Treatment of Decompensated Heart Disease with Digitalis

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us assume that the stage of decompensation has already reached point E in Figure 22-6, and let us proceed to the same point E in Figure 22-7. At this time, digitalis is given to strengthen the heart. This raises the cardiac output curve to the level shown in Figure 22-7, but there is not an immediate change in the venous return curve. Therefore, the new cardiac output curve equates with the venous return curve at point G. The cardiac output is now 5.7 L/min, a value greater than the critical level of 5 liters required to make the kidneys excrete normal amounts of urine. Therefore, the kidneys eliminate much more fluid than normally, causing diuresis, a well-known therapeutic effect of digitalis.

The progressive loss of fluid over a period of several days reduces the mean systemic filling pressure back down to 11.5 mm Hg, and the new venous return curve becomes the curve labeled "Several days later." This curve equates with the cardiac output curve of the digitalized heart at point H, at an output of 5 L/min and a right atrial pressure of 4.6 mm Hg. This cardiac

Figure 22-7
Figure 22-8

Treatment of decompensated heart disease showing the effect of digitalis in elevating the cardiac output curve, this in turn causing increased urine output and progressive shift of the venous return curve to the left.

output is precisely that required for normal fluid balance. Therefore, no additional fluid will be lost and none will be gained. Consequently, the circulatory system has now stabilized, or in other words, the decompensation of the heart failure has been "compensated." And to state this another way, the final steady-state condition of the circulation is defined by the crossing point of three curves: the cardiac output curve, the venous return curve, and the critical level for normal fluid balance. The compensatory mechanisms automatically stabilize the circulation when all three curves cross at the same point.

Graphical Analysis of High-Output Cardiac Failure

Figure 22-8 gives an analysis of two types of highoutput cardiac failure. One of these is caused by an arteriovenous fistula that overloads the heart because of excessive venous return, even though the pumping capability of the heart is not depressed. The other is caused by beriberi, in which the venous return is greatly increased because of diminished systemic vascular resistance, but at the same time, the pumping capability of the heart is depressed.

Arteriovenous Fistula. The "normal" curves of Figure 22-8 depict the normal cardiac output and normal venous return curves. These equate with each other at point A, which depicts a normal cardiac output of 5 L/ min and a normal right atrial pressure of 0 mm Hg.

Now let us assume that the systemic resistance (the total peripheral resistance) becomes greatly decreased because of opening a large arteriovenous fistula (a direct opening between a large artery and a large vein). The venous return curve rotates upward to give the curve labeled "AV fistula." This venous return curve equates with the normal cardiac output curve at point B, with a cardiac output of 12.5 L/min and a right atrial pressure of 3 mm Hg. Thus, the cardiac output has become greatly elevated, the right atrial pressure

Graphical analysis of two types of conditions that can cause highoutput cardiac failure: (1) arteriovenous (AV) fistula and (2) beriberi heart disease.

is slightly elevated, and there are mild signs of peripheral congestion. If the person attempts to exercise, he or she will have little cardiac reserve because the heart is already being used almost to maximum capacity to pump the extra blood through the arteriovenous fistula. This condition resembles a failure condition and is called "high-output failure," but in reality, the heart is overloaded by excess venous return.

Beriberi. Figure 22-8 shows the approximate changes in the cardiac output and venous return curves caused by beriberi. The decreased level of the cardiac output curve is caused by weakening of the heart because of the avitaminosis (mainly lack of thiamine) that causes the beriberi syndrome. The weakening of the heart has decreased the blood flow to the kidneys. Therefore, the kidneys have retained a large amount of extra body fluid, which in turn has increased the mean systemic filling pressure (represented by the point where the venous return curve now intersects the zero cardiac output level) from the normal value of 7 mm Hg up to 11 mm Hg.This has shifted the venous return curve to the right. Finally, the venous return curve has rotated upward from the normal curve because the avitaminosis has dilated the peripheral blood vessels, as explained in Chapter 17.

The two blue curves (cardiac output curve and venous return curve) intersect with each other at point C, which describes the circulatory condition in beriberi, with a right atrial pressure in this instance of 9 mm Hg and a cardiac output about 65 per cent above normal; this high cardiac output occurs despite the weak heart, as demonstrated by the depressed plateau level of the cardiac output curve.

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