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Case

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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 of speech, or seizures. His initial vital signs include blood pressure (BP), 186/104; pulse, 76 bpm; temperature, 97.6°C; and respiratory rate, 18. He is not hypoxic. Initial neurologic examination does not reveal any motor deficits, and brain computed tomography (CT) shows no 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 attributable to arterial BP are most often seen with low, rather than high, BP and are due to impaired cerebral blood flow. Cerebral perfusion pressure (CPP), the pressure gradient that influences blood flow to the brain, is the difference between mean arterial pressure (MAP) and intracranial 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 CPP, due to changes in CVR. Thus, under normal conditions, moderate changes in CPP have little effect on CBF. 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.1-3 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.8-10 CBF autoregulation typically operates when mean systemic BP (SBP) is between 50 and 150 mm Hg and can be modulated by sympathetic nervous activity and the renin-angiotensin system (RAS).2

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

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