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CARDIOVASCULAR ANESTHESIA

Oxygen Delivery During Retrograde Cerebral Perfusion in Humans

Albert T. Cheung, MD^*, Joseph E. Bavaria, MD, Alberto Pochettino, MD, Stuart J. Weiss, MD, PhD^*, David K. Barclay, BA, and Mark M. Stecker, MD, PhD

Departments of *Anesthesiology, Surgery, and Neurology, University of Pennsylvania, Philadelphia, Pennsylvania

Address correspondence and reprint requests to Albert T. Cheung, MD, Department of Anesthesiology, Dulles 7, University of Pennsylvania, 3400 Spruce St., Philadelphia, PA 19104-4283.

Retrograde cerebral perfusion (RCP) potentially delivers metabolic substrate to the brain during surgery using hypothermic circulatory arrest (HCA). Serial measurements of O₂ extraction ratio (OER), PCO₂, and pH from the RCP inflow and outflow were used to determine the time course for O₂ delivery in 28 adults undergoing aortic reconstruction using HCA with RCP. HCA was instituted after systemic cooling on cardiopulmonary bypass for 3 min after the electroencephalogram became isoelectric. RCP with oxygenated blood at 10°C was administered at an internal jugular venous pressure of 20–25 mm Hg. Serial analyses of blood oxygen, carbon dioxide, pH, and hemoglobin concentration were made in samples from the RCP inflow (superior vena cava) and outflow (innominate and left carotid arteries) at different times after institution of RCP. Nineteen patients had no strokes, five patients had preoperative strokes, and four patients had intraoperative strokes. In the group of patients without strokes, HCA with RCP was initiated at a mean nasopharyngeal temperature of 14.3°C with mean RCP flow rate of 220 mL/min, which lasted 19–70 min. OER increased over time to a maximal detected value of 0.66 and increased to 0.5 of its maximal detected value 15 min after initiation of HCA. The RCP inflow-outflow gradient for PCO₂ (slope 0.73 mm Hg/min; P < 0.001) and pH (slope 0.007 U/min; P < 0.001) changed linearly over time after initiation of HCA. In the group of patients with preoperative or intraoperative strokes, the OER and the RCP inflow-outflow gradient for PCO₂ changed significantly more slowly over time after HCA compared with the group of patients without strokes. During RCP, continued CO₂ production and increased O₂ extraction over time across the cerebral vascular bed suggest the presence of viable, but possibly ischemic tissue. Reduced cerebral metabolism in infarcted brain regions may explain the decreased rate of O₂ extraction during RCP in patients with strokes.

Implications: Examining the time course of oxygen extraction, carbon dioxide production, and pH changes from the retrograde cerebral perfusate provided a means to assess metabolic activity during hypothermic circulatory arrest.

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