Progressive changes in cardiac output and right atrial pressure during different stages of cardiac failure.
circulation. The two curves passing through Point A are (1) the normal cardiac output curve and (2) the normal venous return curve. As pointed out in Chapter 20, there is only one point on each of these two curves at which the circulatory system can operate. This point is where the two curves cross at point A. Therefore, the normal state of the circulation is a cardiac output and venous return of 5 L/min and a right atrial pressure of 0 mm Hg.
Effect of Acute Heart Attack. During the first few seconds after a moderately severe heart attack, the cardiac output curve falls to the lowermost curve. During these few seconds, the venous return curve still has not changed because the peripheral circulatory system is still operating normally. Therefore, the new state of the circulation is depicted by point B, where the new cardiac output curve crosses the normal venous return curve. Thus, the right atrial pressure rises immediately to 4 mm Hg, whereas the cardiac output falls to 2 L/min.
Effect of Sympathetic Reflexes. Within the next 30 seconds, the sympathetic reflexes become very active. They affect both the cardiac output and the venous return curves, raising both of them. Sympathetic stimulation can increase the plateau level of the cardiac output curve as much as 30 to 100 per cent. It can also increase the mean systemic filling pressure (depicted by the point where the venous return curve crosses the zero venous return axis) by several millimeters of mercury—in this figure, from a normal value of 7 mm Hg up to 10 mm Hg. This increase in mean systemic filling pressure shifts the entire venous return curve to the right and upward. The new cardiac output and venous return curves now equilibrate at point C, that is, at a right atrial pressure of +5 mm Hg and a cardiac output of 4 L/min.
Compensation During the Next Few Days. During the ensuing week, the cardiac output and venous return curves rise further because of (1) some recovery of the heart and (2) renal retention of salt and water, which raises the mean systemic filling pressure still further— this time up to +12 mm Hg. The two new curves now equilibrate at point D. Thus, the cardiac output has now returned to normal. The right atrial pressure, however, has risen still further to +6 mm Hg. Because the cardiac output is now normal, renal output is also normal, so that a new state of equilibrated fluid balance has been achieved. The circulatory system will continue to function at point D and remain stable, with a normal cardiac output and an elevated right atrial pressure, until some additional extrinsic factor changes either the cardiac output curve or the venous return curve.
Using this technique for analysis, one can see especially the importance of moderate fluid retention and how it eventually leads to a new stable state of the circulation in mild to moderate heart failure. And one can also see the interrelation between mean systemic filling pressure and cardiac pumping at various degrees of heart failure.
Note that the events described in Figure 22-5 are the same as those presented in Figure 22-1, but in Figure 22-5, they are presented in a more quantitative manner.
Graphical Analysis of "Decompensated" Cardiac Failure
The black cardiac output curve in Figure 22-6 is the same as the curve shown in Figure 22-2, a very low curve that has already reached a degree of recovery as great as this heart can achieve. In this figure, we have added venous return curves that occur during successive days after the acute fall of the cardiac output
Right atrial pressure (mm Hg)
Right atrial pressure (mm Hg)
Graphical analysis of decompensated heart disease showing progressive shift of the venous return curve to the right as a result of continued fluid retention.
curve to this low level. At point A, the curve at time zero equates with the normal venous return curve to give a cardiac output of about 3 L/min. However, stimulation of the sympathetic nervous system, caused by this low cardiac output, increases the mean systemic filling pressure within 30 seconds from 7 to 10.5 mm Hg. This shifts the venous return curve upward and to the right to produce the curve labeled "autonomic compensation." Thus, the new venous return curve equates with the cardiac output curve at point B. The cardiac output has been improved to a level of 4 L/min but at the expense of an additional rise in right atrial pressure to 5 mm Hg.
The cardiac output of 4 L/min is still too low to cause the kidneys to function normally. Therefore, fluid continues to be retained, and the mean systemic filling pressure rises from 10.5 to almost 13 mm Hg. Now the venous return curve becomes that labeled "2nd day" and equilibrates with the cardiac output curve at point C. The cardiac output rises to 4.2 L/min and the right atrial pressure to 7 mm Hg.
During the succeeding days, the cardiac output never rises quite high enough to re-establish normal renal function. Fluid continues to be retained, the mean systemic filling pressure continues to rise, the venous return curve continues to shift to the right, and the equilibrium point between the venous return curve and the cardiac output curve also shifts progressively to point D, to point E, and, finally, to point F. The equilibration process is now on the down slope of the cardiac output curve, so that further retention of fluid causes only more severe cardiac edema and a detrimental effect on cardiac output. The condition accelerates downhill until death occurs.
Thus, "decompensation" results from the fact that the cardiac output curve never rises to the critical level of 5 L/min needed to re-establish normal kidney excretion of fluid that would be required to cause balance between fluid input and output.
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