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Course Sample:
Overview
Approximately 4,600,000 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.
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.
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 |
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. |
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.
Left versus right heart failure. The most common cause of chronic heart failure is dysfunction of the heart's pumping chamber, the left ventricle. The left ventricle is an oblong-shaped chamber made up of thick walls of muscular tissue. Normally, during systole the left ventricle contracts and ejects approximately 60% of the blood in the chamber into the aorta. The percentage of blood pumped out of the left ventricle with each contraction is called the ejection fraction. The ejection fraction provides a way to quantify the functioning of the left ventricle. In patients with left ventricular dysfunction, the left ventricle may pump 40%, 30%, 20%, or as little as 10% of the blood it contains with each contraction. Patients with an ejection fraction of approximately 40% to 45% have mildly depressed ejection fractions, those with ejection fractions of approximately 30% to 40% have moderately depressed ejection fractions, and those with ejection fractions of 10% to 25% have severely depressed ejection fractions.
For various reasons, the left ventricle of the heart may become enlarged or dilated (this may occur with the other chambers of the heart, too). When the left ventricle dilates, it pumps blood to the aorta less efficiently, which compounds the problem. Heart failure can also develop if the muscular walls of the left ventricle become too thickened and "stiff," which occurs in diastolic dysfunction and hypertrophic cardiomyopathy.
There are several relatively common causes of left ventricular dysfunction and dilation that lead to heart failure:
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