Effects of aortopulmonary collaterals on cerebral cooling and cerebral metabolic recovery after circulatory arrest.

Abstract

Aortopulmonary collaterals (APC) have been associated with an increased risk of choreoathetosis after deep hypothermic circulatory arrest (DHCA). To study the effects of APC on cerebral hemodynamics and metabolism before and after DHCA, a piglet model was developed. Protocol 1: Eight 4- to 6-week-old piglets underwent placement of a left subclavian-to-main pulmonary artery shunt. Control shunts (n = 4) were ligated, APC shunts (n = 4) were left patent. All animals were placed on cardiopulmonary bypass (CPB) and cooled in identical fashion for 20 minutes. Temperature probes were placed in the nasopharynx, cortex, and deep brain. Control animals achieved significantly lower temperatures in all three areas by the end of cooling (17.5 degrees C versus 20.1 degrees C, 19.0 degrees C versus 22.3 degrees C, and 17.5 degrees C versus 21.0 degrees C, respectively, P < .005). Protocol 2: Six control and six APC animals were instrumented as described. All were placed on CPB, cooled to 18 degrees C, arrested for 90 minutes, and rewarmed to 37 degrees C. Cerebral blood flow (CBF) was measured with radioactive microspheres while warm on CPB, after cooling, and after rewarming. Arterial and sagittal sinus blood gases and CBF were used to calculate the cerebral metabolic rate of oxygen consumption (CMRO2). Both CBF and CMRO2 were significantly higher after rewarming to 37 degrees C in control versus APC animals (28 +/- 3 versus 14 +/- 2 mL/100 g per minute and 1.72 +/- 0.21 versus 1.04 +/- 0.14 mL O2/100 g per minute, respectively, P < .05). APC decrease the rate of cerebral cooling on CPB and even if temperature is controlled result in increased cerebral metabolic derangement after DHCA. Patients with such collaterals may need additional measures to optimize cerebral protection.