Comparison of superoxide dismutase, thiopental, and nimodipine for maintenance of somatosensory evoked responses during aortic cross-clamping and declamping in dogs.

Paraplegia is a potential complication of aortic cross-clamping. The occurrence of this devastating sequela has caused increased interest in the use of somatosensory evoked responses (SER) to monitor spinal cord ischemia during aortic cross-clamping. This study was designed to examine changes in SERs during clamping and declamping of the canine aorta after injection of superoxide dismutase (SOD), thiopental (T), and nimodipine (N). In the control group, cross-clamping the aorta produced an increase in latency and a decrease in amplitude of the SER starting at two minutes. Isoelectric SERs were obtained after 16 minutes of aortic cross-clamping, but recovered with cross-clamp removal. When the aorta was clamped for more than 16 minutes in the control group, the isoelectric SERs obtained were irreversible. After the injection of SOD and T, SER latencies and amplitudes changed to a smaller degree with aortic cross-clamping and did not become isoelectric even after 20 minutes of clamping. During aortic cross-clamp removal in the control group, SERs initially improved and then showed signs of reperfusion ischemia, which disappeared after eight minutes. There were no significant SER changes due to reperfusion when SOD or T or the combination was given prior to aortic cross-clamping. There was no difference in SER changes from the control group during aortic cross-clamping and after release of cross-clamping when N was given. Nimodipine did not alter SER changes from aortic cross-clamping alone. In summary, SOD and T, alone or in combination, protect the spinal cord against ischemia during aortic cross-clamping and declamping.

Superoxide dismutase and hemodynamic changes following aortic crossclamp release.

Release of an aortic crossclamp usually results in hypotension which is mainly due to hypovolemia from sequestration of fluid in the tissues and the release of vasoactive substances (ie, bradykinin, free radicals) that increase capillary permeability. The purpose of this study was to evaluate superoxide dismutase (SOD), a free-radical scavenger, as a pharmacologic technique to prevent hemodynamic changes following aortic crossclamping and release. Fourteen mongrel dogs were studied and divided into two groups. The aorta was clamped for 60 minutes. Group A received NaHCO3, 3.5 mEq/kg, and SOD, 15,000 U/kg; while group B received only NaHCO3, 3.5 mEq/kg, prior to aortic crossclamp release. There was a statistically significant difference in cardiac output, systolic blood pressure, systemic and pulmonary vascular resistances, and arterial oxygen tension between the two groups following aortic crossclamp release. Cardiac output increased from 2.2 +/- .05 to 2.5 +/- .03 L/min (P < .05) after declamping, and returned toward preclamping baseline values after five minutes in group A. In group B, cardiac output decreased from 2.3 +/- .05 to 2.1 +/- .01 (P < .005) after declamping and remained unchanged five minutes later. No statistically significant changes in PaO2 occurred in group A, while there was a significant decrease in PaO2 in group B after crossclamp release. In group B, PaO2 decreased from 95 +/- 7 to 70 +/- 1 mmHg (P < .005) after crossclamp release. Bradykinin levels were almost identical in both groups studied. It is concluded that SOD significantly decreases the cardiovascular changes following aortic crossclamp release.

Pulse oximetry during pulmonary artery banding.

In children with a ventricular septal defect and congestive heart failure, banding of the pulmonary artery (PA) causes equalization of right and left ventricular pressures, reduces the volume of the left-to-right shunt, and diminishes the work of the left ventricle and the engorgement of the pulmonary vessels. However, banding the PA too tightly usually produces hypoxemia by reversing the left-to-right shunt and causes severe hemodynamic changes. A series of 14 infants is reported who underwent PA banding during which a pulse oximeter was used as an early indicator of excessively tight PA banding. Significant hemodynamic changes occurred in eight infants in whom the PA banding was too tight. This consisted of hypotension and bradycardia three to four minutes after the banding. The eight patients also showed significant desaturation of the blood after application of the band, with the arterial hemoglobin saturation (SaO2) dropping from a preband value of 98 +/- 6% to a postband value of 80 +/- 2%. The decrease in SaO2 preceded the hypotension and bradycardia by two to three minutes in all cases. When the band was removed, the hemodynamic and SaO2 changes returned toward baseline. Subsequently, a less tight band was applied; this was associated with a smaller decrease in SaO2, an elevation of blood pressure, and no bradycardia. This was considered to be acceptable banding. The right ventricle/PA pressure gradient significantly decreased after acceptable banding, and a gradient higher than 45 mmHg was usually associated with hypoxemia.

Ventricular fibrillation during general anaesthesia in a seven-year-old patient with mitral valve prolapse.

A case report is presented of a seven-year-old boy who developed ventricular fibrillation during general anaesthesia with atracurium, O2, N2O and halothane, following tracheal intubation for hypospadias revision. He spontaneously defibrillated and the surgery was cancelled. Echocardiography done two days later was normal. The patient returned two weeks later for the same procedure. He developed nodal tachycardia, and premature ventricular contractions, which responded to lidocaine. A second echocardiographic examination done postoperatively while the child was crying showed mitral valve prolapse.