The effect of hypotensive anesthesia on renal hemodynamics

Abstract

Deliberate hypotensive anesthesia (MBP = 36 mm Hg) using Halothane, hyperventilation, and positive pressure respiration (peak inspiratory pressure = 15 cm H 2O) was used in 7 dogs for a 2-hr period. Xenon-133 washout was employed by injection of 800–1500 μCi through a catheter placed under fluoroscopic control in the right renal artery. Washout curves were obtained before hypotensive anesthesia, during and after a return of normal hemodynamics using a collimater placed over the right flank. The curves were analyzed and total renal blood flow plus four components of renal blood flow were developed: I cortex; II juxtamedulla; III inner medulla; and IV hilar fat. Using an indocyanine green indicator dilution curve, cardiac output was measured. Urinary output was collected and blood gases monitored. Total renal blood flow decreased significantly during hypotensive anesthesia only to return toward normal within 30 min of discontinuing deliberate hypotension (328 control → 159 during hypotensive anesthesia → 227 ml/100 g/min after hypotensive anesthesia). This decrease in renal blood flow was associated with a fall in cardiac output which also returned toward normal promptly after discontinuing inhalation anesthesia (3.2 → 1.7 → 3.0 liter/min). The ratio of renal blood flow/cardiac output did not change with hypotensive anesthesia indicating an absence of renal vasoconstriction, and renal vascular resistance actually fell from .427 to .306 mm Hg/ml/100 g/min. During the recovery phase, because the blood pressure and cardiac output returned to the control level before renal blood flow, the ratio of renal blood flow/cardiac output fell from 7.1 to 4.9% and the renal vascular resistance rose from .306 to .611 mm Hg/ ml/100 g/min. It was apparent that during recovery renal vasoconstriction developed. The fall in renal blood flow with hypotensive anesthesia was associated with a significant fall in Component I (cortical) flow (414 → 257 → 330 ml/100 g/min) but no significant change in Component II (outer medullary) flow (72 → 74 → 98 ml/ 100 g/min) or the percent distribution of radioactivity between cortex and medulla. This indicates a selective decrease in cortical flow and an absence of marked intrarenal shunting which is seen with hypovolemic hypotension. Urine output fell during hypotension (65 → 20 → 80 ml/hr) but did not cease entirely in any animal. The explanation for the known renal safety of hypotensive anesthesia rests primarily with the absence on intrarenal shunting and associated vasoconstriction during hypotension.