Does cardioplegic arrest compromise long-term left ventricular function?
This study was undertaken to evaluate the chronic, long-term effect of global ischemia produced by cold potassium cardioplegia during cardiopulmonary bypass. Fifteen dogs underwent either control thoracotomy and chronic instrumentation(Group A) or cardiopulmonary bypass and 60 minutes of cold cardioplegic arrest (Group B). With the dogs conscious, hemodynamic variables and left ventricular studies were recorded weekly for 12 weeks postoperatively, both at rest and during volume overload with saline solution. At rest, the heart rate in Group B was 18% higher and stroke volume was 14% lower than Group A. With volume overload, cardiac output and maximum rate of rise of left ventricular pressure in Group B rose only from 3.7 +/- 0.6 to 7.1 +/- 0.8 liters per minute and 2,410 +/- 220 to 2,730 +/- 130 mm Hg per second, respectively, compared with 3.9 +/- 0.6 to 10.4 +/- 0.8 liters per minute and 2,740 +/- 230 to 3,890 +/- 350 mm Hg, respectively, in Group A (p less than 0.01). In Group B, the other variables reached a plateau sooner than in Group A (48 versus 110 seconds). The left ventricular function curve showed a mild decrease in functional capacity and depressed contractility. Therefore, one hour of cardioplegic cardiac arrest caused no depression of function at rest. Mild depression of left ventricular function was demonstrated up to 7 weeks postoperatively during acute volume overload.
D000818:Animals; D001011:Aorta / Q000502:physiology; D001794:Blood Pressure; D002302:Cardiac Output; D004285:Dogs; D006324:Heart Arrest, Induced / Q000009:adverse effects*; D006339:Heart Rate; D006439:Hemodynamics; D009200:Myocardial Contraction; D011184:Postoperative Period; D013318:Stroke Volume; D013997:Time Factors; D016276:Ventricular Function