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Heart failure is a pathophysiological state in which the heart is unable to pump blood at a rate sufficient to meet the metabolic demands of the body.(1) Some clinicians now prefer to use the term heart failure rather than congestive heart failure because a patient can have the clinical syndrome of heart failure without having symptoms of congestion. Heart failure is not a specific disease entity, but rather a clinical syndrome that may be caused by numerous different cardiac disorders.(2)
Congestive heart failure has been described as low-output heart failure in which the heart is unable to pump all the blood with which it is presented. For example, a normal ejection fraction (EF) is greater than 60 percent; however, a patient with severe CHF may have an EF as low as 20-30 percent. Increased cardiac workload (preload, afterload, contractility, heart rate) and decreased myocardial contractility are factors, which contribute to the development of CHF.
To review; cardiac output (CO) is defined as the volume of blood ejected per unit of time (L/min) and can be determined by multiplying heart rate times stroke volume (CO=HR x SV). Stroke volume is the volume of blood ejected during systole, and is dependent on preload, afterload, and contractility. Preload occurs on the venous side of circulation. As the volume of blood returning to the left ventricle increases, pressure increases and causes an increase in wall tension. The fibers or sarcomeres are stretched, resulting in an increased force of contraction. Left ventricular end diastolic volume (LVEDV) is the primary determinant of preload. Afterload can be viewed as the sum of forces preventing active forward ejection of blood by the ventricle.
Contractility is the intrinsic property of cardiac muscle describing fiber shortening and tension development. The terms contractility and inotropic state are used synonymously. Myocardial contractility is decreased when myocardial fibers are diminished or poorly functioning. This often occurs with myocardial infarction, coronary artery disease, rheumatic heart disease, and persistent arrhythmias. Cardiomyopathy, a generalized term used to describe a deterioration of cardiac muscle function, may also produce CHF. Occasionally, drugs such as beta-blockers or daunorubicin induce CHF by decreasing myocardial contractility.(3)
The heart uses several compensatory mechanisms to maintain adequate cardiac output as cardiac function decreases. One of those mechanisms is tachycardia and increased contractility. When cardiac output decreases, there is decreased perfusion of tissues. The decreased perfusion signals the sympathetic autonomic nervous system to release norepinephrine. The effect of this release is increased inotropy and chronotropy (heart rate), which may initially maintain the cardiac output at near normal. This will preserve perfusion of the myocardium and CNS. The release of norepinephrine also acts to cause vasoconstriction in the skin, GI tract, and kidney, decreasing perfusion in these organs.
When the tachycardia and increased contractility occur, it is important to understand that the time ratio of systole: diastole decreases. The time it takes for systole to occur remains relatively the same; however, in tachycardia, the length of time of diastole, or the resting state, is decreased. Diastolic filling becomes compromised at approximately 170-200 beats per minute in the normal heart; however, in a heart with preexisting or acute diastolic dysfunction, the ventricle's need for a longer diastolic filling results in reduction of effective preload at significantly lower heart rates. Increasing heart rate also increases myocardial oxygen demand. Shortened diastolic time also causes an increase in intracellular calcium levels, since calcium is pumped out of the sarcoplasmic reticulum and into the cells during diastole, increasing actin-myosin i
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