TREATMENT OF SHOCK IN MAN BASED ON HEMODYNAMIC DIAGNOSIS.

Abstract

This study assessed the hemodynamic abnormalities present in an unselected series of patients in shock. 20 patients were studied. The following types of hemodynamic abnormalities could be found: 1) cardiac deficit (cause of shock in 10 patients); 2) blood volume deficit (n=9); and 3) peripheral vascular failure (n=1). The finding that 10/20 patients had low cardiac output with a high central venous pressure or cardiac filling pressure was surprising. The hemodynamic cause of shock in these patients was only suspected clinically in 2/10 with myocardial infarction and corpulmonale respectively. In these patients further transfusions were not indicated since the central venous pressure was elevated to 10-15 cm. Response to cardiac output of isoproterenol was excellent with output of from .8-5.14 1/minute. Isoproterenol increased the cardiac output after vasoconstrictors such as metaraminol had increased blood pressure but had failed to increase cardiac output. Shock is a failure of blood flow not of blood pressure. Drugs which elevate blood pressure without increasing flow are not useful. In this study only 1 patient had a failure of resistance vessels as a cause of hypotension and since a failure of resistance vessels is the main reason for administering vasoconstrictor therapy this study does not support its use. Irreversible shock can be strongly suspected in patients who have a persistently elevated or rising arterial blood lactate level. There was no correlation between clinical diagnosis and hemodynamic abnormality. In bactermic shock for example 2 patients demonstrated a volume deficit; the other patient had a cardiac deficit. 1 probable reason for the high mortality rate of bacteremic endotoxic shock is the failure to identify the precise hemodynamic abnormality present. A useful maxim in treatment of most patients in shock is transfuse until either the blood pressure or central venous pressure rises; if the blood pressure returns to normal 1st a volume deficit probably exists. If the central venous pressure rises 1st a cardiac deficit predominates.