These causes include:
Constrictive pericarditis
Restrictive cardiomyopathy, which includes Amyloidosis (most common restrictive), Sarcoidosis and fibrosis. Pathophysiology
Gross structural abnormalities
Structural changes that occur with HFpEF are often radically different from those associated with heart failure with reduced ejection fraction (HFrEF). Many patients experience increased thickening of the ventricular wall in comparison to chamber size, termed concentric hypertrophy. This leads to increased left ventricular mass and is typically accompanied by a normal, or slightly reduced, end diastolic filling volume. Conversely, HFrEF is typically associated with eccentric hypertrophy, characterized by an increase in cardiac chamber size without an accompanying increase in wall thickness. This leads to a corresponding increase in left ventricular end diastolic volume. Cellular abnormalities
Cellular changes generally underlie alterations in cardiac structure. In HFpEF cardiomyocytes have been demonstrated to show increased diameter without an increase in length; this is consistent with observed concentric ventricular hypertrophy and increased left ventricular mass. HFrEF cardiomyocytes exhibit the opposite morphology; increased length without increased cellular diameter. This too is consistent with eccentric hypertrophy seen in this condition.Changes in the extracellular environment are of significant importance in heart disease. Particularly, regulation of genes that alter fibrosis contribute to the development and progression of HFrEF. This regulation is dynamic and involves changes in fibrillar collagens through increased deposition as well as inhibition of enzymes that break down extracellular matrix components (matrix metalloproteinases, collagenases). While early stage HFrEF is associated with a significant disruption of extracellular matrix proteins initially, as it progresses fibrotic replacement of myocardium may occur, leading to scarring and increased interstitial collagen.
For these procedures, the surgical team will bypass the heart with a heart-lung machine and inject potassium chloride into the heart muscle to stop the heartbeat. Side effects
Side effects can include gastrointestinal discomfort, including nausea and vomiting, diarrhea, and bleeding of the digestive tract. Overdoses cause hyperkalemia, which can lead to paresthesia, cardiac conduction blocks, fibrillation, arrhythmias, and sclerosis.Because of the risk of small-bowel lesions, the US FDA requires some potassium salts containing more than 99 mg (about 1.3 mEq) to be labeled with a warning, while recommending an adult daily intake of 4700 mg (about 63 mEq). History
Slow-K is a 1950s development where the medicine is formulated to enter the bloodstream at delayed intervals. It was first only prescribed to British military forces to balance their diets while serving in Korea. Society
Brand names
Brand names include K-Dur, Klor-Con, Micro-K, Slow-K, Sando-K, and Kaon Cl, most of which are extended release medicine by mouth. Lethal injection
Potassium chloride is used in lethal injection as the third of a three-drug combination. KCl is also sometimes used in fetal intracardiac injections in second- and third-trimester induced abortions. Jack Kevorkians thanatron machine injected a lethal dose of potassium chloride into the patient, which caused the heart to stop functioning, after a sodium thiopental-induced coma was achieved.Cardiac arrest induced by potassium has been used in political assassinations in Iran, by injection or by inserting a potassium suppository into the victims rectum. References
External links
"Potassium chloride". Drug Information Portal. U.S. National Library of Medicine.