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MMCTS
(November 29, 2005). doi:10.1510/mmcts.2004.000729 Copyright © 2005 European Association for Cardio-thoracic Surgery
Procedure Myocardial protection in congenital heart surgeryDepartment of Cardiovascular Surgery, University Hospital Freiburg, Hugstetter Strasse 55, 79106 Freiburg, Germany * Corresponding author: * Tel.: +49-11-761-2702818; fax: +49-11-761-2702368. E-mail: schlensa{at}ch11.ukl.uni-freiburg.de
Modern pediatric cardiac surgery prides itself by performing primary surgical repair of cardiac anomalies. As a consequence, the majority of cases are nowadays performed in neonates and young infants. For the repair of intracardiac malformations the aorta is crossclamped and the heart is arrested (i.e. subjected to ischemia). Cardioplegic solution is administered routinely to arrest the contractile apparatus, decrease energy consumption and thereby increase ischemia tolerance. It is usually combined with hypothermia as another method to extend ischemia tolerance. In pediatric cardiac surgery several different cardioplegic solutions and strategies are currently used. For myocardial protection during crossclamp time either blood or crystalloid solution is administered into the aortic root or retrogradely into the coronary sinus, intermittently or as a single shot. The final concept for myocardial protection is highly dependent on the individual surgeon and his personal preference. There is currently no evidence in favor of one or the other technique. Thus, pediatric protection is currently experience-based.
Key Words: Blood cardioplegia • Myocardial protection • Pediatric cardiac surgery
Although major advances in surgical techniques and technical aspects have been made in the field of congenital cardiac surgery, mortality remains high [1,2,3]. According to the EACTS congenital database [4] the 30-day mortality for all patients with congenital cardiac malformations is 5% (out of 24,637 patients in 2004) and exceeds 11% in neonates (out of 4,951 patients in 2004). Inappropriate myocardial protection during crossclamp time is still considered the main cause of death in the pediatric population [5]. It is interesting to note in this context, that the strategies for pediatric myocardial protection have remained relatively unchanged over the last decade. This is evident in the small number of publications available in the pediatric literature compared to a large number on the same topic in adults. Adopting principles for myocardial protection established in adult patients for the pediatric patient population warrants caution because there are important structural and biochemical differences between the pediatric and adult myocardium. The main differences that relate to clinical practice are:
The pediatric heart utilizes mainly glucose as the oxidative substrate compared to fatty acids in the adult heart [6,7]. A shift towards glucose utilization is considered to improve ischemic tolerance [8]. A lower level of the enzyme 5'nucleotidase as in the pediatric heart is associated with a higher end-ischemic level of AMP (that means preservation of the adenine nucleotide pool), which is a prerequisite for recovery of function [9]. Finally, the calcium metabolism in the pediatric heart is immature. In the pediatric myocardium the sarcoplasmatic reticulum is underdeveloped and has reduced capacity for calcium storage [10]. In the pediatric heart the calcium is mainly provided by influx from the external space [10]. This difference makes it clear why the pediatric myocardium is so much more responsive to postischemic calcium overload. There are several reports describing the detrimental effects of cardioplegia solutions used for neonates containing normal or high calcium concentrations. Therefore most cardioplegia solutions used for the protection of the pediatric myocardium have lower than normal concentrations of calcium [2,11,12,13].
Cardioplegic techniques Most likely due to historical reasons (blood cardioplegia was developed in the US [17,18] and crystalloid cardioplegia was developed in Europe [19,20,21]) cardiac surgeons in North America use blood cardioplegia to protect the pediatric myocardium while most European centers are using crystalloid solution [22]. The principle difference between crystalloid and blood cardioplegia is that for blood cardioplegia the crystalloid solution is mixed with blood in a certain ratio (for example 1:4, crystalloid solution:autologous blood) while for crystalloid cardioplegia the solution is administered as is. Both, crystalloid and blood cardioplegia can be administered antegradely or retrogradely or as a single shot or intermittently.
At our institution in Freiburg we use Buckberg's cardioplegic solution [23] for myocardial protection in neonates and infants. The crystalloid solution is available (MMCTSLink 73). It is mixed through the delivery system of the heart-lung machine with autologous blood in a ratio 1:4 (crystalloid solution:autologous blood) prior to its application (Photo 1).
If the aortic valve is competent the initial infusion is administered into the aortic root. After placement of a purse-string suture on the anterior part of the ascending aorta, the adventitia within the purse-string suture is incised with a No. 11 scalpel blade. Then the adventitia is gripped to both sides of the incision by a pair of forceps, after a No. 11 scalpel blade is advanced through the aortic wall within the purse-string suture. The hole can be closed by the adventitial flap. The cardioplegia cannula can then slide into the incision of the aortic wall and the purse-string suture can be snugged. After de-airing the cardioplegia line, the cannula is connected. The CPB is started and the ascending aorta is crossclamped and the myocardium arrested with cold blood cardioplegia (4 °C) (Photo 2). The initial infusion rate is 30 ml/kg body weight. Infusion pressure is not to exceed 80 mmHg for antegrade delivery. During aortic crossclamp time retrograde re-infusions are given every 20 min.
Subsequent re-infusions are given retrogradely through a catheter which is placed into the coronary sinus. After placement of a purse-string suture around the ostium of the coronary sinus the catheter is connected to the cardioplegia line. Once the cannula is de-aired it is slowly advanced into the coronary sinus. The purse-string suture can be snugged and the cold cardioplegia re-infusion is delivered with 10 ml/kg body weight. This rate is several fold the volume used for cardioplegia of the adult heart, where infusion is based on time rather than body weight. Infusion pressure is not to exceed 50 mmHg for retrograde delivery. The coronary sinus catheter will stay in place during the whole aortic crossclamp time (Video 1). This retrograde perfusion technique has the benefit, that the coronary arteries and the aortic root as well are sufficiently de-aired. If the aortic crossclamp time exceeds 60 min, a terminal warm substrate enriched infusion (‘hot shot’, 36 °C) is given through the coronary sinus catheter before the aorta is unclamped with a rate of 10 ml/kg body weight. During reperfusion the systemic reperfusion pressure is kept low (i.e. 30–40 mmHg) during the initial 5 min after blood flow to the myocardium is restored.
Between January 1999 and June 2005 our strategy of myocardial protection was applied to 624 children presenting with the full spectrum of congenital cardiac malformations. Forty-two percent of our patients were less than 1 year of age. Mean aortic crossclamp time in all patients was 67±48 min (8–235 min). There were 6 hospital deaths (i.e. 1.0% overall mortality rate). None of them was related to inadequate myocardial protection. Our strategy of cardioplegia management did not increase the complexity of the procedure.
For pediatric myocardial protection, different cardioplegic solutions and strategies are currently clinically used. Both, the application and the composition of the solutions are borrowed from protection strategies for the adult heart [14,23,24]. However, the pediatric heart possesses several clinically relevant mechanisms for the conduct of congenital heart surgery. The preference for glucose and the low activity of 5'nucleotidase contribute to the extensive ischemia tolerance of the pediatric heart. In contrast, the increased calcium sensitivity, the reduced enzyme activity of the free radical scavenging system, and unknown factors associated with the presence of cyanotic heart defects, may decrease ischemia tolerance and make the heart more prone to damage during reperfusion [13,25]. Recently, it could be demonstrated that preoperative cyanosis profoundly affects the protection of cardioplegic solutions on the myocardium [25]. In this study the authors showed that cold blood cardioplegia protected the hypoxic hearts in babies from ischemic and reoxygenation injury whereas crystalloid cardioplegia provides inadequate myocardial protection. Additionally, a terminal warm reperfusion (‘hot shot’) could improve myocardial function and preserve the adenine nucleotide pool in cyanotic children [25]. Our own results in Freiburg support this finding. However, evidence-based medicine criteria have not yet shown which cardioplegia is best [16]. Interestingly, most pediatric cardiac surgeons report similar results using different strategies of myocardial protection. It seems reasonable to assume that one technique in the hands of one surgeon may work, although it does not give the same results for another surgeon. Differences in operative techniques, operating times and quality of postoperative care may further camouflage possible differences. It is reasonable to conclude that the effects of these variations are minor with respect to extending the ischemia tolerance. Large randomized trials are required to evaluate the links between basic mechanisms and clinical practice of protection strategies for the pediatric heart. In summary, use of cardioplegia is the standard intraoperative care in most pediatric centers worldwide. Blood cardioplegia provides superior protection, especially in complex and longer cases. Evidence-based medicine criteria, however, have not yet shown which cardioplegia is best.
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