Retrograde continuous warm blood cardioplegia: Maintenance of myocardial homeostasis in humans

Recent clinical reports have suggested that continuous delivery of oxygenated warm blood cardioplegia through the coronary veins (retrograde cardioplegia) produces good myocardial preservation during aortic cross-clamping. No data exist, however, about actual myocardial metabolism/homeostasis during retrograde warm blood cardioplegia. We studied 100 consecutive patients undergoing coronary artery bypass grafting, aortic valve replacement, or both who received retrograde continuous warm blood cardioplegia (4:1 dilution) during aortic cross-clamping for 54 to 174 minutes. We measured pH, oxygen tension, carbon dioxide tension, HCO 3 , base excess, and oxygen content of the inflow cardioplegia and the blood egressing from coronary arteries during each arteriotomy for bypass grafting (arteries act as postcapillary veins with retrograde cardioplegia) or the left and right coronary orifices during aortic valve replacement. We also measured these variables from the coronary sinus effluent 1 minute after release of the aortic cross-clamp. Retrograde cardioplegia flow ranged from 50 to 250 mL/min (mean flow, 150 mL/min). All patients were maintained at normothermia during bypass. A total of 460 samples were analyzed (4.6 per patient). Neither the duration of aortic cross-clamping nor the artery sampled affected myocardial blood gases. The pH dropped from 7.41 ± 0.05 for the inflow cardioplegia to 7.32 ± 0.1 when sampled from coronary arteries, and the oxygen tension fell from 181 ± 25 to 28 ± 5 mm Hg, respectively. Carbon dioxide tension rose from 31.0 ± 4.1 to 41.4 ± 9.8 mm Hg. Coronary sinus blood gases 1 minute after cross-clamp removal showed no acidosis or oxygen debt. These results indicate that (1) myocardial homeostasis is preserved by retrograde continuous warm blood cardioplegia during normothermic aortic cross-clamping for up to 3 hours in humans; (2) normal myocardial metabolism and oxygen uptake can be maintained solely by retrograde cardioplegia in the arrested heart, eliminating oxygen debt and ischemia; and (3) unlike experimental models, the arrested human heart is very active metabolically. Further application of this new clinical technique appears warranted, provided appropriate monitoring is used.