Period Of Cardioplegic Arrest Research Articles

Intraoperative thermographic imaging to assess myocardial distribution of Del Nido cardioplegia.

We describe the intraoperative non-invasive use of an infrared (IR) camera to monitor Del Nido cardioplegia delivery in patients undergoing cardiac surgery. Thermal pictures were taken pre- and post-cardioplegia and at timed points after arrest, and compared to readings from a transseptal temperature probe. There was good concordance between the transseptal probe and the IR camera temperature readings. This non-invasive technique, which assesses cardioplegic distribution, may help to determine when additional doses of Del Nido cardioplegia are required during periods of cardioplegic arrest.

Is the Extracardiac Conduit the Preferred Fontan Approach for Patients With Univentricular Hearts?

With improvements in technology, operative technique, and critical care medicine, more and more children with congenital heart disease are surviving into adulthood. As they age, these patients are providing physicians with new challenges, and we are realizing the long-term consequences of our previous interventions. This oftentimes has changed the mode of treatment for subsequent children. Response by Khairy and Poirier on p 2515 Fontan palliation for single-ventricle patients was first described in 1971.1 The original approach was in the form of a classic atriopulmonary Fontan connection, bypassing the nonfunctional right ventricle. After recognizing the long-term complication of an atriopulmonary connection (right atrial dilation, arrhythmias, and thrombus formation), modifications have been made. The atriopulmonary connection has been abandoned in favor of modified Fontan anatomy and physiology. The modified Fontan can be performed by the use of an extracardiac conduit approach or a lateral tunnel approach. The extracardiac Fontan uses an external conduit to anastomose the inferior vena cava into the pulmonary arteries, whereas a lateral tunnel Fontan uses a baffle within the right atrium (Figure 1). Because the systemic venous pathway is completely separated from the right atrium with the extracardiac Fontan, it is more challenging for the electrophysiologist to access the heart for ablation. My aim is to demonstrate why “the extracardiac conduit is the preferred Fontan approach for patients with univentricular hearts.” Figure 1. Left , Lateral tunnel Fontan shows the Fontan pathway inside of the right atrium. Right , Extracardiac Fontan shows the conduit completely separated from the right atrium. The extracardiac Fontan has several advantages over the lateral tunnel Fontan. Minimizing cardiopulmonary bypass and ischemia may optimize early postoperative outcomes. In multiple studies, both prolonged cardioplegic arrest and extended cardiopulmonary bypass times have been associated with an increased risk of early postoperative death or Fontan failure.2– …

Heparin-Bonded Circuits Decrease Myocardial Ischemic Damage: An Experimental Study

Background. Heparin-bonded cardiopulmonary bypass circuits reduce complement activation, but their effect on myocardial function is unknown. This study was undertaken to determine whether heparin-bonded circuits reduce myocardial damage during acute surgical revascularization.Methods. In 16 pigs, the second and third diagonal vessels were occluded with snares for 90 minutes followed by 45 minutes of cardioplegic arrest and 180 minutes of reperfusion with the snares released. During the period of coronary occlusion, all animals were placed on percutaneous bypass followed by standard cardiopulmonary bypass during the periods of cardioplegic arrest and reperfusion. In 8 pigs, heparin-bonded circuits were used, whereas 8 other pigs received nonbonded circuits.Results. Animals treated with heparin-bonded circuits had the best preservation of wall motion scores (3.5 ± 0.3 versus 2.3 ± 0.2; 4 = normal to −1 = dyskinesis; p < 0.05), least tissue acidosis (change in pH = −0.31 ± 0.02 versus −0.64 ± 0.08; p < 0.05), smallest increase in lung H2O (1.7% ± 0.7% versus 6.1% ± .5%; p < 0.05), and the lowest area of necrosis/area of risk (20.3% ± 2.2% versus 40.4% ± 1.6%; p < 0.05).Conclusions. We conclude that heparin-bonded circuits significantly decrease myocardial ischemic damage during acute surgical revascularization.(Ann Thorac Surg 1997;63:1701–5)

Effects of beta-blockers and Ca2+ -antagonists on the response of the isolated working rat heart to adrenergic stimulants after cardioplegic arrest

During coronary artery bypass graft (CABG) surgery, patients pretreated with the combination of beta-blocking drugs and Ca2+ antagonists for control of myocardial ischemia often respond inadequately to adrenergic stimulants administered after cardioplegic arrest. In this study, the effects of the combination of a beta-blocker (propranolol) and a Ca2+ antagonist (nifedipine) on the spontaneous recovery, as well as the adrenergic response of the isolated, perfused, working rat heart after a period of cardioplegic arrest were evaluated. After pretreatment of the animals with propranolol and/or nifedipine, hearts were removed, perfused in the presence of pretreatment drugs, subjected to 45 minutes of normothermic cardioplegic arrest, reperfused, and finally stimulated with exponentially increasing concentrations of a sympathomimetic drug. Propranolol, and to a lesser extent nifedipine, protected the hearts during cardioplegic arrest, as indicated by the improved recovery and maximum response to adrenergic stimulation after cardioplegia. Isoprenaline, a beta-stimulant, (at a 100 x higher than conventional concentration), elicited an adequate inotropic and chronotropic response. Stimulation by the alpha, beta-stimulant adrenaline or dobutamine improved only the inotropic response of propranolol and combination treated hearts. Cautious extrapolation of the results to human may suggest continuation of drug therapy of patients before CABG surgery.

Detrimental effects of interrupting warm blood cardioplegia during coronary revascularization

Warm blood cardioplegia has emerged as a substitute for cold blood cardioplegia as a method of myocardial protection. However, the continuous infusion of blood in this technique may obscure the operative field and necessitate interruption of warm blood cardioplegia. This experimental study was therefore undertaken to determine whether interrupting warm blood cardioplegia during coronary revascularization would increase myocardial damage. In 30 adult pigs, the second and third diagonal vessels were occluded with snares for 90 minutes. All animals underwent cardiopulmonary bypass and 45 minutes of cardioplegic arrest. During the period of cardioplegic arrest, 10 pigs received intermittent antegrade/retrograde infusion of cold blood cardioplegic solution (4 degrees C) 10 pigs received continuous retrograde infusion of warm blood cardioplegic solution (37 degrees C) at 100 ml/min, and 10 pigs received retrograde infusion of warm blood cardioplegic solution that was interrupted for three 7-minute periods. After aortic unclamping, the coronary snares were released and all hearts were reperfused for 180 minutes. Interrupting retrograde warm blood cardioplegia resulted in more tissue acidosis during cardioplegic arrest (6.20 +/- 0.16 interrupted retrograde warm blood cardioplegia and 6.45 +/- 0.12 continuous retrograde warm blood cardioplegia, both p < 0.05 compared with 6.98 +/- 0.17 intermittent antegrade and retrograde cold blood cardioplegia), decreased echocardiographic wall-motion scores (4 [normal] to -1 [dyskinesis]; 2.06 +/- 0.30 interrupted retrograde warm blood cardioplegia, p < 0.05 compared with 3.30 +/- 0.40 intermittent antegrade and retrograde cold blood cardioplegia, 2.80 +/- 0.40 continuous retrograde warm blood cardioplegia), and increased tissue necrosis as measured by the area of necrosis/area at risk (38% +/- 5% interrupted retrograde warm blood cardioplegia, p < 0.05 compared with 21% +/- 2% intermittent antegrade and retrograde cold blood cardioplegia; 25% +/- 2% continuous retrograde warm blood cardioplegia). We concluded that interrupting warm blood cardioplegia during coronary revascularization diminishes the effectiveness of warm blood cardioplegia and results in increased ischemic damage.

Warm versus cold blood cardioplegia—Is there a difference?

This experimental study sought to compare the effectiveness of warm blood cardioplegia versus cold blood cardioplegia in protecting areas of ischemic myocardium during urgent coronary revascularization. In 40 adult pigs, the second and third diagonal vessels were occluded with snares for 90 minutes. All animals were then placed on cardiopulmonary bypass and underwent 45 minutes of cardioplegic arrest followed by 3 hours of reperfusion during which time the coronary snares were released. During the period of cardioplegic arrest, 10 pigs received antegrade continuous warm blood cardioplegic solution (37 degrees C) at 100 ml/min; 10 animals received retrograde warm blood cardioplegic solution at 100 ml/min; 10 received intermittent, antegrade cold blood cardioplegic solution (4 degrees C), and 10 animals received intermittent, antegrade/retrograde cold blood cardioplegic solution. Hearts protected with antegrade warm blood cardioplegic solution had the lowest pH values in the area at risk (6.59 +/- 0.10 antegrade warm blood cardioplegia versus 6.80 +/- 0.10 retrograde warm blood cardioplegia versus 6.72 +/- 0.18 antegrade cold blood cardioplegia versus 6.85 +/- 0.15 antegrade/retrograde cold blood cardioplegia and the highest area of necrosis (42% +/- 3% antegrade warm blood cardioplegia versus 26% +/- 2% [p < 0.05 from antegrade warm blood cardioplegia] retrograde warm blood cardioplegia versus 31% +/- 2% [p < 0.05 from antegrade warm blood cardioplegia] antegrade cold blood cardioplegia versus 21% +/- 2% [p < 0.05 from antegrade warm blood cardioplegia] antegrade/retrograde cold blood cardioplegia). We conclude that in the presence of an acute coronary occlusion with ischemic myocardium, warm blood cardioplegic solution should be given in a continuous retrograde fashion and does not result in myocardial protection superior to the protection that can be achieved with antegrade/retrograde cold blood cardioplegic solution.

Uso de fósforo 31 ressonância nuclear magnética para avaliação da proteção do miocárdio utilizando cardioplegia sangüínea contínua e normotérmica

Um modelo isolado de coração de porco perfundido com sangue foi adaptado para o uso de fósforo 31 ressonância nuclear magnética (31 pRNM) em estudos de espectroscopia do metabolismo cardíaco durante cardioplegia sangüínea contínua e normotérmica (CSCN). O experimento foi dividido em dois grupos: Grupo I (n=5): os corações foram submetidos a 1 hora de CSCN. Grupo II (n=5): um período de 20 minutos de isquemia normotérmica durante o período de 1 hora de CSCN 17. A função do ventrículo esquerdo (VE) foi avaliada, com o coração batendo, utilizando um balão intraventricular, antes do período de parada cardioplégica e a seguir, quando o coração foi novamente perfundido com sangue normokalêmico. Durante todo o protocolo, análise espectroscópica do metabolismo cardíaco foi obtida utilizando-se 4.7 T/30cm Bruker TM Biospec 31 p RNM com uma resolução de 2 minutos para cada resultado. Ao final dos experimentos biópsias miocárdicas foram obtidas para análise de ATP e fosfocreatina (PCr) utilizando cromatografia liqüida de alta "performance" (HPLC). Não houve perda significante de ATP e PCr durante o período de parada cardioplégica com CSCN (Grupo I). Contudo, no Grupo II, a análise espectroscópica demonstrou perda completa de PCr após 14 ± 2 minutos durante a isquemia normotérmica acompanhada de aumento de fosfato inorgânico (Pi) e diminuição do pH intracelular. Quando reperfundido com CSCN, PCr, pH e Pi retornaram aos valores normais em 3 minutos. A função do VE avaliada através da elastância sistólica final foi mantida em 100 ± 10% dos valores obtidos antes da parada cardioplégica no Grupo I. No Grupo II, a função do VE foi de 88 ± 7% (p<0,05) dos valores precedentes à parada cardioplégica. Os resultados das biópsias do miocárdio demonstraram manutenção dos níveis normais de ATP (24 ± 3 µmol/g dry weight) e PCr (55 ± 14 µmol/g dry weight) no Grupo I, porém no Grupo II, apesar dos níveis normais de PCr após a reperfusão, os níveis de ATP diminuíram para 21 ± 3 µmol/g dry weight ao final do experimento. Este experimento demonstrou que o metabolismo cardíaco deteriorou após 14 minutos de isquemia normotérmica com conseqüente diminuição da função do VE (Grupo II). Porém, quando a cardioplegia sangüínea contínua e normotérmica foi utilizada sem interrupções (Grupo I) o metabolismo cardíaco e a função de VE foram preservadas, sugerindo que essa é a maneira ideal para se proteger o coração durante cirurgia cardíaca.

Oxygen-derived free radical scavengers for amelioration of reperfusion damage in heart transplantation

In this study we tried to define the possible benefits of the oxygen-derived free radical scavengers after 3 hours of cold myocardial global ischemia, as required in the setting of cardiac transplantation. Twenty-one pig hearts were harvested after preservation with a cold cardioplegic solution (St. Thomas' Hospital solution) and topical cooling. Normothermic reperfusion with blood was achieved with a special heart-lung machine preparation, which allows the heart to beat in a working or nonworking mode. Twelve hearts served as control hearts (group I), and nine (group II) were subjected to superoxide dismutase and catalase. Superoxide dismutase was applied at a dose of 40 U/ml of cardioplegic solution and 1500 U/kg body weight with the start of reperfusion. Catalase was added to the cardioplegic solution in a dose of 100 U/kg and 3500 U/kg body weight with the start of reperfusion. After 15 minutes of retrograde reperfusion, both left ventricular developed pressure and its first derivative were significantly higher in group II (137 +/- 7.6 mm Hg, 2467 +/- 162 mm Hg/sec) than in group I (105 +/- 6 mm Hg, 1676 +/- 231 mm Hg/sec, p less than 0.05 for each). In addition, a considerably higher coronary blood flow was observed in group II throughout the 180-minute period of reperfusion (p = 0.047). We therefore conclude that the combined administration of superoxide dismutase and catalase during the initial period of cardioplegic arrest and during early reperfusion of donor hearts submitted to 3 hours of cold ischemia has a beneficial effect on myocardial performance.

Atrial electrical activity and its suppression during cardioplegic arrest in pigs

Right atrial electrical activity and myocardial temperatures of all four chambers were monitored during a 1 hour period of cardioplegic arrest in 20 pigs subjected to different methods of venous cannulation and cardiac cooling. Myocardial protection was provided by systemic hypothermia (28 degrees C) and intermittent intra-aortic administration of cold (4 degrees C) hyperkalemic (20 mEq/L) crystalloid cardioplegia. The use of a single right atrial cannula for venous drainage was associated with sustained atrial activity (50 +/- 5.5 minutes) during cardioplegic arrest and the warmest right atrial (27 degrees +/- 0.2 degrees C) and right ventricular (20.5 degrees +/- 0.4 degrees C) temperatures. Separate caval cannulation with snaring and right atrial venting decreased right atrial and ventricular temperatures marginally (25.3 degrees +/- 0.5 degrees C and 19.1 degrees +/- 0.4 degrees C, respectively, p less than 0.05) but did not significantly alter the duration of atrial electrical activity (42.2 +/- 2.5 minutes, p greater than 0.05). Addition of an extracavitary right atrial drip of cold (4 degrees C) saline, 750 ml for the 1 hour aortic clamping period, reduced right atrial temperature (22.8 degrees +/- 0.4 degrees C) and activity (24.8 +/- 6.3 minutes) to a significant extent. Intracavitary irrigation of the right atrium with cold saline, in the presence of snared double caval cannulas, decreased right atrial and ventricular temperatures most dramatically (17.0 degrees +/- 0.5 degrees C and 17.5 degrees +/- 0.3 degrees C, respectively, p less than 0.05), reduced the duration of atrial electrical activity by 84% (to 8 +/- 3.9 minutes, p less than 0.01), and diminished the total number of atrial contractions per hour of aortic clamping by 88%. It is concluded that intracavitary right atrial cooling with separate snared caval cannulation is the most effective method of ensuring atrial inactivity and prolonged right heart hypothermia during cardioplegic arrest.

Supraventricular conduction abnormalities following cardiac operations: A complication of inadequate atrial preservation

The documented efficacy of cardioplegic myocardial preservation has led to increased application of coronary artery bypass grafting, with an increasing number of grafts being performed under prolonged continuous cardiac arrest. Coincident with these developments has been an increased incidence of postoperative conduction block and supraventricular tachyarrhythmias. The frequent return of atrial electromechanical activity during the aortic cross-clamp period implies an inadequate degree of protection afforded the atria and supraventricular conduction system by current techniques of myocardial preservation and suggests that postoperative conduction abnormalities may be due to ischemic injury of atrial structures. In eight patients undergoing coronary artery bypass grafting, a marked disparity was noted in the ability to cool the atrial septum and ventricular septum (mean temperatures 25.9° ± 1.3° C versus 15.7° ± 1.3° C, respectively, p < 0.05). Moreover, atrial septal temperature returned to the temperature of the systemic perfusate (28° C) within 3 minutes following cessation of cardioplegic infusion while ventricular septal temperature remained at 15° to 20° C. The effect of intermittent topical iced saline slush on atrial septal temperature was transient. Following the period of cardioplegic arrest (average, 29 minutes), all eight patients demonstrated first-degree atrioventricular (AV) block, and prolonged AV conduction persisted for at least 2 hours after release of the aortic cross-clamp. In 10 dogs, similar differences in atrial septal and ventricular septal cooling and rewarming were noted during cardioplegic arrest. The temperature gradients between the atrial septum and the ventricular septum were due in part to differential delivery of the cardioplegic solution, the atrial septum receiving 1.42 ± 0.14 ml/gm compared to 3.01 ± 0.22 ml/gm in the ventricular septum (p < 0.05). Regional atrial and ventricular myocardial blood flow was determined before, during, and after cardioplegic arrest. The atrial and ventricular septae showed similarly diminished blood supply during the cross-clamp period (0.044 ± 0.009 and 0.040 ± 0.004 ml/min/gm, respectively) and reactive hyperemia on reperfusion. Detailed AV node, His bundle, and Purkinje system electrophysiological studies before and after cardioplegic arrest supported the concept that inadequate atrial hypothermia during cardioplegic arrest led to ischemic injury of the supraventricular conduction system. Following the period of cardioplegic arrest, all 10 animals demonstrated conduction delay, the site of the delay being primarily within the AV node. Factors implicated in conduction system dysfunction following cardioplegic arrest are discussed, and emphasis is placed on inadequate atrial and AV nodal hypothermia and subsequent ischemic injury as the major causes of postoperative conduction disturbances.

Relationship between atrioventricular arrhythmias and the concentration of K+ ion in cardioplegic solution

The use of potassium cardioplegia during cardiac operation is associated with various types of arrhythmias such as complete heart block or junctional rhythm following the resumption of coronary blood flow. The purpose of this study was twofold: (I) to determine if a relationship exists between the atrioventricular (AV) dissociation arrhythmias and the quantity of potassium used in cardioplegic solutions and (2) to determine whether reducing the quantity of potassium ion infused would result in depletion of high-energy phosphates (HEPs) during the period of cardioplegic arrest. Patients undergoing myocardial revascularization made up the study group, which consisted of three groups of 20 patients each. Group I was perfused with 20 mEq/L K+ cardioplegic solution both initially and after each distal anastomosis. Group II was perfused with 5 mEq/L K+ both initially and after each distal anastomosis. Group III was perfused initially with 20 mEq/L K+ and then with 5 mEq/L K+ for subsequent anastomoses. There was a statistical difference in the incidence of arrhythmias both at hypothermic (28° C) and normothermic temperatures among the groups. In Group I an average of 29 mEq K+ was infused and an 85% incidence of arrhythmias was noted at 28° C. In Group II 8 mEq K+ was infused and a 15% incidence of arrhythmia (p < 0.001) was observed. Group III had an average of 21 mEq K+ infused, and six of 15 patients had arrhythmias (p < 0.01). At 37° C, Group I patients had a 45% incidence of arrhythmias as compared to Group II (10%) and Group III (10%) (p < 0.05). The level of HEPs, including both adenosine triphosphate (ATP) and creatine phosphate (CP), was 61.2 μmoleslgm and fell to 53.5 μmoles/gm (13%) in Group I (p = NS). By comparison, in Group II the HEP level was 62.7 μmoles/gm at control and fell to 59.7 μmoles/gm (5%) (p = NS). In Group III, the HEP level was 58.9 μmoles/gm at control and fell to 49.4 μmoles/gm (16%) after cardioplegic arrest (p = NS). There was essentially no change in HEPs in any group. This study indicates that excellent myocardial preservation can be obtained with the use of either high concentrations of potassium (20 mEq/L K+) or normal concentrations of potassium (5 mEq/L K+). Significant AV dissociation arrhythmias can be avoided by using an initial infusion of 20 mEq/L K+, followed by repeated infusions with normal concentrations of potassium, while still preserving HEPs during the arrest period.

Effects of various periods of cold potassium cardioplegic arrest upon myocardial contractility and metabolism

A maximal “safe” period of cardioplegic arrest has not been documented. Twenty-five dogs were therefore subjected to 1, 2, and 3 hr of potassium cardioplegic arrest (Groups I, II, and III), using 200 ml at 20-min intervals of D 5 0.2 NS with 20 mEq KCl and 6 mEq NaHCO 3/500 ml at 0–4°C. Results: Myocardial temperature decreased to 13°C after each cardioplegic infusion. Left ventricular pressure volume curves did not decrease significantly in Group I, but did in Group II, from 204 ± 20 mm Hg with 10-ml volume to 140 ± 8 ( P < 0.03). Group III decreased from 117 ± 9 with 5-ml volume to 60 ± 3 ( P < 0.0004), from 160 ± 11 with 10-ml volume to 108 ± 6 ( P < 0.004), and from 181 ± 17 with 15-ml volume to 127 ± 9 ( P < 0.03). Cardiac output was less in Group III than in Groups I and II 60 min after bypass [44 ± 10 vs 76 ± 8 ml/min/kg ( P < 0.08)]. Myocardial ATP was significantly less in Group III than Group I 15 min after reperfusion and 60 min after bypass, being 2.25 ± 0.35 and 2.95 ± 0.81 vs 5.18 ± 0.85 and 5.68 ± 0.60 μmoles/g ( P < 0.05). Myocardial lactate increased from 3.65 to 8.55 ± 0.81 μmoles/g at 60 min of cardioplegia, 9.36 ± 0.67 at 2 hr, and 12.01 ± 2.0 at 3 hr. Myocardial glycogen decreased through the cardioplegic period and remained depressed in Group III 30 min after bypass, being 488 ± 124 mg%, as compared to 901 ± 130 in Group I ( P < 0.05). Conclusions: Hearts subjected to 1 and 2 hr of potassium cardioplegia showed relatively little hemodynamic or metabolic derangement, as compared to those subjected to 3 hr of cardioplegia.