The failing ventricle can be filled to progressively higher pressures, and for a while stroke volume rises. But the curve is not infinite. At some filling pressure the ventricle reaches its plateau: further increases in preload no longer increase stroke volume. Beyond that point the curve may even descend, because excessive stretch and high wall stress impair contraction and because the high pressures themselves increase afterload. Meanwhile, the filling pressure is not confined to the ventricle. It is transmitted backward into the pulmonary veins and capillaries, where it drives fluid into the lung interstitium and alveoli, and into the systemic veins, where it produces peripheral edema and jugular venous distension. The simulation lets you set the filling pressure and observe two outputs simultaneously: stroke volume, which rises then plateaus, and a congestion indicator, which rises monotonically. The teaching point is that there is no filling pressure at which the failing heart achieves normal stroke volume without congestion. The two outcomes are coupled.
Why the Heart Fails and How the Body Compensates
The Frank-Starling Response: Using Preload to Defend Output
Finding the Ceiling: Stroke Volume and Congestion at Different Filling Pressures
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Start with the filling pressure low. Stroke volume is low because the ventricle is underfilled. Now increase the filling pressure gradually. Stroke volume rises — this is the Frank-Starling response, and it is the compensation working. Keep increasing. At some point stroke volume stops rising. You have reached the plateau of the depressed curve. Push further and stroke volume may even fall, because excessive stretch and high wall stress impair contraction. Now watch the second output, the congestion indicator. It has been rising the entire time, because the filling pressure is transmitted backward into the pulmonary and systemic veins. There is no setting on this dial where stroke volume is normal and congestion is absent. The compensation and its cost are inseparable.
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