used for bradycardias). c. Biventricular pacemakers: Pace the rhythm of the ventricles so that the chambers contract simultane-ously; used in patients with heart failure and conduc-tion abnormalities. d. Combination pacemaker: Have pacemaker and defibrillation functions. 3. Implantable cardiac defibrillator: Surgically placed and functions by detecting lethal cardiac arrhyth-mias and delivering electrical shocks until the rhythm normalizes; indicated in VF and/or VT that is uncon-trolled with medication (important prevention for sud-den cardiac death). B. Geriatric considerations. 1. Aging process is associated with the development of arrhythmias, particularly AF. 2. Degenerative changes of the cardiac conduction sys-tem (i. e., SA and AV nodes) are more common in elderly patients, who are more likely to experience heart blocks due to conduction delays. 3. Elderly patients are more likely to have ventricular heart disease and thus a higher risk of arrhythmias sec-ondary to structural abnormalities (especially within the aortic and mitral valves). 4. During the physiologic aging process, the PR interval can be prolonged. 5. Geriatric patients can report vague complaints (i. e., weakness, fatigue, malaise) as presenting symptoms for an arrhythmia. It can be difficult to separate these from the normal aging process. 6. The frequency of PVCs also increases with age. 7. If considering a device for geriatric patients, it is important to address comorbidities, life span, impact on quality of life, maintenance of device, and occurrence of unnecessary shocks during end-of-life care. 8. The use of anticoagulants in the geriatric population should be carefully reviewed with patients (and family members, if necessary) to ensure that risks versus bene-fits of these medications are evaluated. a. Cognitive status (important for medication com-pliance). b. Comorbidities (e. g., is patient already utiliz-ing other antiplatelet or anticoagulant agents, thus increasing the risk of bleeding events?). c. Overall functional status—important to address risk of falls and bleeding complications. Bibliography Agabegi, S. S., & Agabegi, E. D. (2008). Step-up to medicine (2nd ed. ). Philadelphia, PA: Wolters Kluwer. Bashore, T. M., Granger, C. B., Jackson, K. P., & Patel, M. R., Heart dis-ease. In M. A. Papadakis, S. J. Mc Phee, & M. W. Rabow (Eds. ), Current medical diagnosis & treatment 2018 (57th ed., pp. 328-446). New York, NY: Mc Graw-Hill. Gugneja, M., & Kraft, P. L. (2017, April 5). Paroxysmal supraventricular tachycardia. In M. F. El-Chami (Ed. ), Medscape. Retrieved from http: //emedicine. medscape. com/article/156670-overview Med Calc 3000. (2011). Atrial fibrillation CHA2DS2-VASc score for stroke risk. Retrieved from https://reference. medscape. com/calculator/chads-vasc-af-stroke Rosenthal, L., Mc Manus, D. D., & Sardana, M. (2018, July 18). Atrial fibrillation. In J. N. Rottman (Ed. ), Medscape. Retrieved from http: //emedicine. medscape. com/article/151066-overview Sohinki, D., & Obel, O. A. (2014). Current trends in supraventricular tachycardia management. The Ochsner Journal, 14 (4),586-595. Retrieved from https://www. ncbi. nlm. nih. gov/pmc/articles/PMC4295736 Arrhythmias

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48Dyslipidemia Allison Rusgo Definition A. Hyperlipidemia: Elevation of total cholesterol (TC), phospholipids, or triglycerides (TG). B. Hyperlipidemia can be inherited or caused by secondary diagnoses. C. It increases the risk of atherosclerosis, leading to stroke and heart disease. D. Dyslipidemia: Elevation of plasma cholesterol, TGs, or both, or a decreased high-density lipoprotein level (HDL) that augments atherosclerosis. Incidence A. Framingham Heart Study noted an epidemiological link between elevated cholesterol and atherosclerotic cardiovascu-lar disease (ASCVD). B. Current statistics also show that elevated cholesterol is responsible for an estimated 2. 6 million deaths per year worldwide. C. An estimated 31% of U. S. adults have elevated TG (>150 mg/d L). Pathogenesis A. Disease process starts in gastrointestinal tract with hydroxymethylglutaryl-coenzyme A (HMG-Co A). B. HMG-Co A is a precursor that undergoes complex bio-chemical reactions to produce cholesterol. C. Once synthesized, cholesterol travels through the plasma. D. The liver also plays a role, converting very low-density lipoprotein (VLDL) to low-density lipoprotein (LDL), which moves through the plasma. E. Also, dietary cholesterol that moves from the small intestines to the liver through the serum with LDLs must be considered. F. Cholesterol is an important organic molecule for cell membrane integrity and serves as precursor to steroid hor-mones, vitamin D, and bile acid. However, with increased levels of cholesterol, concern is for atherosclerosis. G. Atherosclerosis is an inflammatory process where various cells and mediators undergo a cascade of reactions to form plaques in the vasculature. 1. Various factors trigger inflammation, such as elevated glucose, tobacco by-products, elevated blood pressure (BP), and oxidized LDLs. 2. With increased inflammation, there is increased per-meability and injury to vessel walls. The result is increased accumulation of LDLs within the tunica intima layer of the vasculature. 3. The inflammation causes increased activation of inflammatory mediators (i. e., monocytes and macrophages). 4. Inflammatory mediators uptake the oxidized LDLs, leading to transformation of macrophages into foam cells, also known as “fatty streaks” within the vasculature. 5. Foam cells eventually result in plaque formation with fibrous caps; when the thin top layer of these caps dislodges, exposing highly thrombotic necrotic con-tents, platelet aggregation and cardiac ischemia can result. Predisposing Factors A. Hereditary: Genetic component for the metabolism of LDL. 1. Familial hypercholesterolemia (FH): A type of hyperlipidemia (HLD) caused by genetic mutation (chro-mosome 19) where those affected have TC greater than 300 mg/d L and LDL greater than 200 mg/d L (other vari-ations exist with TC >1,000 mg/d L). B. Diet: Foods high in saturated fat and cholesterol. C. Lifestyle: Physical inactivity, which can lead to increased cholesterol levels. D. Comorbidities. 1. Secondary causes of hyperlipidemia: Hypothy-roidism, diabetes mellitus (DM), nephrotic syndrome, Cushing disease, chronic kidney disease (CKD), and medications (oral contraceptives, diuretics). 2. Secondary causes of elevated TGs: Obesity, DM, alco-hol use, CKD, and medications (estrogen). 3. Concern for metabolic syndrome: Large waist circum-ference, elevated TGs, low HDL level, elevated BP, ele-vated glucose levels. Subjective Data A. Common complaints/symptoms. 1. Rarely any complaints from hyperlipidemia alone. 2. Concern exists from its sequelae, such as cardio-vascular disease, peripheral vascular disease (PVD) sec-ondary to claudication, and neurological diseases (i. e., transient ischemic attack [ TIA] and cerebrovascular accident [ CVA]). B. Common history of present illness (HPI). 1. Determine the duration of a patient's hyperlipidemia diagnosis and how the diagnosis occurred (i. e., detected during routine screening versus after an acute event such as an myocardial infarction [MI] or CVA/TIA). 2. Assess a patient's routine monitoring of his or her cholesterol—when levels were last checked and how they have evolved over time. 3. Assess a patient's past medical history for associated comorbidities such as hypertension (HTN), MI, periph-eral artery disease (PAD)/PVD, coronary artery disease (CAD), carotid artery stenosis, or DM II. It is also impor-tant to assess for any underlying liver disease, which is a contraindication to statin use. 4. If a patient is utilizing lipid-lowering medication, assess for side effects, such as myopathies that are com-monly appreciated in statin use. If a patient is utilizing nonpharmacological interventions, such as diet and exer-cise, those interventions should also be reviewed. 5. Determine if a patient is experiencing any cardiovas-cular or neurological complaints as a result of the hyper-lipidemia. C. Family and social history. 1. Assess for family history of hyperlipidemia, dyslipi-demia, CAD, DM type 2, PVD, PAD, and neurological complications (CVA, TIA). 2. Understand dietary routine, exercise/activity levels, and use of tobacco and alcohol consumption. D. Review of systems. 1. Evidence of weight gain. 2. Skin changes: Yellow deposits (xanthomas). 3. Cardiac symptoms: Chest pain, palpitations, decreased exercise tolerance, shortness of breath, and dyspnea on exertion. 4. Peripheral vascular status: Claudication. 5. Neurological (if concern for CVA or TIA): Changes in mental status, vision, speech, sensation, and strength. 3. Cardiac Guidelines

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49 Physical Examination A. Vital signs: Determine body mass index (BMI) and con-sider comorbid HTN. B. Skin: Check for xanthomas. C. Ophthalmologic: Perform funduscopic examination and check for possible corneal arcus. D. Neck: Auscultate carotid arteries and evaluate for carotid bruits. E. Cardiovascular: Inspect for lifts/heaves/visible pulsations, assess point of maximum impulse (PMI), palpate for thrills, and auscultate using diaphragm and bell for murmurs and extra heart sounds. F. If concern for CVA/TIA—consider complete neurologi-cal examination. Diagnostic Tests A. For the evaluation of dyslipidemia, the U. S. Preventive Services Task Force (USPSTF) strongly recommends (level A evidence) the routine screening of males 35 years old and older and females 45 years old and older for lipid disorders. B. Evaluation should consist of fasting (9-12 hours fast) lipid panel for TC, LDL, and HDL (see Table 3. 3). C. For secondary causes of dyslipidemia, workup should include a complete blood count, complete metabolic panel, fasting glucose, thyroid-stimulating hormone (TSH), and urinary protein. D. Lipid measurement should be accompanied by evaluation for other cardiovascular risk factors, including an ECG, stress testing, and echocardiogram. Differential Diagnosis A. The focus of the differential diagnosis in dyslipidemia is on primary versus secondary causes. 1. Primary causes—inherited disorder. 2. Secondary causes. a. Hypothyroidism. b. Corticosteroids. c. Alcoholism. d. Smoking. e. Obstructive liver disease. TABLE 3. 3 Diagnostic Interpretation of Lipid Panel LDL Cholesterol (mg/d L) <100 Optimal 100-129 Near optimal 130-159 Borderline high 160-189 High >190 Very high HDL Cholesterol (mg/d L) <40 Low >60 High TC (mg/d L) <200 Preferable 200-239 Borderline high >240 High HDL, high-density lipoprotein; LDL, low-density lipoprotein; TC, total cholesterol. f. Renal failure. g. Uncontrolled diabetes. h. Nephrotic syndrome. Evaluation and Management Plan A. General plan. 1. The National Cholesterol Education Program (NCEP) and Adult T reatment Panel (ATP) III have created a process for the management of elevated choles-terol. 2. Determine LDL, TC, and HDL levels. 3. Identify any comorbidities, including cardiovascular disease or its equivalents (DM, PAD, abdominal aortic aneurysm). 4. Identify modifiable and unmodifiable risk factors: Low HDL, tobacco use, HTN, age (males >45 years and females >55 years), and family history of CAD. 5. Assess overall cardiovascular risk and determine goal LDL. 6. Initiate therapeutic lifestyle changes (TLC) plan if LDL is higher than goal: Consists of increased physical activity, weight management, and low trans fat and low cholesterol diet. 7. Utilize medications if LDL remains above goal. 8. Assess for metabolic syndrome and evaluate TGs. 9. T reat elevated HDL and TGs if required. B. Patient/family teaching points. 1. Emphasize medication compliance, use of TLC plan, and elimination of modifiable risk factors (i. e., tobacco cessation). 2. Stress importance of compliance with clinician appointments. C. Pharmacotherapy. 1. Lipid management. a. Statins (HMG-Co A reductase inhibitor). i. Important considerations regarding side effects of statins. ii. Elevation in liver enzymes (usually alanine aminotransferase [ALT]). iii. Myalgias: Occurs in approximately 10% of patients, can be dose dependent; switching to dif-ferent statin can help relieve symptoms. iv. Rhabdomyolysis: Myalgias plus creatine kinase (CK) levels greater than 10,000 U/L can result in renal failure. v. Myositis: Myalgias with CK less than 10,000 U/L. b. Bile acid sequestrants. c. Cholesterol absorption inhibitors. d. Injectable medications (monoclonal antibodies); works by allowing liver to absorb increased level of cholesterol, thus decreasing circulating plasma choles-terol). 2. Medications for high TG. a. Fibrates. b. Niacin. c. Omega-3 fatty acids supplements. Follow-Up A. Check lipid levels per American College of Cardiology (ACC) and American Heart Association (AHA) recommen-dations, which stipulate checking levels at 4 to 12 weeks after initiating (or changing) statin therapy and then every 3 to 12 months thereafter. B. Obtain baseline liver and CK levels before initiating statin therapy (routine monitoring not required). Dyslipidemia

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50 Consultation/Referral A. Consult with lipidologist in the following situations. 1. Suspicion for primary genetic disorder. 2. Unsuccessful treatment plans despite optimal therapy and patient compliance. 3. Comorbid liver disease if limiting therapeutic options. 4. Young adults in whom long-term therapy and moni-toring is a consideration. Special/Geriatric Considerations A. Patients with statin intolerance. Use the following. 1. Lower intensity statin or nondaily moderate intensity statin. 2. Low-dose statin with selective cholesterol-absorption therapy (ezetimibe), bile acid sequestrants, or niacin. 3. Nonstatin monotherapy with goal of 30% reduction in LDL levels. B. Geriatric considerations. 1. Patients at least 65 to younger than 80 years of age with ASCVD or DM: Consider moderate or high inten-sity statin (once risks/benefits assessed by provider and patient). 2. For secondary cardiovascular prevention in patients 80 years of age or older: Consider moderate inten-sity statin once risks/benefits assessed by provider and patient. Bibliography Lloyd-Jones, D. M., Morris, P. B., Ballantyne, C. M., Birtcher, K. K., Daly, D. D., Jr., De Palma, S. M., & Smith, S. C., Jr. (2017, October). 2017 focused update of the 2016 ACC expert consensus decision pathway on the role of non-statin therapies for LDL-cholesterol lowering in the management of atherosclerotic cardiovascular disease risk. Journal of the American College of Cardiology, 70 (14), 1785-1822. doi:10. 1016/j. jacc. 2017. 07. 745 National Cholesterol Education Program, National Heart, Lung, and Blood Institute, National Institutes of Health. (2001, May). NIH Publication No. 01-3670. Retrieved from https://www. nhlbi. nih. gov/files/docs/guidelines/atp3xsum. pdf. Prabhakaran, D., Anand, S., Gaziano, T. A., Mbanya, J.-C., Wu, Y., & Nugent, R. (2017). Disease control prior-ities: Cardiovascular, respiratory, and related disorders (3rd ed., Vol. 5). Washington, DC: World Bank. Retrieved from https://openknowledge. worldbank. org/handle/10986/28875. License: CC BY 3. 0 IGO Reamy, B. V. (2011). Dyslipidemias. In J. E. South-Paul, S. C. Matheny, & E. L. Lewis (Eds. ), CURRENT diagnosis & treatment in family medicine (3rd ed., pp. 224-228). New York, NY: Mc Graw-Hill. Tsai, S. A., Ravenell, J., Fernandez, S., Schoenthaler, A., Kenny, K., & Ogedegbe, G. (2014). Cardiovascular disease prevention. In S. S. Gorin (Ed. ), Prevention practice in primary care. (pp. 120-149). New York, NY: Oxford University Press. Tsao, C. W., & Vasan, R. S. (2015, December 1). Cohort profile: The Fram-ingham Heart Study (FHS): Overview of milestones in cardiovascular epidemiology. International Journal of Epidemiology, 44 (6), 1800-1813. doi:10. 1093/ije/dyv337 Heart Failure Allison Rusgo Definition A. Inability of the heart to meet the metabolic demands of the body. B. Left-sided heart failure (HF): Further classified by the functional capacity of the left ventricle via ejection fraction (EF). 1. Heart failure with preserved ejection fraction (HFp EF). a. EF at least 40%. b. Occurs when the ventricle is unable to properly fill during diastole (muscle has stiffened). c. Amount of available blood for circulation is decreased. 2. Heart failure with reduced ejection fraction (HFr EF). a. EF less than 40%. b. Occurs when ventricle has lost its normal contrac-tile ability. c. Force/amount of blood pumped during systole is decreased. C. Right-sided HF: An additional subtype of HF; usually occurs secondary to HFr EF, but also seen in HFp EF, idio-pathic pulmonary arterial hypertension (IPAH), and chronic obstructive pulmonary disease (COPD). 1. Left ventricular dysfunction causes an increase in fluid pressure that travels into the lungs and affects the right ventricle (RV). 2. This results in fluid accumulation in the peripheral system. D. High-output HF: A subtype of HF where there is an increase in the body's oxygen demands (i. e., chronic anemia, pregnancy, hyperthyroidism). 1. Increased demand forces the heart to work harder to meet these needs. 2. This eventually results in decreased cardiac function. E. HF can be defined by the New York Heart Associ-ation (NYHA) classification, which is a method to cat-egorize severity of HF based on patient symptoms (see Table 3. 4). Incidence A. HF affects approximately 5. 7 million Americans, with 850,000 new cases diagnosed per year. B. Prevalence of HF increases with age, doubling with each decade of life and exceeding 10% in males and females older than 80 years. C. HF is the leading cause of hospital admissions for patients older than 65 years of age. D. HF is the second most common cardiovascular diagnosis evaluated during outpatient primary care visits. E. Overall, the United States spends more than 30 billion dollars per year on HF. TABLE 3. 4 NYHA Classification of HF Class I Nearly asymptomatic; can experience HF symptoms (angina, palpitations, dyspnea) with very vigorous sporting activities Class II Slight limitation of physical activity where ordinary activities (i. e., climbing steps) causes HF symptoms; no symptoms at rest Class III Marked limitation of physical activity where very basic activity (i. e., walking on a flat surface) causes HF symptoms; no symptoms at rest Class IV Unable to perform any activity without symptoms of HF; symptoms also present at rest, disease is Incapacitating HF, heart failure; NYHA, New York Heart Association. 3. Cardiac Guidelines

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51 Pathogenesis A. During the aging process, the heart develops a decreased ability to respond appropriately to normal stressors (i. e., physical activity) or disease states (i. e., hypertension [HTN] or myocardial infarctions [MIs]). B. Four major pathophysiologic changes have been identified. 1. Decreased ability to reach maximum heart rate and contractility under stressful conditions (secondary to impaired beta-adrenergic activity). 2. Increased stiffness of coronary and peripheral vascula-ture: This affects EF and causes increased afterload. 3. Altered diastolic filling ability. 4. Insufficient amount of energy production (on a cel-lular level) to meet the needs of the heart under stressful physiologic and/or pathophysiologic conditions. Predisposing Factors A. Coronary artery disease (CAD; MI/ischemic cardiomy-opathy). B. HTN/hyperlipidemia. C. Valvular heart disease (VHD; atrial stenosis [AS], atrial regurgitation [AR], mitral stenosis [MS], mitral regurgitation [MR]). D. Peripheral vascular disease. E. Connective tissue diseases (i. e., sarcoidosis). F. Arrhythmias (new onset/persistent atrial fibrillation, ven-tricular arrhythmias, bradyarrhythmias). G. Cardiomyopathies (alcohol related; nonischemic, restric-tive, or hypertrophic; medication related). H. Infectious (myocarditis, pericarditis, endocarditis). I. High-output HF (anemia of chronic disease, pregnancy, hyperthyroidism, thiamine deficiency, atrioventricular [ AV] shunting). J. Noncardiac etiologies: Pulmonary embolus, pneumonia, exacerbation of COPD. Subjective Data A. Common complaints/symptoms. 1. Shortness of breath (SOB) or dyspnea (during activity or rest). 2. Fatigue or generalized weakness. 3. Decreased exercise tolerance. 4. Orthopnea: Manifests as difficulty breathing while supine; relieved with head elevation using pillows. 5. Paroxysmal nocturnal dyspnea (PND): Sudden awak-ening during sleep secondary to acute SOB. 6. Nonproductive cough (worse at night). 7. Confusion/change in mental status: Due to inade-quate cerebral perfusion in late stages of HF. 8. Swelling of extremities: Secondary to volume overload. B. History of the present illness. 1. Determine chief complaint that is associated with HF and evaluate the onset, provoking factors, palliative fac-tors, quality, and severity and timing of the symptoms. 2. Determine if this is an initial presentation or exacer-bation of a previously diagnosed HF. 3. Evaluate the past medical history for known HF, pre-vious MI, HTN, HLD, diabetes mellitus (DM), car-diomyopathies, congenital heart defects, sleep apnea, renal disease, or collagen vascular diseases. 4. Determine if a previous cardiac evaluation was per-formed (i. e., ECG, stress test, echocardiogram, cardiac catheterization). C. Family and social history. 1. Determine past and present tobacco use, alcohol con-sumption, and use of illegal substances. 2. Review daily diet and nutrition information. 3. Determine frequency and degree of physical activity routines. 4. Evaluate family history for cardiac diseases such as HF, MI, HTN, hyperlipidemia, CAD, and cardiovascu-lar equivalents (i. e., DM). a. If there is evidence of cardiomyopathy, the Heart Failure Society of America recommends an in-depth three-generation family history evaluation for cardiovascular diseases, especially those related to car-diomyopathies. D. Review of systems. 1. General: Fatigue, malaise, weight changes, appetite changes, and generalized weakness. 2. Skin/nails: Changes in nail shape (i. e., clubbing). 3. Cardiac: Chest discomfort, palpitations, decreased exercise tolerance, and peripheral edema. 4. Pulmonary: Nonproductive cough, SOB, dyspnea on exertion, orthopnea, PND. 5. Gastrointestinal: Bloating, nausea, changes in bowel habits. 6. Genitourinary: Oliguria, nocturia. 7. Neurological: Syncope, near-syncope, confusion, memory impairment, sleep disturbances, headaches. 8. Psychological: Anxiety, irritability. Physical Examination A. Assessment of HF patients can vary based on stage of dis-ease and underlying comorbidities. B. The most common physical examination findings are based on severity (see Table 3. 5). Diagnostic Tests A. The American Heart Association ( AHA), American Col-lege of Cardiology ( ACC), and Heart Failure Society of America recommend the following tests in the evaluation of HF. 1. Complete blood count: Identify anemias or infec-tions as underlying factors of HF. 2. Complete metabolic panel: Identify electrolyte imbalances (especially important for patients using diuretics). 3. Renal function: Identification of underlying kidney dysfunction (decreased renal perfusion) as a marker for HF. 4. Fasting glucose: Helps identify underlying DM as a contributing factor to overall cardiovascular health. 5. Natriuretic peptides (brain natriuretic peptide [BNP] or pro-BNP): Help evaluate ventricular pressure and volume status. 6. Liver function panel: Evaluate aspartate aminotrans-ferase (AST) and alanine aminotransferase (ALT), which can be elevated in cardiac cirrhosis or congestive hep-atomegaly as a result of long-standing HF. 7. Urinalysis: Evaluates for proteinuria, which is a marker of cardiovascular disease. 8. ECG: Somewhat nonspecific but can be useful to detect left ventricular hypertrophy (LVH) or underlying cardiac ischemia or arrhythmias. 9. Chest x-ray: Important evaluation tool for size and shape of the cardiac silhouette and presence of effusions. a. Can appreciate cardiomegaly. Heart Failure

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52 b. May show Kerley B Lines: Short, thin horizontal lines that are noted near the border of the lung and extend outward as a marker of increased interstitial pulmonary fluid. c. Can appreciate pleural effusions or pulmonary edema. 10. Echocardiogram : Diagnostic test of choice for sus-pected HF. a. Utilized to determine type of HF (i. e., HFp EF or HFr EF). b. Useful for determining the EF, where a value less than 40% can help delineate between HF with pre-served versus reduced EF. c. Evaluates for VHD, overall dilatation, and/or hypertrophy: In addition, can consider a stress echocardiogram as a measure of underlying cardiac ischemia/CAD. 11. Cardiac catheterization/coronary angiography. a. Useful in the following scenarios. i. For refractory HF in patients without CAD. ii. For HFr EF with concomitant angina, wall-motion abnormalities on echocardiogram, nuclear evidence of reversible ischemia, or if percutaneous revascularization is considered. iii. If there is a high suspicion of ischemic car-diomyopathy and surgical procedures are a con-sideration. iv. If cardiac transplant or device implantation is being considered. TABLE 3. 5 Common Physical Findings in HF (Grouped by Severity) Mild Crackles in lung bases S3 gallop (best heard at apex with bell) S4 gallop (best heard at left sternal border with bell) Jugular vein distention Generalized weakness Peripheral pitting edema Weight gain/increased abdominal girth Displaced point of maximal impulse (usually leftward) Moderate In addition to the earlier findings: Nonproductive cough Right ventricular heave Loud pulmonic component of second heart sound (best heard at left sternal border due to pulmonary HTN) Crackles in lung bases Dullness to percussion of lung bases and decreased tactile fremitus (secondary to pleural effusions) Tachypnea (especially at rest) Tachycardia Hepatomegaly/ascites/hepatojugular reflex Edema (extremities, sacral, and scrotal) Severe Ascites Central and peripheral cyanosis Decreased level of consciousness Frothy sputum and/or pink sputum Hypotension HF, heart failure; HTN, hypertension. b. Patients can undergo unilateral (right-sided) catheterizations, which provide detailed information regarding cardiac hemodynamics, including cardiac output, ventricular filling pressures, and vascular resistance. Differential Diagnosis A. Acute respiratory distress syndrome (ARDS). B. COPD. C. Pulmonary edema. D. Cirrhosis. E. Idiopathic pulmonary fibrosis. F. Viral pneumonia. G. Bacterial pneumonia. H. Pulmonary embolus. I. MI. J. Nephrotic syndrome. K. Acute kidney injury/insufficiency. L. Acute bronchitis. Evaluation and Management Plan A. General plan: Utilize pharmacologic and nonpharmaco-logic mechanisms to achieve the following goals. 1. Improve overall quality of life. 2. Decrease frequency of HF exacerbations and need for hospitalizations. 3. Extend patient survival. 4. Increase exercise/functional capacity and enhance overall patient well-being. 5. T reat underlying comorbidities that may contribute to HF (i. e., cardiac revascularization for ischemia, valvular replacement for compromising VHD, and treatment of HTN). B. Patient/family teaching points. 1. Strong focus on nonpharmacologic modalities. a. Emphasize importance of medication and clinic appointment compliance. b. Discuss signs and symptoms of worsening HF and when to seek medical care. c. Design daily weight chart for patients with specific instructions regarding weight parameters and when to seek medical care. d. Educate on dietary guidelines. i. Sodium: Less than 2. 3 g/d. ii. Fluid restriction: Less than 2. 0 L/d. iii. Low fat and low cholesterol diet. e. Ensure patients have close follow-up via in-person and phone contact with providers. f. Educate on tobacco cessation and decreased alco-hol intake (if indicated). g. Collaborate with cardiac rehabilitation specialist to design HF-focused exercise program. i. Should contain flexibility, strengthening, and aerobic activities. ii. Encourage daily low to moderate activity with gradual increased intensity over weeks to months with heart monitoring (for most patients). C. Pharmacotherapy. 1. Angiotensin-converting enzyme (ACE) inhibitors: Work by increasing preload and afterload via vascular dilatation; known to decrease morbidity and hospitaliza-tions while alleviating HF-related symptoms and improv-ing quality of life. a. Recommended that all patients regardless of symp-toms receive an ACE inhibitor. 3. Cardiac Guidelines

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53 b. Important to monitor blood pressure, renal func-tion, and electrolytes. c. Advised to start at low dose and titrate. d. Caution to avoid nonsteroidal anti-inflammatory drugs (NSAIDs) in combination with ACE inhibitors because NSAIDs are ACE inhibitor antagonists and will decrease ACE inhibitor effectiveness; in addition, NSAIDs promote sodium and water retention. e. Typically, combination of an ACE inhibitor and diuretic: First-line therapy for most HF patients. i. Patients who cannot tolerate ACE inhibitors should use angiotensin II receptor blockers (ARBs). ii. Patients are intolerant to ACE and ARB ther-apy can utilize a combination of hydralazine and oral or topical nitrates for similar benefits. 2. Beta-blockers: Proven to decrease mortality in post-MI HF patients. a. In the United States, carvedilol and metoprolol succinate are approved for treatment of NYHA HF classes I, II, and III. b. Several contraindications to beta-blocker therapy include NYHA class IV HF, significant pulmonary disease, marked bradycardia, baseline hypotension, and all heart blocks except first degree. 3. Mineralocorticoid antagonists. a. Most commonly used: Spironolactone. b. Function as a potassium-sparing diuretic that affects aldosterone. c. Recommended in NYHA HF classes II to IV HF with EF less than 35% or an EF less than 40% in post-MI HF. d. Contraindicated in patients with renal dysfunction (Cr>2. 5 mg/d L) or known hyperkalemia. e. Caution: In the geriatric population, many patients with underlying renal dysfunction are predis-posed to electrolyte abnormalities. 4. Diuretics. a. Diuretics are the most effective pharmacologic treatment for fluid balance and decreasing symptoms of edema; however, no proven morbidity/mortality benefits. b. Either thiazide (less potent) or loop diuretics (more potent) can be used. c. If the patient is unresponsive to loop or thiazide diuretics, consider the addition of metolazone for enhanced results (caution with metolazone in the elderly, as small doses can result in life-threatening hyponatremia). d. The most important side effect of diuretics is electrolyte imbalance, particularly hypokalemia, hyponatremia, hypomagnesemia, and increased bicarbonate. e. All patients, but especially geriatric individuals, utilizing these medications should have routine elec-trolyte monitoring. 5. Digoxin. a. Has a positive ionotropic effect. b. Beneficial in HF patients with EF less than 30%, NYHA HF class IV, or concomitant AF. c. Has not been shown to decrease morbidity/ mortality. d. Careful monitoring of digoxin levels necessary. e. Can be added to preexisting therapy with diuret-ics, ACE inhibitors, or ARBs in patients with severe disease. D. Additional treatment options. 1. Implantable cardiac defibrillator (ICD) placement: Reduces mortality rate from sudden cardiac death in patients with NYHA class II and III HF and an EF less than 35% (primary prevention) or following cardiac arrest secondary to ventricular arrhythmias (secondary prevention). a. Note that ICDs help prevent sudden cardiac death but do not improve quality of life. 2. Cardiac resynchronization therapy (CRT): Used in patients with systolic (decreased EF) HF to improve clin-ical symptoms, exercise tolerance, and overall survival. a. Procedure requires placement of a biventricular pacemaker (one lead in RV and one lead in the left ventricle via the coronary sinus vein) to assist in pac-ing the left ventricle: Helps by improving cardiac con-tractile ability. b. Works by increasing stroke volume, EF, and car-diac output. c. Indicated in patients with NYHA HF classes II to IV, EF less than 35%, and QRS duration greater than 150 ms on ECG. 3. Considerations for refractory HF: Defined as advanced structural heart disease and marked HF symp-toms at rest or repeated exacerbations despite optimal medical therapy. a. Consider additional supportive devices such as left ventricular assistive devices (LVADs), right ventricular supportive devices (RVADs), or biventricular assistive devices (BIVADs). b. Can also consider advanced intravenous ionotropic therapy to increase cardiac output and strength of contractility (i. e., dobutamine or milri-none). c. Use extracorporeal membrane oxygenation (ECMO) in settings of worsening cardiomyopathy or HF; indicated in persistent NYHA class IV HF as potential bridge to transplantation. 4. Cardiac transplantation: Can be a consideration in patients with refractory cardiogenic shock, constant dependency on intravenous ionotropic therapy, or per-sistent NYHA class IV HF with oxygen consumption less than 10 m L/kg/min. a. However, many contraindications to transplant exist. b. In-depth evaluation and dedicated cardiac trans-plant treatment team are necessary. E. Discharge instructions. 1. Ensure proper transition from inpatient to outpatient management of underlying comorbidities that can exac-erbate HF (DM, HTN, and hyperlipidemia). 2. Ensure adequate understanding of modifiable cardio-vascular risk factors (i. e., smoking cessation, weight loss, and diet/activity restrictions). 3. Prior to discharge: a. Ensure that the patient is at optimal volume sta-tus with proper transition from intravenous to oral diuretic therapy. b. Ensure that the patient has had echocardiogram with documented EF. c. Ensure that the patient has been stable on all oral cardiac medications for 24 hours. d. Ensure that the patient is receiving optimal oral pharmacologic therapy including an ACE inhibitor and beta-blocker (if decreased EF); if optimal therapy is not prescribed, must document reasoning for deviation from accepted practice guidelines. Heart Failure

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54 e. Consult with physical therapy (and occupational therapy) to ensure patient is stable with ambulation and activities of daily living prior to discharge. f. Ensure that the patient has follow-up with outpa-tient cardiologist scheduled for 7 to 10 days postdis-charge. g. Based on the patient's functional status and degree of HF, consider home health nursing or short-term rehabilitation facilities (or long-term care). Follow-Up A. Ensure effective coordination of care between primary care physician and cardiologist. If recent hospitalization: 1. Follow-up within 7 days of discharge, then 1 to 2 weeks until patient is asymptomatic and then every 3 to 6 months thereafter. 2. All providers should ensure efficient communication regarding a patient's current clinical status, medication regimen, diagnostic test results, and goals of care. B. Ensure medication compliance and importance of all clinic visits. C. Create patient-centered exercise plan: Consider referral to cardiac rehabilitation. D. Provide instruction about daily home weight monitoring. 1. If weight gain is more than 2 lb. in 24 hours or 5 lb. above target in 1 week, notify healthcare provider. 2. Discuss weight loss if indicated (body mass index [BMI] ≥30 kg/m2). E. Educate on proper dietary habits including low fat, low cholesterol, and low salt ( <2,300 mg/daily). 1. Consider possibility of fluid restriction. F. Provide smoking cessation and decreased alcohol con-sumption information, if necessary. G. Ensure patient understanding regarding symptoms of worsening HF (cough, weight gain, worsening or rest dysp-nea, orthopnea, and edema) and importance of seeking early medical care. Consultation/Referral A. Recommend consultation with cardiologist and HF specialist. B. Refer to interventional cardiologist and cardiothoracic surgeon for device implantation or if cardiac catheteriza-tion/revascularization is needed. Consider referral to trans-plant surgeon in special cases where cardiac transplantation is a consideration. C. Recommend consultation with nutritionist to assist with dietary restrictions of HF. D. Recommend referral to cardiac rehabilitation for assis-tance with physical activity plan (newly approved for NYHA classes II to IV, EF less than 35%, and on optimal medical therapy for at least 6 weeks). E. Consider consultation with physical therapy, occupa-tional therapy, and case manager during hospitalization to evaluate patients' functional capacity and assist with dis-charge planning. F. Refer to palliative/hospice care for end-stage HF. Special/Geriatric Considerations A. Additional considerations for HF. 1. Considerations for hospitalization. a. Hypotension or other hemodynamic instability. b. Worsening renal function or significant electrolyte disturbance. c. Change in mental status. d. Dyspnea at rest (resting tachypnea) or oxygen sat-uration less than 90%. e. New-onset or worsening arrhythmia such as atrial fibrillation or a ventricular arrhythmia. f. HF with concomitant ACS. g. Evidence of worsening pulmonary congestion on physical examination (rales, jugular venous distention [JVD]). B. Geriatric considerations. 1. HF in the geriatric population can manifest with non-descript symptoms. a. Malaise. b. Weight loss. c. Decreased exercise tolerance. d. Changes in mental status (confusion, changes in mood/irritability, sleep disturbances). e. Gastrointestinal dysfunction (nausea, abdominal pain, anorexia, alterations in bowel habits). 2. Note that geriatric patients also experience typical HF symptoms, especially orthopnea; inquire about sleeping in a recliner (to alleviate SOB) and elevated JVD (noted on physical examination). 3. The mnemonic DEFEAT (Diagnosis, Etiology, Fluid volume status, Ejection fr Action, and Treatment) may be useful in the geriatric population. a. General principle for the treatment of HF in older adults is similar to that of younger adults: Divided between symptom-relieving and disease-modifying treatment. b. All geriatric HF patients should receive an ACE inhibitor or an ARB; can also utilize a low dose beta-blocker such as metoprolol. c. Can also utilize an aldosterone antagonist (i. e., spironolactone) in advanced HF; however, use caution in those with impaired renal function (common in geriatric population) due to risk of hyperkalemia. d. Recommend to avoid digoxin in geriatric patients but could consider in low doses if patient remains symptomatic despite maximal medical therapy with other pharmacologic classes. e. Diuretics should be used to achieve euvolemia using lowest dose possible with careful monitoring of electrolytes. f. Realize that HF is a debilitating condition in the geriatric population: Fewer than 25% will survive greater than 5 years. It is important to: i. Have comprehensive discussions with patients and families regarding end-of-life wishes and ensure that appropriate referrals to palliative care and hospice are made when the patient's condition declines. ii. Understand patients and family members' wishes regarding aggressiveness of clinical inter-ventions before designing treatment plans. 1)Recommend that risk versus benefit anal-ysis for geriatric patients be considered with regard to device implantation. 2)Understand that patients with low life expectancies (12-18 months) are unlikely to benefit from ICDs and patients older than 80 years of age are likely to experience major complications following device placement. 3. Cardiac Guidelines

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55 Bibliography Agabegi, S. S., & Agabegi, E. D. (2008). Step-up to medicine (2nd ed. ). Philadelphia, PA: Wolters Kluwer. Dumitru, I., & Baker, M. M. (2018, May 7). Heart failure. In G. K. Sharma (Ed. ), Medscape. Retrieved from http://emedicine. medscape. com/article/163062-overview Rich, M. W. (2016). Heart failure. In J. B. Halter, J. G. Ouslander, S. Stu-denski, K. P. High, S. Asthana, M. A. Supiano, & C. Ritchie (Eds. ), Hazzard's geriatric medicine and gerontology (7th ed. ). New York, NY: Mc Graw-Hill. Retrieved from http://accessmedicine. mhmedical. com/ book. aspx?bookid=1923 Yancy, C. W., Jessup, M., Bozkurt, B., Butler, J., Casey, D. E., Jr., Colvin, M. M., & Westlake, C. (2017a). 2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guideline for the management of heart failure: A report of the American College of Cardiology/Ameri-can Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America. Circulation, 136, e137-e161. doi:10. 1161/CIR. 0000000000000509 Yancy, C. W., Jessup, M., Bozkurt, B., Butler, J., Casey, D. E., Jr., Colvin, M. M., & Westlake, C. (2017b). 2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guideline for the management of heart failure. Journal of the American College of Cardiology, 70 (6), 776-803. doi:10. 1016/j. jacc. 2017. 04. 025 Hypertension Allison Rusgo Definition A. According to 2017 guidelines from the American Col-lege of Cardiology and American Heart Association, normal blood pressure (BP) is defined as a systolic blood pressure (SBP) less than 120 mm Hg and diastolic blood pressure (DBP) less than 80 mm Hg. An elevated BP is now defined as a SBP between 120 and 129 mm Hg anda DBP less than 80 mm Hg; Stage I hypertension (HTN) is now defined as an SBP between 130 and 139 mm Hg ora DBP between 80 and 90 mm Hg. Stage II HTN is any SBP of 140 mm Hg or more ora DBP of 90 mm Hg or more. B. Condition applies to anyone taking antihypertensive medication or a person who is told by a clinician on two separate occasions that his or her BP is greater than or equal to 140 mm Hg/90 mm Hg. Incidence A. According to the National Health and Nutrition Exam-ination Survey (NHANES), HTN affects 86 million U. S. adults (age ≥20 years) with a prevalence of 34%. B. Majority of patients (90%-95%) are diagnosed with pri-mary (idiopathic) HTN. C. Global prevalence of approximately 972 million individ-uals (26% of world's population). D. Globally, African Americans maintain the highest preva-lence rate of HTN and experience the highest mortality rates from associated complications including cardiovascular dis-ease, end-stage renal disease, and cerebrovascular accidents (CVAs ). Pathogenesis A. Believed to be multifactorial, with many sites of target organ damage. 1. Cardiac: Left ventricular hypertrophy (LVH), myocardial infarctions (MIs), congestive heart failure (CHF), and acceleration of atherosclerosis. 2. Central nervous system (CNS): CVAs, transient ischemic attacks (TIA). 3. Renal: Chronic kidney disease (CKD). 4. Vascular: Peripheral vascular disease (PVD). 5. Ophthalmological: Retinopathy. B. In increased systemic vascular resistance (cardiac after-load), concentric LVH, and decreased left ventricular function secondary to left ventricular dilatation: Leads to a weakened heart muscle and eventual CHF. C. Decreased stroke volume and cardiac output. D. Endothelial cell dysfunction due to altered renin-aldosterone-angiotensin cascade. Predisposing Factors A. Nonmodifiable risk factors. 1. Age: Both SBP and DBP increase with age. 2. Gender. a. Until age 45, more males are affected than females. b. From ages 45 to 64, males and females are affected equally. c. After age 65, more females are affected than males. 3. Race and ethnicity: Most common in African Americans. 4. Hereditary: Heritable component between 33% and 57% according to Framingham Heart Study. B. Modifiable risk factors. 1. Sedentary lifestyle; obesity (BMI ≥30 kg/m2). 2. Increased sodium intake. 3. Increased alcohol consumption (8 oz. wine or 24 oz. beer per day). 4. Tobacco use. 5. Hyperlipidemia: Elevated low-density lipoprotein ( LDL) cholesterol (or total cholesterol ≥240 mg/d L) or low HDL cholesterol. 6. Diabetes mellitus as a component of metabolic syndrome. Subjective Data A. Common complaints/symptoms. 1. Headache (particularly headache upon awakening) and dizziness. 2. Visual changes; subconjunctival hemorrhages. 3. Epistaxis. B. History of the present illness. 1. Documented elevated BP on three separate occasions (three clinic visits required for HTN diagnosis). a. Based on average of two or more readings at each follow-up visit after initial screening. 2. HTN-related comorbidities and evidence of target end-organ damage. 3. Possible evaluation for secondary causes of HTN based on patients' symptomatology. a. Pheochromocytoma: Facial flushing, labile HTN, and palpitations. b. Hypothyroidism: Cold intolerance, lethargy, and bradycardia. c. Hyperthyroidism: Heat intolerance, tachycardia, and diaphoresis. d. Obstructive sleep apnea: Snoring and daytime sleepiness. e. Hyperparathyroidism: Nephrolithiasis, gastroin-testinal symptoms, osteitis fibrosa cystica. f. Cushing disease: Weight gain, hirsutism, abdomi-nal striae. C. Family and social history. 1. Family history of HTN and premature history of cardiovascular disease (males <55 years and females <65 years). 2. Use of alcohol, tobacco, anabolic steroids, and illicit drugs, particularly cocaine and amphetamines. Hypertension

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56 3. Diet (salt, fat, caloric intake), exercise, and life stressors. D. Review of systems (focus should be on target organ damage). 1. General: Weight gain/obesity. 2. Integumentary: Edema and ulcerations. 3. Neurological: Headache, dizziness, lightheadedness, syncope/near-syncope, and weakness. 4. Ophthalmological: Visual changes. 5. Cardiovascular and respiratory: Chest pain, palpita-tions, tachycardia, shortness of breath, and dyspnea on exertion. 6. Gastrointestinal/genitourinary: Abdominal pain and changes in urinary habits. Physical Examination A. Measure accurate BP: Average of three readings taken 2 minutes apart; on first visit, BP should be taken in both arms and one leg to evaluate for coarctation of aorta and sub-clavian artery stenosis. B. Evaluate pulse, oxygen saturation, respiratory rate, and temperature. C. Assess skin for changes related to venous stasis: Brawny appearance with red/blue discoloration and possible venous stasis ulcerations. D. Check the following body systems. 1. Ophthalmological: Perform visual acuity; fundus-copic examination for arteriovenous nicking, copper/sil-ver wiring, cotton wool spots, retinal hemorrhages, and papilledema. 2. Neck: Evaluate thyroid, carotid bruits, and jugular venous distention. 3. Respiratory: Auscultate all lung fields. 4. Cardiac: Assess for point of maximum impulse (PMI) displacement, sustained/enlarged apical impulse, pres-ence of S3or S4, evidence of murmurs, rubs or gallops, femoral pulse abnormalities, and peripheral edema. 5. Abdomen: Evaluate for pulsatile abdominal mass over aorta, presence of bruits (aortic, renal, femoral, and iliac), and assess radial-femoral delay. 6. Neurological: Perform complete mental status exami-nation. Diagnostic Tests A. BP measurement (diagnostic criteria): T wo or more dias-tolic BP measurements on at least two subsequent visits (after initial screening) of greater than or equal to 90 mm Hg or when the average of systolic BP readings on two or more subsequent visits is consistently greater than or equal to 140 mm Hg. B. Initial laboratory evaluation. 1. Complete blood count. 2. Complete metabolic panel, including renal function and glomerular filtration rate (GFR). 3. Fasting lipid panel. 4. Hemoglobin A1C. 5. Urinalysis (microalbumin levels correlate with clinical BP readings). 6. Can also consider ECG, echocardiogram, and stress testing to further evaluate cardiac status. C. Additional diagnostic tests for secondary causes of HTN. 1. Pheochromocytoma: 20-hour urinary metanephrine level. 2. Primary aldosteronism: Plasma aldosterone-to-renin activity ratio. 3. Renal artery stenosis (RAS): Doppler flow ultrasound or computed tomographic angiography (CTA). 4. Obstructive sleep apnea: Sleep study with oxygen sat-uration measurements. 5. Thyroid and parathyroid disease: Thyroid and parathyroid hormone levels. 6. Cushing disease: Dexamethasone suppression test. 7. Coarctation of the aorta: CTA. Differential Diagnosis A. Primary idiopathic HTN. B. Secondary HTN. 1. Drug/toxin: Nicotine, alcohol, cocaine, ampheta-mines, ephedrine-containing decongestants, herbal supplements containing licorice, nonsteroidal anti-inflammatory drugs (NSAIDs), and oral contraceptives. 2. Cardiovascular: MI, CHF. 3. Endocrine: Primary hyperaldosteronism, Cush-ing disease, pheochromocytoma, hyperthyroidism or hypothyroidism, and hyperparathyroidism. 4. Neurological: CVA, TIA, obstructive sleep apnea, intracranial HTN, brain tumor, and serotonin syndrome. 5. Vascular: Coarctation of aorta, vasculitis, collagen vascular diseases, and subclavian artery stenosis. 6. Renal: CKD, polycystic kidney disease (PCKD), and RAS. Evaluation and Management Plan A. General plan. 1. Lifestyle modification. a. Diet modification: Dietary approaches to stop hypertension (DASH) diet; no-added-salt diet (4 g/d) or low-sodium diet (2 g/d). b. Limit alcohol and encourage tobacco cessation. c. Exercise regularly (30 minutes/day for 5-7 days/ week). d. Engage in stress-reduction activities. e. Discontinue unnecessary medications that can raise BP. B. Patient/family teaching points. 1. Encourage family support with regard to lifestyle modifications and medication compliance. C. Pharmacotherapy. 1. Appropriate medications. a. Thiazide diuretics: Initial medication of choice (especially important to use in African Americans). b. Angiotensin-converting enzyme (ACE) inhibitors: Preferred in patients with diabetes mellitus because of its renal protective properties (can use angiotensin II receptor blocker [ARB] if patient intolerant to ACE inhibitor). c. Beta-blockers: Decrease heart rate, cardiac output, and renin release. d. Calcium channel blockers: Work by vasodilatation of atrial vasculature. 2. Patients with HTN and diabetes mellitus often require two medications for control. 3. If BP is greater than 20/10 mm Hg above goal, con-sider use of two agents—one of which is usually a thiazide diuretic. 4. Often a combination drug of a thiazide with either an ACE inhibitor or ARB is used because thiazides increase the effectiveness of other antihypertensive medications. 5. Note that if the patient has poor response to one med-ication, experts recommend changing to another first-line agent in an alternative class before adding a second agent. 3. Cardiac Guidelines

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57 6. Medications such as hydralazine and minoxidil are not commonly used; if initiated, it is typically done with beta-blockers or diuretics for resistant HTN. 7. Caution: With clonidine, it is important to educate about not stopping abruptly due to risk of rebound HTN. Follow-Up A. Encourage patients to monitor BP at home and keep a log. B. Emphasize medication compliance and clinic appoint-ment follow-up with cardiologist or primary care provider. Consultation/Referral A. Consider consultation with a cardiologist for patients with multiple cardiovascular risk factors and/or comorbidi-ties. B. Consider consultation with a nephrologist for patients with resistant HTN and/or comorbid renal disease. C. Based on etiology of secondary HTN, consultation with an appropriate specialist is advised. Special/Geriatric Considerations A. BP goals for special populations. 1. Renal insufficiency: Less than 130/80 mm Hg. 2. Diabetes mellitus: Less than 130/80 mm Hg. 3. Age 65 years or older and high burden comorbidities; provider judgment and patient preferences. 4. HTN/CHF: Less than 130/80 mm Hg. B. Complications 1. Thoracic and abdominal aortic aneurysms. 2. MI. 3. Hypertensive urgency and emergency. 4. CVA, TIA. 5. Target end-organ damage (eyes, kidneys, nervous system). C. Urgent and emergent hypertensive situations. 1. Hypertensive urgency: BP of 180/110 mm Hg or greater without end-organ damage. a. Patients should seek immediate evaluation and treatment. b. Avoid rapid lowering of BP to prevent neuro-logical complications; initiate treatment of BP using oral agents for gradual reduction of BP over 24 to 48 hours. c. Ensure close follow-up and BP monitoring in addi-tion to regulation of antihypertensive medications to prevent future recurrence. 2. Hypertensive emergency: BP greater than 180/120mm Hg with symptoms of end-organ damage. a. Goal is to reduce BP safely to reverse target organ damage without iatrogenic malperfusion. Maintained to less than 180/105 mm Hg for the first 24 hours. b. Hypertensive emergency in pregnancy is defined as acute onset, with BP greater than 160/110 mm Hg persisting more than 15 minutes. c. Patients should be monitored in the ICU with use of intravenous antihypertensive medications until stabilized. D. Geriatric considerations: Structural changes due to aging. 1. Changes in venous system due to aging. a. Reflex alterations in venous vasomotor tone. b. Vasoconstriction. c. Stiffness and loss of elasticity of valves in veins. 2. Arterial changes due to aging. a. Thickening of the intimal and medial layers of the vasculature. b. Lipid deposits. c. Over time, the intimal and medial layers of the arteries acquire collagen deposits that subsequently decrease their elasticity and cause hardening of the vasculature walls. Bibliography Agabegi, S. S., & Agabegi, E. D. (2008). Step-up to medicine (2nd ed. ). Philadelphia, PA: Wolters Kluwer. Benjamin, E. J., Blaha, M. J., Chiuve, S. E., Cushman, M., Das, S. R., Deo, R.,... Muntner, P. (2017, March 7). Heart disease and stroke statistics-2017 update: A report from the American Heart Association. Circula-tion, 135 (10), e146-e603. doi:10. 1161/CIR. 0000000000000485 Chobanian, A. V., Bakris, G. L., Black, H. R., Cushman, W. C., Green, L. A., Izzo, J. L., Jr.,... Roccella, E. J. (2003, December). Seventh report of the Joint National Committee on Prevention, Detection, Eval-uation, and T reatment of High Blood Pressure. Hypertension, 42 (6), 1206-1252. doi:10. 1161/01. HYP. 0000107251. 49515. c2 Institute for Clinical Systems Improvement. (2010). Hypertension diagnosis and treatment. Retrived from https://www. icsi. org/ James, P. A., Oparil, S., Carter, B. L., Cushman, W. C., Dennison-Himmelfarb, C., Handler, J.,... Ortiz, E. (2014). 2014 evidence-based guideline for the management of high blood pressure in adults: Report from the panel members appointed to the Eighth Joint National Com-mittee (JNC 8). Journal of the American Medical Association, 311 (5), 507-520. doi:10. 1001/jama. 2013. 284427 Jermendy, G., Horvath, T., Littvay, L., Steinbach, R., Jermendy, A. L., Tarnoki, A. D.,... Osztovits, J. (2011, November 3). Effect of genetic and environmental influences on cardiometabolic risk factors: A twin study. Cardiovascular Diabetology, 10, 96. doi:10. 1186/1475-2840-10-96 Levy, D., De Stefano, A. L., Larson, M. G., O'Donnell, J., Lifton, R. P., Gavras, H.,... Myers, R. H. (2000, October). Evidence for a gene influencing blood pressure on chromosome 17. Genome scan linkage results for longitudinal blood pressure phenotypes in subjects from the Framingham Heart Study. Hypertension, 36 (4), 477-483. doi:10. 1161/ 01. HYP. 36. 4. 477 Mitchell, G. F., De Stefano, A. L., Larson, M. G., Benjamin, E. J., Chen, M.-H., Vasan, R. S.,... Levy, D. (2005, July 12). Heritability and a genome-wide linkage scan for arterial stiffness, wave reflection, and mean arterial pressure: The Framingham Heart Study. Circulation, 112 (2), 194-199. doi:10. 1161/CIRCULATIONAHA. 104. 530675 Mozaffarian, D., Benjamin, E. J., Go, A. S., Arnett, D. K., Blaha, M. J., Cushman, M.,... T urner, M. B. (2015, January 27). Heart disease and stroke statistics—2015 update: A report from the American Heart Association. Circulation, 131 (4), e29-322. NHANES (n. d. ). National health and nutrition examination survey. Retrieved from http://www. cdc. gov/nchs/nhanes. htm Whelton, P. K., Carey, R. M., Aronow, W. S., Casey, D. E., Jr., Collins, K. J., Dennison Himmelfarb, C.,... Wright, J. T., Jr. (2018). 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APh A/ASH/ASPC/N-MA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults. Jour-nal of the American College of Cardiology, 71 (19), e127-e248. doi:10. 1016/j. jacc. 2017. 11. 006 Pericardial Effusions Allison Rusgo Definition A. An abnormal amount or type of fluid within the peri-cardium of the heart secondary to various etiologies. B. Can be acute or chronic, pathologic or idiopathic, or symptomatic or asymptomatic. C. Arise when there is an increase in production or a decrease in drainage of pericardial fluid; both mechanisms lead to an overabundance of fluid within the pericardial space. The excess fluid leads to inflammation and irritation of the peri-cardium, which is termed pericarditis. Pericardial Effusions

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58 Incidence A. Data from the Framingham Heart Study ( n=5,652) showed that 6. 5% of adults had pericardial effusions from echocardiogram results. B. Pericardial effusions are common after cardiac bypass and valve replacement procedures (self-limiting). C. It is common for patients with underlying hematolog-ical/oncological malignancies to have malignant pericardial effusions (21%). 1. Lung cancer (37%), breast cancer (22%), and leukemia/lymphoma (17%) are the most common can-cers that cause pericardial effusions. D. Evidence of HIV or AIDS increases the risk of pericardial effusions (prevalence between 5% and 43%, depending on the study's inclusion criteria). Pathogenesis A. The pericardium is a double-walled sac that surrounds the heart. Its two layers work together to evenly distribute pressure and volume forces across the heart, allowing for stretching of the myocardium and uniform contractions. The layers are: 1. Visceral pericardium (closer to the heart): Composed of ultrafiltered plasma (pericardial fluid is thought to come from this layer). 2. Parietal pericardium (farther from the heart): Con-tributes to diastolic pressure and pressure within the right side of the heart. B. The pericardium normally contains 15 to 50 m L of peri-cardial fluid, which is used for lubrication for each of the peri-cardial layers. C. Clinical manifestations of pericardial effusions differ based on the rate of accumulation of the fluid. For example: 1. Instant accumulation of less than 80 m L of fluid can cause significant cardiac compromise. 2. Slow accumulation (months-years) requires more than 2 L of fluid before symptoms arise. 3. Acute pericarditis typically involves accumulation of 150 to 200 m L of fluid when symptoms occur. D. Pericardium has an important role during inspiration. 1. As the right atrium and ventricle fill, the pericardium prevents the left atrium and ventricle from expanding. 2. This process stretches the atrial and ventricular sep-tum, decreases left ventricular filling volumes, and reduces cardiac output. 3. If there is a significant accumulation of fluid within the pericardial space, the pressure within the pericar-dial spaces increases, stroke volume declines, and life-threatening cardiac tamponade can result. Predisposing Factors A. Postprocedures (coronary artery bypass grafting [CABG] or valve replacement). B. Post-myocardial infarctions (MIs). C. Neoplastic status. 1. Benign: Atrial myxoma. 2. Primary malignancy: Mesothelioma. 3. Metastatic malignancy: Lung cancer or breast cancer. 4. Hematologic malignancy: Leukemia or lymphoma. D. Congestive heart failure as a result of rheumatic heart dis-ease, cor pulmonale, or cardiomyopathies. E. Connective tissue disorders: Rheumatoid arthritis, sys-temic lupus erythematosus, or scleroderma. F. Chronic renal disease (secondary to uremia) or nephrotic syndrome. G. Severe hypothyroidism with myxedema coma. H. Medications: Procainamide, hydralazine, or status post radiation therapy. I. Infectious pericarditis (most common is viral). 1. HIV/AIDS: Secondary bacterial infection, oppor-tunistic infections, or Kaposi sarcomas. 2. Viral: Coxsackievirus A and B, adenovirus, influenza, and some forms of hepatitis. 3. Fungal: Candida, histoplasmosis, or coccidioidomy-cosis. 4. Protozoal. 5. Parasitic. 6. Pyogenic: Streptococci, pneumococci, Neisseria, Legionella, or staphylococci. 7. T uberculosis. 8. Syphilitic. J. T rauma (blunt or penetrating). Subjective Data A. Common complaints/symptoms. 1. Chest pain/discomfort: Can be relieved by leaning forward and worsened by laying supine (27% of patients). 2. Palpitations. 3. Syncope/lightheadedness. 4. Cough/hoarseness (47% of patients). 5. Dyspnea (78% of patients). 6. Anorexia (90% of patients). 7. Anxiety. 8. Confusion/change in mental status. B. History of the present illness. 1. Inquire about onset, provoking/alleviating factors, quality, severity, and timing of symptoms. a. Especially important regarding chest pain and positioning for pericarditis (sitting up/leaning for-ward improves symptoms while lying flat worsens dis-comfort). b. Chest discomfort often described as pleuritic (worse with inspiration) and sharp/stabbing. 2. Discuss past medical history, particularly connective tissue disorders; neoplastic diseases; cardiac comorbidi-ties; and infectious diseases such as HIV/AIDS, tubercu-losis, or hepatitis. C. Family and social history. 1. Review family history for connective tissue disorders, cardiac diseases, neoplastic diseases, or renal failure. 2. Determine use of tobacco, alcohol, or illegal substances. 3. Obtain information regarding medications, especially procainamide or hydralazine. 4. Ensure vaccinations and screenings are current. a. Influenza vaccine. b. T uberculosis purified protein derivative (PPD), HIV/AIDS, and sexually transmitted infection test-ing (i. e., gonorrhea and syphilis). c. Cancer screenings. 5. Assess for recent travel to wooded areas (exposure to tick-borne illnesses). D. Review of systems. 1. General: Fevers, chills, weight changes, appetite changes, or malaise. 2. Cardiac: Chest pain/discomfort, or palpitations. 3. Pulmonary: Shortness of breath, dyspnea, cough, or hoarseness/change in voice quality. 4. Gastrointestinal: Singultus (hiccoughs). 5. Neurological: Syncope, lightheadedness, confusion, or change in mental status. 6. Psychiatric: Anxiety. 3. Cardiac Guidelines

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59 Physical Examination A. Vital signs: Pulse, blood pressure (BP), respirations, tem-perature, oxygen saturation, and weight. 1. Necessary to assess; possible hypotension, pulsus para-doxus, fever, tachycardia, or tachypnea. B. General: Variable based on patient status; could be asymptomatic or in hemodynamic compromise if positive cardiac tamponade. C. Neck: Possible hepatojugular reflux or jugular venous dis-tention (JVD). D. Pulmonary: Possible tachypnea, decreased breath sounds, Ewart sign (dullness to percussion below left scapula sec-ondary to pericardial fluid near left lung). E. Cardiac: Possible tachycardia, S1 and S2, murmurs, rubs, extra heart sounds (i. e., S3 and S4), pericardial friction rub, and muffled heart sounds. Also assess for increased JVD, hypotension, and muffled heart sounds (Beck's T riad) which is hallmark for cardiac tamponade. F. Peripheral vascular: Possible peripheral edema, decreased pulses, or cyanosis. G. Gastrointestinal: Possible hepatosplenomegaly. H. Neurological: Mental status examination (if necessitated by patient status). Diagnostic Tests A. ECG (abnormal in 90% of cases). 1. Low-voltage QRS. 2. Diffuse nonspecific ST wave changes (can see T-wave flattening) and/or electrical alternans (electrical alternans is usually a sign of a massive effusion). B. Echocardiography (imaging test of choice): Used to assess overall cardiac function and amount of pericardial fluid present; can detect as little as 20 m L of fluid. C. Chest x-ray. 1. Can show a “water-bottle” shaped cardiac silhouette and/or pericardial fat stripe. 2. Can show an associated pleural effusion. D. CT or MRI: Can be helpful in some instances for small effusions or loculated effusions. E. Laboratory studies. 1. Complete metabolic panel: Assess electrolytes and renal function. 2. Complete blood count: Assess for leukocy-tosis and/or underlying HIV/AIDS or malignant process. 3. Cardiac biomarkers: Can see minimal elevation. 4. Thyroid-stimulating hormone (TSH): Assess for hypothyroidism as a cause for pericardial effusion. 5. Rheumatoid factor and/or antinuclear antibody (ANA): Obtain if concern for underlying rheumatologic etiology. 6. HIV/AIDS screening: Obtain if clinically suggested. 7. Rickettsial antibody tests: Obtain if clinically indicated. 8. Throat swab for influenza and adenovirus virus. 9. Blood cultures: Obtain if febrile and clinically indicated. 10. T uberculin skin testing: Perform if indicated. F. Pericardial fluid analysis. 1. Currently under debate: Usually done if poor prognosis, likelihood of purulent effusion, pericardial tamponade, or recurrent and/or large effusions (espe-cially conditions that do not resolve with medical management). 2. Can send fluid for a variety of laboratory studies. a. Cell count and differential. b. Protein and lactate dehydrogenase. c. Glucose. d. Gram stain. e. Cultures: Bacterial, fungal, acid-fast stain, and culture. f. T umor cytology. g. Rheumatoid factor and ANA if collagen vascular disease is suspected. Differential Diagnosis A. Acute pericarditis. B. Chronic pericarditis. C. Myocardial infarction (Dressler syndrome is defined as pericarditis after an MI). D. Pulmonary embolus. E. Cardiac tamponade. F. Constrictive pericarditis. G. Cardiogenic pulmonary edema. H. Dilated cardiomyopathy. Evaluation and Management Plan A. General plan. 1. Goal is to determine underlying etiology and treat accordingly; also important to determine level of care that patient requires (intensive care, inpatient, or outpatient). 2. If positive cardiac tamponade or significant hemody-namic compromise, ICU admission required. 3. Pericardiocentesis is required if hemodynamically unstable; recommended for large effusions or those sec-ondary to bacterial infections or cancerous processes. a. This procedure is considered to be diagnostic and therapeutic. i. Done via open surgical procedure or catheter drainage. ii. Catheter drainage via fluoroscopy, echocar-diography, or CT-guidance is the most common method. b. Following the procedure, an in-dwelling catheter can be placed to prevent fluid reaccumulation: This is removed or replaced within 72 hours. c. A sclerosing agent (i. e., tetracycline or bleomycin) within the pericardium can also be used to prevent reaccumulation. d. Other options to prevent recurrence are surgi-cal intervention (pericardial window, thoracotomy or video-assisted thoracic surgery, or balloon pericar-diotomy). e. If constrictive pericarditis, surgical resection is always indicated. 4. Pharmacologic treatments (see section “Pharma-cotherapy”). B. Patient/family teaching points. 1. Educate regarding symptoms of cardiac compromise and signs and symptoms of worsening effusions; espe-cially important if patient is treated as outpatient. 2. Educate regarding importance of medication compli-ance and follow-up visits with provider. 3. Explain to patients that despite proper diagnostic test-ing, an underlying etiology remains undiscovered in 50% of cases. C. Pharmacotherapy. 1. Aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs): Can be used for acute idiopathic or viral peri-carditis. a. Aspirin is preferred for post-MI pericarditis. Pericardial Effusions

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60 b. NSAIDs are preferred for viral pericarditis (avoid indomethacin in those with coronary artery disease [CAD]). 2. Colchicine: Can be used for acute pericarditis in com-bination with aspirin or NSAIDs. a. Avoid in asymptomatic postoperative pericarditis. b. Discuss with patients regarding side effects: Most common is diarrhea. 3. Steroids: If used early in acute pericarditis, there is an increased risk of reoccurrence once steroids are tapered. a. Consider in recurrent disease that is unresponsive to NSAIDs and colchicine. b. Consider for patients with comorbid connective tissue disorder, uremic pericarditis, or autoreactive pericarditis. c. Recommend to use for at least 1 month with slow taper. 4. Antibiotics. a. If purulent pericardial fluid and bacterial infec-tion, combine urgent drainage and aggressive intra-venous antibiotics (e. g., vancomycin, ceftriaxone, and ciprofloxacin). D. Discharge instructions. 1. Educate regarding pericardial effusions and peri-carditis. 2. Educate on reasons to return to the ED: Specifically signs of hemodynamic instability, cardiac compromise, or worsening infection (if etiology is bacterial or viral). 3. Educate on importance of medication and clinic follow-up compliance. Follow-Up A. Patients will require close monitoring until pericardial effusion and symptoms resolve. B. Patients should have repeat echocardiography to ensure effusion resolution and no evidence of constrictive pericardi-tis (usually within 4 weeks of diagnosis). C. Pericardial effusions usually resolve with treatment and when underlying illness is treated; often reoccur with comor-bid conditions such as neoplasms. Consultation/Referral A. Consult with cardiologist. B. Consult with interventional cardiologist (if cardiac catheterization or minimally invasive pericardiocentesis is indicated). C. Consult with cardiothoracic surgeon (if invasive pro-cedure is required or patient is status post cardiothoracic surgery). D. Consult with infectious disease specialist (if indicated). E. Consult with rheumatologist (if indicated). F. Consult with interventional radiologist (if pericardial drainage procedure via fluoroscopy is indicated). G. Consult with hematologist/oncologist (if indicated). Special/Geriatric Considerations A. It is important to assess the cognitive status and comor-bidities of geriatric patients, especially if invasive procedures may be required. B. Studies have shown that in elderly patients undergoing echocardiography for other purposes, those with incidental small asymptomatic pericardial effusions had a higher mor-tality than those without effusions. C. Elderly patients may present with more vague symptoms (generalized malaise, confusion). D. As with many other diagnoses, elderly patients with peri-carditis and pericardial effusions have poorer outcomes as compared to younger patients with the same disease process. Bibliography Agabegi, S. S., & Agabegi, E. D. (2008). Step-up to medicine (2nd ed. ). Philadelphia, PA: Wolters Kluwer. Olshaker, J. S. (2014). Cardiovascular emergencies in the elderly. In J. H. Khan, B. G. Magauran Jr., & J. S. Olshaker (Eds. ), Geriatric emergency medicine: Principles and practice (pp. 199-206). New York, NY: Cam-bridge University Press. Strimel, W. J., Ayub, B., & Contractor, T. (2019, November 28). Pericar-dial effusion. In T. X. O'Brien (Ed. ), Medscape. Retrieved from http: //emedicine. medscape. com/article/157325-overview Usatine, R. P., Smith, M. A., Chumley, H. S., & Mayeaux, E. J., Jr. (2013). Pericardial effusion. In A. Jawaid & J. Delzell, The color atlas of family medicine (2nd ed., pp. 292-296). New York, NY: Mc Graw-Hill. Retrieved from http://accessmedicine. mhmedical. com/book. aspx? book ID=685 Valvular Heart Disease Allison Rusgo Definition A. Damage or defect in one of the four heart valves: Mitral, aortic, tricuspid, or pulmonary. B. T wo most common abnormalities: Regurgitation and stenosis of the aortic and mitral valves. 1. Regurgitation or insufficiency: Occurs when the valve leaflets do not close tightly; blood leaks backward into the respective chamber instead of flowing forward through the proper circulatory path. 2. Stenosis: Occurs because of stiffening and narrowing of the valve leaflets. a. This prevents the valve from opening properly; the result is not enough blood flowing through the valve and circulatory path, which leads to an outflow-type obstruction during systole. b. Mitral stenosis (MS) results in an increase in left atrial, pulmonary artery, and right ventricular pres-sures. c. Mitral regurgitation (MR) leads to a backflow (or reversal) of blood from the left ventricle to the left atrium during systole; it can be primary or secondary and acute or chronic. i. Acute MR: Typically occurs because of endo-carditis or myocardial infarction (MI) with struc-tural cardiac damage (papillary muscle rupture, chordae rupture). ii. Chronic MR: Can be primary or secondary. iii. Causes of primary MR: Mitral valve prolapse (MVP; subtype of MR where the mitral valve leaflets close improperly and bulge into the left atrium during systole), rheumatic heart disease, MI with resultant structural cardiac damage, or endocarditis. iv. Causes of secondary MR: Left ventricular dysfunction. Incidence A. Globally, the prevalence of valvular heart disease (VHD) is estimated at 2. 5%. B. Prevalence of VHD increases in individuals older than 65 years of age, particularly in those with aortic stenosis (AS) or MR. More than 33% of those older than age 75 have moderate to severe VHD. 3. Cardiac Guidelines

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61 C. AS is the leading cause of clinically significant VHD in geriatric patients (prevalence of 2%-9%). D. Acute aortic regurgitation (AR) is a rare and life-threatening condition. Chronic AR is common in geriatric patients (prevalence of 20%-30% in geriatric patients). E. MS is more common in females as compared to males and usually occurs because of rheumatic heart disease (97%). 1. MS caused by rheumatic heart disease typically presents in the fourth or fifth decade but can occur in individuals older than age 65 years. 2. Only 60% of patients with MS secondary to rheumatic heart disease can recall a previous history of the infection. 3. Among geriatric patients with non-rheumatic heart disease-related MS, the etiology is typically because of age-related calcifications that narrow the valve. F. MR occurs equally in males and females, with a preva-lence of 2%. 1. Most common cause of MR is MVP. 2. MVP can be spontaneous or genetically linked. Pathogenesis A. Stenosis. 1. Senile AS or MS. a. Exact mechanism is still not entirely understood; it is thought to be secondary to a buildup of calcifica-tions within the valve. b. Very similar to the process of atherosclerosis. c. Increase in lipids, inflammation, and calcification of the valve. 2. Bicuspid AS: Secondary to an inherited congenital condition where two (of the normally structured three) leaflets of the aortic valve are fused together. a. This improper fusion of the two valve leaflets results in a bicuspid aortic valve instead of a tricuspid-shaped valve. b. Result is an increase in calcification formation and outflow obstruction. 3. Rheumatic heart disease-related AS or MS: Can affect the aortic or mitral valves via fusion of the leaflets to create narrowing and outflow obstruction. B. Regurgitation. 1. Acute MR: Results in increase in preload and decrease in afterload. a. This causes an increase in end-diastolic volume (EDV) and decrease in end-systolic volume (ESV). b. Thus, stroke volume and left atrial pressures are increased. 2. Chronic MR: Slow deterioration of the valve allows the left atrium and left ventricle to adjust (dilate) to the increased backflow of blood. a. Left atrial pressure is usually normal or slightly ele-vated; end-diastolic pressure is also within an accept-able range. b. Over time, the left ventricle will continue to dilate, further damaging the mitral valve leaflets and worsen-ing the MR. 3. Acute AR: Increased volume in the left ventricle dur-ing diastole; the ventricle does not have sufficient time to dilate appropriately to accommodate the sudden increase in fluid. a. EDV increases quickly, which this causes an eleva-tion in pulmonary artery pressures, affecting coronary and pulmonary circulation. b. With this increase in volume and pressures, patients develop symptoms consistent with pul-monary congestion (i. e., dyspnea). 4. Chronic AR: Results in slow progressing fluid over-load within the left ventricle. a. This condition causes the left ventricle to dilate over time, resulting in left ventricular hypertrophy. b. Initially, the hypertrophy helps mitigate the increased pressure and volume that occurs within the left ventricle. c. In early phase, cardiac contractility (or ejection fraction [EF]) remains normal via compensation mechanisms. d. As the disease progresses and the ventricle con-tinues to dilate, it reaches maximal stretch capacity; beyond this threshold there is an increase in end-diastolic pressures and decrease in perfusion of the coronary system. e. As the left ventricle structure and function wors-ens, the EF decreases and symptoms (i. e., dyspnea) ensue. Predisposing Factors A. Recent MI with resultant structural damage of valve leaflets, chordae, and papillary muscles. B. Most common risk factors for MR: MVP, rheumatic heart disease, infective endocarditis, known coronary artery disease (CAD), and cardiomyopathies. Note the following: 1. Rheumatic heart disease most commonly causes regurgitation of the mitral valve followed by the aortic valve (rarely affects tricuspid or pulmonary valves). 2. Infective endocarditis can technically affect any valve—it most commonly targets the tricuspid but also affects the aortic and mitral valves. C. Possible cause of MS: Age-related degenerative changes or more rare etiologies, including congenital malformations and intracardiac tumors (myxoma). D. AS: Age-related changes, bicuspid aortic valves, and rheumatic heart disease. E. Advanced hypertension (HTN) and atherosclerosis, which can affect valvular function. F. Conditions that can lead to VHD: Autoimmune and connective tissue processes such as systemic lupus erythema-tous and Marfan's syndrome. G. Other conditions that increase risk: Tobacco use, insulin resistance/diabetes mellitus (DM), obesity, and a family his-tory of VHD. H. Acute aortic dissection, which can result in acute life-threatening AR. Subjective Data A. Common complaints/symptoms. 1. AS: Angina, syncope, and findings associated with heart failure (i. e., fatigue, orthopnea, paroxysmal noctur-nal dyspnea, shortness of breath, decreased exercise toler-ance, dyspnea on exertion). 2. AR. a. Acute AR: Dramatic presentation of cardiogenic shock (secondary to infective endocarditis or aortic dissection). b. Chronic AR: Palpitations, angina, heart failure presentation (dyspnea on exertion, peripheral edema, fatigue, paroxysmal nocturnal dyspnea). Valvular Heart Disease

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62 3. MS. a. Often presents with new-onset atrial fibrillation (i. e., fatigue, chest discomfort, palpitations, light-headedness, dizziness). b. Rarely presents with Ortner's syndrome: Occurs with MS where there is compression of the left recur-rent laryngeal nerve due to an enlarged left atrium; results in hoarseness. 4. MR: New-onset atrial fibrillation (similar to MS), anxiety, chest discomfort, dyspnea, fatigue, and/or signs of volume overload consistent with heart failure. B. History of the present illness. 1. Obtain information regarding specific symptom: Onset, provoking/palliative, quality, severity, radiation (if applicable), and timing. 2. Review patient's past medical history: Particularly, recent MIs, known CAD, HTN, or HLD; congenital car-diac abnormalities, previous rheumatic fever, connective tissue disorders, cardiomyopathies, or congestive heart failure (CHF). 3. Determine if the patient ever had a previous car-diac evaluation, especially an echocardiogram, or learned about a heart murmur. 4. Understand that patient scenarios will vary based on the valve affected, type of dysfunction (stenosis or regur-gitation), and underlying etiology. C. Family and social history. 1. Gather information regarding family history of VHD (especially bicuspid aortic valves or MVP), HTN, hyper-lipidemia, CHF, arrhythmias (i. e., atrial fibrillation), or connective tissue disorders. 2. Obtain social history information, especially regard-ing tobacco use, alcohol use, and illegal substance use (very important to document any intravenous drug use due to high risk of infective endocarditis). D. Review of systems. 1. General: Fatigue, malaise, fevers, chills, weight changes, and appetite changes. 2. Skin/Nails: Painful red-purple nodules on hands/feet (Osler nodes of infective endocarditis) and painless red areas on palms/soles (Janeway lesions of infective endo-carditis). 3. Head, ear, eyes, nose, and throat (HEENT): Hoarse-ness. 4. Cardiac: Chest discomfort, palpitations, racing heart-beat, decreased exercise tolerance, peripheral edema, and uncomfortable awareness of heartbeat (associated with AR). 5. Pulmonary: Cough, shortness of breath, dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, and hemoptysis (rare but associated with MS). 6. Gastrointestinal: Increasing abdominal girth. 7. Neurological: Lightheadedness, dizziness, syncope, and near-syncope. 8. Psychological: Anxiety. Physical Examination A. Vital signs: Assess pulse rate and rhythm, blood pressure ( BP), respirations, temperature, and oxygen saturation. 1. Possible tachycardia or bradycardia. 2. Possible irregularly irregular pulse (consistent with atrial fibrillation). 3. Possible hyperthermia (concern for infection) or hypothermia (in geriatric patients with infections who cannot mount fevers). 4. Decreased oxygen saturation (concern for signs of CHF). 5. Possible HTN (acute or long-standing) or hypoten-sion (concern for cardiogenic shock). 6. Widened pulse pressure (associated with AR). 7. Mayne sign: Decrease in BP with arm elevation (asso-ciated with AR). 8. Hill sign: Higher BP in lower as compared to upper extremity (associated with AR). B. General survey: Determine if patient is in acute distress, or asymptomatic. C. Skin/Nails: Assess for Osler nodes and Janeway lesions. D. Head: Possible evidence of head bobbing with each heart-beat (de Musset sign of AR). E. Neck. 1. Consider possible jugular venous distention ( JVD; concern for CHF). 2. Evaluate carotids. a. “Pulsus parvus et tardus” (associated with AS) where there is a weakened and delayed pulse with late carotid upstroke. b. Brisk carotid upstroke (associated with MR). F. Pulmonary: Possible rales or crackles (sign of increased fluid accumulation). G. Gastrointestinal: Possible ascites or hepatomegaly (con-cern for worsening heart failure). H. Cardiac. 1. Inspect for lifts/heaves (concern for ventricular enlargement). 2. Palpate for thrills (grade IV to VI murmurs) and the point of maximum impulse (PMI; if displaced, concern for ventricular hypertrophy). 3. Auscultate for S1, S2, and evidence of extra heart sounds (S3 and S4) and murmurs. a. AS: Harsh late-peaking crescendo-decrescendo systolic murmur that radiates to carotids and best heard over right second intercostal space (ICS), can also have paradoxical splitting of second heart sound. b. Aortic regurgitation: PMI often displaced toward axilla, possible S3, diastolic low-pitched rumbling murmur best heard at left sternal border; can also hear an Austin Flint murmur (severe AR: Low-pitched, rumbling, mid-diastolic murmur; heard best at apex). c. MS: Loud first heart sound, positive high-pitched opening snap after A2 heart sound; nonradiating mid-diastolic murmur best heard at apex. d. MR: Decreased S1, wide splitting of S2, high-pitched holosystolic (can be early systole in acute MR) best heard at cardiac apex and radiates to left axilla. i. MVP: If concern for MVP (associated with MR): Murmur is usually in late systole and associ-ated with the hallmark mid-systolic click that pre-cedes that MR murmur. I. Peripheral vascular: Possible bounding peripheral pulses (water hammer pulse associated with AR), possible peripheral edema. J. Neurological: Mental status examination (if positive mental status changes) and complete neurological examina-tion if concern for associated syncope/near-syncope. Diagnostic Tests A. MS. 1. Routine laboratory studies: Complete blood count, electrolytes, renal function, and liver function. 3. Cardiac Guidelines

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63 2. Chest x-ray: Can see left atrial enlargement, promi-nent pulmonary vasculature, and interstitial edema (Kerley A and B lines). 3. ECG: If severe MS, signs of left atrial enlargement, atrial fibrillation, and right ventricular hypertrophy. 4. T ransthoracic echocardiogram (TTE) to assess overall cardiac function, left ventricular dysfunction, and degree of stenosis. a. Mild: Valve area greater than 1. 5 cm2. b. Moderate: Valve area of 1. 0 to 1. 5 cm2. c. Severe: Valve area less than 1. 0 cm2. d. Consider transesophageal echocardiogram (TEE) if TTE does not produce quality images; there is ques-tion of a left atrial thrombus or prior to surgical inter-vention. 5. Cardiac catheterization is not routine, but can be con-sidered in several circumstances. a. If discrepancy between physical examination and echocardiogram results. b. Patients with severe underlying lung disease and pulmonary HTN who require further evaluation. c. Geriatric patients with severe MS to rule out comorbid CAD. B. AS. 1. Routine laboratory studies: Complete blood count, electrolytes, cardiac biomarkers, renal function, and liver function. 2. ECG: Could be normal, possible left ventricular hypertrophy pattern, and possible atrial fibrillation. 3. TTE. a. Follow recommendations of American Heart Asso-ciation (AHA) for evaluation of grade 3 AS murmurs via TTE. b. Consider stress echocardiogram in asymptomatic patients with severe AS to determine need for clinical intervention. c. Perhaps consider TEE if concern for bicuspid aortic valve. 4. Cardiac catheterization. a. Use if discrepancy between patient presentation and echocardiogram results. b. Consider in patients older than 35 years of age with AS requiring surgical intervention to evaluate for CAD. 5. Exercise stress testing: Absolutely contraindicated in severe symptomatic AS (can be considered in those with asymptomatic severe AS under strict surveillance of car-diologist). 6. CT angiography: Can be used in patients for whom transcatheter aortic valve replacement (TAVR) is being considered. 7. Chest x-ray: Findings vary based on severity of AS. a. In severe AS: May appreciate aortic valve cal-cifications, left atrial enlargement, right-sided heart enlargement, and pulmonary congestion. C. AR: Evaluation is based on clinical scenario and suspected underlying etiology. 1. Laboratory studies. a. For infective endocarditis: Complete blood count, electrolytes, renal function, kidney function, blood cultures, lactate levels, prothrombin time (PT)/partial thromboplastin time (PTT), and international nor-malized ratio ( INR). b. For connective tissue disorders: Consider serologic tests (antinuclear antibody [ ANA], Anti-ds DNA). 2. TTE: Assess valve structure and degree of dysfunc-tion, overall left ventricular function, EF percentage, size of aortic root, and presence of vegetations (TEE may be required if +vegetation on TTE). 3. Cardiac catheterization: Obtain if surgical interven-tion is a consideration, especially if concern for underly-ing CAD. D. MR. 1. Chest x-ray: Possible left ventricular enlargement and increased pulmonary venous congestion (if concomitant CHF). 2. TTE. a. The American College of Cardiology ( ACC) and American Heart Association ( AHA) recommend TTEs for several reasons. i. Evaluate left ventricular size and function. ii. Determine right ventricle and left atrial size, pulmonary artery pressure, and severity of MR. iii. Monitor EF of symptomatic patients with moderate-to-severe MR. iv. Determine etiology of MR. v. Monitor EF and left ventricular size and func-tion if patient has change in clinical status. vi. Evaluate MR integrity and left ventricular function in patients with mitral valve repair or replacement. b. Consider TEE if TTE is nondiagnostic or prior to surgical repair/replacement. Differential Diagnosis A. MS. B. MR. C. MVP. D. AS. E. AR. F. Pulmonic stenosis. G. Acute coronary syndrome. H. T ricuspid stenosis. I. T ricuspid regurgitation. J. Infective endocarditis. Evaluation and Management Plan A. General plan. 1. Determine etiology of given VHD and treat accordingly. 2. Monitor patients for symptoms of worsening VHD. 3. Evaluate patients for determination of management: Medical versus surgical (open approach vs. percutaneous approach, such as TAVR). 4. Manage symptoms associated with given VHD (i. e., CHF). 5. T reat underlying comorbidities that contribute to worsen VHD (i. e., HTN, HLD, DM). B. Patient/family teaching points. 1. Explain underlying etiology and specific type of VHD. 2. Discuss course of therapy: Medical versus surgical and importance of ongoing monitoring. 3. Emphasize importance of compliance with follow-up appointments and medications. a. If utilizing anticoagulation agents: Ensure patients understand not to discontinue drugs prior to any pro-cedures without consulting cardiologist. Valvular Heart Disease

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64 b. If clinically indicated: Educate regarding preinva-sive procedure prophylactic antibiotics. 4. Geriatric patients: Consider involving family mem-bers to help determine best course of treatment. 5. For patients at high risk for endocarditis, discuss use of preprocedure prophylactic antibiotics. 6. Ensure understanding regarding reasons for urgent return to ED such as hemodynamic instability, new or worsening chest discomfort, palpitations, new or worsen-ing difficulty breathing, syncope/near-syncope, or mental status changes. C. Management of specific valvular diseases. 1. AR. a. Surgical intervention via valve replacement: If angina, evidence of CHF, or ventricular failure. b. Medical management: Typically reserved for patients who are not surgical candidates (due to comorbidities) because conservative management of symptomatic patients is rarely successful. i. There is conflicting evidence with regard to use of medical management for asymptomatic patients with AR. ii. With medications: Goal is to reduce after-load via vasodilators such as calcium channel blockers or ACE inhibitors); beta-blockers are not first-line drugs (due to bradycardia) but could benefit patients with significant left ventricular dysfunction. 2. AS. a. According to AHA, there is no acceptable medical management to alleviate AS. b. Available medical therapy is only used to alleviate symptoms and manage comorbidities (diuretics are not indicated due to the possibility of a decrease in cardiac output). i. Beta-blockers (help with HTN and CAD). ii. ACE inhibitors (help with HTN, DM, and left ventricular fibrosis). c. Once patients are symptomatic, considerations should be made for surgery. i. If patient is not a candidate for open (tradi-tional) aortic valve replacement (AVR), consider TAVR. 3. MS. a. Medical management may be useful, although it cannot ameliorate the narrowing of the mitral valve. b. Several classes of medications can be used to assist with symptoms. i. Beta-blockers: Decrease heart rate and improve dyspnea on exertion. ii. Diuretics: Decrease pulmonary edema. c. Symptomatic patients will require surgical inter-vention. There are several options. i. Percutaneous mitral valvuloplasty: Typically used in younger patients and those with mild MS (contraindicated in moderate to severe disease). ii. Surgical procedures: Open repair with com-missurotomy or valve replacement with mechan-ical or bioprosthetic valve (considered high-risk procedures; mortality >20% in geriatric popula-tion with multiple comorbidities). 4. MR. a. Asymptomatic patients with normal BPs and no left ventricular dysfunction do not require treatment. b. Medical therapy can be used for symptom manage-ment (i. e., vasodilators and diuretics to manage BP). c. Symptomatic patients should be considered for surgical repair/replacement. i. If possible, valve repair is preferred to replace-ment: Eliminates requirement of long-term anti-coagulation, improves symptoms, and increases postoperative survival rates. ii. Surgical management indicated if NYHA class II to IV CHF, severe MR regardless of car-diac size and function, or asymptomatic patients with MR and atrial fibrillation, pulmonary HTN, or left ventricular dysfunction. iii. Various percutaneous options are in the devel-opment process. D. Additional pharmacologic considerations. 1. Outpatient anticoagulation. a. INR monitoring is recommended in patients with mechanical prosthetic valves. b. Goal is INR of 2. 0 to 3. 0 in patients with mechan-ical AVR and no other risk of thromboembolism. c. Goal is INR 2. 5 to 3. 5 in patients with a mechan-ical AVR, MVR, and additional risk factors for thromboembolisms (i. e., atrial fibrillation, previous thromboembolism). d. Low-dose daily aspirin is recommended in addi-tion to anticoagulation in patients with a mechanical valve prosthesis. e. Low-dose daily aspirin can be used in patients with a bioprosthetic aortic or mitral valve. f. Anticoagulation can be used for the first 3 months after bioprosthetic MVR or AVR or repair to achieve an INR of 2. 5. g. Can consider clopidogrel 75 mg daily for the first 6 months after TAVR in addition to daily lifelong aspirin. 2. Anticoagulation with bridging. a. Continuation of anticoagulation with a ther-apeutic INR is recommended in patients with mechanical heart valves undergoing minor procedures (i. e., dental extractions or cataract removal) where bleeding is easily controlled. b. Bridging anticoagulation with heparin is rec-ommended for invasive procedures when the INR is subtherapeutic preoperatively in those with a mechanical AVR, any thromboembolism risk factor, older generation mechanical AVRs, or a mechanical MVR. E. Discharge instructions. 1. Ensure patient receives all prescriptions prior to discharge. 2. Arrange timely follow-up appointments with cardiologist. 3. Educate patients about reasons to return to ED with regard to worsening symptoms of VHD. 4. Based on clinical scenario and degree of VHD, pro-vide patients with information regarding physical activity restrictions. Follow-Up A. Patients require monitoring via history/physical examina-tions and echocardiography based on clinical scenario, degree of VHD, and overall cardiac status (i. e., EF and left ventric-ular function). In AS, for example: 1. If mild disease, echocardiograms every 3 to 5 years. 3. Cardiac Guidelines

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65 2. If moderate disease, echocardiograms every 1 to 2 years. 3. If severe disease, echocardiograms every 6 months to 1 year. Consultation/Referral A. Consult with cardiologist for VHD. B. Consult with infectious disease specialist (if concern for underlying infective endocarditis). C. Consult with rheumatologist (if concern for underlying connective tissue disorder). D. Consult with cardiothoracic surgeon (if surgical repair is a consideration). E. Consult with interventional cardiologist (if consideration for TAVR). F. Refer to cardiac rehabilitation following invasive valve repair/replacement procedure. Special/Geriatric Considerations A. Antibiotic prophylaxis. 1. According to AHA, preinvasive procedure prophylac-tic antibiotics (against Streptococcus viridans ) should be used in certain populations and scenarios with risk of infective endocarditis. a. Prosthetic heart valve. b. History of previous infective endocarditis. c. Congenital heart disease (CHD) that is unrepaired and cyanotic, repaired CHD using prosthetic materi-al/device for 6 months, or repaired CHD with a resid-ual defect. d. Cardiac transplant patients with VHD. e. Recommended for patients with MVP or moderate to severe primary MR. f. Procedures: Dental (if manipulation of gingiva, perforation of oral mucosa, or significant teeth manipulation) or respiratory (i. e., tonsillectomy, ade-noidectomy). Amoxicillin (2 g 1-hour preprocedure),clindamycin (600 mg 1-hour preprocedure), or cephalexin (2 g 1-hour preprocedure) may be used. B. Geriatric considerations. 1. Aortic valve disease is the most common type of VHD in this demographic. 2. If surgical intervention is a consideration, it is impor-tant to assess underlying CAD risk, cognitive status, and overall health status. 3. For elderly patients with severe AS who are not sur-gical candidates, consultation should be obtained for TAVR, which is minimally invasive. 4. If valve replacement procedure is indicated, it is nec-essary to assess risk versus benefit regarding use of antico-agulation. 5. It is important to remember that VHD symptoms in this population can be vague (i. e., fatigue and dyspnea) and difficult to differentiate from normal aging. Bibliography Christensen, B. (2018, December 4). Endocarditis prophalaxis, adults. In B. Christensen (Ed. ), Medscape. Retrieved from http://emedicine. medscape. com/article/2172262-overview Dima, C. (2018, February 2). Mitral stenosis. In T. X. O'Brien (Ed. ), Med-scape. Retrieved from http://emedicine. medscape. com/article/155724-overview Hanson, I., & Alfanso, L. C. (2018, November 28). Mitral regurgitation. In T. X. O'Brien (Ed. ), Medscape. Retrieved from http://emedicine. medscape. com/article/155618-overview Karavas, A. N., & Edwards, N. M. (2016). Valvular heart disease. In J. B. Halter, J. G. Ouslander, S. Studenski, K. P. High, S. Asthana, M. A. Supiano, & C. Ritchie (Eds. ), Hazzard's geriatric medicine and gerontology (7th ed. ). New York, NY: Mc Graw-Hill. Retrieved from http://accessmedicine. mhmedical. com. ezproxy2. library. drexel. edu/content. aspx?bookid=1923&sectionid=144524931 Ren, X. (2017, March 23). Aortic stenosis. In T. X. O'Brien (Ed. ), Med-scape. Retrieved from http://emedicine. medscape. com/article/150638-overview Wang, S. S. (2018, November 19). Aortic regurgitation. In T. X. O'Brien (Ed. ), Medscape. Retrieved from http://emedicine. medscape. com/article/150490-overview Valvular Heart Disease

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

67 4 Gastrointestinal Guidelines Catherine Harris Acute Abdomen Shawn Mangan Definition A. Acute abdomen is defined as pain, which arises sud-denly and is usually less than 48 hours duration. Acute abdomen sometimes requires urgent surgical intervention, but not always. B. Nontraumatic pain in the abdominal region with an onset of less than a few days and has worsened progressively until presentation. C. Conditions categorized under acute abdomen. 1. Abdominal aortic aneurysm (AAA). 2. Acute cholecystitis. 3. Acute mesenteric ischemia. 4. Acute pancreatitis. 5. Appendicitis. 6. Diverticulitis. 7. Ectopic pregnancy/ovarian torsion. 8. Intestinal obstruction. 9. Perforated duodenal ulcer. Incidence A. Acute abdomen accounts for approximately 5% to 10% of all ED visits. B. Approximately 20% of these patients will have small bowel obstruction, 14% will be diagnosed with appendici-tis, 5% with cholecystitis, and less than 1% with perforated peptic ulcer. Another 25% will not be able to be diagnosed and will be discharged from the ED. Pathogenesis A. Acute abdomen depends on the origin of the pain: Ischemia, distension, obstruction, ulceration, or inflamma-tion in the affected area. Predisposing Factors A. Previous abdominal surgery. B. Diverticulitis. C. Constipation. D. History of gallstones. E. Abdominal cancers. F. Peptic/duodenal ulcers. G. Crohn's disease or ulcerative colitis. H. Severe endometriosis or ectopic pregnancy. I. Medications including nonsteroidal anti-inflammatory drugs (NSAIDS), steroids. J. Alcohol abuse. 1. Age greater than 50. Subjective Data A. Common complaints/symptoms. 1. Right upper quadrant (RUQ). a. Cholecystitis: Colicky, intermittent waves of pain that come and go. The pain may radiate to back, cause nausea, and worsen after a fatty meal. Pain improves with rest. b. Peptic ulcer disease: Pain worsens after a meal. c. Pancreatitis: Diffuse, burrowing, stabbing pain radiates to mid back. 2. Right lower quadrant (RLQ). a. Appendicitis: Starts in mid abdomen, becoming more acute in RLQ. Sometimes nausea and vomiting occur. 3. Left lower quadrant (LLQ). a. Diverticulitis. B. Common/typical scenario. 1. AAA: If ruptured, patients who do not die immedi-ately present with abdominal or back pain, hypotension, and tachycardia. They may have a recent history of strain-ing (such as lifting a heavy object), and most will also have a history of hypertension. 2. Acute cholecystitis: Abrupt, severe, constant, aching pain in RUQ with radiation to the back and right shoul-der lasting 24 hours or more, associated with nausea and vomiting. 3. Acute mesenteric ischemia: Patients are usually greater than 50 years old. a. Arterial: Sudden onset of severe pain out of pro-portion to physical findings (abdomen soft; little or no tenderness) in patients at risk (coronary artery dis-ease, atrial fibrillation, generalized atherosclerosis, low flow states). Patients may have a history of post pran-dial pain suggesting intestinal angina. However, many patients have no identifiable risk factors. b. Venous: Similar symptoms to arterial, but with a more gradual onset. 4. Acute pancreatitis: Steady, piercing, upper abdomi-nal pain, severe enough to require intravenous (IV) opi-oid pain management. Pain radiates to the back in some patients. Patients may find pain reduction by sitting up and leaning forward. Nausea and vomiting may be present. The pain develops suddenly in gallstone pancre-atitis. In alcoholic pancreatitis, pain usually develops over several days. 5. Appendicitis: In about 50% of patients, epigastric or periumbilical pain is followed by nausea, vomiting, then Acute Abdomen

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

68 pain shifting to the RLQ. Direct and rebound tenderness at Mc Burney's point is present. In other patients, pain may not be localized or may be diffuse. 6. Diverticulitis: Pain or tenderness in the LLQ with fever. Rebound or guarding, nausea, vomiting, and abdominal distention occur if concurrent bowel obstruc-tion is present. 7. Ectopic pregnancy: Sudden, severe pelvic pain and/or vaginal bleeding followed by syncope and signs of hem-orrhagic shock in females of reproductive age. 8. Intestinal obstruction. a. Small bowel: Cramping near epigastrium, vomiting (with some relief in pain), and, if complete obstruction, obstipation. Range of bowel sounds on auscultation from high pitched peristalsis in early presentation to no BS in later presentations. b. Large bowel: Gradual development of consti-pation, then abdominal distention, lower abdomi-nal cramps, and borborygmi (loud prolonged bowel sounds). 9. Perforated duodenal ulcer—sudden agonizing pain usually in patients with history of peptic ulcer disease or NSAID therapy. Frequently occurs in the elderly (60 to 70 year age group). Pain occurs initially in the upper abdomen then becomes diffuse. Patients lay still, in a knee to chest position, breathe shallowly, and are tachy-cardic. Hypotension and fever are late findings. Abdomen appears nondistended with board-like rigidity. C. Family and social history. 1. Smoking. 2. Alcohol abuse. 3. Low fiber or fatty diet. 4. Obesity. 5. Family history may increase risk. D. Review of systems. 1. SOCRATES acronym. a. Site: Ask about location of pain. b. Onset: Inquire about exact time and mode of pain. Did it occur suddenly or gradually? c. Character: How is the pain characterized? Is it con-fined to one area or all around? Is the pain dull or sharp? d. Radiation or referral of pain: Does the pain stay in one place or does it move around? e. Associated symptoms: Is there any weight loss, nausea, vomiting, diarrhea, constipation, pain on uri-nating, skin discoloration, vaginal bleeding? f. Time course: Is the pain continuous or intermit-tent? g. Exacerbating/relieving factors: Does it hurt to cough, eat, or does it feel better to vomit? h. Severity: Can the pain be measured on a scale from 1 to 10, 10 being the worst pain ever felt? Physical Examination A. Vital signs: Check postural VS to assess for hypovolemia or bleeding. B. Inspection: From nipples to knees. 1. Distention. 2. Scars. 3. Ecchymosis such as Grey T urner sign. C. Auscultation. 1. Bowel sounds (hyperactive/hypoactive/absent?). 2. Bruit. D. Palpation. 1. Rebound tenderness. 2. Ask patient to cough to ascertain peritonitis. 3. Guarding. 4. Organomegaly. 5. Hernia. 6. Rectal, pelvic, testicular examination. E. Diagnosis: Specific findings. 1. AAA. a. Abdomen rigid or distended, very tender. b. Shock-like symptoms (pallor, diaphoresis, tachy-cardia). 2. Ectopic pregnancy. a. Appears toxic and shock-like symptoms. b. Lower abdominal tenderness. 3. Appendicitis: Guarding and rebound tenderness, prefers fetal position. 4. Diverticulitis: LLQ pain. 5. Biliary colic cholecystitis: RUQ pain with Murphy's sign. 6. Renal colic: Severe pain, costovertebral angle tender-ness on affected side. 7. Pancreatitis. a. Epigastric tenderness, abdominal distention, fever, and tachycardia. b. Signs of jaundice. c. May develop Cullen or Grey T urner sign. 8. Special abdominal examination maneuvers: Prior to the advent of radiologic imaging, several clinical maneu-vers were utilized to differentiate abdominal pain diag-noses. While most of these tests will be followed by imaging studies today to confirm findings, they are still utilized. a. Iliopsoas sign: Have the patient roll on his/her left side and hyperextend the right hip joint. If pain is present, the test is positive and suggests irritation of the iliopsoas muscle by appendicitis. b. Obturator sign: With the patient supine, passively flex the thigh and rotate inward. If pain is elicited, the obturator muscle is inflamed because of pathology such as appendicitis, diverticulitis, pelvic inflamma-tory disease, or ectopic pregnancy. c. Rovsing sign: Apply pressure to the LLQ. If pain is referred to Mc Burney's Point (RLQ), the test is positive and appendicitis is suspected. d. Murphy's sign: Ask the patient to take a deep breath while palpating the RUQ. If the patient abruptly stops inspiration, the sign is positive and suggests acute cholecystitis. e. Cullen and Grey T urner signs: Both Cullen and Grey T urner signs are associated with ecchymosis on the abdomen. i. Cullen sign is superficial edema and bruising in the subcutaneous tissue around the umbilicus. This is associated with ruptured ectopic pregnan-cies but can be seen in other conditions as well such as pancreatitis or trauma. ii. Grey T urner sign is bruising along the flank associated with retroperitoneal bleeding or intraabdominal bleeding. Diagnostic Tests A. Ordered based on differential diagnosis, but can include: 1. In all women of childbearing age, assume the woman is pregnant unless proven otherwise; use HCG test, or possibly transvaginal ultrasound (US). 2. Complete blood count (CBC) with differential. 3. Metabolic panel. 4. Electrolytes. 5. Amylase and lipase. 4. Gastrointestinal Guidelines

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

69 6. Consider blood culture in elderly with fever or hypothermia for suspected sepsis. 7. Urinalysis. 8. Abdominal x-ray. 9. Chest x-ray. 10. EKG to rule out cardiac cause of pain. 11. Consider abdominal US. 12. Consider CT abdomen with PO and IV contrast. 13. Consider e ndoscopic retrograde cholangiopancre-atography (ERCP) to visualize distal common bile duct. 14. Helicobacter pylori testing. 15. Endoscopy. 16. Stool guaiac. 17. Colonoscopy. Differential Diagnosis A. Location and duration of abdominal pain can often help in narrowing. 1. RUQ pain. a. Acute cholecystitis and biliary colic. i. Biliary tract—Increased serum amylase. ii. Ascending cholangitis presents with fever and jaundice. iii. In acute cholecystitis, pain radiates to scapula associated with nausea, vomiting, and fever. Mur-phy's sign (inspiratory arrest in response to deep RUQ palpation) may be seen. b. Perforated duodenal ulcer: Accompanied by increased serum amylase. c. Acute pancreatitis. i. Bilateral right and left upper quadrant pain. ii. Accompanied by increased serum amylase. d. Myocardial infarction. e. Pulmonary pathology. 2. RLQ pain. a. Appendicitis: Dull, steady periumbilical pain and nausea, which then localizes to the RLQ at Mc Bur-ney's point. b. Abdominal aneurysm. c. Ruptured ectopic pregnancy/ovarian cyst. d. Incarcerated inguinal hernia. e. Diverticulitis. 3. LUQ pain. a. Acute pancreatitis: Epigastric pain which radiates to the back and is associated with nausea. b. Splenic enlargement infarction or aneurysm. c. Myocardial ischemia. d. Left lower lobe pneumonia. 4. LLQ pain. a. Diverticulitis. b. Aortic aneurysm. c. Ruptured ectopic pregnancy/ovarian cyst. 5. Must not miss diagnoses. a. Small bowel obstruction. b. Large bowel obstruction. c. Nonspecific bowel pain. i. Appendicitis. ii. Perforated ulcer. iii. Acute cholecystitis. 6. Common abdominal pain culprits. a. Acute pancreatitis. b. Diverticulitis. c. Acute pyelonephritis. Evaluation and Management Plan A. General plan. 1. Determine if patient is hemodynamically stable and if peritoneal signs are present. 2. Obtain imaging studies and treat based on suspected condition. a. AAA. i. If rupture is suspected, attempts at hemody-namic stability are begun as the patient is opti-mized for surgery. An US provides bedside results to assist in diagnosis (without treatment, mortality rate approaches 100%). ii. Patients who present in shock will need fluid resuscitation but mean arterial pressure should not exceed 65 mm Hg to prevent further bleeding. iii. If the patient is stable, abdominal CT or com-puted tomography angiography (CTA) can more precisely characterize aneurysm size and anatomy to assist with surgical intervention if necessary. 1)Surgical options include endovascular stent grafting VS open repair. 2)Medical management if AAA less than 5 mm includes repeat imaging every 6 to 12 months to monitor for size increase greater than 5 mm or to assess for rapid growth. Both are indications for elective surgical repair. b. Acute cholecystitis. i. On examination, RUQ pain to palpation with inspiratory arrest ( +Murphy's sign). ii. US (showing presence of stones, gallbladder wall thickening, or enlargement) is the study of choice and can often establish the diagnosis. iii. Management. 1)Medical—single episode may not warrant surgery. Counsel patient to avoid fatty foods, fasting, or starvation diets and to see provider for recurrent pain. Tylenol PRN for pain. Acti-gall decreases amount of cholesterol produced by the liver and absorbed by intestines and may be helpful. 2)Surgical management—laparoscopic cholecystectomy. Conversion to open pro-cedure occurs approximately 5% of the time. 3)Surgical cases a need liver and pancreatic enzyme levels assessed, as elevated levels may show common duct stones. c. Acute mesenteric ischemia. i. Clinical diagnosis is more important than testing due to time delay. Increased mortality is observed once intestinal infarction occurs. Intesti-nal infarction can occur as soon as 10 hours after the onset of symptoms. Untreated, mortality approaches 90%. ii. Proceed directly to surgery for diagnosis and treatment in patients with peritoneal signs. CTA is used if diagnosis is unclear. iii. Support blood pressure (BP) with IV fluids (avoid vasopressors), adequate oxygenation, broad spectrum antibiotics, and adequate pain control. Consider anticoagulation. iv. T reatment involves surgical embolectomy and revascularization with possible bowel resec-tion. Angiographic vasodilators (papaverine) or thrombolytics may be used. v. Depending on the severity of bowel ischemia, the patient may require a long inpatient hospital stay, maintaining nil per os (NPO) status, and sup-porting nutrition with total parenteral nutrition. Acute Abdomen

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf

70 vi. Find and treat predisposing causes. vii. Plan for long-term anticoagulation. d. Acute pancreatitis: Condition ranges from mild abdominal pain and vomiting to severe with systemic inflammatory response syndrome (SIRS) response, shock, and multiorgan failure. e. Mortality rates are as high as 40% to 50% of cases. Important to assess the severity of illness on admis-sion utilizing tools (Ranson criteria, others) that pre-dict mortality risk. Early recognition of severe pan-creatitis improves outcomes by risk stratification and correct admission placement of the patient. i. Diagnose based on clinical suspicion, espe-cially in patients with a history of gallstones or chronic heavy alcohol abuse and noting elevated amylase and lipase. ii. Urine dipstick for trypsinogen-2 has sensitiv-ity and specificity of greater than 90%. WBC ele-vation range is 12 to 20,000. Imaging with plain abdominal film shows calcifications within pancre-atic ducts and gallstones. Obtain US if gallstone pancreatitis is suspected. CT abdomen with con-trast is usually done to identify necrosis, fluid col-lection, or cysts once condition is diagnosed. iii. T reatment includes fluid resuscitation (up to 8 L/day), maintaining NPO status (until tender-ness subsides, amylase WNL), pain control, antibi-otic therapy if pancreatic necrosis, and drainage of collections. f. Appendicitis. i. Surgical management: Appendectomy. ii. Medical management: Antibiotics may be used to treat uncomplicated, nonsurgical appendicitis; however, there are recurrences. More studies need to be done in order to determine the efficacy of antibiotic therapy alone. g. Diverticulitis. i. Typical presentation is with LLQ pain with or without peritonitic findings; an absence of vom-iting; fever; and leukocytosis with left shift. May also complain of back pain, flatulence, borborygmi (loud prolonged bowel sounds), diarrhea, or con-stipation. ii. A C-reactive protein greater than 50 mg/L, along with LLQ pain and absence of vomiting, is highly predictive of acute colonic diverticulosis. iii. CT scan of abdomen and pelvis is the current gold standard in confirming the diagnosis of acute diverticulitis if the clinical picture is unclear. iv. US is fast becoming an additional modality in diagnosis of the disease. v. Management. 1)Medical: Bowel rest. nil per os (NPO). NG tube placement to low suction, IV fluid replacement therapy. Antimicrobial therapy covering gram negative organisms and anaer-obes should be initiated when associated with systemic manifestations of infection. If relapse, same regimen ×1 month. 2)Surgical resection for abscess, peritonitis, obstruction, fistula, failure to improve after several days, or recurrence. 3)Nonsurgical cases should be referred for a colonoscopy 4 to 6 weeks after the event. h. Ectopic pregnancy. i. Urine pregnancy test (beta-hcg) is 99% sensi-tive for ectopic and uterine pregnancy. If positive,follow with serum beta-hcg and transvaginal pelvic US. Diagnostic laparoscopy may be necessary for confirmation. ii. Surgical resection is usually necessary to treat. If possible, salpingotomy is done to conserve the tube. Salpingectomy indicates when ectopic preg-nancies are greater than 5 cm, when tubes are severely damaged, or when no future childbearing is planned. iii. Resuscitate if hemodynamically unstable or in hemorrhagic shock and prepare for immediate surgery. iv. Methotrexate may be an option if unruptured tubal pregnancy is less than 3 cm, no fetal heart activity is heard, and beta-hcg level is less than 5,000. Follow-up within 1 week for repeat beta-hcg level. i. Intestinal obstruction. i. Supine and, if possible, upright abdominal x-rays are usually adequate to diagnose obstruc-tion, showing a “coiled spring” sign in a series of distended small bowel loops or right colon. Large bowel obstruction shows distention of the colon proximal to the obstruction. ii. T reatment for both small and large bowel obstruction includes NG decompression and resuscitation with IV crystalloid fluid administra-tion and IV antibiotics covering gram negative and anaerobes if bowel ischemia is suspected. iii. Complete obstruction of small bowel is treated with early laparotomy. iv. Obstructing colon cancers can be treated with resection and anastomosis, with or without a colostomy or ileostomy. j. Perforated duodenal ulcer. i. Upright chest x-ray reveals free air. Upper GI film with water-soluble contrast is also helpful to diagnose perforation and if it has healed sponta-neously. ii. Leukocytosis and elevated amylase usually present. iii. In approximately 50% of cases, the perfora-tion self-heals. Those who are poor surgical can-didates or who present more than 24 hours after perforation and who are stable may be admitted. Provide careful observation for clinical deteriora-tion, IV fluids, NG suction, and broad spectrum antibiotics. Low threshold for surgical repair if condition deteriorates. 1)H. pylori infection is implicated in 70% to 90% of all perforated ulcers. Medical therapy for peptic ulcer disease includes the combination of omeprazole 20 mg BID, plus clarithromycin 500 mg BID, plus metronida-zole 500 mg TID ×14 days; for non-PCN allergic patients. B. Patient/family teaching points. 1. Do not take laxatives, use enemas, or take medi-cations, food, or liquids until consulting a healthcare provider for suspected abdominal pain and the following: a. Increased or unusual looking vomit or stool. b. Hard, swollen abdomen. c. Lump in scrotum, groin, or lower abdomen. d. Missed period or suspected pregnancy. 2. Engage in activity as tolerated. Abdominal pain with nausea and vomiting, fever, or pain that lasts more than4. Gastrointestinal Guidelines

Adult-Gero Acute Care Practice Guideline by Catherine Harris Ph.d. z-lib.org 1.pdf