Left ventricular function and tissue hypoxia in irreversible hemorrhagic and endotoxin shock

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Abstract
Left ventricular contractile capacity was evaluated in intact anesthetized dogs during various phases of shock produced by hemorrhage or endotoxin. Changes of ventricular function were correlated with measurement of systemic 02 debt and with metabolic indices of myocardial anoxia. Ventricular contractile capacity was enhanced by shock as a result of increased sympathetic drive well beyond the point of irreversibility as judged by systemic oxygen debt or supported respiratory failure. Ventricular function was temporarily impaired during early shock after [beta]-blockade. It was concluded that irreversibility of shock is primarily determined by peripheral mechanisms, although the present experiments are also consistent with the conclusion that cumulative myocardial damage or progressive deterioration of sympathetic drive may contribute to the ultimate heart failure observed when shock is prolonged far beyond critical systemic 02 debt.