Studies in Clinical Shock and Hypotension

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Abstract
Renal blood flow was measured by the indicator-dilution technic in 17 patients with shock related to sepsis, myocardial infarction, pulmonary embolism, or pancreatitis. Renal blood flow averaged 225 ml/min/kidney, the renal plasma transit time was prolonged to an average of nearly three times normal, and the renal fraction of cardiac output was reduced to an average of 10.6%. A direct relationship between renal vascular resistance and systematic nonrenal vascular resistance suggested that renal vasocontriction was a manifestation of a more generalized vasoconstrictor process. Since rapid infusion of dextran in patients with normal central venous pressure relaxed renal vasoconstriction and tended to increase the renal fraction, inadequate venous return apparently is an important factor in the reduced renal blood flow in shock. None of the vasoactive drugs used were effective in restoring normal renal perfusion. The vasoconstrictor drugs (norepinephrine, metaraminol, and angiotensin) increased arterial pressure and renal vascular resistance without significantly altering renal blood flow. Isoproterenol and dopamine increased renal blood flow by an average of 26%, but the renal fraction of cardiac output often decreased further. Renal blood flow was increased by an average of 67% during renal arterial infusion of acetylcholine or hydralazine. It is concluded that shock is associated with preferential diversion of blood flow away from the renal bed. Although plasma volume expansion and vasoactive drug therapy may improve perfusion, renal hypoperfusion often persists.