Conventional carbon dioxide application does not reduce cerebral or myocardial damage in open heart surgery.

Abstract

Open heart surgery is associated with a significant risk of cerebral and myocardial dysfunction, which is attributed in part to air embolism from incompletely deaired cardiac chambers. To evaluate the impact of carbon dioxide (CO2) insufflation to the thoracic cavity, a prospective randomized study was designed. A total of 62 elective patients were randomly assigned to CO2 insufflation (group I, n = 31) or control (group II, n = 31). According to the Parsonnet risk score, 16 patients in group I (52%) and 10 patients in group II (32%) were categorized as being at either high risk or extremely high risk. In group II, perioperative mortality was 16.1% (5 patients); in group I, 1 patient died (ns). Creatine kinase MB isoenzyme, as a marker of myocardial damage, was more elevated in group I after surgery (38.0 +/- 4.1 vs 28.0 +/- 2.1, p = 0.02). Neurocognitive test scores did not reveal significant postoperative differences between groups. Although mortality was lower with CO2 insufflation, no benefit could be demonstrated for markers of cardiac ischemic damage or neurocognitive outcome in this high-risk population. As CO2 concentrations in the thoracic cavity did not necessarily reach anticipated levels, our method of application is in question.