As such, it can be caused by a wide number of conditions, including myocardial infarction (in which the heart muscle is starved of oxygen and dies), hypertension (which increases the force of contraction needed to pump blood) and cardiac amyloidosis (in which misfolded proteins are deposited in the heart muscle, causing it to stiffen).

Decreased end diastolic volume results from impaired ventricular filling; this occurs when the compliance of the ventricle falls (i.e. when the walls stiffen).

This translates to the loss of one's cardiac reserve, or the ability of the heart to work harder during strenuous physical activity.

This is caused by the terminally differentiated heart muscle fibers increasing in size in an attempt to improve contractility.

This increases the risk of cardiac arrest (specifically due to abnormal ventricular heart rhythms) and reduces blood supply to the rest of the body.

In chronic disease the reduced cardiac output causes a number of changes in the rest of the body, some of which are physiological compensations, some of which are part of the disease process:[citation needed] The increased peripheral resistance and greater blood volume place further strain on the heart and accelerates the process of damage to the myocardium.

In right-sided heart failure, this commonly starts in the ankles where venous pressure is high due to the effects of gravity (although if the patient is bed-ridden, fluid accumulation may begin in the sacral region).

In systolic dysfunction, the ejection fraction is decreased, leaving an abnormally elevated volume of blood in the left ventricle.

Thus, left-sided heart failure often presents with respiratory symptoms: shortness of breath, orthopnea, and paroxysmal nocturnal dyspnea.

[citation needed] In severe cardiomyopathy, the effects of decreased cardiac output and poor perfusion become more apparent, and patients will manifest with cold and clammy extremities, cyanosis, claudication, generalized weakness, dizziness, and fainting.

In congenital diseases such as Duchenne muscular dystrophy, the molecular structure of individual myocytes is affected.

Toxins and pharmacological agents (such as ethanol, cocaine, doxorubicin, and amphetamines) cause intracellular damage and oxidative stress.

After myocardial infarction, dead myocytes are replaced by scar tissue, deleteriously affecting the function of the myocardium.

However, they are exquisitely sensitive to increases in heart rate, and sudden bouts of tachycardia (which can be caused simply by physiological responses to exertion, fever, or dehydration, or by pathological tachyarrhythmias such as atrial fibrillation with rapid ventricular response) may result in flash pulmonary edema.

Adequate rate control (usually with a pharmacological agent that slows down AV conduction such as a calcium channel blocker or a beta-blocker) is, therefore, of key importance to preventing acute decompensation.