Biomedical subjects
Publications and source records attributed to D A Fullerton.
Described is a simple technique to use partial left heart bypass for repair of aortic transection. Left heart bypass may be instituted through the left thoracotomy incision without need for groin dissection or opening of the pericardium.
Respiratory acid-base status has recently been shown to affect pulmonary vascular resistance (PVR) in adults following cardiac surgery. The purpose of this study was to examine what influence cardiopulmonary bypass has on the pulmonary vascular response to changes in respiratory acid-base status. Fifteen consecutive patients undergoing aortocoronary bypass were studied under general anesthesia both before and after cardiopulmonary bypass. Arterial PCO2 was manipulated by the addition of 5 percent carbon dioxide to the breathing circuit. Both before and after bypass, PVR increased significantly as PCO2 rose from 30 mm Hg to 50 mm Hg (p < 0.05). The PVR returned to baseline as PCO2 was returned to 30 mm Hg. These data suggest that increased PVR induced by hypercarbic acidemia is not simply a result of the effects of cardiopulmonary bypass on the pulmonary circulation. Instead, we conclude that respiratory acid-base status is an important determinant of adult PVR. We believe these data may be helpful in the treatment of mechanically ventilated patients, since patients are at particular risk of having abnormalities develop in respiratory acid-base status.
Pulmonary vascular resistance is significantly increased in the transplanted lung. We hypothesized that the ischemic or reperfusion injuries incurred by the transplanted lung may produce pulmonary vasomotor dysfunction, which in turn may produce increased pulmonary vascular resistance. In a dog model of autologous lung transplantation, the purpose of this study was to examine the following mechanisms of pulmonary vasomotor control and to relate each of them to cold ischemia and to reperfusion: (1) endothelium-dependent cyclic guanosine monophosphate-mediated vasorelaxation (response to acetylcholine 10(-6) mol/L), (2) endothelium-independent cyclic guanosine monophosphate-mediated vasorelaxation (response to sodium nitroprusside 10(-6) mol/L), and beta-adrenergic cyclic adenosine monophosphate-mediated vasorelaxation (response to isoproterenol 10(-6) mol/L). Autologous right lung transplantation was performed in five dogs. At each of three times, two third-order pulmonary arteries were dissected from each transplanted lung and studied: control (immediately after harvest), cold ischemia (3 hours in 4 degrees C saline solution), and cold ischemia plus reperfusion (1 hour after lung reimplantation). The vasorelaxing effects of acetylcholine, sodium nitroprusside, and isoproterenol were studied in isolated pulmonary arterial rings, suspended on fine wire tensiometers in individual organ chambers. Statistical analysis was by analysis of variance. Results demonstrated significant dysfunction of beta-adrenergic cyclic adenosine monophosphate-mediated relaxation after cold ischemia alone, and this dysfunction was exacerbated by reperfusion. Endothelium-dependent cyclic guanosine monophosphate-mediated relaxation was not impaired by cold ischemia alone but was significantly impaired by reperfusion. Endothelium-independent cyclic guanosine monophosphate-mediated relaxation was not impaired by cold ischemia or reperfusion. We conclude that cold ischemia and reperfusion each produce different patterns of pulmonary vasomotor dysfunction. Cumulatively, such dysfunction may contribute to increased pulmonary vascular resistance in the transplanted lung.
From September 1979 to July 1991, a total of 163 patients have undergone valved conduit reconstruction of the right ventricular outflow tract when a right ventricle-pulmonary artery connection was absent or right ventricular outflow tract enlargement was required. From September 1979 through October 1984, 24 porcine valved conduits were implanted with an operative mortality of 38% (9/24). There were no early failures, but by 9 years after the operation 9 of 15 survivors (60%) had severe conduit obstruction, which resulted in death in 2 patients and reoperation in 6. From May 1985 to June 1991, 24 patients received cryopreserved aortic allografts to correct congenital anomalies. Operative mortality was 25% (6/24) and, again, early conduit function was good. There were 4 (22%) late deaths that were not related to the aortic allograft. At a mean follow-up of 3.4 years, 11 of the 13 survivors (85%) had allograft calcification and 8 of the 13 (62%) had mild to moderate conduit stenosis or regurgitation, or both; two of them required conduit replacement. Distal anastomotic problems that might have been avoided with bifurcated pulmonary allografts were apparent in 4 (36%) patients. Cryopreserved pulmonary allografts were placed in 115 patients between April 1985 and January 1991, with 18 (16%) operative deaths. Late deaths that were not allograft related occurred in 7 of 97 surviving patients (7%). Six patients (6%) underwent reoperation, 2 because of primary pulmonary allograft failure. The 84 remaining patients are free of symptoms with little or no allograft calcification or echocardiographic evidence of significant conduit stenosis or regurgitation. Experience with porcine valved conduits and aortic and pulmonary allografts suggests that pulmonary allografts are the conduit of choice for right ventricular outflow tract reconstruction.
Disturbances of respiratory acid-base status are common in patients supported with mechanical ventilation of the lungs after cardiac operations. This study was conducted with two protocols. The purpose was to determine whether respiratory acid-base status influences pulmonary vascular resistance in adults after cardiac operations and whether the influence is mediated by hydrogen ion concentration or carbon dioxide tension. Patients were studied while under general anesthesia immediately after aorta-coronary bypass. In the first protocol, with seven patients, arterial carbon dioxide tension was manipulated by the addition of 5% carbon dioxide to the breathing circuit. Pulmonary vascular resistance index was determined as arterial carbon dioxide tension rose from 30 mm Hg to 50 mm Hg and back to 30 mm Hg. In the second protocol, with 10 different patients, hydrogen ion concentration was manipulated by the addition of 0.2N hydrochloric acid, sodium bicarbonate, or both as arterial carbon dioxide tension was held constant. We used analysis of variance for statistical data. The results of the first protocol showed that pulmonary vascular resistance index rose by 44% (p < 0.05) as arterial carbon dioxide tension rose from 30 to 50 mm Hg. The results of the second protocol showed that changes in pulmonary vascular resistance index were parallel to changes in hydrogen ion concentration as arterial carbon dioxide tension was held constant (p < 0.05). These data demonstrate that respiratory acid-base status is an important determinant of pulmonary vascular resistance in the adult after cardiac operations. Furthermore, these data suggest the effect is mediated by hydrogen ion concentration, not carbon dioxide tension.
BACKGROUND: A major hemodynamic feature of adult respiratory distress syndrome is pulmonary hypertension secondary to avid pulmonary vascular smooth muscle constriction. This study was undertaken to study the hypothesis that this pulmonary vasoconstriction may derive from pulmonary vasomotor dysfunction. METHODS: A rat model of acute lung injury was studied after 2 hours of superior mesenteric arterial occlusion followed by 4 hours reperfusion. Lung neutrophil accumulation was assessed by myeloperoxidase assay, and lung leak was assessed by iodine 125-labeled albumin lung/blood ratio. The following mechanisms of pulmonary vascular smooth muscle relaxation were studied in isolated pulmonary arterial rings: (1) endothelial-dependent cyclic guanosine monophosphate-mediated, (2) endothelial-independent cyclic guanosine monophosphate-mediated, (3) beta-adrenergic cyclic adenosine monophosphate-mediated. Control rats underwent sham laparotomy. Statistical analysis was done with unpaired Student t test. RESULTS: Lung myeloperoxidase increased from 6.2 +/- 2 to 42 +/- 5 units/gm (p < 0.05), and 125I-labeled albumin lung/blood ratio increased from 0.028 +/- 0.02 to 0.063 +/- 0.03 (p < 0.05) after mesenteric ischemia-reperfusion. beta-adrenergic cyclic adenosine monophosphate-mediated pulmonary vascular smooth muscle relaxation was dysfunctional in the lung-injured rats (62% +/- 5% relaxation versus 95% +/- 3% in controls) (p < 0.05). CONCLUSIONS: These data suggest a mechanistic imbalance of pulmonary vascular smooth muscle contraction and relaxation in acute lung injury. Such imbalance may contribute to the pulmonary hypertension found in adult respiratory distress syndrome.
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Mortality for interruption of the aortic arch approaches 100% within the first year of life if untreated. Prostaglandin E1 can stabilize the patient's condition in anticipation of surgical palliation, but total repair is required for long-term survival. Successful complete repair of type B interrupted aortic arch, hypoplasia of the left ventricular outflow tract, and ventricular septal defect was possible using a cryopreserved allograft in a child who previously had undergone unusual palliation.
To determine the effect of heart donor and recipient size mismatches in infant and pediatric heart transplantation, we studied all 69 patients (age 1 day to 11 years) having 71 orthotopic heart transplants from 1985 to 1989. Patients were divided into three groups based on donor to recipient weight ratios. Group I comprised 13 heart transplants with a donor to recipient weight ratio less than 0.95 (mean 0.81, range 0.48 to 0.94); group II comprised 29 heart transplants with a weight ratio between 0.95 and 1.60 (mean 1.28); and group III had 27 heart transplants with weight ratios greater than 1.60 (mean 2.2, range 1.61 to 3.09). All chests were closed primarily. The cardiothoracic ratio by chest radiography was significantly larger in group III (p = 0.0002); 75% of group III patients had periods of lobar or complete lung collapse by chest radiography compared with 28% of group II and 19% of group I patients (p < 0.05). Despite this, there was no difference in the number of days of ventilator support for any group (p = 0.92). There was no difference in graft ischemic time or inotropic drug use among groups, nor were differences found in the cardiac systolic function parameters of left ventricular preejection time (p = 0.975), left ventricular ejection time (p = 0.975), left ventricular fiber shortening (p = 0.97), and left ventricular fractional shortening (p = 0.596). Thus despite a high incidence of transient lobar or complete lung collapse in high donor to recipient weight ratio transplants, large donor heart size produces very little clinical impairment in recipient lung function. Size mismatches do not influence cardiac systolic function. Overall, large size mismatches appear to be very well tolerated in infant and pediatric heart transplantation.
We describe a technique to repair the torn, friable right atriotomy cannulation site. It results in a tension-free, hemostatic repair.
The Bezold-Jarisch reflex is an inhibitory reflex that originates from the heart, is mediated by the vagus nerve, and is manifested by hypotension and bradycardia. We present 4 pediatric cardiac surgical patients, aged 1 day to 9 months, who exhibited cardiovascular collapse in their early postoperative course. In each patient, cardiovascular deterioration was marked by an insidious decrease in arterial blood pressure without an associated change in heart rate, central venous pressure, or airway pressure. Bradycardia followed the decrease in blood pressure. The Bezold-Jarisch reflex was suspected and atropine was administered, first as a bolus injection at 0.01 mg/kg, and later, as a continuous infusion at 0.01 mg.kg-1.h-1. Atropine prevented recurrent episodes of hypotension and bradycardia. We believe the Bezold-Jarisch reflex is more prevalent than previously suspected in postoperative pediatric cardiac surgical patients.
A two-part experiment was designed to test the hypothesis that myocardial oxygen and carbon dioxide tensions, as measured by coronary venous oxygen and carbon dioxide tensions, determine coronary blood flow during increases in myocardial oxygen consumption. The left main coronary artery was pump-perfused at constant pressure in closed-chest, anesthetized dogs. Oxygenators in the perfusion circuit permitted control of coronary arterial gas tensions. The steady-state relation between coronary venous oxygen and carbon dioxide tensions and coronary flow at a constant myocardial oxygen consumption was determined by locally altering coronary arterial oxygen and carbon dioxide tensions. Values of coronary venous oxygen and carbon dioxide tensions and coronary flow were also obtained at normal coronary arterial gas tensions during pacing-induced increases in myocardial oxygen consumption. The data yielded a hyperbolic relation among coronary venous oxygen and carbon dioxide tension and coronary flow during constant myocardial metabolism, suggesting a synergistic interaction between myocardial oxygen and carbon dioxide tensions in determining coronary flow. This relation was then used to predict the coronary flow change during pacing-induced increases in myocardial metabolism. Approximately 40% of the flow response during pacing-induced increases in myocardial oxygen consumption was predicted. In conclusion, coronary venous oxygen and carbon dioxide tensions synergistically interact to produce steady-state changes in coronary flow at a constant myocardial oxygen consumption. Changes in myocardial oxygen and carbon dioxide tensions can account for about 40% of the change in coronary flow during moderate changes in myocardial oxygen consumption.
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The risks of homologous blood transfusion are well known. Herein, we describe the successful preoperative use of human recombinant erythropoietin to correct severe anemia in a patient refusing transfusion. This case report emphasizes the important perioperative role human recombinant erythropoietin may play in the future.
A retrospective chart review was conducted to examine risk factors associated with the occurrence of choreoathetosis, a rare but significant complication of open-heart surgery in children. Ten children were identified as having developed choreoathetosis after cardiac surgery. Their charts were reviewed and compared with 33 age- and diagnosis-matched controls who underwent open-heart surgery during the same time period. Children with choreoathetosis reached lower rectal and esophageal temperatures (p = 0.0018 for both) and spent a greater portion of total bypass time at lower rectal and esophageal temperatures (p < 0.001 for both). Duration of cooling below 20 degrees C esophageal temperature and PaCO2 at the end of the cooling period were significant predictors of choreoathetosis (p = 0.023 and p = 0.0497, respectively) in a logistic regression model, and a greater fraction of choreoathetosis patients had prior developmental delays (p = 0.017). No difference was found in the age at surgery, duration of bypass, aortic cross-clamp time, arterial pH, PaCO2 or mean arterial pressure. The combination of extended exposure to profound hypothermia and alpha-stat pH management strategy and preexisting developmental delay are associated with the development of choreoathetosis following open-heart surgery 61 in children.
Heart transplantation uniquely offers infants with irreversible myopathies and complex congenital heart disease (CCHD) the potential for survival. Heart transplantation in the first year of life has an actuarial 1-year survival rate of 85%. Controlling for the variables that lead to perioperative death can improve 1-year survival rates to 95%. Mortality is also accrued before transplantation, with 15% to 20% of infants dying before a donor organ is available. Because of this cumulative mortality, an algorithm was developed to maximize pre- and posttransplantation survival and thus increase the likelihood that the limited donor supply would have the greatest impact. The risk factors considered in the algorithm include: (1) hemodynamic stability, (2) central venous access/prostaglandin requirements, (3) need for ventilator support, (4) pulmonary blood flow dependent on a critically restricted atrial septal defect, (5) risk for pulmonary hypertension, (6) anomalous pulmonary venous return, and (7) history of sepsis. Overall, patient survival would be maximized by only using transplantation for patients with CCHD who have moderate or less risk of pre- or posttransplantation death (< 20%). Donor organ utilization could be maximized by reserving transplantation for patients without options (myopathies) and for patients with CCHD who have a low predicted risk of death (< 10%). Because the risks of death at transplantation or in the first year after transplantation are low and relatively fixed, changes in risks of palliative surgery or donor availability can be easily used to adjust the decision algorithm.
Ninety-one infants and children, aged 0 days to 12 years, who received 93 hearts from donors aged 2 days to 24 years between November 1985 and September 1990 were retrospectively studied. Forty-three children were less than 1 month of age; 31 children were between 1 month and 6 months of age, and 19 children were between 6 months and 12 years of age. The donor heart ischemic time ranged from 51 minutes to 8 hours 17 minutes (mean, 4 hours 2 minutes). Fifty-one hearts had an ischemic time of less than 4 hours (group 1), and 42 hearts, more than 4 hours (group 2). No significant difference was noted in the age of donor or recipient or in donor/recipient weight ratio. No correlation was found between ischemic time and number of primary graft failures between groups. Inotropic support was required for 3.9 +/- 3.3 and 5.2 +/- 3.7 days for group 1 versus group 2 (not significant). Ventilator status was the same between the groups. A significant decrease of posterior wall movement in diastole (p < 0.01) occurred among patients of group 2 at 1 week after transplantation, but no difference was found between groups at 2 weeks, 1 month, and 3 months after operation. Posterior wall movement of group 2 heart grafts recovered completely by week 2. No difference was noted in the fractional shortening between the groups; but in both groups, fractional shortening significantly increased from week 1 to week 2. We conclude that ischemic times up to nearly 8 1/2 hours are well tolerated by donor hearts used in pediatric transplantation.