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Peyton Roi List (born April 6, 1998) is an American actress and model. List appeared in various films and television episodes as a young child and modeled for tween magazines and companies. In 2011, she joined the cast of Jessie as Emma Ross, the eldest of four siblings that are being cared for by a young nanny. In 2015, she reprised the role in the spinoff series Bunk'd. She is also recognized for playing Holly Hills in the Diary of a Wimpy Kid film series, and for the role of Tory in the television series Cobra Kai. She also starred as Ellie O'Brien in the 2016 Disney Channel Original Movie The Swap. List was born April 6, 1998. She has two brothers, her twin Spencer, and a younger brother, Phoenix, both of whom are actors. She attended The Carroll School (P.S. 58) for elementary school, and the New Voices School for Academic and Creative Arts (M.S. 443) for middle school, both in New York City. She attended Oak Park High School in Oak Park, California, where she graduated in 2016. List first began acting with television and film appearances. She first made an uncredited appearance on the soap opera As the World Turns in 2002. In 2004, she appeared on the television show All My Children as Bess, and in the same year made a cameo appearance in the feature film Spider-Man 2, which was uncredited. She continued to appear in guest roles and cameos as well as making another uncredited appearance on the live show Saturday Night Live until 2008, when she had her first major role in the feature film 27 Dresses, starring as the young version of the character Jane Nichols. The film was a commercial success, and served as List’s acting debut. List began to appear in more feature films, and in 2010 was cast in alongside Robert Pattinson in the film Remember Me, as a girl who bullies Pattinson's character's little sister. The film was a box-office success. In the same year, List had begun her work with Disney, and appeared in the Disney film The Sorcerer's Apprentice, which turned to be a box-office bomb. She also was cast in Lifetime Movie Network's Secrets in the Walls, alongside Jeri Ryan and Kay Panabaker. List starred in and . She had a major role as Holly Hills, the crush of Greg. The cast, including List, had won a Young Artist Award. From 2011 to 2015, she starred as Emma Ross, the eldest of four children, on the Disney Channel series Jessie alongside Debby Ryan and her Diary of a Wimpy Kid co-star Karan Brar. On February 25, 2015, it was announced that Jessie would end after its fourth season, and that List, along with Brar and Skai Jackson, would reprise their roles in the spinoff series Bunk'd. List is an active member of the Disney Channel Circle of Stars. List was a 2011 model for Justice magazine. She has also appeared on the cover of the American Girl's 2009 Back to School issue. She has appeared in over four hundred advertisements in various formats for various companies. She performed with Ingrid Michaelson at one of Michaelson's concerts. In 2018, List released her first single "Liar Liar". Peyton List shares the same name with a fellow actress, Peyton List (born 1986). The younger List was interviewed by Access Hollywood, saying she uses Peyton R. List to avoid confusion. Union SAG-AFTRA's policy avoids actors with the same name; this instance went unnoticed. They appeared in the same scene -- when the older List starred on As the World Turns as Lucy Montgomery. Years later, the younger List cited confusion when they stayed at the same hotel -- they received daily call sheets and voicemails for each other. IndieWire noted the confusion appeared on the website Wikipedia, where both actresses's articles started out with exactly the same introduction text of: "Peyton List is an American actress and model." As of March 2011, List lived with her family in New York. The family had moved to Los Angeles by the time List was 16. Kevin Quinn (born May 21, 1997) is an American actor. He is known for his starring role as Xander in the Disney Channel original series Bunk'd, and his supporting role in the 2016 Disney Channel Original Movie Adventures in Babysitting. Quinn was born in Chicago, and grew up in Wilmette, Illinois. Son of Brian Quinn, an advertising executive, and Tamara Quinn, founder of Pulling Down the Moon. He has a twin sister. Growing up, Kevin Quinn was involved in Musical Theater productions at the Children's Theater of Winnetka, a lesser known theater company near his hometown. He began his professional career by appearing in episodes of Shameless and Chicago P.D. Before being on Disney, he auditioned for season 12 of American Idol. He wound up being one of the top 60 males in the country. He then played Jonny in Steppenwolf Theater's production of Lord of the Flies, and the role of “Boy” in the Chicago Shakespeare Theater adaption of Henry V. In 2015, Quinn was cast on the spinoff Disney Channel series Bunk'd. In 2016, he appeared in the Disney Channel Original Movie Adventures in Babysitting. Christina Moore (born April 12, 1973) is an American actress, comedian, fashion designer, model, and screenwriter. She was part of the main cast of comedians on the sketch comedy series MADtv, and also portrayed Laurie Forman on That '70s Show during the sixth season, and Candy Sullivan on Hawthorne. She had a recurring role in 90210. Christina Moore was born in Palatine, Illinois. She became interested in performing as a young girl at her family's church by getting involved with children. When she was in high school, she toured with a children's musical theatre troupe throughout the city of Chicago. Moore's first professional job was in summer stock in Evansville, Indiana, where she performed in Young Abe: the Abraham Lincoln Boyhood Outdoor Musical Drama. Her theatre credits included roles in stage productions of Annie, Cinderella and Big River. Her father is Carroll Moore and her mother is Joy Moore. She has three older sisters. After graduating from Illinois Wesleyan University School of Theatre Arts, Moore moved to Los Angeles to pursue her acting career. Moore's television credits included the UPN comedy, The Bad Girl's Guide and Hyperion Bay. She had recurring roles on Pasadena and Unhappily Ever After, with additional television credits that include guest appearances on 24, Just Shoot Me!, Friends, and Suddenly Susan. Moore joined the cast of MADtv in 2002, as a feature performer, for the eighth season. Moore was noted for her impressions of Christina Aguilera, Shannon Elizabeth, Sharon Stone, Trista Rehn, and Brittany Murphy. Moore is one out of three former members of the MADtv cast to join the cast of That '70s Show. Mo Gaffney appeared in Seasons 4 and 5 of That '70s Show as Joanne Stupak, Bob Pinciotti's girlfriend. The other MADtv alumnus is Josh Meyers, who played Randy Pearson in That '70s Show during its final season. Christina Moore appeared in Married to Children as the Hideous Woman in the episode "Twisted" (1996). She left the MADtv at the conclusion of the eighth season to join the cast of That '70s Show. She replaced Lisa Robin Kelly as Laurie Forman during the show's sixth season. In 2005, she starred in the TV series Hot Properties, which had aired 13 episodes. Moore also starred in Without a Paddle and Dave Barry's Complete Guide to Guys. Moore also appeared in Two and a Half Men as Cynthia Sullivan in the episode "The Soil is Moist" (2008). Moore played Alan Harper's rebound lover on Two and a Half Men. In 2008, she began a recurring role on The CW's 90210 as Tracy Clark, the sexy and mischievous mother of Naomi Clark. Moore also narrates various audio books, including Diane Duane's Young Wizards series and Yellow Star. She was part of the main cast of Hawthorne playing Candy Sullivan. Moore is a founding member of Bitches Funny, an all-female sketch group that has performed in New York City and Los Angeles for the past five years. She also had a recurring role in the Disney Channel shows Jessie and Bunk'd, as Christina, the mother of the Ross children, as well as Vanessa Baxter's empty-headed sister April on the former ABC sitcom Last Man Standing. Moore has been married to actor John Ducey since 2008. Pray for Rain (2017), Running Wild (2017)

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The 2015 College Football Playoff National Championship was a bowl game that determined a national champion of NCAA Division I FBS college football for the 2014 season, which took place at AT&T; Stadium in Arlington, Texas on January 12, 2015. It was the culminating game of the 2014–15 bowl season as the inaugural College Football Playoff National Championship, replacing the BCS National Championship Game. The national title was contested through a four- team bracket system, the College Football Playoff, which replaced the previous Bowl Championship Series. The game was played between the winners of two designated semi-final bowl games played on January 1, 2015: the No. 4 Ohio State Buckeyes, who upset No. 1 Alabama 42–35 in the 2015 Sugar Bowl, and the No. 2 Oregon Ducks, who defeated previously unbeaten No. 3 Florida State 59–20 in the 2015 Rose Bowl. This was the first championship game since 2006 that did not feature at least one SEC team, and the teams' first meeting since the 2010 Rose Bowl, which the Buckeyes won 26–17. The Ohio State Buckeyes won the game, 42–20, marking the first national championship awarded under the CFP system. Following the game, the AP Poll and Coaches' Poll also named Ohio State as their top team of the season, marking Ohio State's first national championship since 2002 and their 8th overall. AT&T; Stadium (capacity 80,000) was announced as the host site in April 2013. Arlington and Tampa (Raymond James Stadium) were the only cities to submit hosting bids for the inaugural title game. Each team received 20,000 tickets. Premium seat packages for the event cost $1,899 to $3,899 apiece. The packages can include hotel accommodations, game tickets, parking access, pregame hospitality, and an on-field postgame experience. College Football Playoff announced that 1,000 tickets will be made available for purchase to fans who have signed up for a random drawing by May 1, 2014. On March 25, 2014, Dr Pepper was announced as the official championship partner and presenting sponsor of the new College Football Playoff National Championship Trophy. The cost of a thirty-second commercial during the game broadcast reached upwards of $1 million. Before the game, students dressed in all black from the Episcopal School of Dallas and Saint Philip's School held 15 ft. tall banners of every collegiate football team and marched to Fall Out Boy's "Legends." The students then held out a large American Flag while country music band Lady Antebellum performed the "Star Spangled Banner." The students ran off the field carrying the flag. One student tripped while running off and was dragged hanging onto the flag by the rest. then helped him up off field. The teams playing for the national championship were the winners of semifinal bowl games held on January 1, 2015. The semifinal games were the Rose Bowl in Pasadena and the Sugar Bowl in New Orleans. The semifinal participants were chosen and ranked 1–4 by the 13-member playoff selection committee, with 1 playing 4 and 2 playing 3. Ohio State was 20–24 all-time in bowl games. The Buckeyes made their fifth visit to the state of Texas, having won 4 previous games and outscoring four different schools 120–33. Ohio State, all-time, came into the game with an 8-0 record against Oregon. Oregon is 13–15 all-time in bowl games. The Ducks are 6–4 in Texas having won three straight games and played their third game in the Dallas-Fort Worth metroplex (Dallas, Fort Worth and now Arlington). Source: Oregon received the opening kickoff and drove down the field for a touchdown, earning an early 7-0 lead on a 7 yard TD pass from Marcus Mariota to Keanon Lowe. After an exchange of punts, Ohio State started their second possession at their own 5 yard line. On 3rd and 8, Cardale Jones completed a 26 yard pass to wideout Corey Smith for a 1st down. Ohio State then converted a 4th and 3 from the Oregon 38 yard line to keep the drive alive. On the very next play, Ezekiel Elliott broke several tackles for a 33 yard TD scamper, tying the game at 7. A dropped pass on the Ducks next drive led to a punt, which Ohio State returned to the Oregon 46 yard line. A critical pass interference call set Ohio State up near the goal line, and the Buckeyes capitalized with a 1 yard TD pass from Jones to tight end Nick Vanett. The first quarter ended with Ohio State leading Oregon 14-7. After another Oregon punt, the Buckeyes had a chance to stretch their lead, but a mishandled exchange between Jones and Elliott gave Oregon the ball back. The Ducks marched to the goal line, but failed on 4th and Goal from the 3 yard line. Ohio State escaped the shadow of the goal line, and drove 90 yards, but WR Corey Smith fumbled at the Oregon 11-yard line. Despite the reprieve, the Ducks once again had to punt, and this time, Ohio State made them pay. A Cardale Jones QB sneak from a yard out gave Ohio State a 21-7 lead. Oregon closed out the first half scoring with a field goal, leaving the Buckeyes ahead 21-10 at the break. Ohio State got the ball to begin the second half and drove into Oregon territory. However, Jones threw an interception at the Oregon 30 yard line. The Ducks capitalized on this turnover immediately, with Marcus Mariota finding wide receiver Byron Marshall for a 70-yard touchdown on the first play after the turnover, bringing the Ducks within 21-17. On the next Ohio State drive, Tyson Coleman sacked Jones, and recovered the resulting fumble, setting up an Oregon field goal. The 1 point deficit at the 6:39 mark of the 3rd quarter was as close as Oregon would come. Ohio State closed out the quarter with a 75 yard drive, culminating in a 9 yard Ezekiel Elliott 9 yard touchdown run. The 4th quarter began with an Oregon punt, and Ohio State went 76 yards for another touchdown, with Elliott finding paydirt from 2 yards out for a 35-20 Ohio State lead. A desperate Oregon went for it on 4th and 11 at their own 14 with under 3 minutes to play, but failed. The Buckeyes iced the game on Elliott's 4th touchdown run of the game, providing the final 42-20 margin. Completions/attempts Carries Long gain Receptions The game was televised by ESPN with Chris Fowler and Kirk Herbstreit as English commentators, and Heather Cox and Tom Rinaldi as English sideline reporters and on ESPN Deportes with Eduardo Varela and Pablo Viruega as Spanish commentators. ESPN revived the Megacast coverage it had employed during the 2014 BCS National Championship Game: other ESPN networks (including ESPN2, ESPNEWS, ESPN Classic, ESPNU, and ESPN3) supplemented coverage with analysis and additional perspectives of the game. Approximately 33.4 million watched the game. The game set a cable television record for ratings, receiving an 18.5 Nielsen rating. The game was broadcast on nationwide radio by ESPN Radio with Mike Tirico and Todd Blackledge on the call, with Holly Rowe and Joe Schad on the sidelines. Locally, the game was broadcast on radio by the Oregon IMG Sports Network flagshiped by KUGN (NewsTalk 590) in Eugene, Oregon with Jerry Allen (play-by-play) and Mike Jorgensen (color commentator), and by the Ohio State IMG Sports Network flagshiped by WBNS-AM (1460 ESPN Columbus) and WBNS-FM (97.1 The Fan) in Columbus, Ohio with Paul Keels (play- by-play), Jim Lachey (color commentator) and Marty Bannister on the sidelines. Following the game, fans took to the streets of Columbus, Ohio, to celebrate. Fans tore down a temporary goalpost at Ohio Stadium. 89 fires were reported, and members of the Columbus Police Department used tear gas to disperse crowds. Just over a year later, Elliott, who had entered the draft early following his junior season, was brought back to AT&T; Stadium when the Dallas Cowboys selected him with the 4th overall pick. This was the Buckeyes first national championship since 2002 and their 8th in school history. Ohio State lost the turnover battle in this game 4-1, the 4 turnovers being the most ever by a winning team in national championship history, but outgained Oregon in total yards 538-465. The Buckeyes entered 2015 looking to repeat as national champions with the return of Cardale Jones and several other players. However, Jones struggled mightily and was eventually benched for backup JT Barrett. The Buckeyes lost at home to Michigan State in week 13 17-14, ending their chance at another national championship. They were invited to the Fiesta Bowl against Notre Dame, which they won 44-28. The Buckeyes then returned to the playoff in 2016, despite not winning their conference, but lost in the Fiesta Bowl to eventual national champion Clemson 31-0. Meanwhile, the Ducks fell to 0-2 in national championship games, with their other loss to Auburn in 2010. They also fell to 0-9 all time against Ohio State. Marcus Mariota, who won the Heisman Trophy in 2014, declared for the NFL draft after the season. In 2015, without Mariota, the Ducks offense was depleted, as the team lost momentum going forward. The next season, the Ducks finished 9-4, which included a close loss to Michigan State in East Lansing (31-28). However, a home blowout loss to Utah (62-20) and a double overtime loss at home to Washington State (45-38) cost the Ducks a chance at going back to the national championship. They ended the 2015 season with a triple overtime loss to TCU in the Alamo Bowl 47-41 despite having a 31-0 lead at one point. The 31 point blown lead remains the largest blown lead in school history. In 2016, Oregon regressed even further, finishing 4-8 and failing to reach a bowl for the first time since 2004, and Helfrich was fired. In 2017, under new coach Mario Christobal, the Ducks went back to bowl season, losing in the 2017 Las Vegas Bowl to Boise State 38-28. Oregon's appearance in the 2014 playoff was the last time a Pac-12 team appeared in the playoff until Washington did so in 2016, but the Huskies lost in the Peach Bowl to Alabama 24-7. Since Washington's loss in that game, the Pac-12 hasn't returned to the playoffs since. As of the 2019 season, the Pac-12 has the fewest playoff appearances out of all the power 5 conferences, with only 2. The 2 teams have not met since this game. However, they will meet in a home and home series in 2020 and 2021, with the 2020 game occurring in Eugene and the 2021 game occurring in Columbus. Those 2 games will feature different head coaches for each team than the ones that coached against each other in this game, with Ryan Day for Ohio State and Mario Cristobal for Oregon. Urban Meyer announced his retirement from coaching after the 2018 season, and Mark Helfrich was fired after the 2016 season. College football national championships in NCAA Division I FBS The 2017 UCF Knights football team represented the University of Central Florida in the 2017 NCAA Division I FBS football season. The Knights played their home games at the newly renamed Spectrum Stadium in Orlando, Florida, and competed in the East Division of the American Athletic Conference. They were led by second year head coach Scott Frost. The Knights finished the regular season 12–0, the football program's first ever undefeated regular season, second 12-win season, and won the 2017 American Conference Championship. The Knights season culminated in a 2018 Peach Bowl win over Auburn. The effort came just two years after an 0–12 winless season (2015). UCF became the first team in the history of NCAA Division I FBS to improve from a winless regular season to an undefeated regular season in only two years. Despite being the only undefeated team in FBS, UCF did not receive a spot in the College Football Playoff. Frost criticized the College Football Playoff committee, saying that the Knights "deserve[d] more credit from the committee than what they got." Frost believed that the committee deliberately ranked the Knights low enough on a weekly basis that they had no realistic chance of finishing in the top four. The Knights proclaimed themselves national champions at the end of the season. Florida lawmakers proposed passing a resolution declaring UCF the national champions, which Florida Governor Rick Scott proclaimed officially on January 8, 2018. On January 9, UCF was ranked No. 1 by the Colley Matrix, a mathematically based power rating developed by Wes Colley and listed as a NCAA-recognized National Polls Ranking for major selectors. This ranking was later recognized by the NCAA as a valid national championship claim, alongside Alabama's. Head Coach: Scott Frost Assoc. HC/LBs/Special Teams: Jovan Dewitt Defensive Coordinator: Erik Chinander Offensive Coordinator/WR: Troy Walters Offensive Line: Greg Austin TEs/Recruiting Coordinator: Sean Beckton Defensive Line: Mike Dawson Defensive Backs: Travis Fisher Running Backs: Ryan Held Quarterbacks: Mario Verduzco Chief of Staff/Dir. of Ops: Gerrod Lambrecht Asst. Director of Ops: Trent Mossbrucker Dir. of Player Development: Horace Raymond Dir. of Player Personnel: Sean Dillon Ast. Dir. of Player Personnel: Ryan Callaghan Dir. of High School Relations: Mike Cassano Quality Control Administrator: Barrett Rudd Quality Control Administrator: Zach Crespo Offensive Analyst: Frank Verducci Offensive Graduate Assistant: Dustin Haines Defensive Graduate Assistant: Jack Cooper Offensive Graduate Assistant: Drew Davis Dir. of Sports Performance: Zach Duval Senior Administrative Assistant: Megan Taylor Director of Equipment Operations: Rich Worner The 2017 UCF Spring game was held Saturday April 22 at Spectrum Stadium. The team was split into two squads. Team UCFast consisted mostly of the first team offense and defense, and UCFierce was made up of second team players. UCF announced its 2017 football schedule on February 9, 2017. The 2017 schedule originally consisted of seven home and five away games in the regular season. The Knights were set to host conference foes UConn, East Carolina, Memphis, and South Florida and were to travel to Cincinnati, Navy, SMU, and Temple. The Knights also hosted one of their two non-conference opponents, FIU from Conference USA, and traveled to Maryland from the Big Ten. UCF was scheduled to host games against Georgia Tech from the ACC, and Maine from the Colonial Athletic Association, before Hurricane Irma caused the Georgia Tech game to be canceled and the Memphis home game to be rescheduled over the Maine game. On September 21, 2017, UCF added a home game against the FCS Austin Peay Governors for October 28. In just his second season as head coach, and just two years removed from the winless 2015 campaign, head coach Scott Frost aimed to continue the UCF football teams's turnaround. Frost had brought the team six wins in 2016, making them bowl-eligible. Going into 2017, the team looked to build on their momentum. The Knights opened their season with a lopsided victory against FIU; however, days later, the season was temporarily put on hiatus due to Hurricane Irma. Two games were cancelled, and one was able to be rescheduled. After a 22-day layoff, the Knights had an impressive win at Maryland, leading to a much-anticipated intra-conference meeting against 3–0 Memphis. The Knights soundly beat the Memphis Tigers, establishing themselves as the new front- runner in the AAC. The Knights entered both the AP and Coaches Polls, and later in October, they were also ranked in the CFP rankings. Statistically, the Knights were the top scoring team in the nation (48.2 points per game), and finished 5th in yards per game (530). With blowout wins against Cincinnati, East Carolina, and Austin Peay, along with closer, pivotal wins against Navy and SMU, the Knights were 10–0 entering the final game of the regular season. The Knights hosted rival South Florida on Black Friday to decide the AAC East Division crown. In a shootout game described by some observers as one of the best games of the college football season, the Knights won the game 49–42. The Knights finished the regular season 11–0, the program's first ever undefeated regular season. With the win, UCF would host the AAC Championship game. The school set an NCAA mark by becoming the first team to go from a winless regular season (2015) to an undefeated regular season in only two years. The team set school records for most consecutive games won, most points in a single game, and saw many players and coaches receive individual superlative awards. In the latter weeks of the regular season, fueled by the team's success on the field, media reports began surfacing about the possibility of head coach Scott Frost departing UCF for another school. Frost, the former national championship winning quarterback at Nebraska, had expressed personal interest in the Cornhuskers head coaching job, and it incidentally became available in November. Frost was also rumored for some of the many higher-profile vacancies, including Florida, Tennessee, and others. Nebraska athletic officials actively targeted Frost in their coaching search, and after Frost shot down rumors of going to Florida, it became clear Frost's future would be either at Nebraska, or continuing at UCF. Despite the ongoing coaching rumors, UCF went on to win the AAC Championship game in dramatic fashion. The game was a rematch against Memphis, but this time the game was a shootout. The Knights prevailed 62–55 in double overtime. The win cemented UCF as the top Group of Five school in the nation, clinching them an automatic berth in a New Year's Six bowl game. Despite their unblemished 12–0 record up to that point, the Knights were not named to the College Football Playoff top four, and effectively could not play for the CFP National Championship. The Knights were paired against Auburn in the Chick- fil-A Peach Bowl on New Year's Day. A day after winning the AAC, head coach Scott Frost was formally introduced as the new head coach of Nebraska, as had been widely speculated. UCF immediately named offensive coordinator Troy Walters as the interim head coach. Frost would be taking nearly his entire staff with him to Nebraska, potentially leaving UCF without a coaching staff for the bowl season. The newly-introduced NCAA early signing period fueled Nebraska's urgency of hiring Frost, as school officials were anxious for Frost to begin recruiting immediately. Meanwhile, UCF named Josh Heupel their new head coach, but stopped short of committing Heupel to coaching in the bowl. After several days of uncertainty, and mild controversy, an agreement was reached such that Frost and his staff would return to UCF to coach the bowl game. Despite the difficulty of juggling two teams at once, Frost was committed to coaching UCF in the Peach Bowl, and called finishing out the UCF job as the 'right thing to do.' The Knights defeated the Auburn Tigers in the Peach Bowl 34–27, completing a perfect 13–0 season. In the aftermath, UCF athletic director Danny White created a stir when he publicly proclaimed UCF the national champions, despite the CFP championship game still being one week away. Several other outlets followed suit, including the Orlando Sentinel, WYGM, Prince George Journal, and the NCAA-recognized Colley Matrix. Other national media outlets debated the issue over the next several days. UCF received four first place votes in the final AP Poll, and placed 6th overall. The Knights were honored with a parade at Walt Disney World, a block party in downtown Orlando at Church Street Station, and were presented with the Key to the City by Orlando Mayor Buddy Dyer. Florida Governor Rick Scott signed a resolution officially recognizing the Knights as national champions on January 8, and later in the month, the Knights were honored at the 2018 NFL Pro Bowl. Off the field, UCF's home stadium changed its name to Spectrum Stadium, reflecting the acquisition of Bright House Networks by Charter Communications, and subsequent re-branding as Spectrum. The Knights opened the season on Thursday night against FIU. It was the start of the second season for head coach Scott Frost at UCF, as well as the first game for FIU under head coach Butch Davis. The Knights routed the Panthers, as the offense racked up 587 yards, and quarterback McKenzie Milton threw for 360 yards and four touchdown passes (22 yards, 50 yards, 3 yards, 13 yards, respectively). There were four rushing touchdowns, including a 51-yard run by Napoleon Maxwell in the third quarter. The UCF defense forced three fumbles, an interception, a safety, and four 3-and-outs by the Panthers offense. After a 22-day layoff due to Hurricane Irma, UCF was back on the field in Week 4. With the teams coming into the matchup ranked No. 1 and No. 2 in scoring (61 points for UCF and 57 points for Maryland) and having gone to double overtime in their meeting last year, the game was expected to be close. After a slow start for both teams, Maryland's backup quarterback, Kasim Hill, was injured and taken off the field in the first quarter. While the Terrapins were able to score the opening field goal at the end of that drive, they could not contain the Knights offense much longer, as the offense combined for 428 total yards. Meanwhile, the Knights defense overpowered the Terrapins on offense, keeping the Terrapins to 42 rushing yards, while the Knights picked off third string quarterback Max Bortenschlager twice, returning one for a touchdown. After having their scheduled game on September 10 cancelled due to Hurricane Irma, the two schools arranged to reschedule their game for September 30. It was the conference opener for both teams. Both UCF and Memphis came into the matchup undefeated, with Memphis winning three previous games and UCF winning their two previous games. After a slow start to the game, the Knights ended up with 603 total yards and one turnover, versus Memphis' 396 total yards and four turnovers. UCF quarterback McKenzie Milton threw for 253 yards and three touchdown passes, while running back Adrian Killins Jr. scored two rushing touchdowns. Killins set a UCF record with a 96-yard touchdown run, the longest rushing touchdown in school history. After the game, UCF entered both the AP Poll and the Coaches Poll at No. 25. UCF opened the game with two quick touchdowns, with both possessions totaling one minute and 32 seconds of game time, while holding Cincinnati to one touchdown in their first two possession. While the Knights defense let the Bearcats score more points than any of the Knights previous opponents, they also recorded one interception, a blocked PAT and allowed only 391 yards. Meanwhile, the Bearcats defense could not stop the Knights offense, which scored seven touchdowns and set up one field goal over the Knights' eight possessions. The game was stopped with four seconds left in the third quarter due to lightning in the area. Soon after the delay passed the one hour mark, the American Athletic Conference cancelled the rest of the game. Entering the game ranked number one in scoring offense in the nation while facing the worst scoring defense in the nation, the Knights were 33.5 point favorites. The Knights ended up scoring nine touchdowns, including one interception returned for a touchdown and one punt return returned for a touchdown. The 63 points the Knights scored were the most since 2001, when they beat Liberty University 63–0. The Knights also put up 603 yards of offense, making it the first time since 1998 that UCF has put up more than 500 yards of offense in three straight games. With the win, the Knights improved to 5–0 for the first time in program history since moving up to D-1 football, and the first time since 1988. Navy welcomed the Knights to Annapolis following the Midshipmen's first loss of the season, 30–27 at Memphis, while riding a 17-game home win streak. Prior to the game, the Knights practiced against Navy's triple option scheme by having coach Scott Frost, who ran the option offense during his time as quarterback at Nebraska from 1995 to 1997, play as the scout team's quarterback. The game ended up being the Knights closest scoring game yet, with Navy tying the Knights twice and being only three points down for most of the fourth quarter. Both teams offenses racked up over 400 yards. The Midshipmen's defense recorded one fumble, while the Knights defense recorded two interceptions and a fumble. The forced fumble by the Knights was key play of the fourth quarter. With 7:14 left in regulation, facing a 3rd down & 5 at the UCF 38, and trailing by only 3, Navy running back Darryl Bonner took a pitch to the left. A punishing hit by Brandon Moore jarred the ball loose, and Moore recovered for UCF. The Knights then iced the game with a 7-play, clock- burning drive, culminating in Otis Anderson's first career touchdown for the Knights, and a ten-point lead they would not surrender. With the 31–21 win, the Knights improved to 6–0 for the first time in program history. Coming off of their closest game yet, the Knights welcomed the Austin Peay Governors (an FCS program) to Spectrum Stadium. Austin Peay came into the game 5–3, after having snapped their 29-game losing streak earlier in the year. Both teams offenses surged throughout the game, with the Governors putting up 352 yards and 33 points, the most by any UCF opponent in the season at the time. Meanwhile, the Knights offense put up 489 yards and a school record 73 points. The Knights defense forced two turnovers, including a fumble returned for a touchdown by Shaquem Griffin. The game also included a kickoff return for a touchdown by each team, a tipped pass for an Austin Peay touchdown, both teams going two for two on fourth down conversions, Austin Peay guard Ryan Rockensuess recovering a fumble for a touchdown after the Governors offense fumbled twice in a play that started from the UCF 5 yard line, and an unsportsmanlike conduct call on UCF head coach Scott Frost, all in the first half. With rival USF's loss to Houston, combined with losses by TCU and Penn State to Iowa State and Ohio State respectively, the Knights became one of only five teams remaining undefeated after Week 9 (along with Alabama, Georgia, Miami (FL), and Wisconsin). They also rose to first place in the American Athletic Conference. The Knights visited the SMU Mustangs, who started 6–2, their best record post "death penalty". Both teams boasted high powered offenses, leading some to believe the game would be an offensive shootout. Instead, the game became the second-lowest scoring game of the season for the Knights (behind only the Navy game). The game was the closest game yet for the Knights, and the only one to end as a single digit victory, as well as a one possession game. Though the Knights put up a season-high 615 yards on offense, they were unable to convert all of their drives into points. Inside the red zone, they turned over the ball on downs on their opening drive, and later lost a fumble. Knights quarterback McKenzie Milton also threw two interceptions, including one that was returned for a touchdown. The Knights offense was able to make big plays when it mattered, including an 80-yard touchdown reception by Gabriel Davis, a 64-yard touchdown run Adrian Killins Jr., and a 63-yard catch and run by Tre'Quan Smith which set up a field goal. The Knights defense forced a crucial SMU fumble at the goal line, keeping the Mustangs from scoring a touchdown in the second quarter. Late in the fourth quarter, two critical fourth down stops by the defense sealed the game for the Knights. With 5:10 remaining in regulation, facing a 4th down & 3 at the UCF 38, SMU quarterback Ben Hicks threw to Trey Quinn, who dropped the pass as he was turning down field, and the ball was turned over on downs. With 1:24 to go, the Mustangs faced yet another 4th down at their own 34. Hicks pass attempt was incomplete and the Knights took a knee to win the game. UCF hosted UConn, in a matchup once known briefly as the Civil Conflict. With light rain showers in the area, UCF jumped out to a 21–3 lead after the first quarter. The Knights scored an opening drive touchdown run by Otis Anderson, aided by a fourth down conversion resulting from a Huskies offsides penalty as UCF lined up for a punt at their own 29 yard line. Midway through the second quarter, McKenzie Milton threw to Tre'Quan Smith who eluded three defenders untouched for a 41-yard touchdown pass, and UCF enjoyed a 28–10 halftime lead. The Knights, however, sputtered and were held scoreless in the third quarter. Huskies quarterback David Pindell completed a 60-yard pass to Arkeel Newsome, and on the next play, ran the ball in himself for a touchdown, and trimmed the lead to 28–17. Otis Anderson fumbled the ball deep in UConn territory, and later a turnover on downs, and UCF miscues became the focus of attention. The Knights turned the game around in the fourth quarter, however, behind a 65-yard touchdown run by Anderson, and another touchdown run by Milton. With just under 9 minutes remaining, the UCF defense forced a turnover on downs. On the next play from scrimmage, backup quarterback Noah Vedral threw a 35-yard touchdown to Cam Stewart, who was left unguarded, and the Knights sealed a 49–24 victory. With Georgia's loss to Auburn, UCF would be one of four remaining undefeated teams in the country (the others being Alabama, Miami (FL), and Wisconsin). UCF traveled to Philadelphia to take on division opponent Temple. After a tight first quarter, Temple led 10–7 early in the second period. The Knights then scored 24 unanswered points to go ahead, and never surrendered the lead en route to a 45–19 victory. The Owls offense gave up three turnovers (two interceptions, and one fumble) in the second quarter, all of which led to UCF points. With just over three minutes left before halftime, UCF punter Mac Loudermilk pinned the Owls back at their own 8 yard line. On the next play from scrimmage, Owls quarterback Frank Nutile was intercepted by Kyle Gibson, who returned the ball to the 5 yard line. That set up a McKenzie Milton touchdown pass to Gabriel Davis, and capped off an explosive second quarter, and a comfortable 31–10 lead by the Knights at halftime. Both teams traded punts to start the third quarter. Then Milton threw a 22-yard touchdown pass to Tre'Quan Smith to increase the lead. On the next drive, Shaquem Griffin intercepted Frank Nutile, and returned the ball 22 yards close to midfield. Milton drove the Knights down for another touchdown, and a 45–13 lead. The first team offense and first team defense were benched for the duration of the fourth quarter. The second team defense gave up one 74-yard touchdown pass from Frank Nutile to Adonis Jennings, but with three minutes to go Nevelle Clarke intercepted Nutile in the endzone to halt any chance of an Owls rally. The Knights improved to 10–0 on the season. The 13th-ranked Knights welcomed the 22nd-ranked Bulls (9–1) to Spectrum Stadium with the winner of the game claiming the American Athletic Conference East Division title and a spot in the 2017 American Athletic Conference Football Championship Game. The game was the first ranked match-up in the War on I-4 rivalry. The game quickly turned into an offensive shootout, with a total of 1,186 yards of offense between both teams. The game came down to the wire, with UCF taking an eight-point lead (following an earlier missed extra point by South Florida) with 2:21 left in regulation. South Florida then tied the game with an 83-yard touchdown and a two-point conversion with 1:41 remaining. On the ensuing kickoff, UCF's Mike Hughes returned the kickoff 95 yards for a touchdown, giving the Knights a 49–42 lead, with 1:28 left. The Bulls attempted to strike back, but fumbled on the UCF 45 yard line which UCF linebacker Chequan Burkett recovered to seal the game. The game was called one of the best of the season. With Miami and Alabama both losing their respective games, UCF and Wisconsin would be the only two undefeated teams in college football. Memphis fumbled away the ball on the first drive of the game. UCF quarterback McKenzie Milton threw two touchdown passes, and the Knights led 17–7 at the end of the first quarter. Memphis dominated most of the second quarter, highlighted by miscues by the Knights, particularly on offense. Tigers quarterback Riley Ferguson threw two touchdown passes, including a 68-yard bomb to a wide open Anthony Miller. The Knights committed three turnovers in the second quarter, a fumble and two red zone interceptions. Tigers kicker Riley Patterson kicked a 27-yard field goal as time expired in the first half, and Memphis led at halftime 31–24. UCF bounced back in the third quarter. Memphis opened the second half with a surprise onside kick, but the kick attempt failed. McKenzie Milton had two touchdown runs, and threw for another touchdown, and the Knights were back in the lead by the score of 45–34. Trailing by 14 partway through the fourth quarter, Tigers running back Tony Pollard broke away for a 66-yard touchdown run. On their next drive, Memphis tied the game 48–48 with Ferguson's 10-yard touchdown pass to Anthony Miller. With 33 seconds remaining in regulation, Memphis lined up for a potential game-winning 46-yard field goal attempt. The field goal attempt was blocked and recovered by the Knights, but not before the Tigers were called for Delay of Game. The penalty gave the Tigers a second chance at a game-winning field goal attempt. Riley Patterson's 51-yard field goal attempt sailed wide left, and the game would ultimately go to overtime tied 48–48. Both teams scored touchdowns in the first overtime period, and the game was tied 55–55 going into the second overtime. Otis Anderson scored a 1-yard touchdown run to put UCF ahead 62–55. Memphis took over on offense. Facing 2nd down & Goal at the UCF 9 yard line, Riley Ferguson dropped back to pass, but was pressured by Shaquem Griffin. Ferguson's pass was intercepted by Tre Neal at the 4 yard line to end the game. With UCF's victory, along with Wisconsin's loss in the Big Ten Championship, UCF would stand as the only undefeated team in the college football season. The No. 12 Knights, as the highest ranked Group of Five team, were given an automatic bid to play in a College Football Playoff New Year's Six bowl, traveling up to Atlanta to play in the Peach Bowl at Mercedes-Benz Stadium. The Knights were matched up against the No. 7 Auburn Tigers (10–3), the SEC West champion and 10.5 point favorite. For the Tigers, this would be their second of three consecutive games at Mercedes-Benz Stadium, following their 28–7 loss to Georgia in the 2017 SEC Championship Game, while being scheduled to open their 2018 season against the Washington Huskies in the Chick-fil-A Kickoff Game. McKenzie Milton was the offensive MVP for the UCF Knights with 245 passing yards throwing for two touchdowns and a rushing touchdown. Jarrett Stidham had 331 passing yards throwing for one touchdown with two interceptions. UCF had 411 total yards compared to Auburn Tigers 421 total yards. However, the Tigers had three turnovers with Knights only having one. Shaquem Griffin had 12 tackles and one and a half sacks in the win for the Knights. Antwan Collier sealed the game for the Knights with an interception in the end zone with 24 seconds left. Griffin was later named the game's defensive MVP, with Milton the offensive MVP. Following the game, the school claimed a national championship. The team was ranked number 1 by the Colley Matrix, an NCAA-recognized selector of national champions. The NCAA does not officially select a national champion in FBS football. UCF's national championship claim sparked a massive surge of interest in the school and the program. Under new coach Josh Heupel, UCF would not lose again until 2019. Offensive Player of the Year: McKenzie Milton, Coach of the Year: Scott Frost Aaron Evans, OT, Jordan Johnson, C, Jordan Akins, TE, McKenzie Milton, QB, Adrian Killins Jr., RB Jamiyus Pittman, DL, Shaquem Griffin, LB, Mike Hughes, CB, Kyle Gibson, S Tre'Quan Smith, WR, Wyatt Miller, OT, Trysten Hill, DL, Chequan Burkett, LB Matthew Wright, K, Mac Loudermilk, P, Mike Hughes, RS September 4: McKenzie Milton, October 2: Adrian Killins Jr., October 16: McKenzie Milton, November 20: McKenzie Milton, November 27: McKenzie Milton October 2: Matthew Wright, October 16: Mike Hughes, October 30: Mike Hughes, November 27: Mike Hughes Best record to start season: 13–0, Most consecutive victories: 25, Longest rush from scrimmage: 96 yards (touchdown) – Adrian Killins (September 30, 2017 vs. Memphis), Most points scored in single game: 73 vs. Austin Peay (October 28, 2017), Most points scored in a season: 627, Passing yards in a season: 4,037, McKenzie Milton, Passing touchdowns in a season: 37, McKenzie Milton, Rushing yards by a quarterback in a season: 613 yards, McKenzie Milton, Total touchdowns responsible for in a season: 45 (37 passing, 8 rushing), McKenzie Milton, Total offense in a single game: 562 yards (494 passing, 68 rushing), McKenzie Milton (December 2, 2017, American Championship Game vs. Memphis) AFCA Coach of the Year Award – Scott Frost, Archie Griffin Award — McKenzie Milton, Associated Press College Football Coach of the Year Award – Scott Frost, Broyles Award — Troy Walters (semi-finalist), College GameDay "Herbie" Awards, Moment of the Year — Scott Frost winning AAC Championship, Game of the Year — UCF vs. South Florida, Davey O'Brien National Quarterback Award (semi-finalist) — McKenzie Milton, ESPN All-Bowl Team – Shaquem Griffin, George Munger Coach of the Year — Scott Frost (semi-finalist), Home Depot Coach of the Year – Scott Frost, Jason Witten Collegiate Man of the Year (finalist) — Shaquem Griffin, Manning Award Quarterback of the Week (Week 12) — McKenzie Milton, Ray Guy Award Punter of the Week (Week 11) — Mac Loudermilk, Senior CLASS Award – Shaquem Griffin, Touchdown Club of Columbus Male Athlete of the Year — Shaquem Griffin, Walter Camp Award FBS Offensive Player of the Week (Week 13) — McKenzie Milton, Walter Camp Player of the Year Award (semi-finalist) — McKenzie Milton, Woody Hayes Trophy — Scott Frost Shaquem Griffin Mike Hughes Additionally, two players were signed as undrafted free agents: The College Football Playoff (CFP) is an annual postseason knockout invitational tournament to determine a national champion for the National Collegiate Athletic Association (NCAA) Division I Football Bowl Subdivision (FBS), the highest level of college football competition in the United States. Four teams play in two semifinal games, and the winner of each semifinal advances to the College Football Playoff National Championship game. The inaugural tournament was held at the end of the 2014 NCAA Division I FBS football season and was won by the Ohio State Buckeyes, who defeated the Oregon Ducks in the championship game. After the first season, the playoff was dominated for several years by two teams, the Alabama Crimson Tide and the Clemson Tigers; they faced each other in the championship game three times, and in one other year they met in the semifinals. A 13-member committee selects and seeds the four teams to take part in the CFP. This system differs from the use of polls or computer rankings that had previously been used to select the participants for the Bowl Championship Series (BCS), the title system used in FBS from 1998 to 2013. The current format is a Plus-One system, an idea which became popular as an alternative to the BCS after the 2003 and 2004 seasons ended in controversy. The two semifinal games rotate among six major bowl games, referred to as the New Year's Six: the Rose Bowl, Sugar Bowl, Orange Bowl, Cotton Bowl, Fiesta Bowl, and Peach Bowl. In addition to the four teams selected for the playoff, the final CFP rankings are used to help determine the participants for the other four New Year's Six bowls that are not hosting the semifinals that year. The semifinal games, which take place on the same day, are usually scheduled on Friday, Saturday, or Monday close to or on New Years Day, with flexibility allowed to ensure that they are not in conflict with other bowl games traditionally held on New Year's Day. The National Championship game is then played on the first Monday that is six or more days after the semifinals. The venue of the championship game is selected based on bids submitted by cities, similar to the Super Bowl or NCAA Final Four. The winner of the game is awarded the College Football Playoff National Championship Trophy. Playoff officials commissioned a new trophy that was unconnected with the previous championship systems, such as the AFCA "crystal football" trophy which had been regularly presented after the championship game since the 1990s (as the AFCA was contractually obligated to name the BCS champion as the Coaches Poll champion). As the NCAA does not organize or award an official national championship for FBS football (instead merely recognizing the decisions made by any of a number of independent major championship selectors), the CFP's inception in 2014 marked the first time a major national championship selector in college football was able to determine their champion by using a bracket competition. The first College Football Playoff selection committee was announced on October 16, 2013. The group consists of 13 members who generally serve three- year terms, although some initial selections served terms both shorter and longer than three years "to achieve a rotation" of members. , the members of the selection committee are: The committee members include one current athletic director from each of the five "major" conferences—ACC, Big Ten, Big 12, Pac-12, and SEC—also known as the Power Five conferences. Other members are former coaches, players, athletic directors, and administrators, plus a retired member of the media. The goal was for the panel to consist proportionally of current "Power Five" athletic directors, former coaches, and a third group of other voters, excluding current conference commissioners, coaches, and media members. During the selection process, organizers said they wanted the committee to be geographically balanced. Conference commissioners submitted lists totaling more than 100 names from which to select the final committee members. The selection of Condoleezza Rice, a former U.S. Secretary of State and Stanford University provost, was met with some backlash within the sport and the media. Critics questioned her qualifications, citing gender and lack of football experience. The committee releases its top 25 rankings weekly on Tuesdays in the second half of the regular season. The top four teams are seeded in that order for the playoff. During the season, the committee meets and releases rankings six or seven times, depending on the length of the season (the number of games is consistent, but the number of weeks those games are played over can vary from year to year). The group, which meets at the Gaylord Texan hotel in Grapevine, Texas, reportedly meets in person up to 10 total times a year. A team's strength of schedule is one of the most pertinent considerations for the committee in making its selections. Other factors that the committee weighs are conference championships, team records, and head-to-head results, plus other points such as injuries and weather. Unlike the BCS system, the AP Poll, Coaches' Poll, and the Harris Poll, computer rankings are not used to make the selections. Advanced statistics and metrics are expected to be submitted to the committee, though like other analytics, they have no formal role in the decision. Committee members are not required to attend games. Long said the panel considered less frequent rankings, but ultimately decided on a weekly release. "That's what the fans have become accustomed to, and we felt it would leave a void in college football without a ranking for several weeks," he said. Long also noted: "Early on there was some talk that we would go into a room at the end of the season and come out with a top four, but that didn't last long." In analyzing this change in thinking, Stewart Mandel of Sports Illustrated commented: "The whole point of the selection committee was to replace the simplistic horse-race nature of Top 25 polls – where teams only move up if someone above them loses – with a more deliberative evaluation method. Now the playoff folks are going to try to do both." Addressing the "pecking order" nature of traditional polls, George Schrodeder of USA Today wrote that "if it actually works as intended, we could see volatile swings" from week to week, with lower-ranked teams moving ahead of higher-ranked teams without either team losing (a rarity in traditional polls). Both Long and Bill Hancock, the CFP executive director, say they expect that to happen. The committee's voting method uses multiple ballots, similar to the NCAA basketball tournament selection process and the entire process is facilitated through custom software developed by Code Authority in Frisco, Texas. From a large initial pool of teams, the group takes numerous votes on successive tiers of teams, considering six at a time and coming to a consensus on how they should be ranked, then repeating the process with the next tier of teams. Discussion and debate happens at each voting step. All votes are by secret ballot, and committee members do not make their ballots public. Each week's ranking process begins anew, with no weight given to the previous week's selections. In this fashion, the committee selects the four teams to compete for the national championship. Committee members who are currently employed or financially compensated by a school, or have family members who have a current financial relationship (which includes football players), are not allowed to vote for that school. During deliberations about a team's selection, members with such a conflict of interest cannot be present, but can answer factual questions about the institution. All committee members have past ties to certain NCAA institutions, but the committee decided to ignore those ties in the recusal requirements. "We just boiled it down to where we felt this group was fit to its high integrity and would differentiate from those past relationships," Long said. Some football writers, like Dennis Dodd and Mark Schlabach, have said the recusal arrangement isn't transparent or objective, suggesting that members' alma maters and former coaching jobs should be considered disqualifying conflicts of interest. To date, 21 of the 24 teams selected for the College Football Playoff have been undefeated or 1-loss conference champions from Power Five conferences. Two 1-loss Power Five teams have been selected without playing in their conference championship game. One undefeated independent team has been selected. No teams from the "Group of Five" conferences or with two or more losses have been selected. Due to the increased emphasis on strength of schedule, teams have considered playing more challenging opponents during the non-conference portion of their schedules. Some teams have traditionally played three or four "weak" non- conference opponents, but wins against such low-level competition are unlikely to impress the committee. For teams on the cusp of making the playoff four, "I think one of the first things the committee will look at is strength of schedule," said selector Oliver Luck. Teams in the Big Ten, Big 12 and Pac-12 play nine conference games on their twelve-game schedules and thus only have flexibility in choosing their opponents for the three non-league games. Some programs are opting to increase their schedule strength by scheduling high- profile matchups at neutral sites and on weeknights, garnering primetime TV exclusivity. In response to the new playoff system, the Southeastern Conference considered increasing its conference schedule from eight to nine games, with Alabama coach Nick Saban a vocal proponent. According to Jon Solomon of the Birmingham News, "The prevailing opinion among SEC athletics directors: The SEC is difficult enough that there's no need for a ninth game." Some in the conference, like Mississippi State athletic director Scott Stricklin, opined that a nine-game SEC schedule would result in more teams with two losses. Commissioner Michael Slive and Vanderbilt AD David Williams, among others, supported a stronger out-of-league schedule, which would likely impress the committee. In April 2014, the league voted to mandate that all SEC teams must play a Power Five foe (ACC, Big Ten, Big 12, Pac-12, or independent Notre Dame) in its non-conference slate beginning in 2016. Slive noted this rule "gives us the added strength-of-schedule we were seeking". In 2014, the first year of the College Football Playoff, one team (Georgia) played two opponents from the Power Five, nine of the 14 teams played one Power Five conference opponent and three lower-level opponents (including one FCS school), and four teams did not face a Power Five foe. In the spring of 2015, the SEC decided to count games played against Independents BYU and Army toward its Power Five requirement. The ACC, whose teams also play eight conference games (plus Notre Dame at least once every three years), also considered moving to a nine-game conference schedule. However, the league opted to stay with the eight-plus-Notre Dame model, stipulating instead that teams would have to play one Power Five school in their non-league slates beginning in 2017, which would include the Notre Dame game or other ACC schools, as will games against another FBS independent, BYU. Despite the push to increase schedule strength, some ACC coaches preferred the scheduling flexibility available with fewer permanent fixtures on a team's slate. Opinion was split among league athletic directors on moving to a nine-game schedule prior to the vote. An SEC expansion to a nine-game schedule would limit the ACC's opportunities to play Power Five non-conference opponents. The College Football Playoff uses a four-team knockout bracket to determine the national champion. Six bowl games—the Rose Bowl, Sugar Bowl, Orange Bowl, Cotton Bowl, Fiesta Bowl, and Peach Bowl– rotate as hosts for the semifinals. The rotation is set on a three-year cycle with the following pairings: Rose/Sugar, Orange/Cotton, and Fiesta/Peach. The two semifinal bowls and the other four top-tier bowls are marketed as the New Year's Six. Three of these bowls played per day, typically on consecutive days that include New Year's Day. The selection committee seeds the top four teams, and also assigns teams to the at-large bowls (Cotton, Fiesta, and Peach) in years when they do not host semifinals. The four-team format pits the No. 1-ranked team against No. 4 and No. 2 against No. 3. The seeding determines the semifinal bowl game assigned to each matchup; the No. 1 seed chooses its bowl game to prevent it from playing in a "road" environment. There are no limits on the number of teams per conference, a change from previous BCS rules. However, some non- semifinal bowl selections still maintain their conference tie-ins, similarly to the BCS's automatic qualifier berths. A team from one of the "Group of Five" conferences is guaranteed a spot in one of the New Year's Six bowls. Cities around the country bid to host each year's championship game. The playoff group's leaders make a selection from those proposals, in a similar fashion to other large sporting events, such as the Super Bowl or NCAA Final Four. Officials say the championship game will be held in a different city each year, and that bids must propose host stadiums with a capacity of at least 65,000 spectators. Under the system, cities cannot host both a semifinal game and the title game in the same year. The 2018 Championship Game featured SEC teams Alabama and Georgia. The SEC has a record of 8–3 () in games against other conferences. The television broadcast rights to all six CFP bowls and the National Championship are owned by ESPN through at least the 2025 season. ESPN then reached 12-year agreements to retain rights to the Rose Bowl, Orange Bowl, and Sugar Bowl following the dissolution of the Bowl Championship Series. In November, ESPN reached a 12-year deal to broadcast the remaining three bowls, the championship game, as well as shoulder programming such as ranking shows; as a whole, the contract is valued at around $470 million per year, or nearly $5.7 billion for the life of the contract. The inaugural College Football Playoff games in January 2015 generated larger ratings than previous BCS games. The 2015 College Football Playoff National Championship had an 18.9 Nielsen rating and was watched by approximately 33.4 million people, the largest broadcast audience of all time on American cable television (non-broadcast), according to AdWeek. That was a 31 percent audience increase over the previous year's championship game and a 22 percent increase over the BCS title game's best rating on cable (a 16.1 rating in 2011). The semifinal games, the 2015 Rose Bowl and 2015 Sugar Bowl, saw 28.16 million and 28.27 million viewers, respectively. According to ESPN, these games also set (and briefly held) all-time records for cable TV viewership. In 2015, the ratings for the two semifinal games were down from the prior season's equivalents, with the Orange Bowl reaching a 9.7 rating (in comparison to 15.5 for the 2015 Rose Bowl) and the Cotton Bowl reaching a 9.9 rating (in comparison to a 15.3 rating for the 2015 Sugar Bowl). On the online WatchESPN streaming service, excluding 2014 FIFA World Cup games, the Cotton Bowl and the Orange Bowl drew the second and third-largest streaming audiences in the service's history, behind the 2015 national championship. The ratings drops were attributed to the New Year's Eve time slot, as fewer people were at home to watch the game. The decline in ratings was a factor in changes for the scheduling of future CFP semi-final games. In 2012, ESPN reportedly agreed to pay about $7.3 billion over 12 years for broadcasting rights to all seven games, an average of about $608 million per year. That includes $215 million per year which was already committed to the Rose, Sugar and Orange bowls, plus $470–475 million annually for the rest of the package. By comparison, the most recent contract with the BCS and the Rose Bowl had paid approximately $155 million per year for five games. The average revenue to the new system over 12 years is to be about $500 million per year. After $125–150 million in expenses, the Power Five conferences split about 71.5 percent of the remaining money, for an approximate average payout of $250 million a year ($50 million per league) over the life of the contract. The "Group of Five" conferences split 27 percent, about $90 million a year ($18 million per league). Notre Dame receives around one percent, about $3.5-4 million, and other FBS independents get about 0.5 percent of the deal. Extra revenue goes to conferences in contracts with the Rose, Sugar, and Orange bowls, which split revenue 50/50 between their participating leagues. In non- semifinal years, the Rose Bowl's TV revenue would be divided between the Big Ten and Pac-12 conferences; likewise, the Sugar Bowl and Orange Bowl revenue to its participant conferences. When those bowls are semifinal games, the money is distributed by the playoff system to all FBS conferences. ESPN has paid about $80 million a year each for the Rose and Sugar bowls over 12 years. The Orange Bowl deal is worth $55 million per year. For example, in a non- semifinal year, the Big Ten could receive about $90 million (half of its $80 million Rose Bowl deal plus about $50 million from the playoff system). Conferences receive an additional $6 million each year for each team it places in the semifinals and $4 million for a team in one of the three at-large bowls; Notre Dame receives the same amount in either scenario. No additional money is awarded for reaching the championship game. The Power Five conferences and the "Group of Five" have not decided on their respective revenue-sharing formulas, though the SEC initially receives more revenue than the other four Power Five conferences due to its BCS success. Reports say the money is to be divided based on several criteria such as "on-field success, teams' expenses, marketplace factors and academic performance of student- athletes." The playoff system awards academic performance bonuses of $300,000 per school for meeting the NCAA's Academic Progress Rate standard of 930. In a hypothetical 14-team conference, $4.2 million ($300,000 x 14) would be allocated to that league, and if only 12 of the 14 members meet the APR standard, then each of the 12 schools would receive $350,000 ($4.2 million / 12), penalizing schools that fall below the threshold. BCS Properties, LLC holds all properties related to the College Football Playoff. Previous BCS commissioner Bill Hancock is the executive director of the playoff organization, with former ACC Senior Associate Commissioner Michael Kelly as COO. Like the BCS, the playoff system's management committee consists of the conference commissioners from the 10 FBS conferences and Notre Dame's athletic director. The playoff system's headquarters is in Irving, Texas. According to the CFP website, the system's operations are controlled by the Board of Managers, which consists of presidents and chancellors of the playoff group's member universities. The eleven members have sole authority to develop, review and approve annual budgets, policies and operating guidelines. The group also selects the company's officers. Rodney Bennett – President, Southern Mississippi (C-USA), Anthony Frank – President, Colorado State (Mountain West), Burns Hargis – President, Oklahoma State (Big 12), Jack Hawkins – Chancellor, Troy (Sun Belt), Rev. John I. Jenkins – President, Notre Dame (Independent), Mark Keenum – President, Mississippi State (SEC), Roderick McDavis – President, Ohio (MAC), Max Nikias – President, USC (Pac-12), Harvey Perlman (chair) – Chancellor, Nebraska (Big Ten), Donna Shalala – President, Miami (Fla.) (ACC), Steadman Upham – President, Tulsa (The American) According to the CFP website, the Athletics Directors Advisory Group is appointed by the management committee to "offer counsel" on the operations of the system. As an advisory board, it has no authority in the management of the CFP. Gary Barta, Iowa (Big Ten), Tom Bowen, Memphis (The American), Tom Burman, Wyoming (Mountain West), Joe Castiglione, Oklahoma (Big 12), Jeremy Foley, Florida (SEC), Dan Guerrero, UCLA (Pac-12), Chris Massaro, Middle Tennessee State (C-USA), Terry Mohajir, Arkansas State (Sun Belt), Mike O'Brien, Toledo (MAC), Stan Wilcox, Florida State (ACC) Although being generally well received, the College Football Playoff has been criticized much like its predecessor, the Bowl Championship Series, which had several controversies. Because the tournament has four teams, at least one Power Five champion misses the playoffs every season. However, not all teams selected have been conference winners. In the 2016–17 season, one of the teams selected was Ohio State, who did not qualify to the Big Ten Championship Game. As a result, both the Big Ten and Big 12 champions were not selected for the playoffs (although both teams had two losses, while Ohio State only had one). In the 2017–18 season, two of the four selected teams were from the SEC: conference champions Georgia, and Alabama, who lost to SEC runner-up Auburn. Analysts have discussed whether the committee should select conference champions only. Another critique centered around a perceived bias against smaller conferences such as the Big 12 which used to not stage a conference championship game, but was reintroduced for the 2017 season. The American Athletic Conference addressed this issue by adding Navy to its ranks for 2015, bringing its membership to 12 teams, which allowed it to stage a conference championship game under then-current NCAA rules. Since the 2016 season, FBS conferences have been allowed to stage football championship games even if they do not have 12 members. There are opinions labeling the CFP system "just as" or "even more polarizing" than the BCS or the old wire-service poll system. However, most in sports media believe the College Football Playoff Committee got the right foursome for the 2017-18 playoff inasmuch as it included Alabama, a one- loss team excluded from its conference championship on a tiebreaker, instead of Ohio State, a two-loss conference champion. None of the commentators who agreed with the selection made any reference to the exclusion of undefeated UCF, a Group of Five team with a perfect season and a record that was thus better than all four CFP teams, which each had lost once. In 2019 Urban Meyer, head coach of the national champion 2014 Ohio State Buckeyes football team, said that he intentionally ran up the score against Wisconsin in the Big Ten conference championship to help his team be chosen for the playoff. Criticizing the subjectivity of the selection process, Meyer said that he left the starting lineup in the game despite Ohio State being ahead 45-0 in the third quarter—not resting the starters and risking their health, and poor sportsmanship—because "I don't think the 'eye test' and 'people think' is going to get enough to bump TCU and Baylor". He continued, "I had a job to do, and that was to get Ohio State in the playoff. Do I think that's right? That's wrong", proposing a selection system based on defined criteria. The qualifications of selection committee members has also been scrutinized. As an outsider to the sports world, Condoleezza Rice was the focus of some criticism. Former Clemson head coach Tommy Bowden opined that the committee's members should be "people who played the game and preferably coached the game". Former Auburn head coach Pat Dye said that "All she knows about football is what somebody told her ... or what she read in a book, or what she saw on television. To understand football, you've got to play with your hand in the dirt". Former Big East commissioner Mike Tranghese also gained membership on the selection committee despite having never played football in college. Former sportswriter Steve Weiberg and retired U.S. Air Force General Michael Gould are other committee members without significant football playing, coaching, or administrative experience. The semifinal games for the 2015 season were scheduled for December 31; they were expected to have lower television viewership because the date is not a federal holiday, and because the second game faced heavy competition for television viewers in primetime from New Year's Eve specials (such as New Year's Rockin' Eve, which is aired by ESPN's sister broadcast network ABC). Under television contracts with ESPN that predate the College Football Playoff, both the Rose and Sugar Bowl games are guaranteed exclusive TV time slots on January 1 (or January 2 if New Year's Day falls on a Sunday), regardless of whether they are hosting a semifinal game. In an interview with CBS Sports, CFP commissioner Bill Hancock suggested this scheduling issue would "change the paradigm of what New Year's Eve is all about," opining that "if you're hosting a New Year's Eve party, you better have a bunch of televisions around." Although ESPN proposed moving the Thursday, December 31, 2015 semifinal games to Saturday, January 2, 2016, the idea was rejected. The semifinal games' ratings were ultimately down significantly from those of the previous season. In an effort to reduce the impact of their New Year's Eve scheduling, the 2016 semifinal games, which fell on a Saturday, had earlier kickoff times, at 3:00 p.m. and 7:00 p.m. ET respectively. The 2016 Orange Bowl was played in primetime on December 30, 2016, rather than in an early afternoon window on New Year's Eve. Hancock considered the earlier start times to be a compromise to reduce the games' intrusion into New Year's Eve festivities, but reiterated that there were no plans to move the semi-final games from New Year's Eve outside of years where they are hosted by the Rose Bowl and Sugar Bowl. On July 28, 2016, however, Hancock reversed this stance and announced revisions to the scheduling for future College Football Playoff semi-final games. The games were rescheduled so that they will not necessarily be played on New Year's Eve yearly: outside of years when they are hosted by the Rose and Sugar Bowls (where they retain their traditional New Year's Day scheduling), they will now be scheduled primarily on the last Saturday or federally observed holiday of the year. In some years, this date will land on New Year's Eve. In 2021, the games will be played on Friday, December 31, because the day will be observed as a holiday. Viewership of the 2018 semi- finals were down by 25% over the previous semi-finals, which were played on New Year's Day. A common suggestion is for the playoff to expand to an eight-team format, guaranteeing all five major conference champions a spot along with the highest ranked "Group of Five" champion. The remaining two spots would be at-large selections awarded to the next two highest ranking teams. The seed pairings would be ordered to fit the playoff format, with 1 vs. 8, 2 vs. 7, etc. NCAA coaches were polled and asked if they were in favor of a larger playoff system. More than half of the coaches (53 percent) from the Power 5 conferences (ACC, Big 12, Big Ten, SEC and Pac-12) who voted chose an eight- team playoff, compared with 33 percent for the four-team model. CFP executive director Bill Hancock said his group is committed to only four teams for the next 12 years, and "there has been no discussion of expanding." New Year's Six, College football playoff debate, College football national championships in NCAA Division I FBS, List of college bowl games, Mythical National Championship, Plus-One system

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The State Correctional Institution (SCI) at Rockview, commonly referred to as Rockview, is a Pennsylvania Department of Corrections prison located in Benner Township, Pennsylvania, away from Bellefonte. SCI Rockview, which began construction in 1912 and was completed in 1915, was intended to replace Eastern State Penitentiary and Western Penitentiary. Instead it became a branch prison of Western housing lesser security risk prisoners employed in the extensive farm program outside the gates. Rockview is now a medium- security institution for men. Pennsylvania's execution chamber is located on the grounds of Rockview; however, there is no "death row" there. Condemned prisoners are transported to Rockview from death rows in maximum security prisons across the state several days before their scheduled execution. Pennsylvania State University in State College, Pennsylvania, began a research seminar class held at Rockview known as the Inside/Out Program led by Dr. Thomas Bernard. The first class was held in the Spring of 2007, and made up of 15 Penn State students. These students were taken right into the heart of the institution every week to attend class alongside of 15 low-security, hand chosen, Rockview inmates. The inmates and the students would work side by side discussing assigned criminology theories to rate their validity and discuss ways in which policy and programs can reduce crime. Construction of Rockview began in 1912, and the prison opened three years later in 1915. In 1913, the Pennsylvania State Legislature approved electrocution and the electric chair took the place of the gallows. At that time, the Pennsylvania State Legislature selected the new Western Penitentiary in Centre County, now known as Rockview, as the location of the chair. Neither the chair nor the institution were ready for occupancy until 1915. Between 1915 and 1962, 348 men and two women died in Pennsylvania's electric chair. The first woman to die in the electric chair was Irene Crawford Schroeder aka Shrader February 23, 1931. In 1972, the Pennsylvania Supreme Court decision Commonwealth v. Bradley invalidated the administration of the death penalty. In 1974, Pennsylvania drafted new capital punishment legislation, but it was once again invalidated in 1977. The next year, yet again, new capital punishment legislation was drafted and signed into law. On November 29, 1990, amidst debate over whether electrocution was cruel and unusual punishment, the Pennsylvania State Legislature barred further such executions and lethal injection was approved. The film On The Yard (1978) was filmed entirely at this prison and used actual inmates as extras in the film. It stars John Heard, Thomas Waites, and Mike Kellin. Since June 1997, the state execution chamber has been located in a two-story former field hospital located on the prison grounds outside of the perimeter of the main Rockview SCI facility. The hospital was renovated into a maximum security building that houses the execution chamber and a holding area for death row inmates. This allows officials to prepare for and implement an execution without disrupting the operations of the main Rockview facility. In addition, witnesses do not have to enter the main facility to view an execution. The renovated building gained three cells with cell furniture, floor covering, telephones, an electronic monitoring system, and locking mechanisms. Materials transferred from the previous location include the bullet-proof glass room divider, the tables, and the chairs. The first floor houses the death chamber, while the second floor contains offices for other prison-related operations. It is nicknamed the "Death House". George Feigley escaped from SCI-Rockview in 1976. List of Pennsylvania state prisons PA Dept of Corrections Web site, Yahoo movie "On The Yard" link Witness to Innocence, or WTI, is a non-profit organization based out of Philadelphia, PA dedicated to the effort of abolishing the American death penalty. WTI began as a project of The Moratorium Campaign, led by Jené O'Keefe. Kurt Rosenberg took over in 2005 with sponsorship from Sister Helen Prejean, Witness to Innocence is the only nationwide organization composed of exonerated former death row prisoners; men who were sentenced to death only to later have their innocence revealed. WTI supports these exonerated death row survivors through semi-annual retreats and by running a speakers' bureau. Witness to Innocence works to end the death penalty by bringing to light the crisis of wrongful convictions in death sentencing in the United States. In addition, it seeks to provide organizational and peer-to-peer support to exonerated former death row prisoners and their loved ones. The organization, which is composed of, by and for exonerated former death row prisoners and their loved ones, works with national, state and local anti-death penalty groups to educate citizens and spur political action against the death penalty through the personal stories of those who have survived death row. Witness to Innocence's priorities are to help end the death penalty by coordinating educational and political activities featuring those who have been most directly impacted by capital punishment and to assist these individuals and their loved ones in their transition to life after exoneration. WTI began as a project of The Moratorium Campaign founded by Sister Helen Prejean and led by Jene' O'Keefe. In 2005, WTI became its own organization and was founded as the only national organization led by and composed of exonerated ex-death row prisoners and their loved ones. It held its first national gathering in Orlando, Florida for training, outreach, organizing, leadership, and speaking (TOOLS). The organization has since hosted similar gatherings in Wisconsin, North Carolina, Texas, Pennsylvania, and Alabama. The gatherings consist of organizational development, training workshops, educational activities, peer support sessions, and public anti-death penalty actions. Witness to Innocence also launched its Speakers' Bureau in 2005, providing a platform of empowerment for its membership of exonerated death row survivors to share their stories with audiences around the country. Since its foundation, the WTI speakers' bureau has reached over 25,000 people at nearly 500 events in 37 states. Witness to Innocence has also played a collaborative role in the abolition of the New Jersey death penalty in 2007, the successful campaign against reinstating the death penalty in Wisconsin, and – most recently – the repeal of New Mexico's death penalty in 2009. Witness to Innocence utilizes the innocence list compiled by the Death Penalty Information Center, or DPIC, of people exonerated from death row. The criteria for inclusion on the DPIC innocence list states that, "Defendants must have been convicted, sentenced to death and subsequently either a) their conviction was overturned AND i) they were acquitted at re-trial or ii) all charges were dropped b) they were given an absolute pardon by the governor based on new evidence of innocence.". Proponents of the death penalty cast doubt on the validity of this list, partially because not all of the exonerated former prisoners were on death row at the time of exoneration. All of the 138 people currently on the DPIC list were at some time sentenced to death and were exonerated by the aforementioned legal standards. Witness to Innocence and its members have been featured in numerable publications and news articles, including Parade magazine, the Washington Examiner, the Daily Pennsylvanian, the Tucson Weekly, the Nashua Telegraph, the Salem Statesman Journal, the Austin American-Statesman, the Fort Worth Star-Telegram, and the North Carolina Star-News. WTI member and the 100th former death row prisoner to be exonerated, Ray Krone, was also featured on Good Morning America and an episode of Extreme makeover in its third season. The play and made-for cable television film, The Exonerated, features Witness to Innocence members Delbert Tibbs (played by Delroy Lindo) and David Keaton (played by Danny Glover) as two of its characters. Other projects that feature innocent former death row prisoners include John Grisham's first nonfiction work, , Frank Baumgartner's The Decline of the Death Penalty and the Discovery of Innocence, and Stanley Cohen (sociologist)'s The Wrong Men: America's epidemic of wrongful death row convictions. http://www.countytimes.com/articles/2010/04/29/life/doc4bd98e03e8472189030356.txt, http://www.nashuatelegraph.com/news/699481-196/ex-death-row-inmate-shares-story.html?i=1, http://www.statesmanjournal.com/article/20100421/COMMUNITIES/4210329/1107, http://www.tucsonweekly.com/TheRange/archives/2010/04/16/former-death-row-inmate-to-speak-at-ua-law-school, http://www.citybeat.com/cincinnati/article-940-death-by-the-numbers.html, http://www.biconews.com/?p=6417, http://media.www.jhunewsletter.com/media/storage/paper932/news/2006/04/14/Features/Shackled.No.More.And.Speaking.Out-2242131.shtml, http://www.myjournalcourier.com/news/death-20511-row-imprisoned.html *http://jackcentral.com/news/2008/10/exonerated-death-row-inmate-embodies-gaps-in-justice-system/, http://www.cnjonline.com/articles/state-32718-inmate-death.html, http://www.catholic.org/international/international_story.php?id=27183&cb300;=vocations, http://www.beloitdailynews.com/articles/2006/10/07/news/100706news03a.txt, http://www.channel3000.com/news/10020422/detail.html, http://www.dailypennsylvanian.com/node/52871, http://www.washingtonexaminer.com/local/ap/death-penalty-opponents-tour-virginia-63987052.html, http://www.ionline.pt/interior/index.php?p=news-print&idNota;=42355, http://www.westport-news.com/news/article/Ex-death-row-inmate-crusades-against-fatal-flaws-468854.php The following is a list of people executed by the U.S. State of Pennsylvania. A total of 1,043 people have been executed in Pennsylvania since 1693, the third highest of any other state or commonwealth in the Union, after New York (1,130) and Virginia (1,361). Until 1915, hanging was the common method of execution. 1915 saw the first use of the electric chair, even though it was approved by the Pennsylvania General Assembly in 1913. The delay was due to the time needed to finish the Western Penitentiary in Centre County, now the State Correctional Institution – Rockview. On November 29, 1990, Governor Casey changed the form of execution to lethal injection. Since the reinstatement of the death penalty by the U.S. Supreme Court in 1976, three people, all convicted of murder, have been executed by the Commonwealth of Pennsylvania. All were executed by lethal injection, and in all three cases, they waived their appeals and asked that the execution be carried out. Capital punishment in Pennsylvania, Capital punishment in the United States

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Heart failure (HF), also known as congestive heart failure (CHF) and congestive cardiac failure (CCF), is when the heart is unable to pump sufficiently to maintain blood flow to meet the body's needs. Signs and symptoms of heart failure commonly include shortness of breath, excessive tiredness, and leg swelling. The shortness of breath is usually worse with exercise or while lying down, and may wake the person at night. A limited ability to exercise is also a common feature. Chest pain, including angina, does not typically occur due to heart failure. Common causes of heart failure include coronary artery disease, including a previous myocardial infarction (heart attack), high blood pressure, atrial fibrillation, valvular heart disease, excess alcohol use, infection, and cardiomyopathy of an unknown cause. These cause heart failure by changing either the structure or the function of the heart. The two types of left ventricular heart failure – heart failure with reduced ejection fraction (HFrEF), and heart failure with preserved ejection fraction (HFpEF) – are based on whether the ability of the left ventricle to contract, or to relax, is affected. The severity of the heart failure is graded by the severity of symptoms with exercise. Heart failure is not the same as heart attack (in which part of the heart muscle dies) or cardiac arrest (in which blood flow stops altogether). Other diseases that may have symptoms similar to heart failure include obesity, kidney failure, liver problems, anemia, and thyroid disease. Diagnosis is based on symptoms, physical findings, and echocardiography. Blood tests, electrocardiography, and chest radiography may be useful to determine the underlying cause. Treatment depends on the severity and cause of the disease. In people with chronic stable mild heart failure, treatment commonly consists of lifestyle modifications such as stopping smoking, physical exercise, and dietary changes, as well as medications. In those with heart failure due to left ventricular dysfunction, angiotensin converting enzyme inhibitors, angiotensin receptor blockers, or valsartan/sacubitril along with beta blockers are recommended. For those with severe disease, aldosterone antagonists, or hydralazine with a nitrate may be used. Diuretics are useful for preventing fluid retention and the resulting shortness of breath. Sometimes, depending on the cause, an implanted device such as a pacemaker or an implantable cardiac defibrillator (ICD) may be recommended. In some moderate or severe cases, cardiac resynchronization therapy (CRT) or cardiac contractility modulation may be of benefit. A ventricular assist device (for the left, right, or both ventricles), or occasionally a heart transplant may be recommended in those with severe disease that persists despite all other measures. Heart failure is a common, costly, and potentially fatal condition. In 2015, it affected about 40 million people globally. Overall around 2% of adults have heart failure and in those over the age of 65, this increases to 6–10%. Rates are predicted to increase. The risk of death is about 35% the first year after diagnosis, while by the second year the risk of death is less than 10% for those who remain alive. This degree of risk of death is similar to some cancers. In the United Kingdom, the disease is the reason for 5% of emergency hospital admissions. Heart failure has been known since ancient times, with the Ebers papyrus commenting on it around 1550 BCE. Heart failure is a pathophysiological state in which cardiac output is insufficient to meet the needs of the body and lungs. The term "congestive heart failure" is often used, as one of the common symptoms is congestion, or build-up of fluid in a person's tissues and veins in the lungs or other parts of the body. Specifically, congestion takes the form of water retention and swelling (edema), both as peripheral edema (causing swollen limbs and feet) and as pulmonary edema (causing breathing difficulty), as well as ascites (swollen abdomen). Heart failure symptoms are traditionally and somewhat arbitrarily divided into "left" and "right" sided, recognizing that the left and right ventricles of the heart supply different portions of the circulation, however people commonly have both sets of signs and symptoms. The left side of the heart receives oxygen-rich blood from the lungs and pumps it forward to the systemic circulation (the rest of the body except for the pulmonary circulation). Failure of the left side of the heart causes blood to back up (be congested) into the lungs, causing respiratory symptoms as well as fatigue due to insufficient supply of oxygenated blood. Common respiratory signs are increased rate of breathing and increased work of breathing (non- specific signs of respiratory distress). Rales or crackles, heard initially in the lung bases, and when severe, throughout the lung fields suggest the development of pulmonary edema (fluid in the alveoli). Cyanosis which suggests severe low blood oxygen, is a late sign of extremely severe pulmonary edema. Additional signs indicating left ventricular failure include a laterally displaced apex beat (which occurs if the heart is enlarged) and a gallop rhythm (additional heart sounds) may be heard as a marker of increased blood flow or increased intra-cardiac pressure. Heart murmurs may indicate the presence of valvular heart disease, either as a cause (e.g. aortic stenosis) or as a result (e.g. mitral regurgitation) of the heart failure. Backward failure of the left ventricle causes congestion of the lungs' blood vessels, and so the symptoms are predominantly respiratory in nature. Backward failure can be subdivided into the failure of the left atrium, the left ventricle or both within the left circuit. The person will have dyspnea (shortness of breath) on exertion and in severe cases, dyspnea at rest. Increasing breathlessness on lying flat, called orthopnea, occurs. It is often measured in the number of pillows required to lie comfortably, and in orthopnea, the person may resort to sleeping while sitting up. Another symptom of heart failure is paroxysmal nocturnal dyspnea: a sudden nighttime attack of severe breathlessness, usually several hours after going to sleep. Easy fatigability and exercise intolerance are also common complaints related to respiratory compromise. "Cardiac asthma" or wheezing may occur. Compromise of left ventricular forward function may result in symptoms of poor systemic circulation such as dizziness, confusion and cool extremities at rest. Right-sided heart failure is often caused by pulmonary heart disease (cor pulmonale), which is typically caused by difficulties of the pulmonary circulation, such as pulmonary hypertension or pulmonic stenosis. Physical examination may reveal pitting peripheral edema, ascites, liver enlargement, and spleen enlargement. Jugular venous pressure is frequently assessed as a marker of fluid status, which can be accentuated by eliciting hepatojugular reflux. If the right ventricular pressure is increased, a parasternal heave may be present, signifying the compensatory increase in contraction strength. Backward failure of the right ventricle leads to congestion of systemic capillaries. This generates excess fluid accumulation in the body. This causes swelling under the skin (termed peripheral edema or anasarca) and usually affects the dependent parts of the body first (causing foot and ankle swelling in people who are standing up, and sacral edema in people who are predominantly lying down). Nocturia (frequent nighttime urination) may occur when fluid from the legs is returned to the bloodstream while lying down at night. In progressively severe cases, ascites (fluid accumulation in the abdominal cavity causing swelling) and liver enlargement may develop. Significant liver congestion may result in impaired liver function (congestive hepatopathy), and jaundice and even coagulopathy (problems of decreased or increased blood clotting) may occur. Dullness of the lung fields to finger percussion and reduced breath sounds at the bases of the lung may suggest the development of a pleural effusion (fluid collection between the lung and the chest wall). Though it can occur in isolated left- or right-sided heart failure, it is more common in biventricular failure because pleural veins drain into both the systemic and pulmonary venous systems. When unilateral, effusions are often right sided. If a person with a failure of one ventricle lives long enough, it will tend to progress to failure of both ventricles. For example, left ventricular failure allows pulmonary edema and pulmonary hypertension to occur, which increase stress on the right ventricle. Right ventricular failure is not as deleterious to the other side, but neither is it harmless. Viral infections of the heart can lead to inflammation of the muscular layer of the heart and subsequently contribute to the development of heart failure. Heart damage can predispose a person to develop heart failure later in life and has many causes including systemic viral infections (e.g., HIV), chemotherapeutic agents such as daunorubicin, cyclophosphamide, and trastuzumab, and abuse of drugs such as alcohol, cocaine, and methamphetamine. An uncommon cause is exposure to certain toxins such as lead and cobalt. Additionally, infiltrative disorders such as amyloidosis and connective tissue diseases such as systemic lupus erythematosus have similar consequences. Obstructive sleep apnea (a condition of sleep wherein disordered breathing overlaps with obesity, hypertension, and/or diabetes) is regarded as an independent cause of heart failure. Heart failure may also occur in situations of "high output" (termed "high- output heart failure"), where the amount of blood pumped is more than typical and the heart is unable to keep up. This can occur in overload situations (blood or serum infusions), kidney diseases, chronic severe anemia, beriberi (vitamin B/thiamine deficiency), hyperthyroidism, cirrhosis, Paget's disease, multiple myeloma, arteriovenous fistulae, or arteriovenous malformations. Chronic stable heart failure may easily decompensate. This most commonly results from an concurrent illness (such as myocardial infarction (a heart attack) or pneumonia), abnormal heart rhythms, uncontrolled hypertension, or a person's failure to maintain a fluid restriction, diet, or medication. Other factors that may worsen CHF include: anemia, hyperthyroidism, excessive fluid or salt intake, and medication such as NSAIDs and thiazolidinediones. NSAIDs increase the risk twofold. A number of medications may cause or worsen the disease. This includes NSAIDS, COX-2 inhibitors, a number of anesthetic agents such as ketamine, thiazolidinediones, some cancer medications, several antiarrhythmic medications, pregabalin, alpha-2 adrenergic receptor agonists, minoxidil, itraconazole, cilostazol, anagrelide, stimulants (e.g., methylphenidate), tricyclic antidepressants, lithium, antipsychotics, dopamine agonists, TNF inhibitors, calcium channel blockers, salbutamol, and tamsulosin. By inhibiting the formation of prostaglandins, NSAIDs may exacerbate heart failure through several mechanisms including promotion of fluid retention, increasing blood pressure, and decreasing a person's response to diuretic medications. Similarly, the ACC/AHA recommends against the use of COX-2 inhibitor medications in people with heart failure. Thiazolidinediones have been strongly linked to new cases of heart failure and worsening of pre- existing congestive heart failure due to their association with weight gain and fluid retention. Certain calcium channel blockers such as diltiazem and verapamil are known to decrease the force with which the heart ejects blood and are thus not recommended in people with heart failure with a reduced ejection fraction. Certain alternative medicines carry a risk of exacerbating existing heart failure, and are not recommended. This includes aconite, ginseng, gossypol, gynura, licorice, Lily of the valley, tetrandrine, and yohimbine. Aconite can cause abnormally slow heart rates and abnormal heart rhythms such as ventricular tachycardia. Ginseng can cause abnormally low or high blood pressure, and may interfere with the effects of diuretic medications. Gossypol can increase the effects of diuretics, leading to toxicity. Gynura can cause low blood pressure. Licorice can worsen heart failure by increasing blood pressure and promoting fluid retention. Lily of the valley can cause abnormally slow heart rates with mechanisms similar to those of digoxin. Tetrandrine can lead to low blood pressure through inhibition of L-type calcium channels. Yohimbine can exacerbate heart failure by increasing blood pressure through alpha-2 adrenergic receptor antagonism. Heart failure is caused by any condition which reduces the efficiency of the heart muscle, through damage or overloading. Over time these increases in workload, which are mediated by long-term activation of neurohormonal systems such as the renin–angiotensin system, leads to fibrosis, dilation, and structural changes in the shape of the left ventricle from elliptical to spherical. The heart of a person with heart failure may have a reduced force of contraction due to overloading of the ventricle. In a normal heart, increased filling of the ventricle results in increased contraction force by the Frank–Starling law of the heart, and thus a rise in cardiac output. In heart failure, this mechanism fails, as the ventricle is loaded with blood to the point where heart muscle contraction becomes less efficient. This is due to reduced ability to cross-link actin and myosin filaments in over-stretched heart muscle. No system of diagnostic criteria has been agreed on as the gold standard for heart failure. The National Institute for Health and Care Excellence recommends measuring brain natriuretic peptide (BNP) followed by an ultrasound of the heart if positive. This is recommended in those with shortness of breath. In those with worsening heart failure, both a BNP and a troponin are recommended to help determine likely outcomes. One historical method of categorizing heart failure is by the side of the heart involved (left heart failure versus right heart failure). Right heart failure was thought to compromise blood flow to the lungs compared to left heart failure compromising blood flow to the aorta and consequently to the brain and the remainder of the body's systemic circulation. However, mixed presentations are common and left heart failure is a common cause of right heart failure. More accurate classification of heart failure type is made by measuring ejection fraction, or the proportion of blood pumped out of the heart during a single contraction. Ejection fraction is given as a percentage with the normal range being between 50 and 75%. The two types are: 1) Heart failure due to reduced ejection fraction (HFrEF). Synonyms no longer recommended are "heart failure due to left ventricular systolic dysfunction" and "systolic heart failure". HFrEF is associated with an ejection fraction of less than 40%. 2) Heart failure with preserved ejection fraction (HFpEF). Synonyms no longer recommended include "diastolic heart failure" and "heart failure with normal ejection fraction." HFpEF occurs when the left ventricle contracts normally during systole, but the ventricle is stiff and does not relax normally during diastole, which impairs filling. Heart failure may also be classified as acute or chronic. Chronic heart failure is a long-term condition, usually kept stable by the treatment of symptoms. Acute decompensated heart failure is a worsening of chronic heart failure symptoms which can result in acute respiratory distress. High-output heart failure can occur when there is increased cardiac demand that results in increased left ventricular diastolic pressure which can develop into pulmonary congestion (pulmonary edema). There are several terms which are closely related to heart failure and may be the cause of heart failure, but should not be confused with it. Cardiac arrest and asystole refer to situations in which there is no cardiac output at all. Without urgent treatment, these result in sudden death. Myocardial infarction ("Heart attack") refers to heart muscle damage due to insufficient blood supply, usually as a result of a blocked coronary artery. Cardiomyopathy refers specifically to problems within the heart muscle, and these problems can result in heart failure. Ischemic cardiomyopathy implies that the cause of muscle damage is coronary artery disease. Dilated cardiomyopathy implies that the muscle damage has resulted in enlargement of the heart. Hypertrophic cardiomyopathy involves enlargement and thickening of the heart muscle. Echocardiography is commonly used to support a clinical diagnosis of heart failure. This modality uses ultrasound to determine the stroke volume (SV, the amount of blood in the heart that exits the ventricles with each beat), the end-diastolic volume (EDV, the total amount of blood at the end of diastole), and the SV in proportion to the EDV, a value known as the ejection fraction (EF). In pediatrics, the shortening fraction is the preferred measure of systolic function. Normally, the EF should be between 50% and 70%; in systolic heart failure, it drops below 40%. Echocardiography can also identify valvular heart disease and assess the state of the pericardium (the connective tissue sac surrounding the heart). Echocardiography may also aid in deciding what treatments will help the person, such as medication, insertion of an implantable cardioverter-defibrillator or cardiac resynchronization therapy. Echocardiography can also help determine if acute myocardial ischemia is the precipitating cause, and may manifest as regional wall motion abnormalities on echo. Chest X-rays are frequently used to aid in the diagnosis of CHF. In a person who is compensated, this may show cardiomegaly (visible enlargement of the heart), quantified as the cardiothoracic ratio (proportion of the heart size to the chest). In left ventricular failure, there may be evidence of vascular redistribution ("upper lobe blood diversion" or "cephalization"), Kerley lines, cuffing of the areas around the bronchi, and interstitial edema. Ultrasound of the lung may also be able to detect Kerley lines. An electrocardiogram (ECG/EKG) may be used to identify arrhythmias, ischemic heart disease, right and left ventricular hypertrophy, and presence of conduction delay or abnormalities (e.g. left bundle branch block). Although these findings are not specific to the diagnosis of heart failure a normal ECG virtually excludes left ventricular systolic dysfunction. Blood tests routinely performed include electrolytes (sodium, potassium), measures of kidney function, liver function tests, thyroid function tests, a complete blood count, and often C-reactive protein if infection is suspected. An elevated B-type natriuretic peptide (BNP) is a specific test indicative of heart failure. Additionally, BNP can be used to differentiate between causes of dyspnea due to heart failure from other causes of dyspnea. If myocardial infarction is suspected, various cardiac markers may be used. BNP is a better indicator than N-terminal pro-BNP (NTproBNP) for the diagnosis of symptomatic heart failure and left ventricular systolic dysfunction. In symptomatic people, BNP had a sensitivity of 85% and specificity of 84% in detecting heart failure; performance declined with increasing age. Hyponatremia (low serum sodium concentration) is common in heart failure. Vasopressin levels are usually increased, along with renin, angiotensin II, and catecholamines in order to compensate for reduced circulating volume due to inadequate cardiac output. This leads to increased fluid and sodium retention in the body; the rate of fluid retention is higher than the rate of sodium retention in the body, this phenomenon causes "hypervolemic hyponatremia" (low sodium concentration due to high body fluid retention). This phenomenon is more common in older women with low body mass. Severe hyponatremia can result in accumulation of fluid in the brain, causing cerebral edema and intracranial hemorrhage. Angiography is the X-ray imaging of blood vessels which is done by injecting contrast agents into the bloodstream through a thin plastic tube (catheter) which is placed directly in the blood vessel. X-ray images are called angiograms. Heart failure may be the result of coronary artery disease, and its prognosis depends in part on the ability of the coronary arteries to supply blood to the myocardium (heart muscle). As a result, coronary catheterization may be used to identify possibilities for revascularisation through percutaneous coronary intervention or bypass surgery. There are various algorithms for the diagnosis of heart failure. For example, the algorithm used by the Framingham Heart Study adds together criteria mainly from physical examination. In contrast, the more extensive algorithm by the European Society of Cardiology (ESC) weights the difference between supporting and opposing parameters from the medical history, physical examination, further medical tests as well as response to therapy. By the Framingham criteria, diagnosis of congestive heart failure (heart failure with impaired pumping capability) requires the simultaneous presence of at least 2 of the following major criteria or 1 major criterion in conjunction with 2 of the following minor criteria. Major criteria include an enlarged heart on a chest x-ray, an S3 gallop (a third heart sound), acute pulmonary edema, episodes of waking up from sleep gasping for air, crackles on lung auscultation, central venous pressure of more than 16 cm at the right atrium, jugular vein distension, positive abdominojugular test, and weight loss of more than 4.5 kg in 5 days in response to treatment (sometimes classified as a minor criterion). Minor criteria include an abnormally fast heart rate of more than 120 beats per minute, nocturnal cough, difficulty breathing with physical activity, pleural effusion, a decrease in the vital capacity by one third from maximum recorded, liver enlargement, and bilateral ankle swelling. Minor criteria are acceptable only if they can not be attributed to another medical condition such as pulmonary hypertension, chronic lung disease, cirrhosis, ascites, or the nephrotic syndrome. The Framingham Heart Study criteria are 100% sensitive and 78% specific for identifying persons with definite congestive heart failure. The ESC algorithm weights the following parameters in establishing the diagnosis of heart failure: Heart failure is commonly stratified by the degree of functional impairment conferred by the severity of the heart failure (as reflected in the New York Heart Association (NYHA) Functional Classification.) The NYHA functional classes (I-IV) begin with class I, which is defined as a person who experiences no limitation in any activities and has no symptoms from ordinary activities. People with NYHA class II heart failure have slight, mild limitation with everyday activities; the person is comfortable at rest or with mild exertion. With NYHA class III heart failure, there is marked limitation with any activity; the person is comfortable only at rest. A person with NYHA class IV heart failure is symptomatic at rest and becomes quite uncomfortable with any physical activity. This score documents the severity of symptoms and can be used to assess response to treatment. While its use is widespread, the NYHA score is not very reproducible and does not reliably predict the walking distance or exercise tolerance on formal testing. In its 2001 guidelines the American College of Cardiology/American Heart Association working group introduced four stages of heart failure: Stage A: People at high risk for developing HF in the future but no functional or structural heart disorder., Stage B: a structural heart disorder but no symptoms at any stage., Stage C: previous or current symptoms of heart failure in the context of an underlying structural heart problem, but managed with medical treatment., Stage D: advanced disease requiring hospital-based support, a heart transplant or palliative care. The ACC staging system is useful since Stage A encompasses "pre-heart failure" – a stage where intervention with treatment can presumably prevent progression to overt symptoms. ACC Stage A does not have a corresponding NYHA class. ACC Stage B would correspond to NYHA Class I. ACC Stage C corresponds to NYHA Class II and III, while ACC Stage D overlaps with NYHA Class IV. the degree of coexisting illness: i.e. heart failure/systemic hypertension, heart failure/pulmonary hypertension, heart failure/diabetes, heart failure/kidney failure, etc., whether the problem is primarily increased venous back pressure (preload), or failure to supply adequate arterial perfusion (afterload)., whether the abnormality is due to low cardiac output with high systemic vascular resistance or high cardiac output with low vascular resistance (low-output heart failure vs. high-output heart failure). Histopathology can diagnose heart failure in autopsies. The presence of siderophages indicates chronic left sided heart failure, but is not specific for it.It is also indicated by congestion of the pulmonary circulation. A person's risk of developing heart failure is inversely related to their level of physical activity. Those who achieved at least 500 MET-minutes/week (the recommended minimum by U.S. guidelines) had lower heart failure risk than individuals who did not report exercising during their free time; the reduction in heart failure risk was even greater in those who engaged in higher levels of physical activity than the recommended minimum. Heart failure can also be prevented by lowering high blood pressure and high blood cholesterol, and by controlling diabetes. Maintaining a healthy weight as well as decreasing sodium, alcohol, and sugar intake may help. Additionally, avoiding tobacco use has been shown to lower the risk of heart failure. Treatment focuses on improving the symptoms and preventing the progression of the disease. Reversible causes of the heart failure also need to be addressed (e.g. infection, alcohol ingestion, anemia, thyrotoxicosis, arrhythmia, hypertension). Treatments include lifestyle and pharmacological modalities, and occasionally various forms of device therapy and rarely cardiac transplantation. In acute decompensated heart failure (ADHF), the immediate goal is to re- establish adequate perfusion and oxygen delivery to end organs. This entails ensuring that airway, breathing, and circulation are adequate. Immediate treatments usually involve some combination of vasodilators such as nitroglycerin, diuretics such as furosemide, and possibly noninvasive positive pressure ventilation (NIPPV). Supplemental oxygen is indicated in those with oxygen saturation levels below 90% but is not recommended in those with normal oxygen levels on room air. The goals of treatment for people with chronic heart failure are the prolongation of life, the prevention of acute decompensation and the reduction of symptoms, allowing for greater activity. Heart failure can result from a variety of conditions. In considering therapeutic options, it is important to first exclude reversible causes, including thyroid disease, anemia, chronic tachycardia, alcohol abuse, hypertension and dysfunction of one or more heart valves. Treatment of the underlying cause is usually the first approach to treating heart failure. However, in the majority of cases, either no primary cause is found or treatment of the primary cause does not restore normal heart function. In these cases, behavioral, medical and device treatment strategies exist which can provide a significant improvement in outcomes, including the relief of symptoms, exercise tolerance, and a decrease in the likelihood of hospitalization or death. Breathlessness rehabilitation for chronic obstructive pulmonary disease (COPD) and heart failure has been proposed with exercise training as a core component. Rehabilitation should also include other interventions to address shortness of breath including psychological and education needs of people and needs of carers. Iron supplementation appears useful in those with iron deficiency anemia and heart failure. Various measures are often used to assess the progress of people being treated for heart failure. These include fluid balance (calculation of fluid intake and excretion), monitoring body weight (which in the shorter term reflects fluid shifts). Remote monitoring can be effective to reduce complications for people with heart failure. Behavior modification is a primary consideration in chronic heart failure management program, with dietary guidelines regarding fluid and salt intake. Fluid restriction is important to reduce fluid retention in the body and to correct the hyponatremic status of the body. The evidence of benefit of reducing salt however is poor as of 2018. Exercise should be encouraged and tailored to suit individual capabilities. The inclusion of regular physical conditioning as part of a cardiac rehabilitation program can significantly improve quality of life and reduce the risk of hospital admission for worsening symptoms; however, there is no evidence for a reduction in mortality rates as a result of exercise. Furthermore, it is not clear whether this evidence can be extended to people with heart failure with preserved ejection fraction (HFpEF) or to those whose exercise regimen takes place entirely at home. Home visits and regular monitoring at heart failure clinics reduce the need for hospitalization and improve life expectancy. First-line therapy for people with heart failure due to reduced systolic function should include angiotensin-converting enzyme (ACE) inhibitors (ACE-I) or angiotensin receptor blockers (ARBs) if the person develops a long term cough as a side effect of the ACE-I. Use of medicines from this class is associated with improved survival, fewer hospitalizations for heart failure exacerbations, and improved quality of life in people with heart failure. Beta-adrenergic blocking agents (beta blockers) also form part of the first line of treatment, adding to the improvement in symptoms and mortality provided by ACE-I/ARB. The mortality benefits of beta blockers in people with systolic dysfunction who also have atrial fibrillation (AF) is more limited than in those who do not have AF. If the ejection fraction is not diminished (HFpEF), the benefits of beta blockers are more modest; a decrease in mortality has been observed but reduction in hospital admission for uncontrolled symptoms has not been observed. In people who are intolerant of ACE-I and ARBs or who have significant kidney dysfunction, the use of combined hydralazine and a long-acting nitrate, such as isosorbide dinitrate, is an effective alternate strategy. This regimen has been shown to reduce mortality in people with moderate heart failure. It is especially beneficial in African- Americans (AA). In AAs who are symptomatic, hydralazine and isosorbide dinitrate (H+I) can be added to ACE-I or ARBs. In people with symptomatic heart failure with markedly reduced ejection fraction (anyone with an ejection fraction of 35% or lower or less than 40% if following a heart attack), the use of an aldosterone antagonist, in addition to beta blockers and ACE-I (once titrated to the target dose or maximum tolerated dose), can improve symptoms and reduce mortality. Second-line medications for CHF do not confer a mortality benefit. Digoxin is one such medication. Its narrow therapeutic window, a high degree of toxicity, and the failure of multiple trials to show a mortality benefit have reduced its role in clinical practice. It is now used in only a small number of people with refractory symptoms, who are in atrial fibrillation and/or who have chronic low blood pressure. Diuretics have been a mainstay of treatment for treatment of fluid accumulation, and include diuretics classes such as loop diuretics, thiazide-like diuretics, and potassium-sparing diuretics. Although widely used, evidence on their efficacy and safety is limited, with the exception of mineralocorticoid antagonists such as spironolactone. Mineralocorticoid antagonists in those under 75 years old appear to decrease the risk of death. A recent Cochrane review found that in small studies, the use of diuretics appeared to have improved mortality in individuals with heart failure. However, the extent to which these results can be extrapolated to a general population is unclear due to the small number of participants in the cited studies. Anemia is an independent factor in mortality in people with chronic heart failure. The treatment of anemia significantly improves quality of life for those with heart failure, often with a reduction in severity of the NYHA classification, and also improves mortality rates. The European Society of Cardiology guideline in 2016 recommend screening for iron-deficiency anemia and treating with intravenous iron if deficiency is found. The decision to anticoagulate people with HF, typically with left ventricular ejection fractions <35% is debated, but generally, people with coexisting atrial fibrillation, a prior embolic event, or conditions which increase the risk of an embolic event such as amyloidosis, left ventricular noncompaction, familial dilated cardiomyopathy, or a thromboembolic event in a first-degree relative. Vasopressin receptor antagonists can also be used to treat heart failure. Conivaptan is the first medication approved by US Food and Drug Administration for the treatment of euvolemic hyponatremia in those with heart failure. In rare cases hypertonic 3% saline together with diuretics may be used to correct hyponatremia. Sacubitril/valsartan may be used in those who still have symptoms well on an ACEI, beta blocker, and a mineralocorticoid receptor antagonist. Ivabradine is recommended for people with symptomatic heart failure with reduced left ventricular ejection fraction who are receiving optimized guideline directed therapy (as above) including the maximum tolerated dose of beta blocker, have a normal heart rhythm, and continue to have a resting heart rate above 70 beats per minute. Ivabradine has been found to reduce the risk of hospitalization for heart failure exacerbations in this subgroup of people with heart failure. In people with severe cardiomyopathy (left ventricular ejection fraction below 35%), or in those with recurrent VT or malignant arrhythmias, treatment with an automatic implantable cardioverter defibrillator (AICD) is indicated to reduce the risk of severe life-threatening arrhythmias. The AICD does not improve symptoms or reduce the incidence of malignant arrhythmias but does reduce mortality from those arrhythmias, often in conjunction with antiarrhythmic medications. In people with left ventricular ejection (LVEF) below 35%, the incidence of ventricular tachycardia (VT) or sudden cardiac death is high enough to warrant AICD placement. Its use is therefore recommended in AHA/ACC guidelines. Cardiac contractility modulation (CCM) is a treatment for people with moderate to severe left ventricular systolic heart failure (NYHA class II–IV) which enhances both the strength of ventricular contraction and the heart's pumping capacity. The CCM mechanism is based on stimulation of the cardiac muscle by non-excitatory electrical signals (NES), which are delivered by a pacemaker-like device. CCM is particularly suitable for the treatment of heart failure with normal QRS complex duration (120 ms or less) and has been demonstrated to improve the symptoms, quality of life and exercise tolerance. CCM is approved for use in Europe, but not currently in North America. About one third of people with LVEF below 35% have markedly altered conduction to the ventricles, resulting in dyssynchronous depolarization of the right and left ventricles. This is especially problematic in people with left bundle branch block (blockage of one of the two primary conducting fiber bundles that originate at the base of the heart and carries depolarizing impulses to the left ventricle). Using a special pacing algorithm, biventricular cardiac resynchronization therapy (CRT) can initiate a normal sequence of ventricular depolarization. In people with LVEF below 35% and prolonged QRS duration on ECG (LBBB or QRS of 150 ms or more) there is an improvement in symptoms and mortality when CRT is added to standard medical therapy. However, in the two-thirds of people without prolonged QRS duration, CRT may actually be harmful. People with the most severe heart failure may be candidates for ventricular assist devices (VAD). VADs have commonly been used as a bridge to heart transplantation, but have been used more recently as a destination treatment for advanced heart failure. In select cases, heart transplantation can be considered. While this may resolve the problems associated with heart failure, the person must generally remain on an immunosuppressive regimen to prevent rejection, which has its own significant downsides. A major limitation of this treatment option is the scarcity of hearts available for transplantation. People with heart failure often have significant symptoms, such as shortness of breath and chest pain. Palliative care should be initiated early in the HF trajectory, and should not be an option of last resort. Palliative care can not only provide symptom management, but also assist with advanced care planning, goals of care in the case of a significant decline, and making sure the person has a medical power of attorney and discussed his or her wishes with this individual. A 2016 and 2017 review found that palliative care is associated with improved outcomes, such as quality of life, symptom burden, and satisfaction with care. Without transplantation, heart failure may not be reversible and heart function typically deteriorates with time. The growing number of people with Stage IV heart failure (intractable symptoms of fatigue, shortness of breath or chest pain at rest despite optimal medical therapy) should be considered for palliative care or hospice, according to American College of Cardiology/American Heart Association guidelines. Prognosis in heart failure can be assessed in multiple ways including clinical prediction rules and cardiopulmonary exercise testing. Clinical prediction rules use a composite of clinical factors such as lab tests and blood pressure to estimate prognosis. Among several clinical prediction rules for prognosticating acute heart failure, the 'EFFECT rule' slightly outperformed other rules in stratifying people and identifying those at low risk of death during hospitalization or within 30 days. Easy methods for identifying people that are low-risk are: ADHERE Tree rule indicates that people with blood urea nitrogen < 43 mg/dl and systolic blood pressure at least 115 mm Hg have less than 10% chance of inpatient death or complications., BWH rule indicates that people with systolic blood pressure over 90 mm Hg, respiratory rate of 30 or fewer breaths per minute, serum sodium over 135 mmol/L, no new ST-T wave changes have less than 10% chance of inpatient death or complications. A very important method for assessing prognosis in people with advanced heart failure is cardiopulmonary exercise testing (CPX testing). CPX testing is usually required prior to heart transplantation as an indicator of prognosis. Cardiopulmonary exercise testing involves measurement of exhaled oxygen and carbon dioxide during exercise. The peak oxygen consumption (VO2 max) is used as an indicator of prognosis. As a general rule, a VO2 max less than 12–14 cc/kg/min indicates a poor survival and suggests that the person may be a candidate for a heart transplant. People with a VO2 max<10 cc/kg/min have a clearly poorer prognosis. The most recent International Society for Heart and Lung Transplantation (ISHLT) guidelines also suggest two other parameters that can be used for evaluation of prognosis in advanced heart failure, the heart failure survival score and the use of a criterion of VE/VCO2 slope > 35 from the CPX test. The heart failure survival score is a score calculated using a combination of clinical predictors and the VO2 max from the cardiopulmonary exercise test. Heart failure is associated with significantly reduced physical and mental health, resulting in a markedly decreased quality of life. With the exception of heart failure caused by reversible conditions, the condition usually worsens with time. Although some people survive many years, progressive disease is associated with an overall annual mortality rate of 10%. Approximately 18 of every 1000 persons will experience an ischemic stroke during the first year after diagnosis of HF. As the duration of follow-up increases, the stroke rate rises to nearly 50 strokes per 1000 cases of HF by 5 years. In 2015 heart failure affected about 40 million people globally. Overall around 2% of adults have heart failure and in those over the age of 65, this increases to 6–10%. Above 75 years old rates are greater than 10%. Rates are predicted to increase. Increasing rates are mostly because of increasing life span, but also because of increased risk factors (hypertension, diabetes, dyslipidemia, and obesity) and improved survival rates from other types of cardiovascular disease (myocardial infarction, valvular disease, and arrhythmias). Heart failure is the leading cause of hospitalization in people older than 65. In the United States, heart failure affects 5.8 million people, and each year 550,000 new cases are diagnosed. In 2011, heart failure was the most common reason for hospitalization for adults aged 85 years and older, and the second most common for adults aged 65–84 years. It is estimated that one in five adults at age 40 will develop heart failure during their remaining lifetime and about half of people who develop heart failure die within 5 years of diagnosis. Heart failure is much higher in African Americans, Hispanics, Native Americans and recent immigrants from the eastern bloc countries like Russia. This high prevalence in these ethnic minority populations has been linked to high incidence of diabetes and hypertension. In many new immigrants to the U.S., the high prevalence of heart failure has largely been attributed to lack of preventive health care or substandard treatment. Nearly one out of every four people (24.7%) hospitalized in the U.S. with congestive heart failure are readmitted within 30 days. Additionally, more than 50% of people seek re-admission within 6 months after treatment and the average duration of hospital stay is 6 days. Heart failure is a leading cause of hospital readmissions in the U.S. People aged 65 and older were readmitted at a rate of 24.5 per 100 admissions in 2011. In the same year, people under Medicaid were readmitted at a rate of 30.4 per 100 admissions, and uninsured people were readmitted at a rate of 16.8 per 100 admissions. These are the highest readmission rates for both categories. Notably, heart failure was not among the top ten conditions with the most 30-day readmissions among the privately insured. In the UK, despite moderate improvements in prevention, heart failure rates have increased due to population growth and ageing. Overall heart failure rates are similar to the four most common causes of cancer (breast, lung, prostate and colon) combined. People from deprived backgrounds are more likely to be diagnosed with heart failure and at a younger age. In tropical countries, the most common cause of HF is valvular heart disease or some type of cardiomyopathy. As underdeveloped countries have become more affluent, there has also been an increase in the incidence of diabetes, hypertension and obesity, which have in turn raised the incidence of heart failure. Men have a higher incidence of heart failure, but the overall prevalence rate is similar in both sexes since women survive longer after the onset of heart failure. Women tend to be older when diagnosed with heart failure (after menopause), they are more likely than men to have diastolic dysfunction, and seem to experience a lower overall quality of life than men after diagnosis. Some sources state that people of Asian descent are at a higher risk of heart failure than other ethnic groups. Other sources however have found that rates of heart failure are similar to rates found in other ethnic groups. In 2011, non-hypertensive heart failure was one of the ten most expensive conditions seen during inpatient hospitalizations in the U.S., with aggregate inpatient hospital costs of more than $10.5 billion. Heart failure is associated with a high health expenditure, mostly because of the cost of hospitalizations; costs have been estimated to amount to 2% of the total budget of the National Health Service in the United Kingdom, and more than $35 billion in the United States. There is low-quality evidence that stem cell therapy may help. Although this evidence positively indicated benefit, the evidence was of lower quality than other evidence that does not indicate benefit. A 2016 Cochrane review found tentative evidence of longer life expectancy and improved left ventricular ejection fraction in persons treated with bone marrow-derived stem cells. G protein-coupled receptor kinase 2 (GRK2) inhibition is being researched as a potential treatment for heart failure. Heart failure, American Heart Association – information and resources for treating and living with heart failure, Heart Failure Matters – patient information website of the Heart Failure Association of the European Society of Cardiology, Heart failure in children by Great Ormond Street Hospital, London, UK Aortic stenosis (AS or AoS) is the narrowing of the exit of the left ventricle of the heart (where the aorta begins), such that problems result. It may occur at the aortic valve as well as above and below this level. It typically gets worse over time. Symptoms often come on gradually with a decreased ability to exercise often occurring first. If heart failure, loss of consciousness, or heart related chest pain occur due to AS the outcomes are worse. Loss of consciousness typically occurs with standing or exercising. Signs of heart failure include shortness of breath especially when lying down, at night, or with exercise, and swelling of the legs. Thickening of the valve without narrowing is known as aortic sclerosis. Causes include being born with a bicuspid aortic valve, and rheumatic fever; a normal valve may also harden over the decades. A bicuspid aortic valve affects about one to two percent of the population. As of 2014 rheumatic heart disease mostly occurs in the developing world. Risk factors are similar to those of coronary artery disease and include smoking, high blood pressure, high cholesterol, diabetes, and being male. The aortic valve usually has three leaflets and is located between the left ventricle of the heart, and the aorta. AS typically results in a heart murmur. Its severity can be divided into mild, moderate, severe, and very severe, distinguishable by ultrasound scan of the heart. Aortic stenosis is typically followed using repeated ultrasound scans. Once it has become severe, treatment primarily involves valve replacement surgery, with transcatheter aortic valve replacement (TAVR) being an option in some who are at high risk from surgery. Valves may either be mechanical or bioprosthetic, with each having risks and benefits. Another less invasive procedure, balloon aortic valvuloplasty (BAV), may result in benefit, but for only a few months. Complications such as heart failure may be treated in the same way as in those with mild to moderate AS. In those with severe disease a number of medications should be avoided, including ACE inhibitors, nitroglycerin, and some beta blockers. Nitroprusside or phenylephrine may be used in those with decompensated heart failure depending on the blood pressure. Aortic stenosis is the most common valvular heart disease in the developed world. It affects about 2% of people who are over 65 years of age. Estimated rates were not known in most of the developing world as of 2014. In those who have symptoms, without repair the chance of death at five years is about 50% and at 10 years is about 90%. Aortic stenosis was first described by French physician Lazare Rivière in 1663. Symptoms related to aortic stenosis depend on the degree of stenosis. Most people with mild to moderate aortic stenosis do not have symptoms. Symptoms usually present in individuals with severe aortic stenosis, though they may also occur in those with mild to moderate aortic stenosis. The three main symptoms of aortic stenosis are loss of consciousness, anginal chest pain and shortness of breath with activity or other symptoms of heart failure such as shortness of breath while lying flat, episodes of shortness of breath at night, or swollen legs and feet. It may also be accompanied by the characteristic "Dresden china" appearance of pallor with a light flush. Angina in setting of heart failure also increases the risk of death. In people with angina, the 5-year mortality rate is 50% if the aortic valve is not replaced. Angina in the setting of AS occurs due to left ventricular hypertrophy (LVH) that is caused by the constant production of increased pressure required to overcome the pressure gradient caused by the AS. While the muscular layer of the left ventricle thickens, the arteries that supply the muscle do not get significantly longer or bigger, so the muscle may not receive enough blood supply to meet its oxygen requirement. This ischemia may first be evident during exercise when the heart muscle requires increased blood supply to compensate for the increased workload. The individual may complain of anginal chest pain with exertion. At this stage, a cardiac stress test with imaging may be suggestive of ischemia. Eventually, however, the heart muscle will require more blood supply at rest than can be supplied by the coronary artery branches. At this point there may be signs of ventricular strain pattern (ST segment depression and T wave inversion) on the EKG, suggesting subendocardial ischemia. The subendocardium is the region that is most susceptible to ischemia because it is the most distant from the epicardial coronary arteries. Syncope (fainting spells) from aortic valve stenosis is usually exertional. In the setting of heart failure it increases the risk of death. In people with syncope, the three-year mortality rate is 50% if the aortic valve is not replaced. It is unclear why aortic stenosis causes syncope. One theory is that severe AS produces a nearly fixed cardiac output. When a person with aortic stenosis exercises, their peripheral vascular resistance will decrease as the blood vessels of the skeletal muscles dilate to allow the muscles to receive more blood to allow them to do more work. This decrease in peripheral vascular resistance is normally compensated for by an increase in the cardiac output. Since people with severe AS cannot increase their cardiac output, the blood pressure falls and the person will faint due to decreased blood perfusion to the brain. A second theory is that during exercise the high pressures generated in the hypertrophied left ventricle cause a vasodepressor response, which causes a secondary peripheral vasodilation that, in turn, causes decreased blood flow to the brain resulting in loss of consciousness. Indeed, in aortic stenosis, because of the fixed obstruction to blood flow out from the heart, it may be impossible for the heart to increase its output to offset peripheral vasodilation. A third mechanism may sometimes be operative. Due to the hypertrophy of the left ventricle in aortic stenosis, including the consequent inability of the coronary arteries to adequately supply blood to the myocardium (see "Angina" below), abnormal heart rhythms may develop. These can lead to syncope. Finally, in calcific aortic stenosis at least, the calcification in and around the aortic valve can progress and extend to involve the electrical conduction system of the heart. If that occurs, the result may be heart block, a potentially lethal condition of which syncope may be a symptom. Congestive heart failure (CHF) carries a grave prognosis in people with AS. People with CHF attributable to AS have a 2-year mortality rate of 50% if the aortic valve is not replaced. CHF in the setting of AS is due to a combination of left ventricular hypertrophy with fibrosis, systolic dysfunction (a decrease in the ejection fraction) and diastolic dysfunction (elevated filling pressure of the LV). In Heyde's syndrome, aortic stenosis is associated with gastrointestinal bleeding due to angiodysplasia of the colon. Recent research has shown that the stenosis causes a form of von Willebrand disease by breaking down its associated coagulation factor (factor VIII-associated antigen, also called von Willebrand factor), due to increased turbulence around the stenotic valve. Notwithstanding the foregoing, the American Heart Association has recently changed its recommendations regarding antibiotic prophylaxis for endocarditis. Specifically, as of 2007 it is recommended that such prophylaxis should be limited only to those with prosthetic heart valves, those with previous episode(s) of endocarditis, and those with certain types of congenital heart disease. Since the stenosed aortic valve may limit the heart's output, people with aortic stenosis are at risk of syncope and dangerously low blood pressure should they use any of a number of medications for cardiovascular diseases that often coexist with aortic stenosis. Examples include nitroglycerin, nitrates, ACE inhibitors, terazosin (Hytrin), and hydralazine. Note that all of these substances lead to peripheral vasodilation. Under normal circumstances, in the absence of aortic stenosis, the heart is able to increase its output and thereby offset the effect of the dilated blood vessels. In some cases of aortic stenosis, however, due to the obstruction of blood flow out of the heart caused by the stenosed aortic valve, cardiac output cannot be increased. Low blood pressure or syncope may ensue. Aortic stenosis is most commonly caused by age-related progressive calcification (>50% of cases), with a mean age of 65 to 70 years. Another major cause of aortic stenosis is the calcification of a congenital bicuspid aortic valve (30-40% of cases), typically presenting earlier (ages 40+ to 50+). Acute rheumatic fever post-inflammatory is the cause of less than 10% of cases. Rare causes of aortic stenosis include Fabry disease, systemic lupus erythematosus, Paget disease, high blood uric acid levels, and infection. The human aortic valve normally consists of three cusps or leaflets and has an opening of 3.0-4.0 square centimeters. When the left ventricle contracts, it forces blood through the valve into the aorta and subsequently to the rest of the body. When the left ventricle expands again, the aortic valve closes and prevents the blood in the aorta from flowing backward (regurgitation) into the left ventricle. In aortic stenosis, the opening of the aortic valve becomes narrowed or constricted (stenotic) (e.g., due to calcification). Degenerative (the most common variety), and bicuspid aortic stenosis both begin with damage to endothelial cells from increased mechanical stress. Inflammation is thought to be involved in the earlier stages of the pathogenesis of AS and its associated risk factors are known to promote the deposition of LDL cholesterol and lipoprotein(a), a highly damaging substance, into the aortic valve, causing significant damage and stenosis over time. As a consequence of this stenosis, the left ventricle must generate a higher pressure with each contraction to effectively move blood forward into the aorta. Initially, the LV generates this increased pressure by thickening its muscular walls (myocardial hypertrophy). The type of hypertrophy most commonly seen in AS is known as concentric hypertrophy, in which the walls of the LV are (approximately) equally thickened. In the later stages, the left ventricle dilates, the wall thins, and the systolic function deteriorates (resulting in impaired ability to pump blood forward). Morris and Innasimuthu et al. showed that different coronary anatomy is associated with different valve diseases. Research was in progress in 2010 to see if different coronary anatomy might lead to turbulent flow at the level of valves leading to inflammation and degeneration. Aortic stenosis is most often diagnosed when it is asymptomatic and can sometimes be detected during routine examination of the heart and circulatory system. Good evidence exists to demonstrate that certain characteristics of the peripheral pulse can rule in the diagnosis. In particular, there may be a slow and/or sustained upstroke of the arterial pulse, and the pulse may be of low volume. This is sometimes referred to as pulsus parvus et tardus. There may also be a noticeable delay between the first heart sound (on auscultation) and the corresponding pulse in the carotid artery (so-called 'apical-carotid delay'). In a similar manner, there may be a delay between the appearance of each pulse in the brachial artery (in the arm) and the radial artery (in the wrist). The first heart sound may be followed by a sharp ejection sound ("ejection click") best heard at the lower left sternal border and the apex, and, thus, appear to be "split". The ejection sound, caused by the impact of left ventricular outflow against the partially fused aortic valve leaflets, is more commonly associated with a mobile bicuspid aortic valve than an immobile calcified aortic valve. The intensity of this sound does not vary with respiration, which helps distinguish it from the ejection click produced by a stenotic pulmonary valve, which will diminish slightly in intensity during inspiration. An easily heard systolic, crescendo-decrescendo (i.e., 'ejection') murmur is heard loudest at the upper right sternal border, at the 2nd right intercostal space, and radiates to the carotid arteries bilaterally. The murmur increases with squatting and decreases with standing and isometric muscular contraction such as the Valsalva maneuver, which helps distinguish it from hypertrophic obstructive cardiomyopathy (HOCM). The murmur is louder during expiration but is also easily heard during inspiration. The more severe the degree of the stenosis, the later the peak occurs in the crescendo- decrescendo of the murmur. The second heart sound (A) tends to become decreased and softer as the aortic stenosis becomes more severe. This is a result of the increasing calcification of the valve preventing it from "snapping" shut and producing a sharp, loud sound. Due to increases in left ventricular pressure from the stenotic aortic valve, over time the ventricle may hypertrophy, resulting in a diastolic dysfunction. As a result, there may be a fourth heart sound due to the stiff ventricle. With continued increases in ventricular pressure, dilatation of the ventricle will occur, and a third heart sound may be manifest. Finally, aortic stenosis often co-exists with some degree of aortic insufficiency (aortic regurgitation). Hence, the physical exam in aortic stenosis may also reveal signs of the latter, for example, an early diastolic decrescendo murmur. Indeed, when both valve abnormalities are present, the expected findings of either may be modified or may not even be present. Rather, new signs that reflect the presence of simultaneous aortic stenosis and insufficiency, e.g., pulsus bisferiens, emerge. According to a meta-analysis, the most useful findings for ruling in aortic stenosis in the clinical setting were slow rate of rise of the carotid pulse (positive likelihood ratio ranged 2.8-130 across studies), mid to late peak intensity of the murmur (positive likelihood ratio, 8.0-101), and decreased intensity of the second heart sound (positive likelihood ratio, 3.1-50). Other peripheral signs include: sustained, heaving apex beat, which is not displaced unless systolic dysfunction of the left ventricle has developed, A precordial thrill, narrowed pulse pressure Although aortic stenosis does not lead to any specific findings on the electrocardiogram (ECG), it still often leads to a number of electrocardiographic abnormalities. ECG manifestations of left ventricular hypertrophy (LVH) are common in aortic stenosis and arise as a result of the stenosis having placed a chronically high pressure load on the left ventricle (with LVH being the expected response to chronic pressure loads on the left ventricle no matter what the cause). As noted above, the calcification process that occurs in aortic stenosis can progress to extend beyond the aortic valve and into the electrical conduction system of the heart. Evidence of this phenomenon may rarely include ECG patterns characteristic of certain types of heart block such as Left bundle branch block. Cardiac chamber catheterization provides a definitive diagnosis, indicating severe stenosis in valve area of <1.0 cm (normally about 3 cm). It can directly measure the pressure on both sides of the aortic valve. The pressure gradient may be used as a decision point for treatment. It is useful in symptomatic people before surgery. The standard for diagnosis of aortic stenosis is non-invasive testing with echocardiography. Cardiac catheterization is reserved for cases in which there is discrepancy between the clinical picture and non-invasive testing, due to risks inherent to crossing the aortic valve, such as stroke. Echocardiogram (heart ultrasound) is the best non-invasive way to evaluate the aortic valve anatomy and function. The aortic valve area can be calculated non-invasively using echocardiographic flow velocities. Using the velocity of the blood through the valve, the pressure gradient across the valve can be calculated by the continuity equation or using the modified Bernoulli's equation: Gradient = 4(velocity)² mmHg A normal aortic valve has a gradient of only a few mmHg. A decreased valvular area causes increased pressure gradient, and these parameters are used to classify and grade the aortic stenosis as mild, moderate or severe. The pressure gradient can be abnormally low in the presence of mitral stenosis, heart failure, co-existent aortic regurgitation and also ischaemic heart disease (disease related to decreased blood supply and oxygen causing ischemia). Echocardiogram may also show left ventricular hypertrophy, thickened and immobile aortic valve and dilated aortic root. However, it may appear deceptively normal in acute cases. A chest X-ray can also assist in the diagnosis and provide clues as to the severity of the disease, showing the degree of calcification of the valve, and in a chronic condition, an enlarged left ventricle and atrium. Treatment is generally not necessary in people without symptoms. In moderate cases echocardiography is performed every 1–2 years to monitor the progression, possibly complemented with a cardiac stress test. In severe cases, echocardiography is performed every 3–6 months. In both moderate and mild cases, the person should immediately make a revisit or be admitted for inpatient care if any new related symptoms appear. There are no therapeutic options currently available to treat people with aortic valve stenosis; however, studies have indicated that the disease occurs as a result of active cellular processes, suggesting that targeting these processes may lead to viable therapeutic approaches. The effect of statins on the progression of AS is unclear. The latest trials do not show any benefit in slowing AS progression, but did demonstrate a decrease in ischemic cardiovascular events. In general, medical therapy has relatively poor efficacy in treating aortic stenosis. However, it may be useful to manage commonly coexisting conditions that correlate with aortic stenosis: Any angina is generally treated with beta-blockers and/or calcium blockers. Nitrates are contraindicated due to their potential to cause profound hypotension in aortic stenosis., Any hypertension is treated aggressively, but caution must be taken in administering beta-blockers., Any heart failure is generally treated with digoxin and diuretics, and, if not contraindicated, cautious administration of ACE inhibitors. While observational studies demonstrated an association between lowered cholesterol with statins and decreased progression, a randomized clinical trial published in 2005 failed to find any effect on calcific aortic stenosis. A 2007 study did find a slowing of aortic stenosis with the statin rosuvastatin. Aortic valve repair or aortic valve reconstruction describes the reconstruction of both form and function of the native and dysfunctioning aortic valve. Most frequently it is applied for the treatment of aortic regurgitation. It can also become necessary for the treatment of an aortic aneurysm, less frequently for congenital aortic stenosis. In adults, symptomatic severe aortic stenosis usually requires aortic valve replacement (AVR). While AVR has been the standard of care for aortic stenosis for several decades, aortic valve replacement approaches include open heart surgery, minimally invasive cardiac surgery (MICS) and minimally invasive catheter-based (percutaneous) aortic valve replacement. However, surgical aortic valve replacement is well-studied, and generally has a good and well- established longer-term prognosis. A diseased aortic valve is most commonly replaced using a surgical procedure with either a mechanical or a tissue valve. The procedure is done either in an open-heart surgical procedure or, in a smaller but growing number of cases, a minimally invasive cardiac surgery (MICS) procedure. Globally more than 250,000 people have received transcatheter aortic valve replacement (TAVR). For people who are not candidates for surgical valve replacement and most patients who are older than 75, TAVR may be a suitable alternative. For infants and children, balloon valvuloplasty, where a balloon is inflated to stretch the valve and allow greater flow, may also be effective. In adults, however, it is generally ineffective, as the valve tends to return to a stenosed state. The surgeon will make a small incision at the top of the person's leg and proceed to insert the balloon into the artery. The balloon is then advanced up to the valve and is inflated to stretch the valve open. Acute decompensated heart failure due to AS may be temporarily managed by an intra-aortic balloon pump while pending surgery. In those with high blood pressure nitroprusside may be carefully used. Phenylephrine may be used in those with very low blood pressure. If untreated, severe symptomatic aortic stenosis carries a poor prognosis with a 2-year mortality rate of 50-60% and a 3-year survival rate of less than 30%. Prognosis after aortic valve replacement for people who are younger than 65 is about five years less than that of the general population; for people older than 65 it is about the same. Approximately 2% of people over the age of 65, 3% of people over age 75, and 4% percent of people over age 85 have aortic valve stenosis. The prevalence is increasing with the aging population in North America and Europe. Risk factors known to influence disease progression of AS include lifestyle habits similar to those of coronary artery disease such as hypertension, advanced age, being male, hyperlipidemia, diabetes mellitus, cigarette smoking, metabolic syndrome, and end-stage kidney disease. Aortic stenosis was first described by French physician Lazare Rivière in 1663. People on bisphosphonates were found in a 2010 study to have less progression of aortic stenosis, and some regressed. This finding led to multiple trials, ongoing . Subsequent research failed to confirm the initial positive result. Pulmonary edema is fluid accumulation in the tissue and air spaces of the lungs. It leads to impaired gas exchange and may cause respiratory failure. It is due to either failure of the left ventricle of the heart to remove blood adequately from the pulmonary circulation (cardiogenic pulmonary edema), or an injury to the lung parenchyma or vasculature of the lung (non-cardiogenic pulmonary edema). Treatment is focused on three aspects: firstly improving respiratory function, secondly, treating the underlying cause, and thirdly avoiding further damage to the lung. Pulmonary edema, especially acute, can lead to fatal respiratory distress or cardiac arrest due to hypoxia. It is a cardinal feature of congestive heart failure. The term edema is from the Greek (oídēma, "swelling"), from οἰδέω (oidéō, "I swell"). Classically it is cardiogenic (left ventricular) but fluid may also accumulate due to damage to the lung. This damage may be direct injury or injury mediated by high pressures within the pulmonary circulation. When directly or indirectly caused by increased left ventricular pressure pulmonary edema may form when mean pulmonary pressure rises from the normal of 15 mmHg to above 25 mmHg. Broadly, the causes of pulmonary edema can be divided into cardiogenic and non-cardiogenic. By convention cardiogenic refers to left ventricular causes. Congestive heart failure which is due to the heart's inability to pump the blood out of the pulmonary circulation at a sufficient rate resulting in elevation in wedge pressure and pulmonary edema – this may be due to left ventricular failure, arrhythmias, or fluid overload, e.g., from kidney failure or intravenous therapy., Hypertensive crisis can cause pulmonary edema as the elevation in blood pressure and increased afterload on the left ventricle hinders forward flow and causes the elevation in wedge pressure and subsequent pulmonary edema. Negative pressure pulmonary edema in which a significant negative pressure in the chest (such as from an inhalation against an upper airway obstruction) ruptures capillaries and floods the alveoli. Negative pressure pulmonary edema has an incidence in the range of 0.05-0.1% for general anesthesia. The negative pressure causes a significant increase in preload, thereby increasing pulmonary blood volume. There is also a significant increase in left ventricular afterload, which causes a decreased cardiac output. The increase in pulmonary blood volume along with a decrease in cardiac output will increase the pulmonary transudative pressures. With all this occurring, pulmonary vascular resistance increases causing a shift of the intraventricular septum. The ventricular septal shift to the left causes a left ventricular diastolic dysfunction, which further increases pulmonary hydrostatic pressures., Neurogenic causes (seizures, head trauma, strangulation, electrocution)., Acute respiratory distress syndrome Injury to the lung may also cause pulmonary edema through injury to the vasculature and parenchyma of the lung. The acute lung injury-acute respiratory distress syndrome (ALI-ARDS) covers many of these causes, but they may include: Inhalation of hot or toxic gases, Pulmonary contusion, i.e., high-energy trauma (e.g. vehicle accidents), Aspiration, e.g., gastric fluid, Reexpansion, i.e. post large volume thoracocentesis, resolution of pneumothorax, post decortication, removal of endobronchial obstruction, effectively a form of negative pressure pulmonary oedema., Reperfusion injury, i.e. postpulmonary thromboendartectomy or lung transplantation, Swimming induced pulmonary edema also known as immersion pulmonary edema, Transfusion Associated Circulatory Overload (TACO) occurs when multiple blood transfusions or blood-products (plasma, platelets, etc.) are transfused over a short period of time., Transfusion associated Acute Lung Injury (TRALI) is a specific type of blood-product transfusion injury that occurs when the donors plasma contained antibodies against the recipient,such as anti-HLA or anti-neutrophil antibodies., Severe infection or inflammation which may be local or systemic. This is the classical form of ALI-ARDS. Some causes of pulmonary edema are less well characterised and arguably represent specific instances of the broader classifications above. Arteriovenous malformation, Hantavirus pulmonary syndrome, High altitude pulmonary edema (HAPE), Envenomation, such as with the venom of Atrax robustus The most common symptom of pulmonary edema is difficulty breathing, but may include other symptoms such as coughing up blood (classically seen as pink, frothy sputum), excessive sweating, anxiety, and pale skin. Shortness of breath can manifest as orthopnea (inability to lie down flat due to breathlessness) and/or paroxysmal nocturnal dyspnea (episodes of severe sudden breathlessness at night). These are common presenting symptoms of chronic pulmonary edema due to left ventricular failure. The development of pulmonary edema may be associated with symptoms and signs of "fluid overload"; this is a non-specific term to describe the manifestations of right ventricular failure on the rest of the body and includes peripheral edema (swelling of the legs, in general, of the "pitting" variety, wherein the skin is slow to return to normal when pressed upon), raised jugular venous pressure and hepatomegaly, where the liver is enlarged and may be tender or even pulsatile. Other signs include end-inspiratory crackles (sounds heard at the end of a deep breath) on auscultation and the presence of a third heart sound. Flash pulmonary edema (FPE), is rapid onset pulmonary edema. It is most often precipitated by acute myocardial infarction or mitral regurgitation, but can be caused by aortic regurgitation, heart failure, or almost any cause of elevated left ventricular filling pressures. Treatment of FPE should be directed at the underlying cause, but the mainstays are nitroglycerin, ensuring adequate oxygenation with non-invasive ventilation, and decrease of pulmonary circulation pressures. Recurrence of FPE is thought to be associated with hypertension and may signify renal artery stenosis. Prevention of recurrence is based on managing hypertension, coronary artery disease, renovascular hypertension, and heart failure. There is no one single test for confirming that breathlessness is caused by pulmonary edema; indeed, in many cases, the cause of shortness of breath is probably multifactorial. Low oxygen saturation and disturbed arterial blood gas readings support the proposed diagnosis by suggesting a pulmonary shunt. Chest X-ray will show fluid in the alveolar walls, Kerley B lines, increased vascular shadowing in a classical batwing peri-hilum pattern, upper lobe diversion (increased blood flow to the superior parts of the lung), and possibly pleural effusions. In contrast, patchy alveolar infiltrates are more typically associated with noncardiogenic edema Lung ultrasound, employed by a healthcare provider at the point of care, is also a useful tool to diagnose pulmonary edema; not only is it accurate, but it may quantify the degree of lung water, track changes over time, and differentiate between cardiogenic and non-cardiogenic edema. Especially in the case of cardiogenic pulmonary edema, urgent echocardiography may strengthen the diagnosis by demonstrating impaired left ventricular function, high central venous pressures and high pulmonary artery pressures. Blood tests are performed for electrolytes (sodium, potassium) and markers of renal function (creatinine, urea). Liver enzymes, inflammatory markers (usually C-reactive protein) and a complete blood count as well as coagulation studies (PT, aPTT) are also typically requested. B-type natriuretic peptide (BNP) is available in many hospitals, sometimes even as a point-of-care test. Low levels of BNP (<100 pg/ml) suggest a cardiac cause is unlikely. In those with underlying heart disease, effective control of congestive symptoms prevents pulmonary edema. Dexamethasone is in widespread use for the prevention of high altitude pulmonary edema. Sildenafil is used as a preventive treatment for altitude-induced pulmonary edema and pulmonary hypertension, the mechanism of action is via phosphodiesterase inhibition which raises cGMP, resulting in pulmonary arterial vasodilation and inhibition of smooth muscle cell proliferation. While this effect has only recently been discovered, sildenafil is already becoming an accepted treatment for this condition, in particular in situations where the standard treatment of rapid descent has been delayed for some reason. The initial management of pulmonary edema, irrespective of the type or cause, is supporting vital functions. Therefore, if the level of consciousness is decreased it may be required to proceed to tracheal intubation and mechanical ventilation to prevent airway compromise. Hypoxia (abnormally low oxygen levels) may require supplementary oxygen, but if this is insufficient then again mechanical ventilation may be required to prevent complications. Treatment of the underlying cause is the next priority; pulmonary edema secondary to infection, for instance, would require the administration of appropriate antibiotics. Acute cardiogenic pulmonary edema often responds rapidly to medical treatment. Positioning upright may relieve symptoms. A loop diuretic such as furosemide (Lasix®) is administered, often together with morphine to reduce respiratory distress. Both diuretic and morphine may have vasodilator effects, but specific vasodilators may be used (particularly intravenous glyceryl trinitrate or ISDN) provided the blood pressure is adequate. Continuous positive airway pressure and bilevel positive airway pressure (BIPAP/NIPPV) has been demonstrated to reduce the need of mechanical ventilation in people with severe cardiogenic pulmonary edema, and may reduce mortality. It is possible for cardiogenic pulmonary edema to occur together with cardiogenic shock, in which the cardiac output is insufficient to sustain an adequate blood pressure. This can be treated with inotropic agents or by intra-aortic balloon pump, but this is regarded as temporary treatment while the underlying cause is addressed.

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