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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In patients with neuropathologic processes leading to disturbed cerebrovascular autoregulation, sudden increases in arterial blood pressure may lead to a sudden elevation in cerebral blood flow and intracranial pressure. Therefore, sudden increases in arterial pressure should be assiduously avoided in the perioperative period. Hypertensive episodes may occur at any time during anesthesia, but are more likely to occur (1) during laryngoscopy and intubation, (2) at the time of skin incision, (3) at extubation, and (4) during awakening. In patients with cardiovascular disease, such hypertensive episodes may also cause deterioration of the cardiovascular situation. Catecholamines are the principal mediators of such intraoperative hypertensive reactions. There are 2 options available to the anesthesiologist: (1) attempt to suppress this response after it has occurred, or (2) prevent its occurrence at the outset. Treatment of hypertension often relies on agents that relax vascular smooth muscle. In patients with compromised intracranial compliance, however, cerebral vasodilation must be avoided because it leads to an increase in cerebral blood volume. This, in turn, may raise intracranial pressure and result either in herniation of brain contents or a decrease in cerebral perfusion pressure leading to brain ischemia. Different pharmacologic means of preventing or suppressing such intraoperative hypertensive reactions are reviewed. Many of the drugs reviewed resulted in adverse effects that could preclude their use in patients with reduced intracranial compliance. Alpha- and beta-adrenergic receptor blockers can safely be administered to such patients.
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PMID:Treatment of intraoperative hypertensive emergencies in patients with intracranial disease. 264 55

The neurological recovery and histological changes were studied in monkeys after intermittent postischemic arterial hypertension after 16 min of global brain ischemia. Ischemia was produced with a high pressure (1500 mm Hg) neck tourniquet and systemic arterial hypotension. Intensive care and life support, including monitoring of physiological variables, were provided for 7 days. Postischemia all monkeys were immobilized; ventilation was controlled and mean arterial pressure was maintained between 85--115 mm Hg for the first 48 hours. Immediately postischemia in four monkeys, intermittent arterial hypertension (i.e., 150--190 mm Hg) was induced by norepinephrine infusion for 3--5 min. Hypertensive episodes were repeated at 15, 30, 60, and 120 min postischemia, once every hour for the first 24 hours and once every 2 hours between 24 and 48 hours. Thereafter, the monkeys were allowed to breathe spontaneously. Four control monkeys were similarly treated except that arterial hypertension was not induced. Neurological recovery was evaluated by EEG, intracranial pressure, neurological deficit scoring, and histological examination of the brain after killing on day 7 postischemia. The neurological deficit score (100 % = brain death; 50% = vegetative state; 0% = normal) in control monkeys on day 7 was 17.8 +/- 1.8 (SEM) % compared to 46.3 +/- 6.5% (p less than 0.05) in the hypertension group. EEG recovery was delayed and the postischemic increase in intracranial pressure was prolonged in the hypertension group. Histological damage scores in the brain correlated with neurological deficit scores. Severe intermittent hypertension has a deleterious effect on neurological recovery after global brain ischemia.
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PMID:Augmentation of postischemic brain damage by severe intermittent hypertension. 676 25