Heart Failure
DEFINITION
Heart failure is a clinical syndrome caused by the inability of the heart to pump sufficient blood to meet the metabolic needs of the body.
Heart Failure can result from any disorder that reduces ventricular filling (diastolic
dysfunction) and/or myocardial contractility (systolic dysfunction).
PATHOPHYSIOLOGY
- Causes of systolic dysfunction (decreased contractility) are reduction in muscle mass (e.g., myocardial infarction [MI]), dilated cardiomyopathies, and ventricular hypertrophy. Ventricular hypertrophy can be caused by pressure overload (e.g., systemic or pulmonary hypertension, aortic or pulmonic valve stenosis) or volume overload (e.g., valvular regurgitation, shunts, high-output states).
- Causes of diastolic dysfunction (restriction in ventricular filling) are increased ventricular stiffness, ventricular hypertrophy, infiltrative myocardial diseases, myocardial ischemia and infarction, mitral or tricuspid valve stenosis, and pericardial disease (e.g., pericarditis, pericardial tamponade).
- The leading causes of Heart Failure are coronary artery disease and hypertension.
- As cardiac function decreases after myocardial injury, the heart relies on the following compensatory mechanisms: (1) tachycardia and increased contractility through sympathetic nervous system activation; (2) the Frank-Starling mechanism, whereby increased preload increases stroke volume; (3) vasoconstriction; and (4) ventricular hypertrophy and remodeling. Although these compensatory mechanisms initially maintain cardiac function, they are responsible for the symptoms of Heart Failure and contribute to disease progression.
- The neurohormonal model of Heart Failure recognizes that an initiating event (e.g., acute MI) leads to decreased cardiac output but that the Heart Failure state then becomes a systemic disease whose progression is mediated largely by neurohormones and autocrine/paracrine factors. These substances include angiotensin II, norepinephrine, aldosterone, natriuretic peptides, arginine vasopressin, proinflammatory cytokines (e.g., tumor necrosis factor α, interleukin-6 and interleukin-1 β), and endothelin-1.
- Common precipitating factors that may cause a previously compensated patient to decompensate include noncompliance with diet or drug therapy,coronary ischemia, inappropriate medication use, cardiac events (e.g., MI, atrial fibrillation), pulmonary infections, and anemia.
- Drugs may precipitate or exacerbate Heart Failure because of their negative inotropic, cardiotoxic, or sodium- and water-retaining properties.