Ann Thorac Surg 1998;66:1358-1364
© 1998 The Society of Thoracic Surgeons
Original articles: cardiovascular
The importance of cardioplegic infusion pressure in neonatal myocardial protection
Michael Kronon, MDa,
Kirk S. Bolling, MDa,
Bradley S. Allen, MDa,
Ari O. Halldorsson, MDa,
Tingrong Wang, MDa,
Shaikh Rahman, PhDa
a Division of Cardiothoracic Surgery, University of Illinois at Chicago, Chicago, Illinois, USA
Address reprint requests to Dr Allen, Division of Cardiothoracic Surgery, University of Illinois at Chicago, Suite 417 CSB (M/C 958), 840 South Wood St, Chicago, IL 60612-7238
Presented at the Poster Session of the Thirty-fourth Annual Meeting of The Society of Thoracic Surgeons, New Orleans, LA, Jan 26–28, 1998.
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Abstract
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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.
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Introduction
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Antegrade cardioplegia is often delivered without directly monitoring the infusion pressure. The surgeon or perfusionist can therefore only estimate the actual perfusion pressure [1, 2]. This may result in cardioplegia being delivered at a pressure which is higher or lower than desired. Furthermore, even if the pressure is monitored, the optimal cardioplegia infusion pressure remains essentially unknown, especially in neonates. Few people have investigated this subject even in adults, and it has never been addressed in the neonatal heart, which, because of structural, functional, and metabolic differences, may be more prone to a pressure injury than the adult [3–7]. Although a high cardioplegic perfusion pressure is thought to be deleterious, especially to ischemic tissue, the definition of high remains undefined [1, 3, 5]. An adequate cardioplegic pressure is needed, however, to ensure distribution to all areas of the myocardium [1]. What pressure is required, and the consequences of even moderate elevation of cardioplegic infusion pressure in neonatal hearts are unknown, especially in the hypoxic (stressed) heart, which may be more prone to pressure injury [3, 8–11]. This study therefore used nonhypoxic and hypoxic neonatal hearts to investigate (1) whether lower infusion pressures (30 to 50 mm Hg) allow adequate cardioplegia distribution to ensure reliable neonatal myocardial protection, and (2) if even slightly higher pressures (80 to 100 mm Hg), which in the absence of direct aortic monitoring may occur without the surgeon’s knowledge, are hazardous.
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Material and methods
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Twenty neonatal (5- to 18-day-old) piglets (3.5 to 5 kg) were premedicated with 40 mg/kg ketamine intramuscularly and anesthetized with 30 mg/kg pentobarbital intraperitoneally, followed by 5 mg/kg intravenously each hour. The lungs were ventilated via a tracheotomy using a volume ventilator (Servo 900B; Siemans/Elema, Solna, Sweden), at an inspired oxygen fraction of 1.0. All animals received humane care in compliance with the "Principles of Laboratory Animal Care" formulated by the National Society for Medical Research and the "Guide for the Care and Use of Laboratory Animals" prepared by the National Academy of Sciences and published by the National Institutes of Health (NIH publication no. 96-03, revised 1996). The experimental preparation, including cannulation for bypass and blood procurement, is comparable to that previously described [8, 9]. The cardiopulmonary bypass (CPB) circuit was heparinized, primed with packed red cells from donor pigs, and made normocalcemic with CaCl2. The hematocrit value was adjusted to 25% to 35% with 0.9% normal saline solutions. A Baxter Univox membrane oxygenator (Baxter Healthcare Corporation, Irvine, CA) was used, and the systemic flow was adjusted to approximately 100 mL/kg per minute to maintain a continuously monitored aortic root pressure of 30 to 50 mm Hg.
Cardioplegia protocol
Cardioplegia solutions (CAPS Service, Research Medical, Salt Lake City, UT) are shown in Tables 1 and 2. The aorta was cross-clamped for 70 minutes and cardioplegia delivered using a protocol of 5 minutes of warm (37°C) followed by 5 minutes of cold (4°C) blood cardioplegic induction, a 2-minute cold (4°C) multidose cardioplegic infusion every 20 minutes, and a 4-minute warm (37°C) cardioplegic reperfusate ("hot shot") before aortic unclamping. Immediately after the aorta was cross-clamped, all piglets were cooled to a systemic temperature of 25°C, and rewarming to 37°C was initiated 16 minutes before aortic unclamping. All piglets were weaned from CPB with no inotropic support 30 minutes after aortic unclamping. Final functional and biochemical measurements were made 30 minutes later, after arterial blood gases, calcium, and potassium levels were normalized.
Experimental groups
Nonhypoxemic (uninjured) studies
Five minutes after initiating CPB, 10 piglets underwent 70 minutes of cardioplegic arrest using the cardioplegia protocol outlined earlier. Five piglets (group 1, low pressure) had the cardioplegia infused at a continuous measured aortic pressure of 30 to 50 mm Hg and five piglets (group 2, high pressure) at an aortic pressure of 80 to 100 mm Hg.
Hypoxemic (stress) studies
Ten other piglets underwent 60 minutes of ventilator hypoxia by lowering the fraction of inspired oxygen to 8% to 10%, producing an arterial PO2 of 25 to 35 mm Hg and an oxygen saturation (SaO2) of 65% to 70%. Before hypoxemia, piglets were transfused as necessary to increase their hematocrit to greater than 35%. This simulates the chronic adaptive change of erythrocytosis that occurs in the cyanotic infant and increases oxygen-carrying capacity, thereby allowing ischemia to be avoided during hypoxia [8, 12]. All piglets remained hemodynamically stable during the entire 60 minutes of ventilator hypoxia. At the end of 60 minutes all piglets were placed on cardiopulmonary bypass at an inspired oxygen fraction of 1.0 for 5 minutes to produce a reoxygenation injury [12, 13]. The aorta was cross-clamped and the heart underwent 70 minutes of cardioplegic arrest using the cardioplegic protocol outlined earlier at either a low infusion pressure (30 to 50 mm Hg, group 3, n = 5) or high infusion pressure (80 to 100 mm Hg, group 4, n = 5).
Myocardial performance
Left ventricular pressure and conductance catheter signals were amplified and digitized to inscribe left ventricular pressure volume loops after first correcting for parallel conductance (myocardial tissue and blood viscosity) using hypertonic saline according to the method of Baan, Van Der Velde, and Steendijk [14]. A series of pressure volume loops was generated under varying conditions by transient occlusion of the inferior vena cava during an 8-second period of apnea. Measurements were made before hypoxia (baseline) and 30 minutes after CPB was discontinued.
The end-systolic pressure–volume relationship, end-diastolic pressure–volume relationship, and preload recruitable stroke work relationship were analyzed with the use of a computer graphics program (Spectrum, Bowman-Gray School of Medicine, Winston-Salem, NC) on a 486-33-mHz Dell personal computer. Left ventricular systolic performance was determined from the descending slope of the end-systolic pressure–volume relationship using linear regression analysis and designated as end-systolic elastance. End-diastolic compliance was determined from the exponential regression of the end-diastolic pressure–volume relationship. Overall myocardial performance was assessed by preload recruitable stroke work which was calculated as the integral of left ventricular transmural pressure and cavity volume over each cardiac cycle. Functional measurements were expressed as percent recovery of baseline values with each piglet acting as its own control. After final hemodynamic measurements, all piglets again received CPB and were cooled to 25°C. Hearts were then arrested with cold (4°C) blood cardioplegia and transmural left ventricular biopsy specimens were obtained. Endocardial and epicardial portions were separated, frozen quickly in liquid nitrogen, and stored for biochemical analysis. Separate samples were obtained for myocardial water.
Physiologic measurements
Coronary vascular resistance (CVR) was determined during each cardioplegic infusion by measuring coronary sinus pressure and cardioplegic flow once a constant infusion rate and aortic root pressure were achieved. Coronary vascular resistance was calculated using the formula:
where CIP = cardioplegia infusion pressure; CFR = cardioplegia flow rate; and CSP = coronary sinus pressure.
Biochemical analysis
Myocardial samples were crushed in a liquid nitrogen–cooled mortar and pestle and lyophilized (Savant Speed Vac Systems, Farmingdale, NY). The adenosine pool was determined according to the method of Sarin and associates as described previously [8, 9, 15]. Adenosine triphosphate (ATP) levels were expressed as micrograms per gram of dry tissue.
Myocardial water
Ventricular samples were placed in preweighed vials and dried to a constant weight at a temperature of 85°C. The percent myocardial water was calculated using the formula:
Statistics
Data were analyzed using JMP V2.0 software (SAS Institute, Cary, NC) on a Macintosh IIVX computer (Apple, Cupertino, CA). Group data are expressed as mean ± standard error of the mean. Paired Student’s t test and two-way analysis of variance with interaction (factorial analysis) were used for comparison of variables among experimental groups. When the analysis of variance revealed a significant interaction, a pairwise test of individual group means was contrasted by way of multiple comparisons (Tukey’s test), using a level of significance of p less than 0.01.
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Results
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There was no difference between groups for prebypass baseline values of left ventricular contractility (end-systolic elastance, 38 ± 2), diastolic compliance (0.05 ± 0.01), or preload recruitable stroke work (62 ± 3). Hypoxia resulted in an increase in heart rate from 130 to 150 to 190 to 220 beats per minute, a decrease in systemic vascular resistance, and an increase in pulmonary vascular resistance. All piglets tolerated 60 minutes of hypoxia with stable hemodynamics.
Hemodynamic and physiologic measurements
Results are depicted in Figures 1 to 4. There was no change or difference in the X axis intercept point (Vo) for end-systolic elastance (before, 6.5 ± 0.1; after, 6.6 ± 0.1) or preload recruitable stroke work (before, 10.0 ± 0.2; after, 10.2 ± 0.2) between values before (baseline) and after bypass in any experimental group. Therefore, the change in slope of end-systolic elastance and preload recruitable stroke work can be interpreted to express variability in the contractile state of the myocardium compared with control values. In normal hearts, cardioplegic infusion pressure (groups 1 and 2) had no statistical effect (p < 0.2) on myocardial function, as both groups had complete preservation of postbypass systolic function (101 ± 2% versus 104 ± 3%) and preload recruitable stroke work (102 ± 2% versus 100 ± 1%); and minimal increase in diastolic stiffness (159 ± 2% versus 153 ± 12%). Conversely, in hypoxic hearts, infusing cardioplegia at a slightly higher pressure (80 to 100 mm Hg, group 4) resulted in a marked reduction in postbypass systolic function (28 ± 4% versus 101 ± 1%; p < 0.001), increased diastolic stiffness (274 ± 9% versus 162 ± 3%; p < 0.001), and decreased preload recruitable stroke work (31 ± 3% versus 102 ± 2%; p < 0.001), compared with low-pressure cardioplegia (group 3), which resulted in complete functional recovery. There was no statistically significant difference (p > 0.2) in CVR among groups 1, 2, and 3 (Fig 4). In contrast, there was a marked increase in CVR in hypoxic hearts receiving a high-pressure (80 to 100-mm Hg) cardioplegia solution (group 4; p < 0.001), suggesting that these hearts had sustained a vascular injury.
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Fig 1. Left ventricular systolic function as measured by the end-systolic elastance (EES) and expressed as percent recovery of baseline values. There is complete preservation of systolic function independent of the cardioplegic infusion pressure in nonhypoxic hearts. In contrast, there is marked loss of systolic function when slightly higher cardioplegic infusion pressures are used in hypoxic hearts. (*p < 0.001.)
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Fig 2. Left ventricular diastolic compliance as measured by the end-diastolic pressure–volume relationship and expressed as percent increased stiffness compared to baseline values. There is only minimal increase in diastolic stiffness in nonhypoxic independent of cardioplegic infusion pressure. Conversely, in hypoxic hearts there is a significant increase in diastolic stiffness with the use of higher cardioplegic infusion pressure. (*p < 0.001.)
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Fig 3. Overall left ventricular myocardial function measured by preload recruitable stroke work and expressed as percent recovery compared with baseline values. In nonhypoxic hearts there is complete preservation of global myocardial function independent of the cardioplegia infusion pressure. Conversely, overall myocardial function is significantly diminished in hypoxic hearts receiving cardioplegia at a slightly higher pressure. (*p < 0.001.)
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Fig 4. Coronary vascular resistance (CVR) measured during each cardioplegic infusion. There is no difference in CVR in nonhypoxic hearts independent of cardioplegia infusion pressure (Press), indicating preservation of vascular function. In hypoxic hearts, use of a low infusion pressure resulted in CVRs that were similar to nonhypoxic hearts, implying similar vascular function. Conversely, there was a marked rise in CVR when high infusion pressures were used in hypoxic hearts, indicating that higher pressures caused a vascular injury. (*p < 0.001; High Press = high pressure; Low Press = low pressure.)
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Tissue studies
Results are summarized in Table 3. There was no significant difference in ATP levels among groups 1, 2, and 3. In contrast, hypoxic hearts receiving higher-pressure infusions (80 to 100 mm Hg, group 4) had significantly lower ATP levels. The ATP to adenosine diphosphate (ADP) ratio, which reflects the ability of the mitochondrial to phosphorylate ADP to ATP, was also markedly reduced in group 4. This suggest mitochondrial damage and may explain why the ATP levels were lower in this group of hearts. Group 4 also had the highest percentage of myocardial water of any experimental group, indicating the greatest degree of myocardial cell damage. However, there was also an increase in myocardial edema in nonhypoxic hearts given a high cardioplegia infusion pressure (group 2), suggesting that pressures of 80 to 100 mm Hg cause some damage even in normal hearts.
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Comment
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This study demonstrates that in a clinically relevant intact neonatal animal model, simulating the operating room, (1) hypoxic hearts are very sensitive to cardioplegic infusion pressure; (2) even moderate elevations (80 to 100 mm Hg) cause significant injury, resulting in increased edema in normal hearts, and in hypoxic hearts myocardial depression and vascular dysfunction; (3) this injury is avoided by low (30 to 50 mm Hg) cardioplegic infusion pressure; and (4) pressures of 30 to 50 mm Hg appear to be ideal, as they provide excellent myocardial protection without causing injury.
Cardioplegic infusion pressure must be adequate to ensure distribution to all areas of the myocardium, but not so high as to cause cellular damage [1, 3]. The principle is simple, but what pressure is adequate and what pressure causes myocardial damage are unknown, especially in neonatal hearts. Because the neonatal heart is structurally, functionally, and metabolically different from that of the adult, the effects of elevations in cardioplegic infusion pressure may be dramatically altered [3–7]. Although most surgeons usually avoid excessively high cardioplegic infusion pressures, the pressure must also be high enough to ensure adequate myocardial distribution. It is safer to cross-clamp the aorta for 4 hours with adequate cardioplegic distribution than for as little as 30 minutes when cardioplegic distribution is suboptimal [1]. Just as low perfusion pressure may be deleterious by limiting distribution, high perfusion pressure may be equally harmful [1, 5]. Cardioplegic infusions may cause myocardial edema if perfusion pressure is allowed to become excessive, especially if the myocardial cells are ischemic [1, 3]. The extent of edema which can be produced during cardioplegic infusions is determined by interaction of the Starling forces which govern fluid flux. These include the perfusion pressure as well as the oncotic and osmotic pressures of the solution, the electromechanical status of the myocardium, and the integrity of the capillary bed [1, 16, 17]. The surgeon or perfusionist should therefore always be aware of the actual or estimated perfusion pressure to avoid producing edema.
Because of structural differences, the neonatal heart may be even more prone to a pressure injury [3, 4, 6, 7]. Although most surgeons would agree that marked elevations of cardioplegic infusion pressure are detrimental, what is high and the effects of even moderate elevations remain untested. Sawatari and associates demonstrated that using very low initial cardiopulmonary bypass pressures (20 mm Hg) when first removing the aortic cross-clamp was beneficial in neonatal hearts after cardioplegic arrest [5]. Although the effect of cardioplegia infusion pressure was not studied, this study suggests that pressures that are generally lower than what are currently used may be desirable. Our study therefore attempted to determine whether currently accepted cardioplegic infusion pressures (30 to 50 mm Hg) are safe while still ensuring adequate cardioplegic distribution to provide myocardial protection, and whether even moderate elevations (80 to 100 mm Hg) are detrimental.
In nonhypoxic (noninjured) hearts, there was complete preservation of myocardial function using either low or high cardioplegia infusion pressure (Figs 1 to 3). There was also no change in CVR (Fig 4) or ATP levels, indicating that either cardioplegic infusion pressure provides good protection. However, it is important to note that there was still an increase in myocardial edema even in normal (nonhypoxic) hearts when an infusion pressure of 80 to 100 mm Hg was used (group 1 versus group 2). Although function was preserved, this implies some myocardial damage as a result of higher infusion pressure. Furthermore, the ischemic (cross-clamp) time was relatively short. Because myocardial injury is dependent on the duration of ischemia, and the nonhypoxic neonatal myocardium is more tolerant of ischemia than the adult, this may have accounted for the lack of greater differences seen between these two groups [3, 4]. It is possible that greater differences would have been seen had the cross-clamp time been extended. In addition, in clinical practice congenital lesions usually result in hypoxia or a pressure–volume overload, and therefore, normal hearts are probably uncommon, especially in the neonatal population.
An increasing number of infants with cyanotic congenital heart disease are undergoing primary repair. Although this may be preferable to palliation, it subjects the immature hypoxic heart to cardiopulmonary bypass and high levels of oxygen, which have been shown to cause unintended reoxygenation injury [8, 12, 13, 18]. This injury is mediated by oxygen free radicals, results in postbypass myocardial depression, and may explain why impairment of ventricular function is common after apparently satisfactory surgical correction of cyanotic congenital defects [3, 12, 18–22]. Despite the prevalence of this condition, no studies have investigated the effects of cardioplegic infusion pressure in a clinically relevant (stress) hypoxic model. Including stressed hearts in any investigation of cardioplegia solutions is important as the results may be dramatically altered. This is why adult studies often impose a preischemic stress when examining cardioplegia solutions [1]. However, because pediatric hearts rarely undergo preoperative ischemia, the injury must be changed to reflect a clinically relevant stress such as hypoxia.
Subjecting the neonatal heart to hypoxia profoundly altered the effect different cardioplegia infusion pressures had on the myocardium. Low cardioplegia infusion pressure not only protected the heart from further damage, but allowed the cardioplegia to facilitate repair of the injury caused by hypoxia and reoxygenation, resulting in complete preservation of myocardial and vascular endothelial cell function (Figs 1 to 4). This supports the safety of a cardioplegic infusion pressure of 30 to 50 mm Hg and implies it is high enough to ensure adequate myocardial distribution; without adequate distribution, myocardial protection is poor. Conversely, hypoxia altered the myocardium, resulting in an increased cellular injury when the cardioplegic infusion pressures were slightly higher (80 to 100 mm Hg). This injury was manifest by postbypass myocardial and vascular dysfunction, increased edema, and decreased ATP levels. Although our model of acute hypoxia does not allow for the chronic adaptive changes that may occur to cyanotic newborns, several studies have documented a similar oxygen-mediated injury with reoxygenation of the chronically hypoxic infant, and using the same biochemical test we recently demonstrated the identical injury in cyanotic infants [18, 23, 24]. Furthermore, this increased sensitivity to cardioplegia arrest after acute hypoxia parallels findings in cyanotic infants and chronically hypoxic animals, leading us to believe that our experimental model is clinically relevant [3, 8, 10, 11, 19, 25]. Our model of acute hypoxia also does not result in ischemia [8, 9, 12]. Conversely, the cyanotic infant may be predisposed to ischemia with energy depletion before surgical correction [26, 27]. Because ischemia may make the heart even more sensitive to elevated cardioplegia pressure, use of a lower infusion pressure may be even more important in cyanotic infants [1, 3].
Vascular endothelial cell function was determined by measuring CVR during each cardioplegic infusion when the heart was arrested and the flow and infusion pressure were constant. Although the myocardial metabolic demands and CVR may change between warm and cold cardioplegia, they should be identical for each heart at any given temperature. Furthermore, because our experimental model of hypoxia does not result in ischemia, restoration of normoxemic perfusion should result in similar coronary vascular resistance in nonhypoxic and hypoxic hearts. As expected, this occurred when a low infusion pressure was used or the heart was not subjected to hypoxia. In contrast, there was a marked increase in CVR during each cardioplegic infusion in hypoxic hearts protected with a slightly higher infusion pressure (group 4). This increased CVR may be caused by a primary vascular injury or vascular compression resulting from increased myocardial edema. However, because edema was not significantly different among hypoxic groups or nonhypoxic hearts given a higher pressure, the increased CVR in group 4 appears to reflect a vascular injury. This injury probably occurs because high shear stress damages vascular endothelium, leading to increased adherence by activated white blood cells which then release proteases and oxygen free radicals [1, 3, 28, 29]. A higher CVR may also result in less homogenous cardioplegia distribution during arrest, thereby compromising myocardial protection. A drawback of this study was that we did not measure vascular function after discontinuing bypass. However, because myocardial function was still depressed after bypass in hypoxic hearts protected with a higher pressure, it is likely that vascular function was similarly affected.
A pressure port is integrated into most commercial cardioplegia systems to allow monitoring of the cardioplegia delivery line. Before the availability of antegrade (and retrograde) cannula with a lumen for direct pressure monitoring, intravascular pressures were estimated by observing the pressure recorded on the pressure port of the cardioplegic delivery system, and subtracting from it the known pressure drop in the delivery system. This requires the perfusionist to calibrate the system intermittently (especially if different sized cannulae are used) and makes it necessary to calculate intravascular pressure with each change in cardioplegic flow rate.
Direct intravascular pressure measurement is the only reliable method for determining either aortic or coronary sinus pressure during cardioplegic delivery [1, 30]. This conclusion was reached in adults by obtaining simultaneous measurement of intravascular pressure in either the aorta or coronary sinus during cardioplegic infusions and comparing it to calculated pressure from the known pressure drop in the tubing system at flow rates ranging from 50 to 300 mL/min [1, 2, 17, 30]. This demonstrated that (1) calculated pressure does not accurately reflect the measured intravascular pressure during either antegrade or retrograde delivery, and (2) the variability between calculated and measured intravascular pressure increases as either antegrade or retrograde cardioplegic flow rate is raised. This discrepancy between the calculated and measured intravascular pressure probably results from differences related to calibration with roller pumps and wide fluctuations in cardioplegic delivery system pressure which can develop when temperature, flow, and viscosity are varied in systems containing rigid and compliant components. Direct intravascular measurement circumvents this problem and provides the surgeon with a more reliable pressure measurement [1, 2, 17, 30]. With smaller cannula and vascular beds, errors in calculating the cardioplegia infusion pressure may be magnified and change quicker in neonates. Because this study demonstrates that even small changes in pressure may significantly affect neonatal myocardial protection, especially in the hypoxic heart, the surgeon must always be able to measure the aortic infusion pressure accurately to prevent inadvertent elevations in pressure.
This study demonstrated that (1) the hypoxic neonatal heart is very sensitive to cardioplegic infusion pressures, (2) a pressure of 30 to 50 mm Hg provides excellent myocardial protection, and (3) even small increases in cardioplegia infusion pressure can result in significant myocardial injury. Pediatric surgeons therefore need to pay careful attention to the actual infusion pressure, especially if the patient is hypoxic. Furthermore, because estimation of cardioplegia infusion pressure may be inaccurate and does not provide the surgeon with a reliable or constant method to monitor the intravascular myocardial pressure, we believe direct aortic monitoring should be used in pediatric patients.
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Acknowledgments
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This work was supported in part by the Pillsbury Fellowship.
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The role of leukodepletion in limiting ischemia/reperfusion damage in the heart, lung and lower extremity
Perfusion,
March 1, 2002;
17(2_suppl):
11 - 22.
[Abstract]
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M. T. Kronon, B. S. Allen, A. Halldorsson, S. Rahman, M. J. Barth, and M. Ilbawi
Delivery of a nonpotassium modified maintenance solution to enhance myocardial protection in stressed neonatal hearts: A new approach
J. Thorac. Cardiovasc. Surg.,
January 1, 2002;
123(1):
119 - 129.
[Abstract]
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Abstract
Introduction
