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These are (1) dilation (Frank-Starling mechanism) purchase 35mg actonel amex, (2) sympathetic stimulation and an increase in circulating catecholamines purchase actonel 35 mg free shipping, and (3) increased heart rate cheap 35mg actonel with visa. The effect of two of these mechanisms on the ventricular function curve is shown in Figure 22. During the process of heart failure, the left ventricle has moved from point A on the normal curve down to point B on a depressed and failing curve. Since cardiac output is the product of stroke volume and heart rate, an increase in heart rate will also tend to maintain cardiac output when stroke volume is reduced. Chronic compensatory mechanisms include (1) hypertrophy, which occurs with both volume and pressure overload, and (2) increased extraction of oxygen from the blood. This latter effect increases oxygen delivery to body tissues at a given cardiac output. The patient begins at point A on a normal ventricular function curve and shifts down to point B with the development of heart failure. The responses of the ventricle to volume or pressure overload are shown in Figures 22 and 23. The passive-pressure volume relations of the ventricle are usually altered by pressure or volume overload (Fig. In volume overload such as occurs with aortic or mitral valvular regurgitation, the ventricle tends to dilate and the curve is shifted to the right with an increase in compliance. In pressure overload such as occurs with aortic stenosis, the curve is often shifted to the left. The wall hypertrophies with a reduction in intraventricular volume (decreased compliance). Figure 23: Changes in the passive-pressure volume relation of the ventricle in response to volume overload (increased compliance) and pressure overload (decreased compliance). An important principle relating to the onset of heart failure is that there may be preservation of ventricular function at rest although the reserve of the heart in response to stress or exercise is markedly reduced. In response to an increase in arterial pressure, there is a tendency for stroke volume to be reduced because of the increased afterload. The ventricle, therefore, increases its contractility by responding to increased systemic and local norepinephrine secretion to maintain stroke volume. This results in a shift upward in function as shown by the dashed line (A) to the higher function curve. This represents a normal integrated response to an increase in arterial pressure in a compensated ventricle. The upper control curve of patient B has resting measurements similar to the resting measurements of patient A. In response to the same increase in arterial pressure, however, this patient has little reserve. Therefore, as afterload is increased, there is a reduction in left ventricular performance and cardiac dilation. This results in a marked shift of function down and to the right (dashed line), as illustrated. Thus, although resting measurements of performance were similar in the two patients, patient A had relatively normal ventricular reserve, whereas patient B had a marked reduction in ventricular reserve. Patient B, therefore, would probably also be limited by symptoms of shortness of breath and fatigue during exercise. It appears that some depletion of high energy phosphates may occur in heart failure, although this is probably not the cause of the heart failure. The oxygen consumption of the heart has an important relationship to pressure development and to shortening. As a general rule, pressure development requires more oxygen than does shortening. Therefore, increases in stroke volume require less of an increase in oxygen consumption than an increase in pressure development. The major determinants of myocardial oxygen consumption are: heart rate, left ventricular pressure, heart size, and contractile state. When any or all of these are increased, there is an increase in oxygen consumption. Minor determinants of oxygen consumption include the basal levels required to maintain cellular integrity, the minor cost of activation, and the direct metabolic effects of catecholamines. Cardiac muscle can increase its performance by an increase in muscle length and/or an increase in contractile state. The primary determinants of myocardial performance are preload, afterload, contractile state, and heart rate. The increase in performance produced by an increase in muscle length probably relates to optimal overlap of cross-bridge formation. Cardiac muscle has a stiff passive length tension relation that prevents over distension of the muscle with increasing stretch. Isometric contraction of cardiac muscle occurs when the ends of the muscle are fixed. Maximum rate of force development (max dF/dt) is a good index of contractility during isometric contraction. Both the distance shortened and the velocity of shortening are inversely related to the load against which the muscle shortens. The maximum velocity of shortening at zero load (V max, a hypothetical extrapolation) is another index of contractility, since it is altered by changes in contractile state but is little affected by changes in initial muscle length. The total force line determined by isometric contractions in isolated heart muscle also represents the endpoint of contraction for all isotonic afterloaded contractions.

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