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Why the Heart Fails and How the Body Compensates

1Cardiac Output and the Determinants of Pump Performance2What Heart Failure Is and Why the Pump Fails3The Frank-Starling Response: Using Preload to Defend Output4Sympathetic Activation: Raising Rate and Contractility5The Renin-Angiotensin-Aldosterone System: Defending Volume and Pressure6Cardiac Remodeling: When Compensation Becomes the Disease
The Frank-Starling Response: Using Preload to Defend Output

Filling the Failing Ventricle: Where the Extra Preload Comes From

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Watch the sequence unfold. First, the kidney retains sodium and water. This happens because the body senses that the effective circulating volume is too low, even when total body fluid is normal or elevated. The retained fluid expands the plasma volume. Second, the veins narrow. Venoconstriction reduces the capacity of the venous reservoir, so the same volume of blood now occupies a smaller space. Both changes converge on the same result: pressure in the veins draining into the heart rises. That pressure is transmitted backward to the right ventricle, then through the pulmonary circulation to the left ventricle. The ventricle is now stretched further along its depressed curve, and stroke volume rises. The compensation works — but look at the pressure required. It is far above what a normal heart would ever need.
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If the failing ventricle needs a higher filling pressure to defend stroke volume, the body must supply that pressure. Two mechanisms do the work. First, the kidney retains sodium and water. Reduced effective circulating volume is sensed as underfilling even when total body fluid is normal or high, and the result is a positive sodium balance that expands plasma volume. Second, venoconstriction — narrowing of the veins — reduces the capacity of the venous reservoir, so the same blood volume occupies a smaller space and venous pressure rises. Together, expanded volume and reduced venous capacitance raise the pressure in the veins draining into the right atrium, which raises right ventricular filling pressure, which in turn raises left ventricular filling pressure. The ventricle is now operating further to the right on its depressed Frank-Starling curve, and stroke volume rises toward the defended value. The animation traces this sequence: volume expansion and venoconstriction raise venous pressure, the ventricle fills more, and stroke volume increases — but the pressure required to achieve this is far above normal.

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