Journal of neurosurgical anesthesiology
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J Neurosurg Anesthesiol · Oct 1992
End-tidal carbon dioxide as an indicator of arterial carbon dioxide in neurointensive care patients.
The relationship between the arterial partial pressure of carbon dioxide (Paco2) and the end-tidal carbon dioxide partial pressure (PEtco2) was evaluated in 11 critically ill adult neurointensive care patients during mechanical ventilation. It was hypothesized that the Paco2 to PEtco2 gradient, or P(a-Et)co2, was maintained and that PEtco2 can be used to determine Paco2 accurately in these patients. After approval by the Clinical Investigations Committee, when clinically indicated arterial blood gases (with Paco2) were measured, the PEtco2 was determined from the capnograph (Hewlett Packard 78520A infrared capnometer). ⋯ The direction of Paco2 change was inaccurately predicted by PEtco2 changes in 31.9% of measurements. PEtco2 does not provide a stable reflection of Paco2 in all neurointensive care patients. Arterial blood gases cannot be eliminated when monitoring respiratory acid-base balance in mechanically ventilated neurointensive care patients.
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J Neurosurg Anesthesiol · Jul 1992
Cerebral blood flow at constant cerebral perfusion pressure but changing arterial and intracranial pressure: relationship to autoregulation.
Therapeutic agents for reducing raised intracranial pressure (ICP) may do so at the expense of reduced mean arterial pressure (MAP). As a consequence, cerebral perfusion pressure (CPP) = (MAP - ICP) may not improve. It is unknown whether the level of MAP alters cerebral blood flow (CBF) when MAP and ICP change in parallel so that CPP remains constant. ⋯ At a CPP of 40 mm Hg, CBF showed a linear correlation with blood pressure (BP) (r = 0.57, p <0.05). These results demonstrate that when autoregulation is impaired, there is a functional difference between autoregulating and nonautoregulating cerebral vessels despite similar MAP and CPP. These results also show that at a CPP of 40 mm Hg when autoregulation is impaired, CBF depends more on arterial driving pressure than on CPP.
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J Neurosurg Anesthesiol · Apr 1992
Autoregulation of cerebral blood flow in response to adenosine-induced hypotension in dogs.
During induced hypotension for surgical procedures, cerebral blood flow (CBF) autoregulation and cerebrovascular responsivity to CO2 may be impaired-changes that appear to be agent-specific. Adenosine is a potent endogenous systemic vasodilator and has been investigated as a hypotensive agent. In this study in dogs we investigated cerebral vascular responses to graded decreases of cerebral perfusion pressure (CPP) (100%, 60%, 45%, and 35% of control CPP) during normocapnia (PaCO2 = 37 mm Hg) and hypocapnia (PaCO2 = 21 mm Hg). ⋯ CBF was significantly greater during normocapnia compared with hypocapnia at all levels of CPP, except at 35% of control when the values were similar. Cerebral metabolic rate was unchanged throughout the study. We conclude that neither CBF nor CO2 responsivity is appreciably altered during adenosine-induced hypotension when GPP remains above the lower limit of autoregulation of CBF.
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J Neurosurg Anesthesiol · Apr 1992
Electroencephalogram, cerebral metabolic, and vascular responses to propofol anesthesia in dogs.
Previous studies on the cerebral effects of propofol report conflicting results regarding the cerebral metabolic rate for oxygen (CMRO2), cerebral blood flow (CBF), autoregulation of CBF, intracranial pressure, and cerebral perfusion pressure (CPP). The present studies were designed to examine these issues as well as propofol effects on the CBF responses to hypocapnia and on the electroencephalogram (EEG) in a well-known canine model that permits continuous determination of EEG activity, CMRO2, CBF, and cerebrospinal fluid (CSF) pressure. Dogs were studied at normocapnia (n = 6) and at hypocapnia (n = 6) during three doses of propofol (12, 24, and 48 mg kg(-1) h(-1)) and during a combination of propofol and elevated (20-25 mm Hg) CSF pressure. ⋯ The authors conclude that low and moderate doses of propofol decrease EEG activity and CMRO2, causing an associated decrease of CBF and CSF pressure. Autoregulation of CBF and cerebral vascular CO2 reactivity are preserved at these propofol doses. In contrast, high dose propofol significantly decreases CPP, resulting in impaired autoregulation of CBF.