Congestive Heart Failure

Etiology

Risk factors for developing CHF in the United States include coronary artery disease, high blood pressure (hypertension), defective heart valves, diabetes mellitus, cardiac dysrhythmias, and cardiomyopathy. Cardiomyopathy can be idiopathic or caused by drugs, infection, thyroid disease, or alcohol.

The most common cause of CHF is left ventricular (LV) systolic dysfunction, resulting from damage to the heart muscle primarily from coronary artery disease. Damage to the LV decreases its strength, measured as the ejection fraction (EF) or proportion of blood that is pumped through the heart with each contraction (systole). A reduced ejection fraction results in decreased forward blood flow with each systole and, therefore, diminished perfusion of other organs. Remodeling of the undamaged heart muscle also occurs, leading to changes in the size and function of the left ventricle that can further decrease LV systolic function. Remodeling of the heart and organ hypoperfusion lead to activation of systemic neurohumoral pathways, such as the plasma rennin–angiotensin–aldosterone system, which can cause further decompensation of cardiac function, creating a vicious cycle of multisystem failure.

As LV systolic function (and therefore EF) declines, an increase in heart rate typically occurs to increase cardiac output. However, the increased rate strains an already weakened heart by increasing myocardial oxygen demand, resulting in further decompensation of function. The rapid heart rate also decreases LV filling time and can, paradoxically, decrease cardiac output.

However, not all heart failure results from LV systolic dysfunction. In community studies, approximately half of patients with symptomatic heart failure had preserved systolic function of the left ventricle. In the Cardiovascular Health Study, heart failure with preserved LV systolic function was common (55%), especially in [Page 116]women and older adults. Although the pathophysiology is not well understood, poor compliance is a likely mechanism. Compliance is the ability of the heart muscle to relax between contractions (diastole). Poor compliance reduces the size of the LV that can be filled with blood prior to the next contraction. Impaired diastolic filling results in decreased forward blood flow (although the EF remains normal) and decreased perfusion of organs similar to LV systolic dysfunction.

Symptoms

The cardinal symptoms of CHF include shortness of breath (dyspnea), cough, swelling of the feet and ankles (peripheral edema), and chronic fatigue. The impaired ability of the heart to pump blood results in blood “backing up” into the pulmonary veins, with leaking of fluid into the lung tissue (pulmonary edema). Pulmonary edema contributes to dyspnea and cough. Fluid leaks out from other veins, causing peripheral edema. Reduced perfusion of muscles, as the body attempts to direct impaired blood flow to more vital organs such as the brain and kidneys, contributes to fatigue. Other symptoms include nighttime urination (nocturia) and disordered breathing during sleep.

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