Heart failure (HF) is a chronic contractile dysfunction characterized by myocyte loss and increased interstitial collagen deposits associated with structural cardiac diseases.8,17,20 Cardiac output is decreased resulting in reduced renal perfusion. Reduced renal perfusion leads to increased renin-angiotensin-aldosterone synthesis. Decreased hepatic perfusion leads to decreased aldosterone clearance. Increased aldosterone concentrations lead to coronary artery and renovascular fibrosis, endothelial cell and baroreceptor dysfunction, and decreased myocardial norepinephrine uptake.
The most common cause of HF is left ventricular (LV) dysfunction.17,20 LV dysfunction develops as a complication of HTN, CAD, cardiomyopathy, and most forms of congenital heart defects. It may manifest as tachycardia, fatigue on exertion, dyspnea on mild exercise, and intolerance to cold. Paroxysmal nocturnal dyspnea and nocturnal cough reflect the redistribution of excess fluid into the lungs with the recumbent position. Occasionally, bronchospasm, wheezing and hemoptysis are present.
Right-ventricular (RV) dysfunction is usually a consequence of either LV dysfunction, tricuspid valve regurgitation, valve stenosis (mitral or pulmonary), pulmonary hypertension, or pulmonary emboli. 17,20 Cardinal symptoms include fatigue; an awareness of fullness in the neck, i.e., jugular vein distension; fullness in the abdomen with an enlarged liver with tenderness in the right upper quadrant; and, in advanced cases, abdominal swelling secondary to ascites and pitting edema of the lower extremities.
The clinical classification of HF, i.e., New York Heart Association Class I, II, III, and IV, is based on the patient’s functional capacity (FC).20 FC is expressed in metabolic equivalents (METs).20 One MET equals the resting or basal oxygen requirement (i.e., 3.5 ml of O2 per kg per minute) of a 40–year-old, 70-kg man. FC can be classified as excellent (>10 METs), good (7-10 METs), moderate (4-7 METs), and poor (<4 METs).21-23 A functional capacity <4 METs is predictive of increased cardiac risks in association with noncardiac procedures.24
Patients with Class I heart failure are typically asymptomatic at rest and ordinary physical activities do not cause fatigue, dyspnea, palpitations, or acute angina pectoris. These patients can complete physical activities requiring a FC of ≤7 METs, e.g., run a short distance; do heavy work around the house such as scrubbing floors or moving furniture; and participate in recreational activities such as golfing, bowling, dancing, or playing basketball.
Patients with Class II heart failure are typically asymptomatic at rest; however, ordinary physical activities can cause fatigue, dyspnea, palpitations, or acute angina pectoris. These patients can only complete physical activities requiring a FC ≤5 METs, e.g., do light work around the house such as dusting and washing dishes; garden; climb a flight of stairs or walk up a hill; walk on level ground at 4 mph (6.4 km per h): and run a short distance.
Patients with Class III heart failure are typically asymptomatic at rest; however, ordinary physical activities can cause fatigue, dyspnea, palpitations, or acute angina pectoris. These patients can only complete physical activities requiring a FC ≤2 METs, e.g., walk indoors around the house, dress, eat, and use the toilet. Patients with Class IV heart failure are typically symptomatic at rest and either cannot complete or perform physical activities requiring a FC ≤2 METs.
The treatment of HF includes: (1) an angiotensin receptor neprilysin inhibitor (ARNI), ACE inhibitor, or ARB, (2) a βeta-blocker, (3) a mineralocorticoid receptor antagonist (MRA), and (4) an a SGLT2 inhibitor. If the patient is volume overloaded, a diuretic is added. Black patients recalcitrant to initial therapy are often prescribed isosorbide dinitrate and hydralazine. 25 When pharmacological strategies fail, a patient with HF becomes a candidate for heart transplantation.