Circulation
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Comparative Study
Myocardial acidosis associated with CO2 production during cardiac arrest and resuscitation.
Previous studies from our institution demonstrated significant hypercarbic acidosis in the mixed venous (pulmonary artery) blood in animals and human patients during cardiac arrest and cardiopulmonary resuscitation (CPR). In the present study, the acid-base state of the myocardium during cardiac arrest was investigated. Cardiac arrest was electrically induced in 11 pentobarbital-anesthetized and mechanically ventilated domestic pigs. ⋯ The PCO2 in cardiac vein blood was significantly greater than that of mixed venous blood, demonstrating disproportionate myocardial production of CO2 during CPR. Accordingly, it is CO2 production during ischemia that is implicated as the predominant mechanism accounting for myocardial [H+] increases during cardiac arrest. Important clinical implications for buffer therapy during CPR and, in particular, treatment with bicarbonate emerge from these observations.
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Deep-hypothermic cardiopulmonary bypass with selective cerebral perfusion (SCP) was used in 34 consecutive patients with aneurysms involving the aortic arch or the adjacent part of the aorta. The ages ranged from 25 to 79 years (mean, 56 years). Atherosclerotic aneurysms were present in 14 patients, dissecting aortic aneurysms in 16, and other lesion types in four. ⋯ Neurological sequelae occurred in one patient (cerebral infarction), but significant respiratory and hemorrhagic problems were not encountered. For the SCP protocols, we advise that perfusion pressures at bilateral superficial temporal arteries be kept at approximately 50 mm Hg and that venous oxygen saturation of the superior vena caval line or internal jugular vein be kept at above 90%. With appropriate monitoring, this method can be performed in aortic arch or related surgeries with low morbidity results.
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Comparative Study
Effects of cardiopulmonary bypass on cerebral blood flow in neonates, infants, and children.
Cardiopulmonary bypass (CPB) management in neonates, infants, and children requires extensive alterations in temperature, pump flow rate, and perfusion pressure, with occasional periods of circulatory arrest. The effect of these alterations on cerebral blood flow (CBF) are unknown. This study was designed to determine the relation of temperature and mean arterial pressure to CBF during hypothermic CPB (18 degrees-32 degrees C), with and without periods of total circulatory arrest. ⋯ In group C, no significant increase in CBF was observed during rewarming after total circulatory arrest (32 +/- 12 minutes) or after weaning from CPB. During moderate-hypothermic CPB (25 degrees-32 degrees C), there was no association between CBF and mean arterial pressure. However, during deep-hypothermic CPB (18 degrees-22 degrees C), there was an association between CBF and mean arterial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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Comparative Study
Organ blood flow and somatosensory-evoked potentials during and after cardiopulmonary resuscitation with epinephrine or phenylephrine.
Pure alpha-adrenergic agonists, such as phenylephrine, and mixed alpha- and beta-adrenergic agonists, such as epinephrine, raise perfusion pressure for heart and brain during cardiopulmonary resuscitation (CPR). However, with the high doses used during CPR, these drugs may directly affect vascular smooth muscle and metabolism in brain and heart. We determined whether at equivalent perfusion pressure, continuous infusion of phenylephrine (20 micrograms/kg/min) or epinephrine (4 micrograms/kg/min) leads to equal organ blood flow, cerebral O2 uptake, and cerebral electrophysiologic function. ⋯ During CPR and at 2 hours after resuscitation, there were no differences between drug groups in the level of regional cerebral or coronary blood flow, cerebral O2 uptake, or evoked potentials. Therefore, with minimal delay in the onset of CPR and with equipotent pressor doses of phenylephrine and epinephrine, we found no evidence that one agent provides superior coronary or cerebral blood flow or that epinephrine by virtue of its beta-adrenergic properties adversely stimulates cerebral metabolism at a critical time that would impair brain electrophysiologic function. Moreover, epinephrine did not preferentially impair subendocardial blood flow as might be expected if it enhanced the strength of fibrillatory contractions.
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Little is known regarding specific biologic and pharmacologic differences between human internal mammary arteries and saphenous veins. To better define the role of alpha-adrenoceptor-mediated vasoconstriction in human internal mammary arteries and saphenous veins, we obtained fresh specimens of both vessels from 32 patients undergoing coronary artery bypass surgery. Dose-response curves were generated for the relatively selective alpha 1-receptor agonist phenylephrine, the alpha 2-receptor agonist BHT-920, and the alpha 1- and alpha 2-receptor agonist norepinephrine. ⋯ Dose-response curves for phenylephrine and BHT-920 were shifted to the right for both vessels in the presence of the alpha 1-receptor antagonist prazosin and the alpha 2-receptor antagonist yohimbine, respectively. Norepinephrine elicited contraction at a lower concentration in saphenous veins than in internal mammary arteries with a mean EC50 of 7.8 X 10(-8) M for saphenous veins and a mean EC50 of 3.4 X 10(-7) M for internal mammary arteries (p less than 0.05). The results suggest that alpha-adrenoceptor-mediated vasoconstriction is caused primarily by alpha 1-receptors in human internal mammary arteries and by alpha 1- and alpha 2-receptors in human saphenous veins.