Congestive heart failure (CHF) is a clinical syndrome characterized by an inability of the heart to pump enough blood and oxygen to meet the energy needs of the body. Heart failure is a common and costly disease that has a great impact on quality of life, mortality, and functional status. Approximately 5 million people in the United States have CHF, which affects mainly older adults (6% to 10% of those age 65 years and older). Approximately 5% of all medical admissions to the hospital are attributable to CHF, and it is the most common reason for admission for older adults. Fully 30% to 40% die within the first year after diagnosis, and 60% to 70% die within 5 years. CHF accounts for approximately 2% of all U.S. health care expenditures—$28 billion in direct and indirect health care costs.(Harlan, 2005)
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.
Major risk factors for developing CHF include coronary artery disease, high blood pressure, diabetes, and left ventricular hypertrophy (LVH). Risk factors for prematurely developing CHF include high cholesterol, chronic inflammation, smoking, and genetic factors.(Kitzman 2003) Obesity additively clusters risk factors and can result in premature manifestation of CHF. Additionally, obesity causes LVH by increasing blood pressure and viscosity. Overall, obesity is associated with an 8 percent population-attributable risk of developing CHF. Prevention of CHF involves prevention of major risk factors.
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.(Harlan, 2005)
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 women and older ...