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Douglas M. Behrendt
Marvin M. Kirsh
Herbert Sloan
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Ann Thorac Surg 1978;26:499-506
© 1978 The Society of Thoracic Surgeons


Articles

Effects of Cardioplegic Solution on Human Contractile Element Velocity

Douglas M. Behrendt, M.D.*, Marvin M. Kirsh, M.D., Kenneth E. Jochim, Ph.D., Herbert Sloan, M.D.

Department of Surgery, Section of Thoracic Surgery, and the Department of Physiology, University of Michigan Medical Center, Ann Arbor, MI 48109

* Address reprint requests to Dr. Behrendt, University Hospital, C7079 Outpatient Building, Ann Arbor, MI 48109.

A technique for measuring the maximum contractile element velocity (Vpm) of the myocardium was developed, verified, and employed in patients to allow accurate intraoperative assessment of the adequacy of myocardial protection. Four groups of patients were studied. Ten patients had coronary artery bypass grafts (CABG) with cardioplegia; 13 had CABG with coronary perfusion, ventricular fibrillation at 28°, and aortic clamping for distal anastamoses; 6 had aortic valve replacement (AVR) with cardioplegia; and 7 had AVR with coronary perfusion to the beating heart. For cardioplegia, a solution of 5% dextrose in 0.2% saline at 4° with 25 mEq of potassium chloride and 12.5 gm of mannitol was infused initially, followed by 500 ml every 30 minutes.

Clinically all patients did well, and there were no deaths. Patients having CABG with intermittent coronary perfusion during ventricular fibrillation had significant (p < 0.01) depression of Vpm from 38.3 to 30.8 sec-1 while Vpm in patients having CABG with cardioplegia was unchanged. Patients having AVR with continuous coronary perfusion or with cardioplegia (average anoxia time, 70.4 minutes) had no significant change in Vpm.

We conclude that this cardioplegic solution provided adequate protection of myocardial function for up to 105 minutes of continuous aortic clamping in humans. The depression in Vpm observed following CABG with intermittent coronary perfusion is consistent with previous suggestions that this combination is detrimental because of maldistribution of coronary blood flow during ventricular fibrillation.




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