Metabolic changes induced by ischemia and cardioplegia: a study employing cardiac microdialysis in pigs.

OBJECTIVE: The present study investigates dynamic changes of myocardial metabolism in response to ischemia, cardioplegia, and extracorporeal circulation (ECC) in order to differentiate between the contributing effects of each of these interventions. Furthermore, warm blood cardioplegia versus empty beating of the heart were compared as methods to resuscitate the ischemic myocardial metabolism. METHODS: Swedish Landrace pigs on ECC (ECC) were compared with pigs on ECC with warm ischemic cardiac arrest (ischemia) or on ECC with warm ischemic arrest followed by warm blood cardioplegia (ischemia-cardioplegia), using sham-operated pigs as controls (n=7 in each group). Microdialysis probes were placed on the surface of the left ventricle and in the femoral artery for serial evaluation of metabolites in the intracardiac extracellular fluid and arterial blood. When hearts started in ventricular fibrillation (VF), it was electroconverted after 10 min of normal blood reperfusion. If VF started after 10 min of reperfusion electroconversion was immediately performed. RESULTS: There were no differences between groups in arterial contents of serine, citrulline, arginine, inosine, hypoxanthine, guanosine, aspartate, glutamate, pyruvate, or asparagine throughout the observation period. Systemic lactate increased in pigs subjected to ischemia (P<0.001) or ischemia and cardioplegia (P=0.002), highest in the ischemia only group (P=0.002). In left ventricular microdialysates, lactate increased in pigs subjected to ischemia alone (P<0.001 vs. ECC) and ischemia and cardioplegia (P=0.004 vs. ECC). Guanosine increased in ischemia versus ECC (P=0.002), while hypoxanthine was increased in microdialysates of both ischemic (P=0.002) and ischemic-cardioplegic (P=0.001) pig hearts. Inosine was increased in pigs subjected to ischemia and cardioplegia (P<0.001 vs. ECC). All ischemic hearts started with VF, but while in the warm ischemia group VF started within 10 min of reperfusion, the ischemia-cardioplegia group had a longer asystolia with VF starting 11-22 min of blood reperfusion. CONCLUSION: The heart should be allowed to start empty beating rather than by the use of warm continuous blood cardioplegia. Microdialysis and sampling of interstitial metabolites may be advantageous when an increased sensitivity is needed or when repeated blood sampling is difficult or contraindicated in monitoring of the myocardium.     

Potassium-induced cardioplegia. Additive protection against ischemic myocardial injury during coronary revascularization.

Potassium-induced cardioplegia during anoxic arrest was utilized in a study of 190 consecutive patients undergoing revascularization (average 2.8 grafts per patient) from August, 1975, through August, 1976. Surgical technique, moderate systemic hypothermia with intermittent anoxic arrest, and the surgeon were the same for all patients. One hundred thirty-five patients (KC1-treated) received a bolus (150 ml.) of potassium solution injected into the proximal aortic root whenever the aortic cross-clamp was applied; 55 others served as control subjects. The mortality rate was 2.2% (three of 135) in the KCl-treated group and one of 55 in the control group. New Q waves appeared in 5.9% (eight of 135) of the KCl-treated patients and 11% (6 of 55) of control subjects (p = N.S.). Catecholamine drips were required after bypass in 4.4% (six of 135) of patients given potassium and 18% (10 of 55) of control patients (p less than 0.05). Profound myocardial relaxation was of added technical value with potassium. It is our impression that hearts treated with potassium exhibited more prompt cardioversion, separated from cardiopulmonary bypass with less need for inotropic support, and exhibited less myocardial injury during the revascularization procedure.     

Regional changes in myocardial acid production during ischemic arrest: a comparison of sanguineous and asanguineous cardioplegia

Regional differences in myocardial acid production have not been characterized during administration of either asanguineous or sanguineous cardioplegia. To investigate this, miniature glass pH electrodes were placed in the right ventricular (RV) myocardium, the left ventricular subendocardial (LV endo) region, and the subepicardial (LV epi) region in a canine model. Multiple doses of either blood cardioplegia (Group 1; N = 11) or crystalloid cardioplegia (Group 2; N = 11) were administered during 4 hours of aortic cross-clamping. The accumulation of hydrogen ions during the cross-clamp period was greater in Group 2 than Group 1 in the LV endo region (629 +/- 79 nm/L versus 66 +/- 31 nm/L; p less than 0.001), the LV epi region (623 +/- 66 nm/L versus 72 +/- 32 nm/L; p less than 0.001), and the RV myocardium (814 +/- 296 nm/L versus 150 +/- 54 nm/L; p less than 0.05). Within each group, the time course of myocardial pH and the accumulation of hydrogen ions did not differ among the LV endo region, LV epi region, and the RV myocardium (p = not significant). These data indicate that transmural and interventricular differences in myocardial pH and hydrogen ion accumulation are not produced in the vented, arrested canine heart. In addition, when compared with asanguineous cardioplegia, blood cardioplegia globally and transmurally reduces acid accumulation during ischemic arrest.     

Potassium-induced cardioplegia during normothermic cardiac arrest. Morphologic study of the effect of varying concentrations of potassium on myocardial anoxic injury.

Most corrective procedures as well as myocardial revascularization require a period of cardiac arrest, and numerous methods have been proposed to protect the myocardium during this ischemic episode. Potassium-induced cardioplegia is one method that appears to be of benefit in this setting. Since it is recognized that myocardial necrosis may result at very high doses of potassium, we examined the effect of varying concentrations of potassium on myocardial anoxic injury. Using an isolated rat heart preparation, we evaluated anoxic injury occurring with cardioplegic solutions containing various concentrations of K+, ranging from 15 to 200 mEq. per liter, during a 50 minute normothermic arrest followed by 60 minutes of reperfusion. The transverse histologic sections of the left ventricular myocardium were analyzed for contraction band injury by morphometric and qualitative methods. Among the 62 animals studied the least severe anoxic injury was seen with K+ cardioplegia at concentrations of 25 and 30 mEq. per liter. At lower and higher concentrations there was little difference between the hearts exposed to anoxia with or without K+ cardioplegia. Potassium administered in very high doses, i.e., 100 or 200 mEq. of K+ per liter, led to contracture and extensive myocardial cell injury. This study suggests that potassium-induced cardioplegia is effective in reducing cell injury due to anoxia, and in this model an optimal concentration range was 25 to 30 mEq. per liter.     

Nicorandil pretreatment and improved myocardial protection during cold blood cardioplegia.

OBJECTIVE: The present study was designed to assess whether pretreatment with nicorandil enhanced myocardial protection provided by cold (15 degrees C) high-potassium (25 mmol/l) blood cardioplegia during open heart surgery. METHODS: Subjects were 40 patients with a variety of acquired heart diseases undergoing cardiac surgery involved cardiopulmonary bypass. They were randomly divided into two groups, 25 pretreated nicorandil (0.3 mg/kg) 30 minutes before aortic cross clamping, 15 not pretreated. After aortic cross clamping, the initial dose of cardioplegic solution (10 ml/kg) was administered through the ascending aorta and supplemental doses of cardioplegia (5 ml/kg) given each 30 minutes thereafter. Preoperative and postoperative cardiac troponin-T, myosin light chain 1 and cardiac enzymes were measured and hemodynamic data recorded. RESULTS: Postoperative serum creatine kinase and myosin light chain 1 were significantly lower in the nicorandil pretreatment group than in controls. Serum glutamic oxalacetic transaminase and troponin-T were lower and cardiac output was higher after surgery in the nicorandil group, although not statistically significant. CONCLUSION: This data suggests that pretreatment with nicorandil enhances the myocardial protection achieved by cold blood cardioplegia.     

Metabolic monitoring during continuous warm- and cold-blood cardioplegia by means of myocardial tissue pH and Po2

Objectives

To study the changes in myocardial tissue pH and Po₂ during cold- and warm-blood cardioplegic arrests.

Design

An experimental study in dogs.

Methods

Nine dogs underwent the following procedures: 30 minutes with an empty heart beating under cardiopulmonary bypass (control period); 30 minutes of warm (33 °C) cardioplegic arrest with a 1:4 mix of crystalloid in blood solution administered continuously at 150 mL/min; 30 minutes of cold (15 °C) cardioplegic arrest; and 30 minutes of myocardial reperfusion. The cardioplegic blood solution was administered antegradely through the ascending aorta.

Main outcome measures

Tissue pH and Po₂. Arterial and coronary sinus oxygen content and myocardial consumption calculated.

Results

There was a modest but significant increase in the left anterior descending (LAD) and circumflex (Cx) tissue pH throughout the experiment. Pmo₂ in the LAD territory averaged 44 (7) mm Hg (mean and standard error of the mean) during the bypass period, 123 (23) mm Hg at the termination of warm cardioplegic arrest, 146 (28) mm Hg at the end of cold arrest and 66 (17) mm Hg after reperfusion. Oxygen consumption averaged 0.65 (0.15) mL/min during the bypass period, 0.3 (0.18) mL/min at the end of warm arrest, 0.25 (0.16) mL/min at the end of cold arrest and 0.45 (0.08) mL/min after reperfusion (p < 0.05). Oxygen delivery to the LAD territory was greater than myocardial oxygen consumption by an average of 2.02 (0.4) mL/min during bypass, 2.02 (0.62) mL/min after warm arrest, 2.12 (0.5) mL/min after cold arrest and 1.55 (0.25) mL/min after reperfusion (p > 0.05).

Conclusions

During cardioplegic arrest, tissue Po₂ increased and oxygen consumption decreased significantly, whereas tissue pH remained normal, suggesting that continuous warm- and cold-blood cardioplegia maintained aerobic glycolysis during myocardial arrest. Thus, the increase in myocardial tissue Pmo₂ during cardioplegic arrest reflects the decrease in myocardial oxygen consumption while maintaining oxygen supply.     

Myocardial perfusion during warm antegrade and retrograde cardioplegia: a contrast echo study.

BACKGROUND: We evaluated distribution of warm antegrade and retrograde cardioplegia in patients undergoing coronary artery bypass grafting (CABG). METHODS: Myocardial perfusion was evaluated pre- and post-CABG using transesophageal echocardiography with injection of sonicated albumin microbubbles (Albunex) during warm antegrade and retrograde cardioplegia. The left ventricle (LV) was evaluated in five segments and the right ventricle (RV) was evaluated in two segments. Segmental contrast enhancement was graded as absent (score = 0), suboptimal or weak (score = 1), optimal or excellent (score = 2), or excessive (score = 3). RESULTS: Pre-CABG cardioplegic perfusion correlated weakly with severity of coronary artery stenoses (r = -0.331 and 0.276 for antegrade and retrograde cardioplegia, respectively). Antegrade cardioplegia administration resulted in 98% and 96% perfusion to the left ventricle pre- and post-CABG, respectively. Retrograde cardioplegic administration resulted in reduced LV perfusion, with 86% (p = 0.032 from antegrade) and 59% (p<0.001 from antegrade) pre- and post-CABG, respectively. The average LV perfusion score (mean +/- SEM) was greater with antegrade than retrograde cardioplegia both pre-CABG (1.93+/-0.04 vs. 1.53+/-0.11, p<0.001) and post-CABG (1.63+/-0.07 vs. 1.19+/-0.13, p = 0.004). RV perfusion was poor with both techniques pre-CABG, but improved significantly with antegrade cardioplegia post-CABG. CONCLUSIONS: We conclude that warm antegrade cardioplegia results in better left ventricular perfusion than warm retrograde cardioplegia. Right ventricular cardioplegic perfusion was suboptimal, but the best delivery was achieved with antegrade cardioplegia after coronary bypass. We therefore recommend construction of the saphenous vein graft to the right coronary artery early in the operative procedure.     

Continuous cold blood cardioplegia improves myocardial protection: a prospective randomized study

BACKGROUND: To assess the influence on myocardial protection of the rate of infusion (continuous vs intermittent) of cold blood cardioplegia administered retrogradely during prolonged aortic cross-clamping. The end-points were ventricular performance and biochemical markers of ischemia. METHODS: Seventy patients undergoing myocardial revascularization for three-vessel disease were prospectively randomized to receive intermittent or continuous retrograde cold blood cardioplegia. Hemodynamic measurements were obtained using a rapid-response thermodilution catheter and included right ventricular ejection fraction, cardiac output, left and right ventricular stroke work index, and systemic and pulmonary vascular resistance. Blood samples were obtained from the coronary sinus before cross-clamp application and immediately after cross-clamp removal for determinations of lactate and hypoxanthine. RESULTS: The left ventricular stroke work index trend was significantly superior (p = 0.038) by repeated-measures analysis in continuous cardioplegia. Other hemodynamic measurements revealed a similar trend. The need for postoperative inotropic drugs support was reduced in continuous cardioplegia. The release of lactate in the coronary sinus after unclamping was 2.30 +/- 0.12 mmol/L after intermittent cardioplegia and 1.97 +/- 0.09 mmol/L after continuous cardioplegia (p = 0.036). The release of hypoxanthine was 20.47 +/- 2.74 micromol/L in intermittent cardioplegia and 11.77 +/- 0.69 micromol/L in continuous cardioplegia (p = 0.002). CONCLUSIONS: Continuous cold blood cardioplegia results in improved ventricular performance and reduced myocardial ischemia in comparison with intermittent administration.     

Preservation of myocardial ATP during cardioplegia: comparison of techniques

Preservation of myocardial ATP enhances the heart's ability to resume normal function following aortic crossclamping (AXC). Preservation of this high energy substrate during 4 cardioplegia delivery techniques was evaluated and compared with changes occurring during 4 hours of continuous coronary perfusion. Dogs (31) were placed on cardiopulmonary bypass and transmural left ventricular biopsies obtained for control ATP measurements. Animals were then divided into five groups: Group I (n = 6): 4 hrs. of continuous coronary perfusion (CCP); Group II (n = 6): 3 hrs. continuous AXC, multidose blood cardioplegia (MBC); Group III (n = 6): 3 hrs. continuous AXC, multidose crystalloid cardioplegia (MCC); Group IV (n = 6): 2 hrs. intermittent AXC, single dose BC (SBC); Group V (n = 7): 2 hrs. continuous AXC, continuous perfusion BC (CBC). In each group, where applicable, myocardial biopsies were taken at 30 minute intervals during AXC, before and after cardioplegia injection, and 30 minutes following final unclamping and rewarming. Hearts in Group II (MBC) and V (CBC) showed greatest preservation of ATP stores (increases 1.1 +/- 1.2%, increases 1.8 +/- 0.9% respectively; p greater than .05) ATP levels rose as high as 23 +/- 2% (p less than .005) above control immediately following cardioplegia injection in Group II (MBC). Group IV showed poorest preservation of ATP (decreases 26 +/- 5%, p less than .01) with levels falling as much as 37 +/- 10% (p less than .01) during the period of AXC. Hearts in Group I (CCP) demonstrated a 15.6 +/- 7.5% decrease in ATP from control (p less than .05). Group III (MCC) also showed a steady decline in ATP declining 18 +/- 3% (p less than .005) from control. These data indicate that multidose blood and continuous-blood cardioplegia techniques will maintain normal myocardial ATP stores throughout the period of AXC. These groups actually show a slight rise in ATP as compared to 4 hrs. of continuous coronary perfusion.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cold cardioplegia versus hypothermia for myocardial protection. Randomized clinical study.

Seventeen of 34 consecutive patients undergoing coronary artery bypass grafting were randomly assigned to one of two methods of myocardial preservation. With the cold cardioplegic method (Group A), a 4 degrees C. asanguineous solution with 30 mEq. of potassium per liter was infused into the aortic root for about 2 minutes immediately after aortic cross-clamping and again after about 45 minutes or when myocardial temperature rose above 19 degrees C. External cardiac cooling was provided by constant infusion of 4 degrees C. Ringer's solution into the pericardium. Seventeen patients were assigned to simple cardiac cooling by hypothermic systemic perfusion before aortic cross-clamping plus external cardiac cooling (Group B). Electromechanical activity ceased within 1 to 2 minutes in Group A but continued throughout the ischemic period in 14 patients in Group B. Myocardial temperature (mean for all observations) during aortic cross-clamping was 17.2 +/- 0.44 degrees C. In Group A and 24.0 +/- 0.70 degrees C. in Group B. Operating conditions were better in Group A. Card-ac function early postoperatively was good in both groups clinically and according to measurements, but only in the cold cardioplegic group (A) was cardiac index not adversely affected by longer cross-clamp time. Myocardial necrosis occurred in both groups but was probably less in the cold cardioplegic group. Thirteen patients (76 percent) in Group A had no electrocardiographic evidence of myocardial injury, compared with eight (47 percent) in Group B (p = 0.08). Eleven (65 percent of Group A had no or short-lived appearance of ceatine phosphokinase isoenzyme (CK-MB), compared with six (35 percent) of Group B (p = 0.08). Time-related CK-MB and SGOT mean levels were consistently lower in Group A.     

Free radicals and cardioplegia: allopurinol and oxypurinol reduce myocardial injury following ischemic arrest

Oxygen-derived free radicals generated by xanthine oxidase may represent a major cause of myocardial injury during ischemia and reperfusion. We have used the isolated working rat heart model of cardiopulmonary bypass and ischemic arrest to assess whether allopurinol or oxypurinol, which should prevent free radical formation through their ability to inhibit xanthine oxidase, can improve postischemic myocardial recovery when the drugs are administered either chronically (pretreatment) or acutely (as an addition to the cardioplegic or reperfusion solution). With normothermic ischemic arrest, both drugs, when given either chronically or acutely, significantly improved postischemic recovery of function. However, under hypothermic conditions, allopurinol conferred no protection when given either as pretreatment or during reperfusion, but it was effective when added to the cardioplegic solution. When administered under the appropriate conditions, both allopurinol and oxypurinol enhanced the protective effect afforded by the St. Thomas' Hospital cardioplegic solution, possibly by inhibiting xanthine oxidase activity and preventing the formation of oxygen-derived free radicals.     

Comparison of myocardial temperatures with multidose cardioplegia versus single-dose cardioplegia and myocardial surface cooling during coronary artery bypass grafting

Myocardial hypothermia with multidose cardioplegia has not been compared with single-dose cardioplegia and myocardial surface cooling with a cooling jacket in patients having coronary artery bypass grafting. In this study, 20 patients with three-vessel disease undergoing coronary bypass at 28 degrees C with bicaval cannulation, caval tapes, and pulmonary artery venting (4.9 +/- 0.7 grafts per patient) were prospectively randomized equally into group I (multidose cardioplegia) and group II (single-dose cardioplegia with a cooling jacket). The initial dose of cardioplegic solution was 1000 ml. Group I then received 500 ml of cardioplegic solution every 20 minutes, delivered into the aortic root and available grafts. In group II, after the cardioplegic solution had been administered, a cooling jacket covering the right and left ventricles was applied. In both groups temperatures were recorded every 30 seconds at five ventricular sites: (1) right ventricular epicardium; (2) right ventricular myocardium or cavity, 7 mm; (3) left ventricular epicardium; (4) left ventricular myocardium or cavity, 15 mm; and (5) septum, 20 mm. Group mean temperatures at each site at various times were compared within each group and between the two groups by analysis of variance. Aortic crossclamp time was 60.3 +/- 12.1 minutes in group I and 52.8 +/- 7.3 minutes in group II (p = 0.12); cardiopulmonary bypass time was 103.7 +/- 11.1 minutes in group I versus 87.7 +/- 12.7 minutes in group II (p less than 0.01). One minute after the cardioplegic solution was initially given, temperatures between groups at each site were not statistically different, but left ventricular epicardial temperatures within both groups were significantly higher than in the other four sites. Nineteen minutes after administration of the cardioplegic solution, temperatures in group I at all sites were higher than in group II. Similarly, throughout the entire period of aortic crossclamping, mean temperatures (except left ventricular myocardial site), maximum temperatures, and percentage of time all temperatures were 15 degrees C or higher were greater in group I than in group II. The following conclusions can be reached: 1. Initial myocardial cooling with 1000 ml of cardioplegic solution is not significantly limited by coronary artery disease but is suboptimal (16 degrees or 17 degrees C) in the inferior left ventricular epicardium because of continual warming from the aorta and subdiaphragmatic viscera. 2. Without myocardial surface cooling, excessive external myocardial rewarming to 18 degrees to 22 degrees C occurs within 20 minutes at all sites after delivery of the cardioplegic solution.(ABSTRACT TRUNCATED AT 400 WORDS)     

Metabolic changes following thermal injury

Patients with extensive thermal injuries have a tremendous, long-lasting increase in transcutaneous heat loss by increased evaporation, radiation, and convection. Their ability to regulate skin temperature and heat loss is limited, and the core-skin insulation is inadequate. The corresponding posttraumatic metabolic response is a massive catabolic drive revealed as insulin insufficiency and increased release of catecholamines and glucagon. This stimulates lipolysis, proteolysis, substrate flow to the liver, and gluconeogenesis of amino acids. The increased heat production is related to an endogenous reset in metabolic activity and is further influenced by environmental conditions. Extensively burned patients cannot overcome the cold stress to which they are exposed by an increased functional heat insulation or by tolerating decreasing body temperature without reacting with a costly increase in heat production and without shivering. If the burn patients are permitted to control the heat supply from infrared heaters until they feel comfortable and all kinds of external environmental disturbances are eliminated, it is possible to reduce their metabolic rate to the normal value for the actual core temperature. The daily caloric requirements can be estimated and, in patients receiving a combined parenteral-enteral dietary program and infrared heat, weight loss can be entirely avoided. Infrared radiation is a practical and inexpensive way of distributing energy from the environment to the patient, suitable also in disaster situations. The ambient air temperature can be kept comfortable with respect to the patient's airways and to the nursing staff.

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Résumé Les patients atteints de brûlures étendues ont, pendant longtemps, des pertes thermiques extrêmement importantes par evaporation accrue, radiation et convection. Ils ont perdu en partie leur capacité de régulation de la température cutanée et des pertes thermiques. L'isolation de l'organisme devient donc inadéquate. En même temps, la réponse métabolique posttraumatique est un hypercatabolisme considérable qui se marque par un déficit en insuline et une libération accrue de catécholamines et de glucagon. Il y a donc augmentation de la lipolyse, de la protéolyse, de l'influx de substrats vers le foie et de la néoglycogenèse à partir d'acides aminés. La production accrue de calories est en rapport avec les perturbations métaboliques et est, de plus, influencée par l'environnement. Les malades atteints de brûlures étendues ne peuvent surmonter le stress par le froid auquel ils sont soumis: ils ne peuvent accroître leur isolation thermique fonctionnelle; ils réagissent à toute baisse de la température corporelle par une production accrue de chaleur et par des frissons. Si on laisse des brûlés contrôler eux-mêmes, selon leur degré de confort, la température dégagée par des lampes à infrarourge, si de plus on élimine toutes les perturbations de l'environnement, leur métabolisme basai peut étre ramené à des valeurs normales pour leur température centrale. Les besoins caloriques peuvent être estimés et il est possible d'éviter complètement les pertes de poids en alimentant les malades à la fois par voies entérale et parentérale et en les plaçant sous une lampe à rayons infrarouges. Celle-ci fournit de l'énergie au patient, de façon pratique et économique, dans ces situations désastreuses. La température ambiante peut rester dans des limites satisfaisantes pour les voies respiratoires du malade et pour l'équipe soignante.

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Supported by the Swedish Medical Research Council (Project Nos. 40X-676 and 40Y-2370).     

A biochemical and ultrastructural study on myocardial changes during aorto-coronary bypass surgery: St. Thomas Hospital cardioplegia versus intermittent aortic cross-clamping at 34 and 25 degrees C

The changes induced by continuous aortic cross-clamping in combination with multidose ice-cold St. Thomas Hospital cardioplegia (myocardial temperature below 16 degrees C), or intermittent aortic cross-clamping at 34 or 25 degrees C were evaluated in a randomized study on 72 patients undergoing extensive aorto-coronary bypass surgery. The cumulative release of heart-specific enzymes was very small and no marked ultrastructural changes in mitochondria of both the subepi- and the subendocardial layer of the left ventricular free wall occurred. No differences between the three operation techniques could be observed on the basis of the above-mentioned parameters. Myocardial ATP and glycogen contents were decreased in post-ischaemic tissue in both the normothermic and hypothermic intermittent aortic cross-clamp groups. This decrease was associated with a release of lactate and inorganic phosphate during the repetitive periods of reperfusion. No change in myocardial ATP and glycogen content could be observed in the cardioplegia-treated hearts. St. Thomas Hospital cardioplegia is obviously most effective in preventing changes in myocardial metabolism such as reduction of ATP and carbohydrate stores during the reversible phase of ischaemic insult.     

Metabolic changes during impending and manifest cerebral hypoxia in traumatic brain injury

The objective was to measure metabolic changes monitored by bedside microdialysis during impending and manifest hypoxia in traumatic brain injury. In 41 patients, a PtiO2-catheter (Licox; 1/min) was placed into non-lesioned frontal white matter together with a microdialysis catheter (CMA, hourly). Data were analysed for identification of episodes of impending (PtiO2 < 10 - 15 mmHg > 5 min) and manifest cerebral hypoxia (PtiO2 < 10 mmHg, > 5 min). In 69% of patients hypoxic episodes occurred, most frequently associated with hyperventilation (p < 0.001). During impending hypoxia, glutamate was increased (p = 0.03), while the energy metabolites remained stable. Manifest hypoxia was reflected by significant increases of glutamate (p = 0.007) and lactate (p = 0.044), but normal lactate-pyruvate ratios. We conclude that hyperventilation had a potential adverse effect on cerebral metabolism and was most frequently associated with cerebral hypoxia. A PtiO2 < 10 mmHg can induce metabolic changes with increase of glutamate and lactate. The presence of anaerobic cerebral metabolism probably depends on duration and severity of the hypoxic episode.     

St. Thomas' Hospital cardioplegia for myocardial preservation during prolonged aortic cross-clamping

The effectiveness of St. Thomas' Hospital cardioplegia for myocardial preservation during prolonged aortic cross-clamping was analyzed in a clinical series of 100 consecutive cardiac surgical patients identified as having aortic cross-clamp times greater than 120 minutes. Hospital mortality from all causes was 8%, but only one of these 8 patients succumbed from immediate primary failure of the myocardial preservation protocol. Severe but reversible low cardiac output syndrome occurred in 5 patients, and in 4 of them there had obviously been a primary failure in cardiac protection. Peri-operative, clinically "silent" myocardial infarction could be demonstrated in retrospect by electrocardiographic criteria in 3 other patients. Post-operative complications occurred in 26 patients, many of them having several complications at the same time. Paired left ventricular and right ventricular prebypass and post-bypass biopsies processed for cytochemical and biophysical investigation were available from one third of the patients. Only 2 cases showed a severe deterioration. There was lack of correlation between the duration of aortic occlusion and operative mortality rate, incidence of peri-operative infarction, and occurrence of low cardiac output syndrome post-operatively. The results thus indicate that St. Thomas' Hospital cardioplegia is a very effective means of myocardial protection during prolonged periods of aortic cross-clamping.