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J Thorac Cardiovasc Surg 1997;114:1079-1080
© 1997 Mosby, Inc.
CARDIOPULMONARY BYPASS, |
Division of Cardiovascular Surgery, University of Toronto, Toronto, Ontario, Canada
National Research Council, Winniped, Manitoba, Canada
Dr. Carias de Oliveira and colleagues performed an elegant evaluation of intermittent warm blood cardioplegia and found that 15 minutes of cardioplegic interruption with 15 minutes of reperfusion was well tolerated by the normal canine heart. They also found that 30 minutes of cardioplegic interruption with 15 minutes of reperfusion resulted in substantial metabolic and functional deterioration that persisted at least 2 hours after cardioplegic arrest. They recommend that cardiac surgeons should limit warm cardioplegic interruptions, particularly in patients with poor preoperative left ventricular function, preoperative ischemia, or left ventricular hypertrophy.
This is an excellent study, which deserves careful consideration by cardiac surgeons interested in warm cardioplegia. The authors used magnetic resonance spectroscopy (MRS) to assess myocardial pH and high-energy phosphates during intermittent warm cardioplegia and reperfusion. MRS is a revolutionary assessment tool that allows noninvasive quantification of tissue metabolites in vivo.
1 However, a number of cautions must be exercised in the interpretation of the results of this study. The authors used blood-perfused isolated canine hearts. The tolerance of normal canine myocardium to interrupted cardioplegia may differ, as the authors suggest, from that of a heart with coronary disease and preoperative ischemia. In this study, an intraventricular balloon was used to assess ventricular function. The authors found a significant increase in left ventricular end-diastolic pressure and a decrease in diastolic function after cardioplegic interruptions of 20 or 30 minutes. This alteration in diastolic compliance renders the assessment of systolic function difficult. They found a decrease in end-systolic elastance after 30 minutes of cardioplegic interruption. Maximal elastance was not measured. A better measure of cardiac function would have been preload recruitable stroke work, which could have been calculated from pressure-volume loops. Unfortunately, the authors did not assess this measure of cardiac function.
Their evaluation of cardiac high-energy phosphates and myocardial acidosis provides clear evidence of progressive ischemia during cardioplegic interruptions. These results suggest cardiac surgeons should limit warm cardioplegic interruptions to less than 30 minutes. Altering the method of delivering cardioplegic solutions may decrease cardioplegic interruption times. In our experience, optimal visualization of distal anastomoses required interruption of warm antegrade cardioplegia for 10 to 20 minutes in 90% of patients, corresponding to 42% of the crossclamp period. 2 The use of warm retrograde blood cardioplegia, in contrast, decreased cardioplegic interruptions to only 27% of the duration of crossclamping. This does not necessarily mean, however, that retrograde cardioplegia results in less ischemia. Retrograde cardioplegia may decrease cardioplegic interruption time simply by decreasing tissue perfusion, which in turn leads to decreased effluent from coronary arteriotomies and improved visualization of the anastomosis. Indeed, retrograde cardioplegia results in increased levels of inorganic phosphate and decreased levels of creatine phosphate compared with antegrade cardioplegia. 3 Using a combination of antegrade and retrograde cardioplegia (i.e., simultaneous cardioplegia administration retrograde through the coronary sinus and antegrade through saphenous vein grafts) may be the optimal method of reducing the duration of cardioplegic interruption without significantly impairing visibility. 4 In addition, lowering the temperature of the cardioplegic solution from 37° C to 29° C ("tepid" cardioplegia) may reduce myocardial oxygen requirements and improve the preservation of myocardial metabolism and ventricular function. 4 These strategies may minimize the deleterious effects of cardioplegic interruption during cardiac surgery.
We have used arterial and coronary sinus serum samples to evaluate myocardial metabolism during cardioplegic delivery. We measured lactate production after resumption of antegrade or retrograde cardioplegia after interruptions of up to 15 minutes (unpublished data). Interruption of antegrade warm blood cardioplegia results in moderate lactate washout with resumption of cardioplegia; the magnitude of this lactate production is not related to the duration of cardioplegic interruption. In contrast, interruption of retrograde warm blood cardioplegia results in greater lactate production at all times, compared with antegrade cardioplegia, and lactate production and oxygen consumption increase significantly after only 7 minutes (implying washout of lactate accumulated during anaerobic metabolism, and repayment of an oxygen debt).
In addition to metabolic measurements, we have also assessed clinical outcomes during warm blood cardioplegia. A randomized clinical trial comparing normothermic and hypothermic blood cardioplegia was performed in 1732 patients at the University of Toronto. 5 It demonstrated a significant reduction in the incidence of low cardiac output syndrome and perioperative enzymatic myocardial infarction in patients randomized to warm blood cardioplegia. The effects of cardioplegic interruption was subsequently assessed post hoc in 720 patients derived from the warm treatment arm. 6 Intermittency was analyzed as cumulative ischemic time as a percentage of total crossclamp time, or as the single longest ischemic interval. Longest ischemic time (highest quartile > 13 minutes) was an important predictor of adverse cardiac outcomes (mortality, myocardial infarction, or low output syndrome, p = 0.053), but no consistent relationship was identified for cumulative ischemic time. We concluded that repeated interruptions of warm blood cardioplegia followed by sufficient cardioplegic reinfusion is a safe method of myocardial protection provided single interruptions are 13 minutes or less. Dr. Carias de Oliveira and colleagues used a model of ischemia with 15 minutes of reperfusion between each ischemic episode. Although the length of interruptions is compatible with clinical practice (average longest ischemic interval 11.4 ± 4.0 minutes for 732 patients from the Warm Heart Trial), 6 15 minutes of reperfusion may represent an ideal rather than reflect routine practice. Additional studies testing shorter periods of reperfusion would provide valuable information that may more closely mimic typical surgeon behavior. It would appear from closer inspection of the first panel of Fig. 2, in conjunction with other animal data, 7 that shorter periods of reperfusion would also be acceptable.
In summary, this is a well-designed study assessing the effects of warm intermittent blood cardioplegia. The results suggest that 15 minutes of repeated warm ischemia is safe, but that cardioplegic interruptions of 30 minutes are probably harmful. This length of time is clinically feasible in the majority of coronary bypass operations, particularly if combinations of antegrade and retrograde cardioplegia are used. Our myocardial metabolic and clinical data would also suggest that this length of warm ischemic time is well tolerated in coronary bypass surgery.
References
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