Acute Effects of Moderate Cardiac Failure

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If a heart suddenly becomes severely damaged, such as by myocardial infarction, the pumping ability of the heart is immediately depressed. As a result, two main effects occur: (1) reduced cardiac output and (2) damming of blood in the veins, resulting in increased venous pressure.

The progressive changes in heart pumping effectiveness at different times after an acute myocardial infarction are shown graphically in Figure 22-1. The top curve of this figure shows a normal cardiac output curve. Point A on this curve is the normal operating point, showing a normal cardiac output under resting conditions of 5 L/min and a right atrial pressure of 0 mm Hg.

Immediately after the heart becomes damaged, the cardiac output curve becomes greatly lowered, falling to the lowest curve at the bottom of the graph. Within a few seconds, a new circulatory state is established at point B rather than point A, illustrating that the cardiac output has fallen to 2 L/min, about two-fifths normal, whereas the right atrial pressure has risen to +4 mm Hg because venous blood returning to the heart from the body is dammed up in the right atrium. This low cardiac output is still sufficient to sustain life for perhaps a few hours, but it is likely to be associated with fainting. Fortunately, this acute stage usually lasts for only a few seconds because sympathetic nerve reflexes occur immediately and compensate, to a great extent, for the damaged heart, as follows.

Compensation for Acute Cardiac Failure by Sympathetic Nervous Reflexes. When the cardiac output falls precariously low, many of the circulatory reflexes discussed in Chapter 18 are immediately activated.The best known of these is the barore-ceptor reflex, which is activated by diminished arterial pressure. It is probable that the chemoreceptor reflex, the central nervous system ischemic response, and even reflexes that originate in the damaged heart also contribute to activating the sympathetic nervous system. But whatever the reflexes might be, the sympathetics become strongly stimulated within a few seconds, and the

Partially recovered heart — Damaged heart + sympathetic stimulation

Partially recovered heart — Damaged heart + sympathetic stimulation

Right atrial pressure (mm Hg)

Figure 22-1

Right atrial pressure (mm Hg)

Figure 22-1

Progressive changes in the cardiac output curve after acute myocardial infarction. Both the cardiac output and right atrial pressure change progressively from point A to point D (illustrated by the black line) over a period of seconds, minutes, days, and weeks.

parasympathetic nervous signals to the heart become reciprocally inhibited at the same time.

Strong sympathetic stimulation has two major effects on the circulation: first on the heart itself, and second on the peripheral vasculature. If all the ventricular musculature is diffusely damaged but is still functional, sympathetic stimulation strengthens this damaged musculature. If part of the muscle is nonfunctional and part of it is still normal, the normal muscle is strongly stimulated by sympathetic stimulation, in this way partially compensating for the nonfunctional muscle. Thus, the heart, one way or another, becomes a stronger pump. This effect is also demonstrated in Figure 22-1, showing after sympathetic compensation about twofold elevation of the very low cardiac output curve.

Sympathetic stimulation also increases venous return because it increases the tone of most of the blood vessels of the circulation, especially the veins, raising the mean systemic filling pressure to 12 to 14 mm Hg, almost 100 per cent above normal. As discussed in Chapter 20, this increased filling pressure greatly increases the tendency for blood to flow from the veins back into the heart. Therefore, the damaged heart becomes primed with more inflowing blood than usual, and the right atrial pressure rises still further, which helps the heart to pump still larger quantities of blood. Thus, in Figure 22-1, the new circulatory state is depicted by point C, showing a cardiac output of 4.2 L/min and a right atrial pressure of 5 mm Hg.

The sympathetic reflexes become maximally developed in about 30 seconds. Therefore, a person who has a sudden, moderate heart attack might experience nothing more than cardiac pain and a few seconds of fainting. Shortly thereafter, with the aid of the sympathetic reflex compensations, the cardiac output may return to a level adequate to sustain the person if he or she remains quiet, although the pain might persist.

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