Effects of rapid blood pressure reduction on cerebral blood flow

doi:10.1016/0002-8703(86)90585-5

American Heart Journal

Volume 111, Issue 1, January 1986, Pages 226-228

https://doi.org/10.1016/0002-8703(86)90585-5 Get rights and content

Abstract

The changes that occur in the cerebral circulation wiht chronic hypertension are important when considering the therapeutic possibilities in treating patients with severe hypertension. Care must be taken not to lower the blood pressure below the lower limit of autoregulation, no matter what drug is used. In patients with severe, chronic hypertension, blood pressure should be lowered carefully. Rapid blood pressure reduction to a level that is below the lower limit of autoregulation may result in central nervous system dysfunction due to cerebral hypoperfusion. This is especially true in patients with increased intracranial pressure and cerebral edema such as those with hypertensive encephalopathy.

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Citation Excerpt :
Clinical surveillance in a short-stay observation unit is usually appropriate, without the need of hospital admission, and a short-term outpatient visit by hypertension specialist is strongly suggested. The gradual reduction in BP is beneficial, while potential harm may derive from a rapid BP decrease, due to an impairment of coronary, cerebral and renal autoregulation [33–36]. All guidelines recommend against the sublingual administration of nifedipine; the degree of BP decrease cannot be anticipated and often is too fast and larger than desirable [37,38].
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Les complications graves après chirurgie intracrânienne surviennent chez 13 à 27 % des patients. Les causes de ces complications sont multiples mais les modifications hémodynamiques systémiques et cérébrales du réveil jouent très probablement un rôle important pour certaines d'entre elles. D'un point de vue physiologique, le réveil s'accompagne d'une augmentation de la consommation d'oxygène de l'organisme, de la sécrétion de catécholamines, du débit cardiaque, de la pression artérielle et de la fréquence cardiaque. Après craniotomie, en l'absence d'hypothermie, l'augmentation de la consommation d'oxygène est faible, en moyenne inférieure à 20 % de la valeur sous anesthésie. En revanche, les modifications de la pression artérielle sont retrouvées chez 70 à 90 % des patients. Un réveil différé de deux heures après la fin de la chirurgie ne permet pas d'atténuer ces modifications. Au niveau cérébral, l'extubation s'accompagne d'une hyperémie cérébrale avec une augmentation de 60 % des vitesses circulatoires enregistrées au doppler transcrânien. L'esmolol permet d'atténuer ces modifications, qui sont donc probablement liées à l'hyperactivité sympathique du réveil. Les conséquences de cette hyperémie ne sont pas connues mais elle pourrait participer à l'aggravation d'un œdème ou d'une hémorragie cérébrale.
Major complications after intracranial surgery occur in 13–27% of patients. Among multiple causes, haemodynamic and metabolic changes of anaesthesia recovery may be responsible for intracranial complications. Recovery from neurosurgical anaesthesia is followed by an increase in body oxygen consumption and catecholamines concentrations. However, in normothermic patients, theses changes are usually mild and not prevented by a 2-h recovery delay. Systemic hypertension is common after neurosurgery and a link between perioperative hypertension and intracranial haemorrhage has been established. The cerebral consequences of recovery associate cerebral hyperaemia and increased ICP in patients with a tight brain at the end of surgery. Cerebral hyperaemia may promote or exacerbate cerebral haemorrhage or oedema. This has been demonstrated in patients operated for subdural haematoma removal or undergoing carotid surgery. Prevention of hypothermia and pain are key factors to prevent metabolic changes. Beta-blockers seem to be suitable agents to obtain haemodynamic control in neurosurgical patients.
The diagnosis and management of hypertensive crises
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Citation Excerpt :
Similarly, IV hydralazine may result in severe, prolonged, and uncontrolled hypotension, and it is therefore not recommenced. Rapid and uncontrolled reduction of BP may result in cerebral, myocardial, and renal ischemia/infarction.29,30,37 The immediate goal of IV therapy is to reduce the diastolic BP by 10 to 15%, or to about 110 mm Hg.
Severe hypertension is a common clinical problem in the United States, encountered in various clinical settings. Although various terms have been applied to severe hypertension, such as hypertensive crises, emergencies, or urgencies, they are all characterized by acute elevations in BP that may be associated with end-organ damage (hypertensive crisis). The immediate reduction of BP is only required in patients with acute end-organ damage. Hypertension associated with cerebral infarction or intracerebral hemorrhage only rarely requires treatment. While nitroprusside is commonly used to treat severe hypertension, it is an extremely toxic drug that should only be used in rare circumstances. Furthermore, the short-acting calcium channel blocker nifedipine is associated with significant morbidity and should be avoided. Today, a wide range of pharmacologic alternatives are available to the practitioner to control severe hypertension. This article reviews some of the current concepts and common misconceptions in the management of patients with acutely elevated BP.
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1998, Neurologic Clinics
Organ transplantation traces its birth to a landmark operation performed by Murray in Boston in 1954 in which an identical twin received a donated sibling kidney.⁷² Over the decades since that seminal procedure, the field of organ transplantation has grown exponentially, largely fertilized by the advent of ever more powerful and precise immunosuppressive agents. With the increase in organ transplantation, health professionals have seen a considerable number of associated neurologic complications. In some instances, these complications are a function of the individual nature of the transplant surgery, whereas in others, neurologic dysfunction is the result of exposing an ill patient to a prolonged, often difficult operation. Complications may be familiar, such as perioperative encephalopathy or seizure, or they may be unique, such as suture line embolus in lung transplantation.
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Cerebral cortex regional blood flow and tissue oxygen tension during the trigeminal depressor response in rabbits
1997, Journal of the Autonomic Nervous System
The trigeminal depressor response (TDR) is characterized with profound hypotension caused by sympathetic outflow decreases. The purpose of this study was: (1) to compare the hemodynamic changes during acute hypotension induced by the TDR with those induced by electrical stimulation of the vagal nerve (VS) as models of sympathetic inhibition and vagal activation and (2) to investigate the effects of nitrous oxide (N₂O), a well-known sympathomimetic, on the hemodynamic changes during the TDR. Male Japan White rabbits were anesthetized with halothane in oxygen and mechanically ventilated. The electrode pair for the TDR was inserted into the submucosal tissue of the animal's tongue. The pair for the VS was applied to the isolated left vagal trunk. Both the TDR and the VS produced similar decreases in mean arterial pressure (MAP) and cerebral cortex regional blood flow (rCBF), although the decreases in heart rate (HR) and aortic blood flow were greater during the VS. Cerebral cortex tissue oxygen tension in both groups decreased slightly. 50% N₂O, producing MAP elevation and HR decrease, ameliorated the hemodynamic changes including rCBF reduction during the TDR. A sudden diminution of sympathetic tone following noxious stimulation of the orofacial area, as in the case of the TDR, may be a possible trigger mechanism for vasodepressor reactions in dental patients. The sympathomimetic and possible antinociceptive effects of N₂O may explain, at least in part, the preventive effects on vasodepressor reactions during dental procedures.

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Symposium on The Practical Management of Patients With Severe Hypertension and Hypertensive EmergenciesEffects of rapid blood pressure reduction on cerebral blood flow

Abstract

Effects of acutely induced hypertension in cats on pial arteriolar caliber, local cerebral blood flow, and the blood brain barrier

Circ Res

Regulatory responses of cerebral vasculature after sympathetic denervation

Am J Physiol

Effects of decreasing arterial blood pressure on cerebral blood flow in the baboon

Circ Res

Autoregulation of cerebral circulation in hypertension

Acta Neurol Scand

Cerebral blood flow in rats with renal and spontaneous hypertension; resetting of the lower limit of autoregulaton

J Cereb Blood Flow Metab

Autoregulation of brain circulation in severe arterial hypertension

Br Med J

Autoregulation of cerebral blood flow in hypertensive patients. The modifying influence of prolonged antihypertensive treatment on the tolerance to acute, drug-induced hypotension

Circulation

Effect of chronic hypertension on the blood brain barrier

Hypertension

Sympathic nerves protect aganist blood-brain barrier disruption in the spontaneously hypertensive rat

Stroke

Symposium on The Practical Management of Patients With Severe Hypertension and Hypertensive Emergencies
Effects of rapid blood pressure reduction on cerebral blood flow