Hypertension

Published on 07/03/2015 by admin

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Chapter 41 Hypertension

Stuart L. Linas, MD , Shailendra Sharma, MD

1 What are the hemodynamic determinants of blood pressure (BP)?

Arterial BP is the product of cardiac output (CO) and systemic vascular resistance (SVR).

image

Malignant hypertension is caused by increased SVR.

2 What is hypertensive crisis?

Hypertensive crisis is the turning point in the course of hypertension in which immediate management of the elevated BP has a decisive role in the eventual outcome. It is a condition of severe and uncontrolled increase in the BP. An acute increase in BP can occur in the absence or presence of acute or chronic target organ dysfunction.

3 What are the target organs affected by hypertensive crisis?

Four organs are the usual target of severely elevated BP:

image Kidneys: acute kidney injury caused by proliferative endarteritis and fibrinoid necrosis of afferent artery

image Brain: hypertensive encephalopathy, cerebrovascular accidents (CVA)

image Eye or retina: retinal hemorrhage or exudates or papilledema

image Heart: acute coronary syndrome, decompensated heart failure, aortic dissection, and acute intravascular hemolysis

4 What are malignant hypertension and accelerated hypertension?

Both are syndromes in which a markedly elevated BP is associated with hypertensive neuroretinopathy. In accelerated hypertension, there may be flame hemorrhages or cotton wool exudates. Malignant hypertension is diagnosed when papilledema occurs as well.

5 What are hypertensive urgency (HU) and nonemergent hypertension (NEH)?

When severe hypertension occurs in the absence of any acute end-organ damage, it is classified as HU-NEH. Because the complications from HU are not immediate, this condition can be treated safely outside the intensive care unit and hospital with gentle reduction in BP achieved over hours to days.

6 What is hypertensive encephalopathy?

Hypertensive encephalopathy occurs in the setting of sudden and sustained elevation in BP. It occurs in both benign and malignant hypertension. The clinical presentation is that of altered mental status and/or seizures, but focal neurologic findings are uncommon. This condition can be difficult to distinguish from a primary neurologic event.

7 What are the causes of malignant and accelerated hypertension?

In contrast to ambulatory hypertension (over 90% essential) as many as 50% of patients with malignant or accelerated hypertension have secondary causes. The most important of secondary causes are medications, chronic kidney disease, and renal artery stenosis (RAS).

8 What is the short-term treatment of hypertension and hypertensive emergency?

The short-term treatment of choice is intravenous (IV) sodium nitroprusside. The initial dose is 0.5 mcg/kg/min, and this should be increased by 0.5 mcg/kg/min every 2 to 3 minutes until a diastolic BP < 110 mm Hg has been attained. Further acute decreases in BP should be avoided to prevent hypoperfusion to vital organ(s) because blood flow autoregulation may have been altered to accommodate chronically elevated BP. Acceptable alternative parenteral drugs for the short-term treatment of malignant hypertension include labetalol, nicardipine, enalaprilat, or fenoldopam. Extreme caution should be taken while using agents known to cause or further worsen intravascular volume status because patients with hypertensive emergency often present with intravascular volume depletion.

9 Outline the typical long-term antihypertensive regimen after successful treatment of malignant hypertension or hypertensive crisisss

Because malignant hypertension is mediated by increased SVR, it is recommended that long-term therapy include a vasodilator such as hydralazine or minoxidil. Vasodilators cause reflex tachycardia and sodium retention; therefore it is usually also necessary to include a β-blocker (labetalol) and a diuretic agent. In some cases, long-term BP reduction may be achieved with less potent vasodilators, such as angiotensin-converting enzyme (ACE) inhibitors or calcium channel blockers.

10 What is the appropriate short-term treatment for hypertension in a patient with pheochromocytoma?

Hypertension from pheochromocytomas is caused by vascular smooth muscle α1-receptor activation, which results in vasoconstriction. Thus the best short-term treatment is IV administration of the α1-blocker phentolamine. Sodium nitroprusside is also a reasonable choice. β-Blockers should initially be avoided because they cause both unopposed peripheral α1-receptor stimulation and decreased CO.

11 Describe the short-term treatment of cocaine-induced hypertensive crisis

Cocaine-induced hypertensive crisis falls under “catecholamine-associated hypertension.” Cocaine causes hypertension by inhibiting catecholamine reuptake at nerve terminals. Therefore drugs that can block α1-receptors such as labetalol or phentolamine are effective. Selective β-blockers without α1 blockade such as propranolol are not recommended because of the risk of unopposed α1 action. If hypertension is severe, sodium nitroprusside is the drug of choice. In the setting of cocaine-related myocardial ischemia, nitroglycerin and benzodiazepines are effective against both cocaine-induced hypertension and vasoconstriction of the coronary arteries. Cocaethylene is a compound formed in vivo when cocaine and ethyl alcohol (EtOH) have been ingested simultaneously. It produces greater increases in heart rate, rate-pressure product, and euphoria compared with the effects of cocaine alone. Therefore the treatment of hypertension tends to pose greater therapeutic challenge in patients consuming EtOH as well as cocaine.

Cocaine-induced hypertension should be treated with extreme caution and treatment regimens reviewed with passage of time because the condition undergoes spontaneous resolution when cocaine is metabolized.

12 How is hypertension treated in the short term in patients with aortic dissection?

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