Raising pressures inside or outside the heart shifts pressure-flow curves and raises zero flow pressure by increasing coronary venous pressure, with effects most prominent in the subendocardial muscle layer.
Animal data on chamber-specific pressure effects on coronary P(zf) warrant clinical caution; leaves open human translation and mechanistic validation.
Increasing pressures to 30 mmHg in right (RV) and left (LV) ventricles and surrounding heart (SH) in isolated, arrested, maximally vasodilated, blood-perfused dog hearts shifted pressure-flow (PF) curves rightward and increased zero flow pressure (P(zf)) by an amount equal to the RV applied pressure, SH applied pressure, or two-thirds of the LV applied pressure. There were comparable increases in coronary venous pressures. Increasing LV or SH pressures decreased coronary blood flows, especially in the subendocardium. Decreases in driving pressure decreased flows in all layers, but even with driving pressure of 5 mmHg, a few subepicardial pieces had flow. We conclude with the following: 1) raising pressures inside or outside the heart shifts PF curves and raises P(zf) by increasing coronary venous pressure; 2) the effects are most prominent in the subendocardial muscle layer; and 3) as driving pressures are decreased, there is a range of P(zf) in the heart with the final P(zf) recorded due to the last little piece of muscle to be perfused.
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Aldea et al. (2000) studied this question.
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