Hypertension

Published on 07/03/2015 by admin

Filed under Critical Care Medicine

Last modified 22/04/2025

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Chapter 41 Hypertension

13 Why is BP elevated in patients with CVA?

Patients with CVA often have a severe increase in BP potentially resulting from a central mechanism and/or compensatory increase in response to increased intracranial pressure. Stress responses to hospitalization, headache, urinary retention, or concomitant infection may lead to abnormal autonomic activity and raised levels of circulating catecholamines. Greater than 60% of patients with CVA will have an acute hypertensive response.

The primary cause is damage or compression of specific regions in the brain that mediate autonomic control. Increased sympathoadrenal tone and subsequent release of renin, each in isolation or together, can also contribute to high BPs.

With acute brain injury, the ability of the brain to autoregulate and maintain cerebral blood flow is impaired. Autoregulation is a mechanism by which the brain can maintain a constant cerebral blood flow despite a wide fluctuation in cerebral perfusion pressure (CPP) (from the range of 60-180 mm Hg).

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CPP is the difference between mean arterial pressure (MAP) and ICP. Under physiologic circumstances cerebral venous pressure (backflow in the cerebral venous system) is the primary determinant of ICP. In absence of any pathologic condition, cerebral venous pressure is zero; thus the arterial pressure determines CPP.

When the ICP goes up because of increase in cerebral venous pressure (as in CVA), MAP goes up in an attempt to maintain adequate CPP.

14 How should hypertension be treated in patients with CVA?

The goal is gradual and careful reversal of vasogenic subcortical edema. MAP should be cautiously reduced by no more than 15% over a 2- to 3-hour period. Severe neurologic complications have occurred with MAP reductions at 40% or more.

The goal is salvation of ischemic penumbra. For patients thought to be candidates for reperfusion therapy, systolic BP (SBP) > 185 mm Hg and diastolic BP (DBP) > 110 mm Hg warrant treatment. For the subset of patients who are not candidates for reperfusion therapy, the expert opinion is to treat SBP > 220 mm Hg and DBP > 120 mm Hg with a goal of 15% to 25% reduction in MAP over the first 24 hours.

Poorly controlled BP increases the risk of rebleeding. The presence of blood in the subarachnoid space induces intense vasospasm and increases the risk of severe ischemia 4 to 12 days after the first bleeding. The goal is 20% to 25% reduction in BP over a 6- to 12-hour period but not less than 160 to 180/100 mm Hg.

The consensus guidelines on treatment of intracerebral bleeding:

22 What are the causes of primary aldosteronism, and how should they be distinguished?

The major causes are unilateral aldosterone-producing adenoma (APA) and bilateral idiopathic adrenal hyperplasia (IAH). Primary aldosteronism should be suspected in a patient with hypokalemia and hypertension with metabolic alkalosis. It is necessary to first demonstrate renal potassium wasting (high urine K+ in association with low serum K+) followed by a decrease in renin and an elevated aldosterone level. The plasma aldosterone/renin ratio (> 40) is often used. If the ratio is elevated, the aldosterone response to either NaCl infusion or fludrocortisone is used and considered positive if the plasma aldosterone level remains elevated (> 10 pg/mL). Treatment of APA is surgical adrenalectomy, whereas mainstays of treatment of IAH are mainly medical. Adrenal imaging can sometimes distinguish between APA and IAH, but it is often necessary to pursue a more definitive study to verify the diagnosis of APA. By far, selective adrenal vein sampling is the most validated technique used to differentiate APA from IAH.