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Intravenous infusions are required to maintain ventricular preload after uneventful coronary bypass operation. During the early postoperative period, when myocardial metabolic recovery is incomplete, volume loading is intended to stabilize ventricular function and metabolism and to prevent progressive ischemic injury. This study attempts to define the optimal preload for both metabolism and performance. Thirty-seven patients recovering from elective coronary bypass operations and cold potassium cardioplegia underwent volume loading with whole plasma. The initial response (VLA) from a low left atrial pressure (LAP = 7.3 +/- 3.3 mm Hg) was compared with the subsequent response (VLB) from a higher filling pressure (LAP = 10.9 +/- 2.7 mm Hg). Both VLA and VLB produced a similar increase in cardiac index, stroke work index, and end-diastolic volume index (EDVI), and a decrease in ejection fraction (measured by nuclear angiography). Myocardial lactate extraction increased with VLA, but myocardial lactate production resulted with VLB. A careful analysis of these volume loading studies suggested that myocardial performance and compliance were not altered in the early postoperative period. The decrease in ejection fraction with volume loading may have resulted from a combination of increased wall tension and decreased inotropic stimulation. After uneventful coronary bypass surgery, an LAP between 5 and 12 mm Hg corresponded to an EDVI between 30 and 80 ml/m2 and produced adequate cardiac index, stroke work index, and lactate extraction. A lower or higher preload did not improve function and resulted in abnormal metabolism.

Cardioplegia provides excellent protection for the left ventricle, but the right atrium may be poorly protected. Myocardial temperatures, right atrial electrical activity, and postoperative arrhythmias were assessed in 103 patients participating in two consecutive randomized trials comparing blood cardioplegia (n = 36), crystalloid cardioplegia (n = 38), and diltiazem crystalloid cardioplegia (n = 29). Both right atrial and right ventricular temperatures were significantly warmer (p less than 0.05) during delivery of the blood cardioplegic solution than during delivery of either the crystalloid or the diltiazem crystalloid cardioplegic solutions; the aortic root temperatures were 9 degrees +/- 2 degrees C with blood cardioplegia and 5 degrees + 1 degrees C with both crystalloid and diltiazem crystalloid cardioplegia. Atrial activity during cardioplegic arrest was greatest with blood cardioplegia (12 +/- 3 beats/min), lower with crystalloid cardioplegia (10 +/- 2 beats/min), and minimal with diltiazem crystalloid cardioplegia (5 +/- 1 beats/min, p less than 0.05). Perioperative ischemic injury (by creatine kinase MB isoenzyme analysis) was greatest with crystalloid cardioplegia (p less than 0.05). Postoperative supraventricular arrhythmias (both treated and untreated) were more frequent after crystalloid cardioplegia (crystalloid, 63%; blood, 40%; diltiazem, 47%; p less than 0.05). Patients in whom supraventricular arrhythmias developed had significantly more postoperative ischemic injury (by creatinine kinase MB isoenzyme analysis, p less than 0.05). Blood cardioplegia reduced supraventricular arrhythmias by reducing ischemic injury despite warmer intraoperative temperatures and more right atrial activity. Diltiazem crystalloid cardioplegia reduced postoperative arrhythmias by improving intraoperative myocardial protection and suppressing intraoperative and postoperative atrial activity. Crystalloid cardioplegia cooled but did not arrest the right atrium intraoperatively, resulted in the most perioperative ischemic injury, and yielded the highest incidence of postoperative supraventricular arrhythmias.

A prospective, randomized trial was instituted to determine whether blood cardioplegia (BC) could reduce the morbidity and mortality for patients undergoing urgent coronary bypass for unstable angina. One hundred forty patients who came to the hospital with prolonged angina at rest and who required urgent revascularization because their symptoms were resistant to medical therapy were randomized to receive BC (n = 70) or crystalloid cardioplegia (CC) (n = 70). The operative mortality rate was 2.8%, the incidence of myocardial infarction was 8.6%, the incidence of low output syndrome was 18% and morbidity (myocardial infraction or low output syndrome) was 23%. Patients who received BC had a significantly lower mortality rate (BC, 0%; CC, 5%; p less than 0.05) and incidence of myocardial infarction (BC, 4%; CC, 13.5%; p less than 0.05) or low output syndrome (BC, 10%; CC, 19%; p less than 0.05). The highest postoperative CK-MB level was less after BC (BC, 31 +/- 17 U/L; CC, 56 +/- 13 U/L; p less than 0.05). Preoperative predictors of postoperative morbidity in addition to the type of cardioplegia included the response to medical therapy, persistent ischemic electrocardiographic changes, left ventricular ejection fraction, and age. A multivariate analysis identified the type of cardioplegic protection (p = 0.008) and age (p = 0.05) as significant independent predictors of postoperative morbidity. BC reduced the risk of urgent revascularization for unstable angina.

Calcium channel blockers may prevent myocardial injury during cardioplegia and reperfusion. A prospective, randomized trial was instituted to evaluate the hemodynamic and myocardial metabolic recovery in 40 patients undergoing elective aorta-coronary bypass with either diltiazem in crystalloid potassium cardioplegia (n = 20) or crystalloid potassium cardioplegia (n = 20). In a preliminary trial, doses between 150 and 250 micrograms/kg reduced the period of heart block after cross-clamp removal (90 +/- 110 minutes) from that found with higher doses and improved myocardial metabolism. In the randomized trial, diltiazem cardioplegia (150 micrograms/kg) produced coronary vasodilatation during cardioplegia and produced less reactive hyperemia during reperfusion. Myocardial oxygen extraction was lower and myocardial lactate production was less after diltiazem cardioplegia during reperfusion. Tissue adenosine triphosphate and creatine phosphate concentrations were preserved better after diltiazem cardioplegia. The postoperative creatine kinase MB levels were less (p less than 0.05) after diltiazem cardioplegia, which indicated less myocardial injury. Postoperative volume loading demonstrated that systolic function (the relation between systolic blood pressure and end-systolic volume index) was depressed after diltiazem cardioplegia compared to crystalloid cardioplegia, but cardiac index was higher because afterload (mean arterial pressure) was lower and preload (end-diastolic volume index) was higher. Diltiazem cardioplegia preserved high-energy phosphates, improved postoperative myocardial metabolism, and reduced ischemic injury after elective coronary bypass. However, diltiazem was a potent negative inotrope and produced prolonged periods of electromechanical arrest. Diltiazem cardioplegia may be of value in patients with severe ischemia but should be used with caution in patients with ventricular dysfunction, and a dose-response relation must be established at each institution before clinical use.