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Cerebral blood flow and its pathophysiology in hypertension
1Department of Medicine, Glostrup Hospital, Denmark.
Insights
Antihypertensive treatments generally prevent stroke by adjusting cerebral blood flow (CBF) autoregulation. However, risks of cerebral ischemia exist in specific patient groups, with potential reversibility in younger individuals.
Area of Science:
- Neurology
- Cardiology
- Pharmacology
Background:
- Chronic hypertension shifts cerebral blood flow (CBF) autoregulation, impairing hypotension tolerance.
- Antihypertensive therapy prevents stroke but carries risks in specific clinical scenarios.
Purpose of the Study:
- To analyze the impact of antihypertensive treatments on CBF autoregulation.
- To classify drugs based on their effects on CBF and intracranial pressure.
- To explore the brain's oxygen reserve in relation to hemodynamic changes.
Main Methods:
- Review of existing literature on hypertension, CBF autoregulation, and antihypertensive drug effects.
- Classification of emergency blood pressure-lowering drugs based on cerebral circulation impact.
- Analysis of jugular venous oxygen saturation data.
Main Results:
- Antihypertensive treatment is largely protective against stroke, with risks concentrated in severe hypertension or specific patient populations.
- Drugs affecting CBF and intracranial pressure were categorized into four groups.
- The brain's higher oxygen saturation compared to the heart suggests a greater capacity to tolerate pressure reduction without ischemia.
Conclusions:
- Adaptive changes in CBF autoregulation due to hypertension may be reversible, particularly in younger patients.
- The brain's oxygen reserve may explain why antihypertensive treatment prevents stroke more effectively than myocardial infarction.
- Hypertensive encephalopathy involves autoregulatory failure, leading to increased CBF, blood-brain barrier dysfunction, and edema.
Abstract:
In chronic hypertension, the lower limit of autoregulation of cerebral blood flow (CBF) is shifted towards high blood pressure with a consequent impairment of the tolerance to acute hypotension. Despite this, antihypertensive treatment in the great majority of patients prevents stroke and the risk for treatment-induced cerebral ischemia is only real in a limited number of clinical settings such as malignant hypertension, hypertension in the elderly, and hypertension associated with acute stroke. During long-term treatment adaptive hypertensive changes in CBF autoregulation may be reversible, especially in young patients. Drugs used for emergency lowering of blood pressure may be classified into four groups according to their effect on CBF and intracranial pressure: (1) drugs with no pharmacological action in the cerebral circulation; (2) cerebral vasodilators; (3) alpha-adrenergic and ganglionic blockers; and (4) angiotensin-converting enzyme (ACE) inhibitors. Oxygen saturation in the jugular venous blood is of the order of 60% to 70% and is considerably higher than in the coronary sinus. It is hypothesized that this oxygen reserve enables the brain better than the heart to take hemodynamic advantage of pressure lowering without risking tissue ischemia. This may explain why antihypertensive treatment prevents stroke but not myocardial infarction. Acute hypertensive encephalopathy is probably caused by failure of autoregulatory vasoconstriction with focal or generalized dilatation of small arteries and arterioles. This is associated with a high CBF, dysfunction of the blood-brain barrier, and the formation of brain edema that is thought to cause the clinical symptoms.