Elevated Venous Pressure The Cardinal Sign of Heart Failure

As was explained in Chapter 14, a decrease in contractility moves the cardiac function curve down and to the right, as shown in Fig. 1. The immediate effect is a rise in venous pressure and a decrease in cardiac output. The decreased cardiac output causes these patients to have the characteristic symptoms of a limited capacity for physical activity and chronic fatigue. A rise in venous pressure is a key feature of the failure syndrome and is the most prominent clinical sign of a failing heart. The elevated venous pressure distends the veins and thus raises the capillary pressure, leading to fluid filtration into the tissue. This combination is often referred to as venous congestion. In fact, the edema from the venous congestion may be more of a threat to the patient than the reduced cardiac output. There are two sides to the heart, and either may fail independently. Venous pressure rises in the side of the heart that is failing; thus, if the left ventricle fails, then pressure will be elevated in the pulmonary veins. If the right heart is failing, systemic venous pressure will be elevated. If both chambers fail together, as in myopathic diseases, then both systemic and pulmonary venous pressures may rise equally.

Fluid

Fluid

FIGURE 1 The venous function curve and the cardiac output curve are co-plotted for a normal and a failing heart. The starting cardiac output is given by point A. As the heart fails, the cardiac output falls and the venous pressure rises (point B). Sympathetic reflexes constrict the veins and further increase venous pressure (point C). The kidneys retain fluid to increase the blood volume; in this case, they were able to restore the cardiac output to the resting level (point D) but with a further increase in venous pressure to 13 mm Hg. Although this patient's cardiac output would be adequate at rest, he would be unable to increase his cardiac output during physical activity.

Atrial pressure (mmHg)

FIGURE 1 The venous function curve and the cardiac output curve are co-plotted for a normal and a failing heart. The starting cardiac output is given by point A. As the heart fails, the cardiac output falls and the venous pressure rises (point B). Sympathetic reflexes constrict the veins and further increase venous pressure (point C). The kidneys retain fluid to increase the blood volume; in this case, they were able to restore the cardiac output to the resting level (point D) but with a further increase in venous pressure to 13 mm Hg. Although this patient's cardiac output would be adequate at rest, he would be unable to increase his cardiac output during physical activity.

When the left ventricle fails, pulmonary edema can become a life-threatening complication. The alveoli can quickly fill with edema fluid, causing the patient to literally drown in his own transudate. Pulmonary edema becomes likely only when left atrial pressure exceeds 25 mm Hg. But, the analysis in Fig. 1 would suggest that a decrease in contractility could never increase the venous pressure above the mean circulatory filling pressure of 7 mm Hg. Three factors, however, can cause the pressure to become much higher. The first is the anatomic arrangement that puts the left and right heart in series with each other. Imagine that the heart is suddenly failing because a blood clot has formed in a coronary artery supplying a large portion of the left ventricle. In that case, the left ventricle will be depressed while the right ventricle is relatively unaffected. The right heart will then force blood through the pulmonary circulation and into the left atrium, causing the diastolic pressure (preload) of the left ventricle to continue to rise beyond the mean circulatory filling pressure until the stroke volume again equals that from the right heart. Under those conditions, left atrial pressure can exceed 25 mm Hg within seconds, even though systemic venous pressure may have changed only slightly.

The second process that elevates venous pressure involves the reflex response to lowered arterial pressure. As predicted by Fig. 1, cardiac output will fall with failure and so will arterial pressure. The baroreceptors will sense the falling pressure and activate the sympathetic nerves, causing an intense venous constriction that raises the mean circulatory filling pressure and hence venous pressure. The sympathetics also stimulate the heart, causing the right ventricle to beat even more strongly.

The third factor involves the long-term adaptation to a reduced cardiac output. In Chapter 15, we learned that the kidney is the long-term controller of blood pressure and does so by adjusting blood volume. A chronically low cardiac output reduces arterial pressure and will cause fluid retention by the kidney. In a healthy individual, fluid retention would stop when the cardiac filling pressure has been sufficiently increased to restore the cardiac output. In the patient with heart failure, however, that mechanism may be ineffective at restoring cardiac output. Rather, the increased blood volume will only shift the venous function curve further to the right (as shown in Fig. 1) and raise venous pressure to dangerous levels.

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