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The contributions of metabolic acidosis, coronary perfusion pressure (CPP) and adrenergic support to left ventricular performance during hemorrhagic shock at aortic pressure (AP) of 30 ± 5 mm Hg were evaluated in cats in which AP, cardiac output (CO), and heart rate (HR) were controlled, and arterial pH, Po2 and Pco2 were continuously monitored. After 2 hours of shock, the stroke volume (SV), ejected at end-diastolic pressure of 10 cm H2O (SV10), was irreversibly reduced to 46 ± 4% (P < .001) of initial values (arterial pH 6.93 ± .05). In control animals SV10 after 2 hours was 86 ± 6% (pH 7.32 ± .07). Eight animals were subject to shock, but their CPP was held at 100 mm Hg. These showed no difference in SV10 from controls after 2 hours, although the pH had fallen to 6.90 ± .05. Reduction of CPP in these animals without correction of pH resulted in a rapid fall of SV10. In 10 animals subjected to shock for 2 hours, the arterial pH was maintained near 7.40 by infusion of Tris buffer. Five showed no greater reduction of SV10 than the controls, and five became severely depressed. In five cats subjected to beta-receptor blockade, hemorrhagic shock (pH 7.40) produced a rapid fall of SV10 which initially could be reversed by reelevation of AP. In less than 15 minutes, the SV10 depression became irreversible. Thus, shock (2 hours) and associated metabolic acidosis is detrimental to ventricular contractility only if CPP is also reduced. The contribution of acidosis may be related to the amount of sympathetic support during shock. With beta-receptor blockade, shock results in a marked reduction in SV10, even in the absence of metabolic acidosis.

circulation research

Contributions of Coronary Perfusion Pressure, Metabolic Acidosis and Adrenergic Factors to the Reduction of Myocardial Contractility during Hemorrhagic Shock in the Cat