Previous studies by this group and others using the mass spectrometer to monitor myocardial gas tensions have described a rapid fall in tissue oxygen tension (PmO2) and a steady increase in tissue carbon dioxide tension (PmCO2) during periods of induced cardiac ischemia. In the present investigation, 32 patients undergoing aortic valve replacement between 1975 and 1976, utilizing hypothermic ischemic arrest, were studied by continuous monitoring of myocardial PmO2 and PmCO2 during the period of aortic cross-clamp and the subsequent reperfusion period. These patients were divided into three groups according to their postoperative courses: group I (N = 17), lived, had no significant left ventricular (LV) failure; group II (N = 11) lived, developed early LV failure requiring inotropic drug support; group III (N = 4), died as a result of severe low cardiac output. During arrest, patients in group III had significantly lower PmO2 and higher PmCO2 levels than did patients in groups I and II. In addition, PmCO2 clearance during reperfusion was delayed in group III patients. Compared to patients without LV failure, subjects in group II demonstrated greater increases in PmCO2 during early reperfusion and significantly prolonged PmCO2 washout. Thus myocardial PmCO2 levels during early reperfusion appear to correlate with left ventricular function after operation. In addition, evidence of most severe ischemic injury during and following aortic cross-clamping correlated with the greatest degree of myocardial hypertrophy as indexed by left ventricular wall thickness. Postarrest PmCO2 curves demonstrate poor tissue perfusion and ongoing ischemia in patients with moderate and severe low output states and may provide an explanation for the postoperative LV failure observed in these patients.
|Original language||English (US)|
|Number of pages||8|
|State||Published - Jul 1979|
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