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Background: In adult cardiac operations, a warm cardioplegic reperfusate ("hot shot") before removing the aortic cross-clamp improves postbypass myocardial function and metabolic recovery. This modality, however, is rarely used in infants, despite the fact that postbypass cardiac dysfunction remains problematic, especially in cyanotic ("stressed") patients., Methods: To produce stress, 15 neonatal piglets underwent 60 minutes of ventilator hypoxia (fraction of inspired oxygen, 8% to 10%). All piglets then received similar protection with multidose cold blood cardioplegic solution during 70 minutes of arrest and were separated into three groups to examine the role of a warm reperfusate as well as possible augmentation by aspartate and glutamate enrichment. In 5 piglets (group 1), the cross-clamp was simply removed; in 5 (group 2), an unsupplemented warm blood cardioplegic reperfusate was given; and in 5 (group 3), the warm reperfusate was enriched with aspartate and glutamate. Myocardial function was assessed using pressure-volume loops and expressed as a percentage of control., Results: Compared with hearts receiving reperfusion with unmodified blood (group 1), a warm unsupplemented cardioplegic reperfusate (group 2) slightly improved systolic contractility (end-systolic elastance, 41% versus 50%; p < 0.05 versus group 1) and preload recruitable stroke work (41% versus 52%; p < 0.05 versus group 1), reduced diastolic stiffness (263% versus 245%; p < 0.05 versus group 1), and increased adenosine triphosphate (10.7 versus 11.9 microg/g tissue, p < 0.05 versus group 1). However, if aspartate and glutamate was included in the warm reperfusate (group 3), there was complete recovery of systolic function (end-systolic elastance, 105%+/-3%; p < 0.001 versus all groups) and preload recruitable stroke work (103%+/-2%; p < 0.001 versus all groups), a minimal rise in diastolic stiffness (154%+/-7%; p < 0.001 versus all groups), and preservation of adenosine triphosphate (15.5+/-0.5 microg/g; p < 0.001 versus all groups)., Conclusions: A warm cardioplegic reperfusate helps reduce the reperfusion injury, resulting in improved myocardial function and metabolic recovery in hypoxic (stressed) neonatal hearts, and this effect is maximized if the reperfusate is enriched with aspartate and glutamate, which completely preserves myocardial function.

Background: Cardioplegia infusion pressure is usually not directly monitored during neonatal heart operations. We hypothesize that the immature newborn heart may be damaged by even moderate elevation of cardioplegic infusion pressure, which in the absence of direct aortic monitoring may occur without the surgeon's knowledge., Methods: Twenty neonatal piglets received cardiopulmonary bypass and the heart was protected for 70 minutes with multidose blood cardioplegia infused at an aortic root pressure of 30 to 50 mm Hg (low pressure) or 80 to 100 mm Hg (high pressure). Group 1 (n = 5, low pressure), and group 2 (n = 5, high pressure) were uninjured (nonhypoxic) hearts. Group 3 (n = 5, low pressure) and group 4 (n = 5, high pressure) first underwent 60 minutes of ventilator hypoxia (FiO2 8% to 10%) before initiating cardiopulmonary bypass to produce a clinically relevant hypoxic stress before cardiac arrest. Function was assessed using pressure volume loops (expressed as a percentage of control), and coronary vascular resistance was measured with each cardioplegic infusion., Results: In nonhypoxic (uninjured) hearts (groups 1 and 2) cardioplegic infusion pressure did not significantly affect systolic function (end systolic elastance, 104% versus 96%), preload recruitable stroke work (102% versus 96%) diastolic compliance (152% versus 156%), or coronary vascular resistance but did raise myocardial water (78.9% versus 80.1%; p < 0.01). Conversely, if the cardioplegic solution was infused at even a slightly higher pressure in hypoxic hearts (group 4), there was deterioration of systolic function (end systolic elastance, 28% versus 106%) (p < 0.001) and preload recruitable stroke work (31% versus 103%; p < 0.001), rise in diastolic stiffness (274% versus 153%; p < 0.001), greater myocardial edema (80.5% versus 79.6%), and marked increase in coronary vascular resistance (p < 0.001) compared to hypoxic hearts given cardioplegia at low infusion pressures (group 3), which preserved function., Conclusions: Hypoxic neonatal hearts are very sensitive to cardioplegic infusion pressures, such that even moderate elevations cause significant damage resulting in myocardial depression and vascular dysfunction. This damage is avoided by using low infusion pressures. Because small differences in infusion pressure may be difficult to determine without a direct aortic measurement, we believe it is imperative that surgeons directly monitor cardioplegia infusion pressure, especially in cyanotic patients.

Objective: We previously demonstrated that calcium can be harmful to the hypoxic neonatal heart. Despite the fact that magnesium inhibits membrane transport of calcium, few studies have examined whether magnesium can prevent the deleterious effects of calcium in cardioplegic solutions., Methods: Twenty neonatal piglets (5 to 18 days old) underwent 60 minutes of ventilator hypoxia (inspired oxygen fraction 8% to 10%) followed by reoxygenation with the use of cardiopulmonary bypass before cardioplegic arrest to produce a clinically relevant hypoxic "stress" injury. The aorta was then crossclamped for 70 minutes with multidose blood cardioplegia. Ten piglets received a hypocalcemic (0.2 to 0.4 mmol/L) cardioplegic solution without (group 1, n = 5) or with magnesium (10 mEq/L) (group II, n = 5) supplementation. Ten other piglets were protected with a normocalcemic (1.0 to 1.2 mmol/L) cardioplegic solution without (group III, n = 5) or with magnesium (group IV, n = 5). Myocardial function was assessed by means of pressure volume loops and expressed as a percentage of control. Coronary vascular resistance was assessed during each cardioplegic infusion., Results: Adding magnesium to a hypocalcemic cardioplegic solution (groups I and II) had no effect: Both groups had complete preservation of postbypass systolic function (end-systolic elastance 101% vs 104%) and preload recruitable stroke work (101% vs 102%), minimal increase in diastolic stiffness (159% vs 153%), and no difference in myocardial tissue edema (78.8% vs 78.9%) or coronary vascular resistance. Conversely, when a normocalcemic cardioplegic solution was administered without magnesium supplementation (group III), the results were markedly poorer than results obtained with magnesium supplementation (group IV). Without magnesium, there was a marked reduction in postbypass systolic function (end-systolic elastance 49% vs 101%; p < 0.05), increased diastolic stiffness (276% vs 162%; p < 0.05), decreased preload recruitable stroke work (53% vs 102%; p < 0.05), increased myocardial tissue edema (80.0% vs 78.9%; p < 0.05), and a rise in coronary vascular resistance (p < 0.05). Magnesium supplementation of the normocalcemic cardioplegic solution, by contrast, resulted in complete functional recovery., Conclusions: This study demonstrates that (1) magnesium does not alter the cardioprotective effects of a hypocalcemic cardioplegic solution, (2) a normocalcemic cardioplegic solution is detrimental to neonatal myocardium subjected to a previous hypoxic stress, and (3) magnesium supplementation of normocalcemic cardioplegic solutions prevents the deleterious effects of calcium.

Objectives: Blood cardioplegia predominates in the adult because it provides superior myocardial protection, especially in the ischemically stressed heart. However, the superiority of blood over crystalloid cardioplegia in the pediatric population is unproved. Furthermore, because many pediatric hearts undergo a preoperative stress such as hypoxia, it is important to compare the different methods of protection in both normal and hypoxic hearts., Methods: Twenty neonatal piglets were supported by cardiopulmonary bypass and subjected to 70 minutes of cardioplegic arrest. Of 10 nonhypoxic hearts, five (group 1) were protected with blood cardioplegia and five (group 2) with crystalloid cardioplegia (St. Thomas' Hospital solution). Ten other piglets underwent 60 minutes of ventilator hypoxia (inspired oxygen concentration 8% to 10%) before cardioplegic arrest. Five (group 3) were then protected with blood cardioplegia and the other five (group 4) with crystalloid cardioplegia. Myocardial function was assessed by means of pressure volume loops and expressed as a percentage of control. Coronary vascular resistance was measured with each infusion of cardioplegic solution., Results: No difference was noted between blood (group 1) or crystalloid cardioplegia (group 2) in nonhypoxic hearts regarding systolic function (end-systolic elastance 104% vs 103%), diastolic stiffness (156% vs 159%), preload recruitable stroke work (102% vs 101%), or myocardial tissue edema (78.9% vs 78.9%). Conversely, in hearts subjected to a hypoxic stress, blood cardioplegia (group 3) provided better protection than crystalloid cardioplegia (group 4) by preserving systolic function (end-systolic elastance 106% vs 40%; p < 0.05) and preload recruitable stroke work (103% vs 40%; p < 0.05); reducing diastolic stiffness (153% vs 240%; p < 0.05) and myocardial tissue edema (79.6% vs 80.1%); and preserving vascular function, as evidenced by unaltered coronary vascular resistance (p < 0.05)., Conclusion: This study demonstrates that (1) blood or crystalloid cardioplegia is cardioprotective in hearts not compromised by preoperative hypoxia and (2) blood cardioplegia is superior to crystalloid cardioplegia in hearts subjected to the preoperative stress of acute hypoxia.