Treatment of low output after cardiac surgery.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to D M Behrendt.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Epicardial and left ventricular endocardial activation were assessed in 5 patients (aged 4 months to 9.5 years) with endocardial cushion defect (ECD) during surgical repair. Epicardial activation was recorded from 40 to 47 sites over the epicardium; left ventricular endocardial activation was measured at 3 sites immediately after institution of cardiopulmonary bypass. Compared with the reported activation sequence in normal hearts, the pattern of excitation in hearts of patients with ECD was abnormal; epicardial excitation began at the left ventricular diaphragmatic surface and spread laterally and anteriorly over the anterobasal left ventricle. It then merged with right ventricular wavefronts ending along the right ventricular anterior atrioventricular groove and outflow tract. Left ventricular endocardial activation also occurred earliest in the diaphragmatic segment of the left ventricle with later wavefronts recorded laterally and anteriorly. This study demonstrates, for the first time in human subjects, correlation between left ventricular epicardial and endocardial activation in patients with ECD. The data indicate that earliest endocardial and epicardial activation occurs at the left ventricular diaphragmatic segments of the heart, and are consistent with the known posterior and inferior displacement of the specialized atrioventricular conduction system in patients with ECD.
Explore the source record for details and available documents.
After obtaining samples at open heart surgery, serum and right atrial digoxin concentrations were measured in 25 children by a nonspecific, direct radioimmunoassay method (NS) and by a specific method in which digoxin was separated from its metabolites by HPLC before radioimmunoassay was applied to the digoxin fraction (S). Digoxin was detectable by S assay (sensitivity 0.1 ng/g) in 16 heart specimens and 22 serum samples. The mean and range of the S/NS ratio was 0.74 (0.23 to 2.63) for serum and 0.81 (0.068 to 1.38) for atrial tissue. By NS assay the mean and range of the atrial/serum ratio was 78.1 (2.4 to 340, n = 21) and by S assay the corresponding values were 100 (10.7 to 318, n = 15). A multiple linear regression indicated that 72.5% of the variance of the heart digoxin concentrations measured by S assay were accounted for by the variables height, body weight, daily digoxin dose before operation, plasma digoxin concentration by S assay, and BUN.
The degradation of adenine nucleotide levels and impairment of functional recovery associated with exposure to hypothermic (20 degrees C) cardioplegia was studied in 84 isolated working rat hearts. After a 1-hour control period, hearts were exposed to 1 hour of cardioplegia that consisted of increasingly longer periods of cardioplegic solution (CPS) infusion (30 seconds and 10, 30 and 60 minutes), followed by increasingly shorter periods of global ischemia (591/2 minutes and 50, 30 and 0 minutes). Hearts were then reperfused for 1 hour with control perfusate, during which recovery of cardiac output was monitored. Additional hearts were freeze-clamped at various points in the protocols to determine adenine nucleotide levels (ATP, ADP, AMP and their sum TAN). Exposure to increasingly longer periods of CPS perfusion resulted in proportionally greater degradation of nucleotides and poorer recovery of cardiac output. Addition of inosine to the recovery perfusate as well as the CPS further improved nucleotide levels and recovery of cardiac output. These results suggest that washout of nucleotide degradation products in the CPS or reperfusion prevents their salvage for nucleotide resynthesis and impairs functional recovery from cardioplegia.
A 15-year-old girl was found to have severe liver fibrosis on liver biopsy at the time of cholecystectomy, 5 1/2 years following a modified Fontan procedure (right atrial-right ventricular conduit) for tricuspid atresia. Postoperative right atrial pressures were consistently elevated above 13 mm Hg and this, in part, may have been due to progressive mild conduit stenosis. Because of increasing symptoms, the patient underwent successful revision of the conduit at the age of 15 years. It is suggested that sustained systemic venous hypertension caused the striking morphologic changes in the liver and that this serious complication may significantly affect the long-term prognosis of patients surviving the Fontan procedure.
To examine the excitation of the double chamber right ventricle and the possibility that it results from a displaced, hypertrophied moderator band, seven patients with double chamber right ventricle were studied. All seven had pre- and postoperative electrocardiograms. Intraoperative right ventricular epicardial maps were obtained in three; right ventricular endocardial activation maps performed at postoperative catheterization were obtained in four. In the three patients studied at operation the breakthrough point of right ventricular epicardial activation was demonstrated in a normal inferior location well below the obstructing muscle band. Two patients with right bundle branch block after operation and two others with only right ventricular conduction delay on postoperative electrocardiogram demonstrated high normal right ventricular time with prolongation of activation in the right ventricular outflow or inflow region, or both, suggesting only peripheral injury. These data suggest that activation of the double chamber right ventricle is similar to that of the normal heart. In addition, the observed normal activation sequence militates against the hypothesis that the moderator band is the obstructing bundle.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
We studied the effectiveness of a computer program based on a mathematic model of warfarin dynamics in assisting with the initial phases of anticoagulation. In retrospective evaluations the program was successful in predicting prothrombin complex activity (PCA) responses for three different groups of subjects, indicating that the model is a good representation of the physiologic system. In a prospective evaluation of the program a computer-assisted group of 10 patients was compared with a control of 10 patients who did not receive computer assistance. Because of the program's very conservative upper limits for warfarin dosage in the first few days of therapy, the computer-assisted patient require slightly more time (6 days), on the average, to first reach PCA values in the 20% to 30% therapeutic range than did the control patients (4.8 days). After the desired PCA had been achieved, however, the computer-assisted group remained within the therapeutic range for 83% of the time compared to only 60% for the control group. This difference was due primarily to much less overanticoagulation of the computer-assisted patients than of the controls.
Ventricular pacing was performed in forty-one children ranging from one day to twenty years of age (median age = 10). Weight of the recipient at implant ranged from 2 kg. to 86 kg. Indications included presyncope, syncope, dyspnea on exertion, congestive heart failure, postoperative infra-Hisian heart block, and inadequate cardiac rate during pharmacotherapy. Four patients died during follow-up, but no deaths were attributable to pacemaker management. In contrast, 66% of the patients required more than one pacemaker related-operative procedure, and 43% of leads implanted failed by 48 hours. Indications for permanent cardiac pacing in this population at this time are symptomatic congenital AV block, symptomatic sinus node disease, and AV block in the postoperative period. Technological developments which might reduce complications seen in this population and electrophysiologic techniques which may better define indications for pacing in children are also reviewed.
During a 31/2 year period, 11 consecutive infants with total anomalous pulmonary venous connection younger than 6 months of age underwent repair at our institution. Early mortality was 19% (one of 11) and long-term mortality 18% (two of 11), yielding an overall survival of 73%. One late death was due to bradyarrhythmia and the other was due to recurrent pulmonary venous obstruction. Postoperative catheterization in seven of eight survivors and in three additional patients disclosed normal or nearly normal pulmonary artery pressure and pulmonary arteriolar resistance. Left ventricular diastolic volume was normal before operation (n = 5) and on follow-up study (n = 9). Mild left ventricular outflow obstruction or coarctation or both developed during follow-up in two patients. Sinus node function was normal in all seven late survivors studied, and atrioventricular conduction was normal in three of four. This experience indicates that total anomalous pulmonary venous connection can be repaired early in infancy, with preservation of normal hemodynamics and electrophysiologic state.
Successful correction of truncus arteriosus in two neonates, both 4 days of age, is described. Nonvalved polytetrafluoroethylene (PTFE) conduits were used because of the small size of the infants. Both recovered from operation with no signs right ventricular failure and remain well. Catheterization data on one patient show satisfactory hemodynamics 1 year after operation with only residual branch pulmonary artery stenosis. These data suggest that a conduit valve is not essential in the correction of truncus arteriosus even in the neonate.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.