v' Measurements of cerebral blood flow (CBF), mean intraventricular pressure (MIVP), CSF acid-base status, and tests of autoregulation and CO2 reactivity of 43 patients were made at varying times after severe closed head injury. There was a distinct hyperemia or "luxury perfusion" in the acute phase of 1 to 14 days, followed by recovery to normal or below normal values. Metabolic CSF acidosis was found with hyperemia and probably reflected severe, diffuse cortical injury. Distinct regional CBF abnormalities, either ischemic or hyperemic, were only observed in regions of focal pathology. Severe ischemia, hyperemia, persistent elevation of MIVP, or generalized "vasoparalysis" indicated an unfavorable prognosis. Autoregulation was impaired and CO2 reactivity was reduced after injury, but both had usually returned to normal by 14 days.
Abstract:A Paradoxical Cerebral Hemodynamic Effect of Hydralazine• Hydralazine is shown to have a very complex cerebral hemodynamic effect. It raises the intracranial pressure which, together with its effect upon systemic blood pressure, reduces the cerebral perfusion pressure. In spite of this and a concomitantly induced hyperventilation by hydralazine, CBF increases with some delay. The conclusion is that hydralazine is a cerebral vasodilator acting immediately upon cerebral capacitance vessels but later upon the resistance vessels as well. Additional Key Wordsregional cerebral blood flow intracranial pressure cerebral capacitance vessels cerebral resistance vessels• Hydralazine has a widespread use in treatment of arterial hypertension and especially in treatment of acute hypertensive encephalopathy. Little is known about the cerebral hemodynamic effect of the drug and nothing about its effect upon intracranial pressure, which probably plays an important role in the pathogenesis of acute hypertensive encephalopathy.On this background we studied the effect of hydralazine in a series of patients where monitoring of the intraventricular pressure (MIVP) was clinically indicated. MethodsRegional cerebral blood flow (rCBF) was measured in 35 areas of the hemisphere by the 133 Xe intra-arterial injection method.1 During each measurement an arterial blood sample was drawn for determination of carbon dioxide tension (Pacoj) using a Severinghaus electrode. The arterial blood pressure (MABP) was measured intra-arterially using an electromanometer connected to the carotid catheter. The logarithmically displayed clearance curves were used for evaluation of regional differences in flow. In the normal brain these curves are linear and it is then possible to calculate rCBF inltln i quantitatively. In damaged brain tissue the two-minute curves are often nicked, and, if so, a more quantitative estimation of flow values is impossible by this method. As this situation occurred in most of the patients in the present series, we preferred to calculate flow from the linearly recorded clearance curves averaging all 35 detectors over ten minutes. The calculation was done by the height over area method. These are the figures given in table 1 and figure 1. The reproducibility by this method is about 5% expressed as the coefficient of variation. 2The intraventricular pressure was measured through a Seletz cannula inserted into a lateral ventricle through a precoronal burr hole. The cannula was connected to an electromanometer (Elema 35) and recorded continuously on a paper writer. Recording included amplitude as well as mean intraventricular pressure (MIVP). Mean arterial pressure *Department of Neurosurgery, The University Hospital, Odense, Denmark. tProfessor, Department of Neurology, Bispebjerg Hospital, Copenhagen, Denmark.(MABP) and MIVP were recorded simultaneously and both registrations were calibrated to the same water column.Autoregulation was tested either by increasing MABP by intravenous (I.V.) infusion of synthetic angiotens...
✓ A series of comatose young patients with head injuries is presented in whom early regional cerebral blood flow (rCBF) is correlated with neurological outcome, and the critical threshold of rCBF compatible with recovery of responsive communicative interaction with the environment is estimated. Within the 1st week following injury, 63 patients had rCBF studies performed with radioactive xenon by the intracarotid bolus-injection technique and 35-channel external counting. A comparison was made between 2724 rCBF values from this group of patients with 381 from nine controls. Surviving patients were followed for 2 years to determine their eventual neurological outcome. When histograms of the frequency distribution of rCBF values were examined, it was evident that there was both a wider spread of rCBF and a shift to the left in all outcome groups. In awake controls, no rCBF values were less than 40 ml/100 gm/min, whereas in comatose patients the threshold for recovery of communicative brain function (with or without neurological deficits) was between 17 and 20 ml/100 gm/min. There was a clear difference, however, between patients who recovered communicative brain function (with or without neurological deficit) and those who did not (dying or surviving in a persistent vegetative state). In the latter two outcome groups, 14.5% of rCBF values were less than 20 ml/100 gm/min, with the highest incidence in those examined within the first few hours of injury. The distribution of ischemic rCBF was mainly in the frontal and parietal lobes. These investigations confirm previous postmortem pathological studies in revealing that cerebral ischemia in the frontoparietal “watershed” areas antemortem is a major factor leading to telencephalic brain death in the early hours after head injury. The pathophysiological mechanisms of this localized ischemia in patients with head injury are not well understood, but probably hemodynamic alterations resulting from increased intracranial pressure are a major factor. The critical threshold for survival of cortical function seems to be similar to that of normal brain, about 17 to 20 ml/100 gm/min.
The effect of althesin 0.5 ml/10 kg on arterial blood pressure, intracranial pressure, cerebral blood flow and oxygen uptake was studied on 19 occasions in 16 patients with varied cerebral pathology. Cerebral blood flow (CBF) was measured using the intracarotid 133xenon method and a 35-channel scintillation detector after cannulation of the internal carotid artery, the internal jugular bulb and the lateral cerebral ventricle. Arterial and intracranial pressures were recorded continuously. Blood gas tensions were measured in simultaneously drawn samples from the internal carotid artery and the jugular bulb. Cerebral oxygen uptake was calculated from the product of CBF and arteriovenous oxygen content difference. Control values were obtained with the patients under a basic general anesthesia, consisting of N2O/O2 pancuronium. The effect of a bolus injection of althesin was then studied 1 and 20 min after the injection. A significant reduction in intracranial pressure, cerebral blood flow and metabolism at 1 min was found to have essentially subsided 20 min after the injection. In patients with focal brain damage, regional flow analysis revealed a paradoxical increase in flow after althesin in the areas corresponding to the focus.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.