Myocardial circulatory and metabolic effects of halothane when used to control intraoperative hypertension in patients with coronary artery disease

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Abstract
The effect of halothane on regional myocardial metabolism and blood flow, when used as an adjunct to fentanyl‐nitrous oxide anaesthesia, to treat intraoperative hypertension was investigated. Fifteen patients with two‐ or three‐vessel coronary artery disease with an ejection fraction >0.5 and on beta‐blockers up to the morning of surgery were studied during elective coronary artery by‐pass grafting. Systemic and pulmonary haemodynamics, global (coronary sinus, CSF) and regional (great cardiac vein, GCVF) myocardial blood flow were measured. Measurements were made: 1) after induction of anaesthesia but prior to skin incision, 2) during sternotomy, and 3) during halothane administration after its use to reduce arterial pressure to the pre‐sternotomy level. The increase in systemic arterial pressure during sternotomy was due to an increase in systemic vascular resistance index (SVRI), and was accompanied by an increase in pulmonary capillary wedge pressure (PCWP), regional myocardial oxygen consumption and extraction, GCFV and CSF. Halothane reduced arterial blood pressure to pre‐sternotomy levels within 7.1 ± 0.6 min at an end‐tidal concentration of 0.96 ± 0.11%. Halothane caused a decrease in SVRI, total coronary vascular resistance, regional myocardial oxygen consumption and extraction, while cardiac index, heart rate and GCVF/CSF ratio remained unchanged. Mean regional myocardial lactate extraction was not affected by sternotomy or halothane. During halothane administration one patient developed regional myocardial lactate production which was not present during sternotomy. However, another two patients, who had regional myocardial lactate production during sternotomy, did not produce lactate or had less negative value of regional myocardial lactate extraction during halothane administration.

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