Critical closing pressure as the arterial downstream pressure with the heart beating and during circulatory arrest.

摘要

BACKGROUND: Calculation of systemic vascular resistance, used for hemodynamic decision-making, is based on central venous pressure taken as the downstream pressure. However, during circulatory arrest, arterial pressure decreases to a plateau higher than central venous pressure, the critical closing pressure (Pcrit). The authors assessed in humans undergoing arrest whether two-compartment and pressure-dependent conductivity models better estimate arterial pressure decay and Pcrit than a single-compartment model, and whether Pcrit corresponds to Pcrit calculated with the heart beating. METHODS: Aortic pressure decay was fitted to single-compartment, two-compartment, and pressure-dependent conductivity models using specified time intervals during arrest and natural diastole in 10 patients during defibrillator implantation. RESULTS: Although all models closely predicted Pcrit with an arrest of > or = 7s, both two-compartment and pressure-dependent conductivity models better estimated pressure decay than a single-compartment model. However, Pcrit calculated from natural diastolic pressure decay was greater (53 mmHg +/- 15.6) than Pcrit 15 s (26.6 mmHg +/- 7.8, P = 0.001) and 30 s (23.9 mmHg +/- 7.1, P = 0.001) during arrest, and also greater than Pcrit calculated for the same time interval during initial arrest. CONCLUSIONS: Thus, during arrest, Pcrit can be closely predicted after > or = 7 s, regardless of the model; two-compartment and pressure-dependent conductivity models provide a better fit than a single-compartment model, and actual Pcrit is much less than Pcrit calculated with the heart beating. Irrespective of uncertainties in whether Pcrit calculated with the heart beating or during arrest is the "true" Pcrit prevailing physiologically, linear vascular resistance is markedly less when substituting Pcrit for central venous pressure as the downstream pressure.