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Introduction

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A 57-year-old man with a 5-year history of hypertension (HTN) presents to the emergency department with the assistance of family. They report progressive confusion and lethargy for 2 days. The patient has not been eating well or taking his home medications for 2 weeks. Home medications include clonidine 0.3 mg three times a day, atenolol 100 mg daily, escitalopram 20 mg daily, and hydrochlorothiazide 25 mg daily. The patient and his family deny any other symptoms including fevers, shortness of breath, slurring, or seizures. His initial vital signs include blood pressure (BP) of 186/104 mm Hg, pulse of 76 bpm, temperature of 36.5°C (97.6°F), and a respiratory rate of 18 breaths/min. He is not hypoxic. Initial neurologic examination and brain computed tomography (CT) do not reveal any motor deficits or acute anatomic abnormality.

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Is uncontrolled hypertension responsible for the patient's acute change in mental status?

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Mental status changes in the setting of poor cerebral blood flow are most often seen with low arterial BP. Cerebral perfusion pressure (CPP), the pressure gradient that influences blood flow to the brain, is the difference between mean arterial pressure (MAP) and intra-cranial pressure (ICP) and is represented by the formula:

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CPP = CBF × CVR

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where CBF is cerebral blood flow and CVR is cerebrovascular resistance.

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Cerebrovascular autoregulation maintains a constant blood flow over a wide range of CPPs. Normally, moderate changes in CPP have little effect on CBF. This is secondary to changes in CVR. An increase in CPP produces vasoconstriction and a decrease produces vasodilation. Typically for adults, CPP ranges between 50 and 100 mm Hg, though some research suggests 70 to 90 mm Hg to be a more accurate number.1,2,3 In chronically hypertensive individuals, the cerebral arterioles develop medial hypertrophy and lose their ability to dilate effectively at lower pressures.4 This can lead to decreased cerebral perfusion when systemic BP falls, even though BP may remain within a range that would provide adequate cerebral perfusion in patients without hypertension.

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The mechanisms governing CBF autoregulation are controversial.5 Most likely, the autoregulatory vessel caliber changes are influenced by arterial smooth muscle and metabolic mechanisms.6,7 Perivascular nerves and the vascular endothelium may also play a role.8,9,10 CBF autoregulation typically operates when mean systemic blood pressure is between 50 and 150 mm Hg2 and can be modulated by sympathetic nervous activity and the renin-angiotensin system (RAS).

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Central nervous system (CNS) trauma or acute ischemic stroke may impair CBF autoregulation, leaving surrounding CNS tissue vulnerable to over- or underperfusion. Likewise, autoregulation may be lost in the setting of a space-occupying brain lesion such as tumor or hematoma.11 Autoregulation may be regained by hyperventilatory hypocapnia.12 Patients with diabetes may have impaired CBF autoregulation, probably due to diabetic microangiopathy.13...

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