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Course Sample:
Overview
Approximately 4,800,000 of the U.S. population have heart failure (HF), with 550,000 new cases each year. The prevalence of HF rises with age. There is a 5-10% annual fatality rate in patients with mild symptoms and up to 30-40% in patients with advanced disease. The 5 year mortality rate is approximately 50%. Recent analyses of the last 50 years have shown that the incidence of HF is decreasing among women, although this does not appear to be occurring among men. Survival rates among both men and women have improved with a decrease in death risk of 12% per decade. Heart failure is the leading cause of hospitalization in patients over 65 years of age. It has been estimated that 20 to 40 billion dollars are spent for HF annually in the U.S. alone. Half of the patients diagnosed with CHF will be dead within 5 years. Each year, there are an estimated 400,000 new cases. The annual number of deaths directly from CHF increased from 10,000 in 1968 to 42,000 in 1993 (figure 1), with another 219,000 related to the condition. CHF is the first-listed diagnosis in 875,000 hospitalizations, and the most common diagnosis in hospital patients age 65 years and older. In that age group, one fifth of all hospitalizations have a primary or secondary diagnosis of heart failure.
Survival following diagnosis of congestive heart failure is worse in men than women, but even in women, only about 20 percent survive much longer than 8 to 12 years. The outlook is not much better than for most forms of cancer. The fatality rate for CHF is high, with one in five persons dying within 1 year. Sudden death is common in these patients, occurring at a rate of six to nine times that of the general population. Thus, CHF remains a highly lethal condition. Advances in the treatment of hypertension, myocardial ischemia, and valvular heart disease have not resulted in substantial improvements in survival once CHF ensues.
The leading cause of HF due to left ventricular systolic dysfunction is coronary artery disease. Non-ischemic causes include hypertension (HTN), valvular heart disease, thyroid disease, myocarditis, and alcohol consumption.
Figure 1
Figure 2
Classification. Treatment of chronic heart failure (HF) is based upon the classification of HF into four stages by the American College of Cardiology/American Heart Association (ACC/AHA) Task Force on Practice Guidelines. It is the intent of the ACC/AHA recommendations to be used in conjunction with the New York Heart Association (NYHA) functional classification that estimates the severity of disease based on patient symptoms. Goals of therapy for HF include improved symptoms, increased functional capacity, improved quality of life, slowed disease progression, decreased need for hospitalization, and prolonged survival.
Table 1. ACC/AHA Guidelines for the
Evaluation and Management of HFa
DISEASE
PROGRESSION
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Stage A: Patients who are high risk for
developing HF, but do not have structural heart disease |
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Stage C: Patients with past or current
HF symptoms and evidence of structural heart damage |
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Stage D: Patients with end-stage
disease, requiring special interventions |
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a
Adapted from Hunt SA, Baker DW, Chin MH, et al. ACC/AHA guidelines for the
evaluation and management of chronic heart failure in the
adult: a report of the American College of Cardiology/American Heart Association
Task Force on Practice guidelines (Committee to
Revise the 1995 Guidelines for the Evaluation and Management of Heart Failure).
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Table 2. NYHA Functional Classification and Objective Assessment of HFa
FUNCTIONAL CAPACITY
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Class I: No limitation of physical activity. Ordinary physical activity
does not cause undue
fatigue,
palpitation, dyspnea, or angina. |
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Class II: Slight limitation of physical activity. Ordinary physical
activity results in fatigue,
palpitation,
dyspnea, or angina. |
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Class III: Marked limitation of physical activity. Comfortable at rest,
but less than ordinary
physical
activity results in fatigue, palpitation, dyspnea, or angina. |
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Class IV: Unable to carry on any physical activity without discomfort.
Symptoms are present
at rest.
With any physical activity, symptoms increase. |
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a
Adapted from the Criteria Committee of the American Heart Association. 1994
revisions to the classification of functional capacity and
objective assessment of patients with disease of the heart. Circulation
1994;90:644-5. |
Pathophysiology
Congestive heart failure, or heart failure, is a term used to describe any condition in which the heart is unable to adequately pump blood throughout the body and/or unable to prevent blood from "backing up" into the lungs. These conditions cause symptoms such as shortness of breath (dyspnea), fatigue, weakness, and swelling (edema) of the legs and sometimes the abdomen.
In order to understand the development of these symptoms, it is important that the reader grasp the concepts of cardiac physiology and the variables related to stroke volume. Stroke volume is the amount of blood ejected by the left ventricle during systole. This is, in essence, the cardiac output. The variables that influence stroke volume are the heart rate, preload, afterload, and contractility. Preload is the term that refers to how much the myocardial muscle fibers stretch just before systole (contraction). Preload is determined by the volume of blood within the ventricle at the end of diastole; preload is also known as left ventricular end-diastolic volume (LVED). The more the ventricle fills the more the muscle fibers are stretched and tension is increased resulting in a more forceful contraction (Starling's law). However, excessive filling over time, therefore stretching, will result in hypertrophy of the ventricle and thickening of the ventricular wall ultimately reducing stroke volume. On the other hand afterload represents the resistance or pressure that the ventricles must overcome to eject blood through the aortic and pulmonic valves into the peripheral and pulmonary circulation. That pressure is directly related to the arterial blood pressure. As arterial blood pressure increases, the resistance (afterload) is increased and exerts a greater work load on the heart muscle. Other factors that affect afterload include compliance of the aortic heart valve, blood viscosity, and total vascular resistance. Stroke volume reduction results in an increase in afterload if compensatory mechanisms are not responding. Stroke volume is increased by contractility controlled by sympathetic stimulation or decreased by hypoxia and acidemia.
As afterload increases the symptoms of fluid overload will occur as the vascular bed is overtaxed and peripheral edema results. As preload increases there may be "backup" of fluid in the pulmonary circulation producing shortness of breath and ultimately pulmonary edema (discussed later).
There are several clinical categories of heart failure. They can be divided in acute versus chronic heart failure, left versus right heart failure, high versus low output failure and systolic versus diastolic failure.
Acute versus chronic heart failure. The mechanisms by which one develops heart failure are usually that of a progressive state wherein the myocardium weakens and the patient develops all of the symptoms of heart failure (shortness of breath, edema etc). However, although unusual, the onset maybe abrupt wherein the patient suffers a catastrophic event such as massive myocardial infarction and the heart is unable to adequately pump and thereby symptoms of failure rapidly develop. In addition, rupture of the chordae tendineae that regulate the valves can lead to a sudden inability of the heart to adequately pump blood out, again leading to a rapid rather than insidious progression to heart failure.
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