The Journal of thoracic and cardiovascular surgery
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J. Thorac. Cardiovasc. Surg. · Nov 1993
Cerebral vascular reactivity to carbon dioxide before and after cardiopulmonary bypass in children with congenital heart disease.
We examined cerebral vascular reactivity to carbon dioxide before and after cardiopulmonary bypass in 15 pediatric patients aged 2 to 9 years undergoing cardiac operations. Cerebral vascular reactivity was noninvasively assessed by transcranial Doppler ultrasonography. The cerebral blood flow velocity was plotted as a function of arterial carbon dioxide partial pressure. ⋯ For the entire series, we obtained best-fit curves of y = 2.8e0.046x (r = 0.91) and y = 3.4e0.031x (r = 0.89) (x; arterial carbon dioxide partial pressure, y; percent changes of cerebral blood flow velocity) before and after cardiopulmonary bypass. We conclude that the cerebral vascular reactivity to carbon dioxide was preserved before and after cardiopulmonary bypass in children undergoing cardiac operations. These results suggest that cerebral perfusion before and after cardiopulmonary bypass is not critically compromised.
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J. Thorac. Cardiovasc. Surg. · Nov 1993
Correction of total anomalous pulmonary venous connection in infancy.
From January 1985 through January 1993, 41 patients less than 1 year of age underwent operative correction of isolated total anomalous pulmonary venous connection. There were 24 boys and 17 girls. The median age at operation was 13 days (range 1 to 282 days) and weight was 3.6 kg (2.5 to 5.2 kg). ⋯ All other patients are alive and well with a mean follow-up of 26 months (range 3 to 77 months). One patient required two subsequent reoperations for persistent pulmonary venous obstruction, and another patient had superior vena cava obstruction necessitating reoperation. Operative treatment of total anomalous pulmonary venous connection in infants can be performed with low mortality and an infrequent need for reoperations.
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J. Thorac. Cardiovasc. Surg. · Oct 1993
Comparative StudyRecovery of cerebral blood flow and energy state in piglets after hypothermic circulatory arrest versus recovery after low-flow bypass.
A miniature piglet model that replicates clinical hypothermic (14 degrees C nasopharyngeal) circulatory arrest and low-flow (50 ml/kg per minute) bypass was used to study carotid blood flow with electromagnetic flow probe, cerebral blood flow by microsphere injection, cerebral metabolic rate by arteriovenous oxygen and glucose extractions, lactate production by cerebral arteriovenous difference, and cerebral edema. Data from five animals that underwent circulatory arrest and five animals that underwent low-flow bypass (aged 28.8 +/- 0.4 [mean +/- standard error of the mean] days) were analyzed. The duration of circulatory arrest and low-flow bypass was 1 hour. ⋯ After 3 hours of normothermic reperfusion, phosphocreatine and adenosine triphosphate recovered to 98.6% +/- 9.0% and 90.1% +/- 13.5% of baseline, respectively, and pH was 7.087 +/- 0.051, similar to baseline (7.1755 +/- 0.041). In the low-flow bypass group, the disparity between the depressed level of cerebral oxygen consumption and normal high-energy phosphate levels may reflect incomplete cerebral rewarming or decreased energy consumption. In the circulatory arrest group, the parallel recovery of oxygen consumption and high-energy phosphates eventually achieving baseline levels suggests that the degree of hypothermia used provides adequate protection for acute cerebral recovery after 1 hour of circulatory arrest.(ABSTRACT TRUNCATED AT 400 WORDS)
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J. Thorac. Cardiovasc. Surg. · Oct 1993
Contracture of the newborn myocardium after prolonged prearrest cooling.
Profound hypothermic circulatory arrest is frequently used to facilitate the surgical repair of congenital heart defects in neonates. Deep hypothermia is achieved by a period of core systemic cooling during cardiopulmonary bypass before cardioplegic arrest. There have been conflicting reports with respect to the consequence of perfusing a nonarrested newborn heart under hypothermic conditions. ⋯ These results suggest that prolonged cold perfusion of the nonarrested newborn heart impairs functional recovery and is therefore detrimental. When followed by a period of ischemic arrest, it further potentiates the myocardial injury and induces severe contracture. This preceding adverse effect of prolonged myocardial cold perfusion before cardiac arrest may, in part, explain the suboptimal protective effect of cardioplegia in neonates.