Pediatric sedation: short-term effects.

A prospective investigation on the short-term effects of various sedation regimens on 549 nonhospitalized magnetic resonance (MR) patients was performed. The drugs evaluated were chloral hydrate, pentobarbital, midazolam, and diazepam (fentanyl was used for enhancement after any of these drugs). The overall safety and efficacy were quite good with all the regimens. Overall, 84% of children slept less than 8 h after the examination, 90% were drowsy and/or unsteady for less than 8 h after they awoke, and 97% resumed their usual activities by 24 h. Significant hyperactivity was seen only with pentobarbital and occurred in 8.4% of children over 8 years of age. The multiple-dose regimen of pentobarbital and fentanyl had a significant short-term effect on the children less than 8 years of age, with 35% sleeping longer than 8 h after the MR. Ten children who had needed the multiple-dose pentobarbital regimen or who had failed prior pentobarbital sedation presented for repeat sedation. Midazolam was effective in 9 of these 10 children.

Mathematical simulation of cerebral blood flow in focal ischemia.

A computer model was developed to describe regional cerebral blood flow and tissue oxygenation with autoregulation during focal ischemia produced by occlusion of th middle cerebral artery (MCA). This steady state model described the distribution of blood flow in the cerebral arterial system including the circle of Willis as well as the pial arterial anastomoses, and included a simplified form of autoregulation based on the local control of pressure and flow in the pial and intracerebral arteries, respectively. Preliminary simulation studies with the model yielded the following results. Less effective autoregulation was predicted by the model at low blood pressure in focal ischemia. Passive dilatation of the pial vasculature produced a leftward shift in the autoregulatory curve. Simulations with occlusion of the MCA revealed the ultimate importance of the pial anastomoses in providing adequate blood and oxygen supply in the ischemic territories including the specially vulnerable lenticulostriate area. The volume of the ischemic (pO2 less than 1 mmHg) brain tissue in the MCA-cortex estimated by using a concurrent Krogh cylinder model was 50% when the pial anastomoses were 80 micrometers in diameter and the ischemic area disappeared at 170 micrometers diameter. With relatively small anastomoses (less than 200 m) the model demonstrated intracerebral steal during intracerebral vasodilation. Passive dilation of the pial arteries including the pial anastomoses caused the steal to disappear and to reverse. These results suggest that both autoregulatory shift and steal reversal can be explained by passive dilatation of the pial vasculature.

A critical evaluation of oxygen disappearance during stop flow in the gerbil brain.

The rate of oxygen disappearance from the gerbil cerebral cortex was measured during bilateral carotid artery occlusion with an oxygen microelectrode at normal tissue PO2 and under hyperbaric oxygenation. The oxygen disappearance rate (ODR) was found to be heavily dependent on the PO2 at occlusion due to the desaturation of hemoglobin-bound oxygen. When the tissue PO2 was elevated to a level high enough to saturate hemoglobin, the ODR reflected the oxygen consumption rate which was calculated to range from 1.6-7.4 cc O2/100 cc tissue-min. for ten barbiturate-anesthetized animals. The fall in PO2 was found not to be totally linear to zero in many cases, but instead consisted of a linear phase followed by a period of decreasing slope. We believe this phase of changing slope represents a diminishing oxygen consumption rate. The exact nature of this decrease is not known but perhaps is an inhibitory response to the accumulation of metabolites as a result of the circulation arrest.

Experimental and theoretical analysis of oxygen transport in fetal brain.

Based on the results obtained in this study and the results of others it seems safe to conclude the following: 1) Fetal brain PO2 values are considerably lower than those found in adult brain. 2) Administration of 100% oxygen to the mother can (but not always) significantly raise the PO2 at a specific point in the fetal cortex. 3) The response of fetal brain PO2 to changes in maternal arterial PO2 is delayed by a finite quantity of time of the order of magnitude of 38 seconds. 4) The time required for the fetal brain PO2 to reach a minimum following a decrease in the PO2 of maternal arterial blood coincides closely with the time required for the maternal arterial PO2 to reach its minimum plus the pure transport delay time (38 seconds). 5) The fetus has available a control mechanism which acts to compensate for periods of reduced PO2 in the microenvironment of the fetal cortex.