Methods of the 7th National Audit Project (NAP7) of the Royal College of Anaesthetists: peri-operative cardiac arrest.

Cardiac arrest in the peri-operative period is rare but associated with significant morbidity and mortality. Current reporting systems do not capture many such events, so there is an incomplete understanding of incidence and outcomes. As peri-operative cardiac arrest is rare, many hospitals may only see a small number of cases over long periods, and anaesthetists may not be involved in such cases for years. Therefore, a large-scale prospective cohort is needed to gain a deep understanding of events leading up to cardiac arrest, management of the arrest itself and patient outcomes. Consequently, the Royal College of Anaesthetists chose peri-operative cardiac arrest as the 7th National Audit Project topic. The study was open to all UK hospitals offering anaesthetic services and had a three-part design. First, baseline surveys of all anaesthetic departments and anaesthetists in the UK, examining respondents' prior peri-operative cardiac arrest experience, resuscitation training and local departmental preparedness. Second, an activity survey to record anonymised details of all anaesthetic activity in each site over 4 days, enabling national estimates of annual anaesthetic activity, complexity and complication rates. Third, a case registry of all instances of peri-operative cardiac arrest in the UK, reported confidentially and anonymously, over 1 year starting 16 June 2021, followed by expert review using a structured process to minimise bias. The definition of peri-operative cardiac arrest was the delivery of five or more chest compressions and/or defibrillation in a patient having a procedure under the care of an anaesthetist. The peri-operative period began with the World Health Organization 'sign-in' checklist or first hands-on contact with the patient and ended either 24 h after the patient handover (e.g. to the recovery room or intensive care unit) or at discharge if this occured earlier than 24 h. These components described the epidemiology of peri-operative cardiac arrest in the UK and provide a basis for developing guidelines and interventional studies.

Stentless vs. stented aortic valve bioprostheses: a prospective randomized controlled trial.

AIMS: We sought to assess the haemodynamic profile of the Freedom stentless aortic valve compared with a stented bioprosthesis in a randomized controlled trial using echocardiography. METHODS AND RESULTS: Sixty patients (mean age 73 years) undergoing bioprosthetic aortic valve replacement (AVR) were randomized to either Sorin Freedom stentless (n=31) or Sorin More stented (n=29) valves. The primary endpoints were left ventricular mass index (LVMI) reduction at 6 and 12-months. We also assessed post-operative effective orifice area index (EOAI), aortic gradient and operative time. There were no significant differences in baseline characteristics. The stentless valve was associated with a lower post-operative gradient [PG 17 (12) vs. 31 (13) mmHg, P<0.0001] and greater EOAI [1.1 (0.3) vs. 0.8 (0.2) cm2/m2, P<0.0001]. A highly significant reduction in LVMI occurred by 6 months in both groups, but LVMI was significantly lower in the stentless group [LVMI 119 (39) vs. 135 (30) g/m2, P=0.05]. However, there was continued regression of left ventricular hypertrophy (LVH) in the stented but not in the stentless group, resulting in no significant difference in LVMI at 12 months [119 (36) vs. 126 (31) g/m2, P=0.42]. CONCLUSION: The use of the Sorin Freedom stentless bioprosthesis for AVR results in lower PG and greater EOA when compared with a Sorin More stented valve. This is associated with earlier regression of LVH.

A case of a periaortic lymphoma presenting with the features of descending thoracic aorta dissection.

We report the case of a 68-year-old male in whom an intrathoracic non-Hodgkin's lymphoma was diagnosed late after he presented with the clinical and radiological features of a descending aortic dissection due to penetrating ulcer. An endovascular stent was implanted in the descending aorta. At follow up, a CT scan showed the presence of a mediastinal mass thought to be a periaortic haematoma as a consequence of the endovascular stent implantation. A further CT scan showed an increase in size of the mediastinal mass encasing the whole descending aorta. A biopsy of the mass was performed which was shown to be non-Hodgkin's lymphoma. This is the first report of a penetrating ulcer of the descending aorta due to lymphoma, which probably caused the dissection.

Right ventricular function in orthotopic total atrioventricular heart transplantation.

BACKGROUND: Total orthotopic heart transplantation was recently introduced into clinical practice as an alternative technique of orthotopic heart transplantation, adding bicaval and left and right pulmonary vein anastomoses to pulmonary artery and ascending aorta connection (total technique). The conventional technique (ventricular transplantation with atrioplasty) is compared with the total technique with particular emphasis on right ventricular performance. METHODS: Forty-eight mongrel dogs (23 to 31 kg) were used for 12 total and 12 standard orthotopic heart transplantations. Right ventricular (RV) function and atrial systole were analyzed with the use of micromanometry, sonomicrometry, and ultrasonic flow probes (preload-independent RV recruitable stroke work, RVPRSW). Fourier analysis was used to calculate RV power and pulmonary vascular impedance. RESULTS: There was no significant difference in cardiac ischemic and bypass times between the two groups. After transplantation, sinus rhythm was preserved after all total transplantations and after only one standard transplantation; no significant hemodynamic differences were observed. RVPRSW in the total group was conserved after transplantation; however, RVPRSW decreased by 39% (+/-8, p < .05) in the standard group. There was also a significant decrease in the rate of RV filling in the standard group after transplantation, suggesting decreased right atrial function. Pulmonary vascular impedance and RV power output were not significantly different after transplantation between the two groups. CONCLUSIONS: Total atrioventricular transplantation is a feasible alternative and conserves normal sinus rhythm. Ischemic and bypass times were not significantly different when the superior vena cava anastomosis is performed last after the release of the aortic cross-clamp. The insignificant decrease in the rate of RV filling with the use of the total technique suggests conserved RV diastolic function after transplantation with less decreased RV function in the total group.

Right ventricular function in the donor heart.

OBJECTIVES: Early morbidity and mortality post cardiac transplantation is frequently caused by right ventricular failure; this is usually attributed to an elevated pulmonary vascular resistance in the recipient. Brain death in the donor is recognised as causing left ventricular dysfunction, but its effects on the right ventricle have not previously been studied. The aim of this study was to investigate right ventricular function following brain death, using a canine model. METHODS: The hearts of 33 dogs were instrumented with micromanometers, flow probes and dimension transducers to measure minor/major axes, and right and left ventricular free wall to septal distances. Left ventricular volume was calculated according to the prolate ellipsoid model and right ventricular volume was calculated according to the shell subtraction method. Systolic function for left and right ventricles was analysed by plotting ventricular stroke work vs. end-diastolic volume during a caval occlusion (preload-independent recruitable stroke work PRSW). Brain death was instigated by inflation of a subdurally placed intracranial balloon; subsequently blood pressure was maintained with intravenous fluid whilst no inotropic medications were given. Data were collected at baseline, and at 2 and 4 h thereafter. A two-tailed paired Student's t-test was applied to compare post-brain death data with baseline measurements. RESULTS: All animals had an initial hyperdynamic response post brain death ensued by the development of diabetes insipidus. Brain stem death was validated by neuropathological examination at the termination of the experiments. Right and left ventricular systolic function had deteriorated significantly 2 h post brain death by 34.4% (+/- 5.1%, P < 0.001) and 20.4% (+/- 3.4%, P < 0.001), respectively, from baseline PRSW [RV = 23.6 erg.10(3) (+/- 1.5), LV = 76.2 erg.10(3) (+/- 3.5)]. This deterioration remained at 4 h post brain death (29.4% (+/- 4.9%, P < 0.001) and 21.2% (+/- 4.3%, P < 0.001), respectively). (The results are expressed as mean and S.E.M.). CONCLUSIONS: Brain death causes a significant decrease in left and right ventricular function. The injury to the right ventricle is more prominent than the left ventricle, and at 2 h post brain death it is significantly greater. Failure of the right ventricle post transplantation in clinical practice may be related to this brain death induced injury. Further studies are required to investigate the mechanisms of this injury.

Brain death alters cardiopulmonary hemodynamics and impairs right ventricular power reserve against an elevation of pulmonary vascular resistance.

Right ventricular (RV) failure, which is a leading cause of early morbidity and mortality following cardiac transplantation, is attributed to the inability of the donor RV to acutely compensate for the recipient's elevated pulmonary vascular resistance (PVR). Furthermore, the effect of donor brain death (BD) on RV function is unclear. The purpose of this study was to investigate the effects of donor BD on RV function in the setting of elevated PVR. The interactions of the RV and its afterload, the pulmonary vasculature, and left atrial pressure were assessed by measurements of pulmonary vascular energetics and their oscillatory nature using proximal ultrasonic pulmonary artery (PA) flow probe and micromanometers in the proximal and distal PA in 20 mongrel dogs (25.8 +/- 0.4 kg, five control animals). A band was placed around the distal PA (PA-systolic gradient > 15 mm Hg). BD was induced by rising intracranial pressure and was validated neuropathologically. Data were collected at 0, 2, 4, and 6 h after BD in both banded and control animals. Fourier analysis was used to calculate RV oscillatory power, mean power, and total power (TP). Comparison of changes due to banding were made to baseline measurements using multivariate analysis and paired Student's t test (p < 0.05). A significant twofold to fourfold increase in pulmonary impedance and PVR occurred with an acute rise in PA gradient. Control animals tolerated acute increases in PVR without significant changes in TP. There was a significant increase of RV TP from 73 (+/-11) to 98 (+/-10) mW at baseline after the acute rise in PVR and impedance. After BD, the response to increased PVR and impedance was abolished significantly compared with baseline and control animals, suggesting a significant loss of compensatory TP to sustain pulmonary vascular blood flow. The data indicate that BD is detrimental to RV mechanical function.

Evaluation of routine postoperative chest X-rays in the management of the cardiac surgical patient.

OBJECTIVES: To evaluate the role of routine chest X-rays in the management of patients post cardiac surgery. METHODS: 340 adult patients undergoing cardiac surgery were studied in three consecutive groups (A, B, C) of 100 patients each. Forty patients were excluded due to the intensive care stay greater than 36 h (n = 35), or early mortality within 36 h (n = 5). Routine chest X-rays were performed according to different protocols in Groups A and B. In group C there were no routine chest X-rays during the entire postoperative period [corrected]. In all three groups chest X-rays were performed where clinically indicated. Group A had three routine chest X-rays post-operation. Group B had one routine chest X-ray on day 4 post-operation. Group C had chest X-rays only when indicated. The X-rays were evaluated in terms of their assistance value and the resultant number of interventions. RESULTS: The three groups were similar preoperatively for age, sex, preoperative left ventricular function, presence of chronic obstructive airway disease and type of operation performed. The total number of chest X-rays in groups A, B and C were 304, 133 and 36, respectively. The number of chest X-rays leading to interventions were five, four and four in groups A, B and C, respectively. Chest X-rays that helped in management were 36, 28, and 28, respectively, in the same groups. There was no mortality or morbidity attributable to non-performance of routine chest X-ray. CONCLUSIONS: Routine chest X-rays post-cardiac surgery are of very little value and patients are adequately managed by performing chest X-rays only when clinically indicated. There was no increased mortality or morbidity attributed to lack of routine chest X-rays in any of these groups. We recommend performing chest X-rays only when clinically indicated in satisfactorily recovering adult cardiac surgical patients.

Total atrioventricular cardiac transplantation preserves atrial systole and ventricular diastolic filling.

BACKGROUND: Total orthotopic heart transplantation was recently introduced into clinical practice as an alternative technique for orthotopic cardiac transplantation. Total cardiac transplantation uses separate bicaval and left and right pulmonary anastomoses, whereas the standard technique of cardiac transplantation uses atrioplasty. Because the anatomic differences between total and standard orthotopic heart transplantation occur at the atrial level, this study compares atrial systolic function and biventricular filling (dV/dt) between the standard and total transplantation techniques. METHODS AND RESULTS: Forty-eight mongrel canines (23 to 31 kg) were used for 12 total and 12 standard orthotopic cardiac transplantations. Right and left ventricular (RV/LV) function and AV synchrony were analyzed with micromanometry, sonomicrometry, ultrasonic flow meters, and intraoperative echocardiography. Results are expressed as mean +/- SEM (ANOVA, paired and unpaired t tests, and chi 2 test). There were no significant differences in baseline function (pretransplantation), bypass times, and cardiac ischemic times between the two groups. Posttransplantation sinus rhythm was preserved in all total (P < 0025) and in only one standard transplantation recipient (all required atrial diastole pacing). Significant decreases in RV/LV dV/dt from 113 +/- 13 and 123 +/- 14 mL/s to 69 +/- 6 and 85 +/- 10 mL/s after transplantation were measured in the standard group. No significant changes occurred in the total group after transplantation with respect to RV/LV diastolic filling. After transplantation, left atrial contractility and relaxation (-dP/dt) decreased significantly in the standard group by 43% and 70%, respectively, whereas in the total transplantation group, there were no observed changes in left atrial contractility and-dP/dt. A significant increase in the septum to RV free wall dimension in the standard group suggests altered geometry. CONCLUSIONS: Total AV transplantation is a feasible alternative to standard cardiac transplantation and conserves both normal sinus rhythm and synchronized beating of the atria and ventricles. Ischemic and bypass times are comparable in patients undergoing either method. These data suggest that RV/LV diastolic function and geometry and atrial systole are better preserved in the total AV transplantation technique.

The combined effects of brain death and cardiac graft preservation on cardiopulmonary hemodynamics and function before and after subsequent heart transplantation.

BACKGROUND: The combined effects of brain death and graft preservation on right and left ventricular function and on pulmonary hemodynamics after subsequent heart transplantation have not been previously studied. METHODS: Fifty-seven dogs (25.5 +/- 0.3 kg) were divided into three groups and underwent a total of 20 brain death experiments and 16 orthotopic complete atrioventricular transplantations with the use of a validated brain death organ donor model, hypothermic heart preservation, and right and left ventricular functional analysis (preload-independent recruitable stroke work, Fourier analysis). In the first group, changes in cardiopulmonary function were assessed over a period of 6 to 7 hours after brain death. In the second group, the hearts were procured from a donor with brain death and immediately transplanted whereas in the third group cardiac graft preservation for a period of 4 hours followed harvest from a donor with brain death before heart transplantation and assessment of heart transplant function. RESULTS: After brain death alone, a significant increase in right and left ventricular end-diastolic pressures and a decrease in systemic and pulmonary resistance and pulmonary impedance occurred. Furthermore, right and left ventricular function decreased significantly by 35% and 19%, respectively, and subsequent transplantation did not cause further cardiac dysfunction. Preservation in combination with brain death led to further significant decreases in right ventricular function after subsequent transplantation compared with brain death alone, necessitating the use of dopamine to wean four animals from cardiopulmonary bypass. CONCLUSION: Brain death causes a significant loss of right and left ventricular function. These injuries are greater in the right ventricle and may contribute to early right ventricular failure after transplantation. Brain death and cardiac graft preservation have significantly additive deleterious effects on right ventricular function after transplantation.

Hormonal and hemodynamic changes in a validated animal model of brain death.

OBJECTIVE: To examine the hormonal and hemodynamic changes in a validated animal model of brain death. DESIGN: Prospective, controlled study. SETTING: Experimental research laboratory. SUBJECTS: Adult male mongrel dogs (n = 10). INTERVENTIONS: Brain death was induced by inflation of a subdural balloon in ten mongrel dogs weighing 23 to 30 kg and validated neuropathologically. The hearts were instrumented with micromanometers and ultrasonic flow probes to measure cardiovascular changes. No inotropic or vasoactive support was given. Hemodynamic stability was maintained with intravenous fluids. Blood samples and hemodynamic readings were collected before and after the induction of brain death. MEASUREMENTS AND MAIN RESULTS: A Cushing reflex, followed by a hyperdynamic response and diabetes insipidus, occurred in every animal following brain death. Mean arterial pressure, heart rate, contractility, and cardiac output increased to > 350 mm Hg, 230 beats/min, 4200 mm Hg/sec, and 2.8 L/min, respectively, at the peak of this phenomenon before returning to baseline. A plasma catecholamine surge was observed in every animal 15 mins after brain death, while the circulating concentrations of the pituitary gland hormones vasopressin and adrenocorticotrophic hormone decreased significantly after 15 and 45 mins of brain death, respectively, and continued to decrease throughout the experiments. Circulating triiodothyronine, thyroxine, and glucagon concentrations decreased significantly (p < .01) from 0.58 +/- 0.05 ng/mL, 2.20 +/- 0.15 micrograms/dL, and 49.7 +/- 9.1 pg/mL, respectively, to 0.34 +/- 0.03 ng/mL, 1.14 +/- 1.14 micrograms/dL, and 6.9 +/- 1.4 pg/mL, respectively, 420 mins after brain death. The hematocrit increased significantly 15 mins after brain death and then gradually decreased throughout the duration of the experiments. CONCLUSIONS: In a validated animal model of brain death, significant decreases in the circulating concentrations of stress hormones, as well as hemodynamic instability, occurred after brain death. Measurements of plasma adrenocorticotrophic hormone and vasopressin values may be useful as diagnostic predictors of brain death. Furthermore, the observed changes may contribute to organ dysfunction after brain death and may necessitate hormonal as well as inotropic and vasoactive support to maintain donor organ function in the clinical setting.

Nitric oxide in brain death related cardiovascular dysfunction.

PURPOSE: Nitric oxide (NO) is a major regulator of vascular tone, blood pressure, and blood flow, and plays a significant role in disease states associated with hemodynamic alterations. However, the role of NO in association with the effects of brain death (BD) has not yet been evaluated. METHODS: In 17 mongrel dogs (23 to 31 kg), right atrial serum measurements of nitrite and L-arginine as well as NO ex vivo tissue nitrite extraction were performed at baseline (0), and 120, 240, and 360 minutes after BD. The hearts were instrumented with micromanometers, transonic flow probes, and ultrasonic dimension transducers to determine systolic function and to analyze the pulmonary vasculature flow characteristics by Fourier analysis. Brain death was induced by inflation of a subdurally placed balloon and validated neuropathologically. The results are expressed as mean and standard error of the mean (+/- SEM) (P < .05, paired t-test). RESULTS: Right and left ventricular function deteriorated significantly (P < .001) by 37% (+/- 10) and 22% (+/- 7) respectively following BD. Pulmonary and systemic vascular resistance as well as pulmonary impedance decreased significantly over 6 hours after BD. Pulsatile flow, a potent stimulant of NO release, converted significantly to more steady flow. Myocardial NO extraction values remained unchanged after BD and serum L-arginine decreased from 12.84 mu g/L (+/- 0.60) to 11.77 mu g/L (+/- 0.55). CONCLUSIONS: The decreases in pulmonary and systemic vascular resistance, pulmonary impedance, and cardiac function associated with BD are not related to major changes in the NO pathway. NO may not play a key role in the early changes after BD.

Myocardial beta-adrenergic receptor function and high-energy phosphates in brain death--related cardiac dysfunction.

BACKGROUND: Cardiac failure remains an important problem after heart transplantation and may be associated with events that occur during brain death (BD) before transplantation. In this study, cardiac function is studied after BD, and biochemical evaluation of myocardial high-energy phosphates and the beta-adrenergic receptor system is presented. METHODS AND RESULTS: The hearts of 17 mongrel dogs (23 to 31 kg) were instrumented with flow probes, micromanometers, and ultrasonic dimension transducers to measure ventricular pressure and volume relationships. In a validated canine BD model, systolic right and left ventricular (RV/LV) function was analyzed by load-insensitive measurements during caval occlusion (preload-recruitable stroke work, PRSW). The beta-adrenergic receptor (BAR) density, adenylate cyclase (AC) activity, and myocardial ATP and creatine phosphate (CP) were measured before and 6 to 7 hours after BD. Results are expressed as mean +/- SEM (*P < .05 versus baseline, paired two-tailed Student's t test). Myocardial function deteriorated significantly from baseline PRSW (RV, 22 +/- 1 erg x 10(3); LV, 75 +/- 4 erg x 10(3)) by 37 +/- 10% for the RV (P < .001) and 22 +/- 7% for the LV (P < .001). BAR density increased from 282 +/- 42 to 568 +/- 173 fmol/mg for the RV and from 291 +/- 64 to 353 +/- 56 fmol/mg for the LV. Isoproterenol-stimulated AC activity was also significantly enhanced after BD. ATP and CP, however, remained unchanged after BD compared with baseline values before BD. CONCLUSIONS: BD causes significant systolic biventricular dysfunction. The loss of ventricular function after BD was more prominent in the right ventricle and may contribute to early postoperative RV failure in the recipient. These injuries occurred despite BAR system upregulation after BD. Global myocardial ischemia is unlikely, since ATP and CP remained normal before and after BD.

The effects of brain death on cardiopulmonary hemodynamics and pulmonary blood flow characteristics.

Deterioration of donor lung function contributes to the shortage of donor organs and early postoperative failure after transplantation. A decrease in donor pulmonary function is associated with opacification of lung fields on radiographs, rendering the lungs unsuitable for transplantation, which may be related to the effects of brain death (BD) on pulmonary hemodynamics. Twenty mongrel canines (25.5 +/- 0.7 kg) underwent 20 BD experiments using a previously validated BD organ donor model. An ultrasonic flowmeter was applied on the pulmonary artery and micromanometers were inserted into the right ventricle, pulmonary artery, and left atrium to measure, which allowed the hemodynamic assessment and impedance profile analysis of the pulmonary vasculature by Fourier transformation. Characteristic impedance (Zo) was compared with input resistance (RIN) and with calculated pulmonary vascular resistance (PVR), the conventional index. Right ventricular hydraulic power was analyzed and divided in its components oscillatory and steady power. The results are expressed as means and SEM (analysis of variance, paired two-tailed t tests). Cushing reflex, hemodynamic response, and diabetes insipidus were consistent findings following BD. PVR, Zo, and RIN decreased significantly (p < 0.05) from 367 +/- 40 dyne.s.cm-5, 226 +/- 13 dyne.s.cm-5, and 771 +/- 52 dyne.s.cm-5 to 261 +/- 25 dyne.s.cm-5, 159 +/- 10 dyne.s.cm-5, and 651 +/- 69 dyne.s.cm-5 6 h after BD. Pulmonary artery blood flow increased significantly from 1,499 +/- 107 mL/min to 2,064 +/- 209 mL/min (p < 0.05) after BD. Hydraulic power increased from 69 +/- 6 mW to 104 +/- 13 mW (p < 0.05) and the oscillatory power to steady power ratio of 33%/67% changed to 23%/77% following BD. Extravascular pulmonary water content increased significantly by 10% after BD. BD causes a significant change in pulmonary vascular hemodynamics. The decrease in impedance and right ventricular afterload may lead to significant pulmonary overflow injury and edema. The increase in steady power represents an important reserve of the right ventricle to sustain pulmonary blood flow following BD.

Complete atrioventricular cardiac transplantation: improved performance compared with the standard technique.

BACKGROUND: There has been renewed clinical interest in an alternative technique to orthotopic cardiac transplantation involving six anastomoses: left pulmonary veins, right pulmonary veins, inferior vena cava, pulmonary artery, aorta, and superior vena cava (complete technique). In this study, the results of the complete technique are compared with those of the standard operation (ventricular transplantation with atrioplasty). METHODS: Dogs were used for ten acute standard and ten acute complete atrioventricular transplantations. There were no significant differences in the baseline cardiac function (preload-independent right and left ventricular recruitable stroke work), bypass times, and cardiac ischemic times between the two groups. RESULTS: After transplantation, sinus rhythm was preserved after all ten complete and after only one standard transplantation but no significant hemodynamic differences were observed. The right and left ventricular preload-independent recruitable stroke work in the complete group and the left ventricular preload-independent recruitable stroke work in the standard group were conserved after transplantation, but the right ventricular preload-independent recruitable stroke work decreased by 39% +/- 8% (p < 0.05) in the standard group. There was also a significant decrease in the rate of biventricular filling in the standard group after transplantation. CONCLUSIONS: Complete atrioventricular transplantation is a feasible alternative technique and conserves normal sinus rhythm. The ischemic and bypass times are comparable for both methods. The insignificant change in the rate of biventricular filling in the dogs undergoing the complete technique indicates right and left ventricular diastolic function may be conserved after transplantation.

Myocardial performance after graft preservation and subsequent cardiac transplantation from brain-dead donors.

BACKGROUND: This study examined the effects of brain death and graft preservation on right and left ventricular function after subsequent cardiac transplantation. METHODS: Seventy-eight dogs underwent 34 orthotopic complete atrioventricular transplantations using a validated brain-dead organ donor model, hypothermic cardiac preservation, and right and left ventricular function analysis (preload-independent recruitable stroke work). Four groups were studied: controls, transplantation from brain-dead organ donors, graft preservation without brain death, and donor brain death and graft preservation before transplantation. RESULTS: Without brain death, cardiac arrest alone as well as the combination of cardiac arrest and preservation did not significantly decrease cardiac function after transplantation. After brain death alone, right ventricular and left ventricular function decreased significantly by 30% and 25%, respectively, but subsequent transplantation did not cause further cardiac dysfunction. Preservation after brain death led to a further significant decrease in right ventricular function after subsequent transplantation, and dopamine hydrochloride was required to wean 4 animals from cardiopulmonary bypass. CONCLUSIONS: Brain death causes a significant loss of right and left ventricular function. These injuries are greater in the right ventricle and may contribute to early right ventricular failure after transplantation. Brain death and cardiac preservation interact significantly to impair right ventricular function further. Future studies of graft preservation should use brain-dead organ donors.

Endocrine changes and metabolic responses in a validated canine brain death model.

PURPOSE: Endocrinologic and metabolic changes after brain death (BD) have not yet been investigated in a validated animal model. Therefore, the effects of BD on hormonal and metabolic function were studied in 10 dogs (23 to 31 kg). METHODS: BD was induced by intracranial pressure increase and validated neuropathologically. Plasma concentrations of pituitary, thyroid, adrenal, and pancreatic hormones were measured pre/post BD. The results are expressed as mean (+/- SEM). RESULTS: A Cushing reflex and diabetes insipidus occurred after BD. Elevated catecholamine levels were documented after 15 minutes whereas the pituitary gland hormones vasopressin and adrenocorticotrophic hormone (ACTH) decreased significantly after 15 and 45 minutes of BD respectively. Thyroxine, triiodothyronine, and glucagon decreased significantly (P < .01) from 0.58 ng/mL (+/- 0.05), 2.20 micrograms/dL (+/- 0.15), and 49.7 pg/mL (+/- 9.1) respectively to 0.34 ng/mL (+/- 0.03), 1.14 micrograms/dL (+/- 1.14), and 6.9 pg/mL (+/- 1.4) respectively 420 minutes after BD. The hematocrit increased significantly after BD and declined toward the end of all experiments. Metabolic acidosis occurred immediately after BD and at the end of the experiments. CONCLUSIONS: In a simple, reproducible, and reliable animal model of BD, a catecholamine storm, vasopressin and ACTH cessation, and diabetes insipidus were consistent findings. The decrease in cortisol and vasopressin levels warrant consideration of hormonal therapy.

Mechanisms of transplant right ventricular dysfunction.

OBJECTIVE: Right ventricular (RV) dysfunction remains the leading cause of early mortality after cardiac transplantation. The effect of brain death and subsequent hypothermic cardioplegic arrest and storage on subsequent post-transplant right ventricular function was examined. SUMMARY BACKGROUND DATA: Right ventricular dysfunction in the donor heart usually is attributed to failure of the donor right ventricle to adapt to the sudden increase in afterload (pulmonary vascular resistance) in the recipient. Strategies to improve ventricular mechanics in the postoperative period are aimed at reducing pulmonary vascular resistance with vasodilators or augmenting right ventricular contractility with inotropic agents. Events occurring in the donor heart (brain death, hypothermic cardioplegic arrest, and storage) also may be directly related to post-transplant RV dysfunction. METHODS: A canine model of brain death and orthotopic cardiac transplantation was used. A dynamic pressure-volume analysis of RV mechanics was performed using micromanometers and sonomicrometric dimension transducers. Systolic function was assessed by measurement of preload recruitable stroke work (PRSW). Brain death was induced in 17 dogs by inflation of an intracranial balloon. Right ventricular function then was assessed serially to 6 hours (PRSW). Right ventricular adrenergic beta receptor density and function was sampled at control and after 6 hours of brain death. The effect of cardioplegic arrest and hypothermic storage was assessed in a second group of 17 dogs, using the same instrumentation and method of RV analysis. RESULTS: A significant decrease in right ventricular PRSW occurred after brain death, with the average decrease being 37% +/- 10.4% from the control. The RV myocardial beta adrenergic receptor density did not significantly change (253 +/- 34 fmol/ng control vs. 336 +/- 54 fmol/ng after brain death). The adenylyl cyclase activity of the RV beta receptor was assessed and was not altered by brain death. Orthotopic transplantation after cardioplegic arrest and hypothermic storage significantly decreased RV PRSW from 23.6 +/- 2.0 x 10(3) erg to 13.5 +/- 1.4 x 10(3) erg. CONCLUSIONS: These data indicate that the donor right ventricle is exposed to factors significantly detrimental to its mechanical performance well before facing an increased afterload in the recipient. Strategies to reduce RV dysfunction associated with brain death and hypothermic storage could positively impact post-transplant survival.

A valid experimental brain death organ donor model.

BACKGROUND: This study was designed to establish a validated canine brain death model. Ten consecutive dogs were studied to investigate the effects of brain death on hemodynamic, metabolic, and hormonal function. METHODS: Brain death was induced by inflation of a subdurally placed balloon and was validated neuropathologically. Functional data and blood samples were collected before and 15, 45, 90, 240, 360, and 420 minutes after the induction of brain death. No inotropic or vasoactive support was given. The results are expressed as mean +/- standard error of the mean. RESULTS: The Cushing reflex occurred in all animals and lasted 13.3 +/- 1.5 minutes. Raised catecholamine levels were documented at 15 minutes, whereas the pituitary gland hormones vasopressin and adrenocorticotrophic hormone decreased significantly after 15 and 45 minutes, respectively. Triiodothyronine, thyroxine, and glucagon decreased significantly from 0.58 +/- 0.05 ng/ml, 2.20 +/- 0.15 micrograms/dl, and 49.7 +/- 9.1 pg/ml to 0.34 +/- 0.03 ng/ml (p < 0.05 versus baseline; paired two-tailed t-test), 1.14 +/- 1.14 micrograms/dl (p < 0.05), and 6.9 +/- 1.4 pg/ml (p < 0.05). Insulin and lactate dehydrogenase showed a moderate increase after brain death. Diabetes insipidus occurred after 45 minutes in nine animals (urine output 13.5 +/- 1.8 ml/kg/hour). Left and right ventricular end-diastolic pressure increased significantly toward the end of all experiments. Cardiac output increased and systemic and pulmonary vascular resistance decreased, but heart rate remained unchanged. CONCLUSION: This simple, reproducible, moderately invasive, and reliable model of brain death in animals assesses donor organ function and preservation. Cushing reflex, hyperdynamic state, catecholamine storm, vasopressin and adrenocorticotropic hormone cessation, total cerebral necrosis, and diabetes insipidus were consistent findings.

Topical aprotinin in cardiac operations.

We performed a prospective, randomized, double-blind trial of topical aprotinin versus placebo in 100 patients undergoing cardiac operations with cardiopulmonary bypass. Fifty-five patients received aprotinin. Forty underwent coronary artery bypass grafting (CABG) and 15 valve replacement +/- CABG. Of 45 patients in the control group 38 underwent CABG and 7 valve replacement +/- CABG. Aprotinin (50 mL; 70 mg) or placebo was applied topically to the heart, pericardium, and mediastinum before sternal closure. There were five reentries for bleeding with a surgical site identified in four. Mean blood loss was significantly less in the aprotinin group (653 versus 903 mL; p = 0.002), and fewer aprotinin patients received blood as a volume expander (67.5% versus 88%; p = 0.03). In coronary patients alone when aspirin administration was continued until the day of operation there was no difference between treatment and placebo groups (768 versus 879 mL). When aspirin administration was discontinued 2 weeks before operation there was a significant difference (558 versus 884 mL; p = 0.016) as in the group overall. This provides the potential for intrapericardial instillation for patients with excessive postoperative bleeding.

Radiological evaluation of the ascending aorta following repair of type A dissection.

A patient with persistent chronic dissection proximal to an aortic interposition graft for repair of a type A dissection prompted us to review the computed tomographic (CT) findings in 14 other such patients 5-47 months after surgery. No other case of proximal aortic dissection was identified although dilatation of the aortic root proximal to the graft was present in 8 patients (57%). Persistent dissection distal to the graft in 11 patients (79%) was in keeping with that reported by other workers. Chronic dissection proximal to the surgical repair of a dissection seems a rare although important complication.