When Is Hypertension a True Crisis, and How Should It Be Managed in the Intensive Care Unit?

Systemic hypertension remains a global priority because it is common and serious. Hypertension affects approximately 1 billion people worldwide and is responsible for over 9 million deaths each year. It is estimated that systemic hypertension accounts for approximately 50% of deaths due to cardiovascular disease and stroke. A hypertensive crisis is typically defined as acute severe hypertension characterized by a diastolic blood pressure (BP) of 110 mm Hg or higher or a systolic BP of 180 mm Hg or higher. New or worsening end-organ dysfunction was observed in 59% of patients with hypertensive crises requiring hospitalization, and the associated mortality at 90 days was 11%.

Since the advent of effective antihypertensive therapy, the prevalence of hypertensive crises has significantly declined. Although the incidence of hypertensive crises in the intensive care unit (ICU) has not been precisely measured, it remains common in medical and perioperative patients in the hospital. In light of the above considerations, it follows that a hypertensive crisis is an often-encountered ICU complication. This chapter outlines a clinical approach to the diagnosis and management of this hemodynamic emergency in the ICU.

Clinical Classification of an Acute Hypertensive Crisis: Emergency Versus Urgency

Hypertensive crises may be divided into hypertensive emergencies or hypertensive urgencies. A hypertensive urgency lacks apparent or threatened end-organ damage. Nonetheless, treatment is indicated. An approach to the management of hypertensive urgencies is outlined in Table 52-1 . In contrast, a hypertensive emergency, the focus of this chapter, is severe hypertension with actual or threatened acute end-organ damage ( Table 52-2 ) and is, by definition, life threatening, mandating immediate therapy in an ICU with titratable, short-acting intravenous vasodilators ( Table 52-3 ).

Table 52-1

Suggested Clinical Approach to a Hypertensive Urgency ^∗

Step 1: Confirm that the BP elevation is truly severe

Step 2: Confirm that there are no clinical indications of threatened or actual end-organ damage

Step 3: Detect and manage triggering factors such as

•

Pain—administer analgesia
•

Anxiety and stress—consider anxiolytics
•

Delirium—consider antipsychotics
•

Drug withdrawal—treat accordingly
•

Intracranial hypertension
•

Urinary retention—drain bladder
•

Hypoxia/hypercapnia—treat cause, administer oxygen, support ventilation
•

Hypoglycemia—treat cause, administer glucose

Step 4: If still hypertensive after above measures, then consider antihypertensive therapy to lower BP to desired range in a gradual fashion

BP , blood pressure.

Adapted from: Salgado DR, Silva E, Vincent JL. Control of hypertension in the critically ill: a pathophysiologic approach. Ann Intensive Care . 2013;3:17.

∗ Defined as severe hypertension with no real or threatened end-organ damage.

Table 52-2

Clinical Scenarios in Which Severe Hypertension Is an Emergency

Neurologic

Hypertensive encephalopathy
Intracranial hemorrhage
Subarachnoid hemorrhage
Thrombotic stroke with severe hypertension

Cardiovascular

Left ventricular failure
Unstable angina
Myocardial infarction
Aortic dissection
Postoperative period after cardiac or vascular surgery (threatened suture lines)

Renal

Gross hematuria
Acute renal injury/failure

Severe Catecholamine Excess

Pheochromocytoma
Recreational drug exposure
Drug withdrawal (e.g., beta blockers, clonidine)
Interactions with MAOIs

MAOIs , monoamine oxidase inhibitors.

Table 52-3

Drugs for Intravenous Management of a Hypertensive Crisis

Agent	Dose	Onset	Duration	Adverse Effects	Comments
Nitroglycerin	25 to 200 μg/min	2 to 5 min	5 to 10 min	Headache, vomiting, tolerance, methemoglobinemia	Consider in myocardial ischemia and cocaine intoxication
Sodium nitroprusside	1 to 10 μg/kg/min	Immediate	1 to 2 min	Vomiting, cyanide poisoning	Caution in raised intracranial pressure, spinal cord ischemia, and azotemia
Nicardipine (calcium channel blocker)	5 to 15 mg/h	5 to 10 min	15 to 30 min but may last 4 h	Headache, vomiting, tachycardia	Caution in acute heart failure
Clevidipine (calcium channel blocker)	2 to 16 mg/h	1 to 2 min	5 to 10 min	Tachycardia	Intralipid vehicle limits total dose in 24 h
Diltiazem (calcium channel blocker)	5 to 15 mg/h	5 to 10 min	2 to 4 h but may persist past 6 h	Hypotension, heart failure, bradycardia, heart block	Caution in bradycardia, heart block, and heart failure
Esmolol (beta-blocker)	50 to 100 μg/kg/min	1 to 2 min	10 to 30 min	Bronchospasm, heart block, and heart failure	Consider in aortic dissection; avoid in cocaine intoxication
Labetalol (beta-blocker)	1 to 5 mg/min	5 to 10 min	3 to 6 h	Bronchospasm, heart block, and heart failure	Caution in acute heart failure; avoid in cocaine intoxication
Enalapril (angiotensin converting enzyme inhibitor)	1.25 to 5 mg every 6 to 8 h	15 to 30 min	6 to 12 h	Hypotension in high rennin states	Acute ventricular failure; caution in azotemia and renal artery stenosis
Fenoldopam (dopamine-1 agonist)	0.1 to 0.3 μg/kg/min	2 to 5 min	30 min	Headache, vomiting, and tachycardia	Caution with glaucoma
Hydralazine	10 to 20 mg	10 to 20 min	1 to 4 h	Headache, vomiting, and tachycardia	Consider in eclampsia
Phentolamine	5 to 15 mg bolus	1 to 2 min	10 to 30 min	Headache, vomiting, and tachycardia	Consider in catecholamine excess states

Adapted from: Marik PE, Rivera R. Hypertensive emergencies: an update. Curr Opin Crit Care . 2011;17:569–580.

Clinical Features of Selected Hypertensive Emergencies

Neurologic Hypertensive Emergencies

Neurologic hypertensive emergencies may have overlapping features ( Table 52-4 ). Hypertensive encephalopathy is often the most difficult to diagnose. There is apparent disruption of the blood–brain barrier and loss of cerebral autoregulation, resulting in diffuse cerebral edema and neurologic dysfunction. The diagnosis of hypertensive encephalopathy requires exclusion of stroke, intracranial hemorrhage, seizures, and mass lesions, usually through neuroimaging. There are no large clinical trials examining the optimal treatment for hypertensive encephalopathy. Expert opinion suggests that therapy for hypertensive encephalopathy includes careful titration of a vasodilator in an ICU setting. Recommendations for first-line vasodilator drugs and BP goals for neurologic hypertensive emergencies are summarized in Table 52-5 . It has been observed that pharmacologic relief is associated with significant neurologic improvement. The patient requires close clinical observation because changes in the neurologic examination may reflect a secondary process—a new stroke or hypotensive overshoot—requiring immediate intervention.

Table 52-4

Clinical Features of Selected Neurologic Hypertensive Emergencies

Clinical Feature	Hypertensive Encephalopathy	Subarachnoid Hemorrhage	Intraparenchymal Hemorrhage	Acute Infarction
History of hypertension	Universal	Common	Common	Common
Symptom duration	Usually subacute	Acute	Acute	Acute
Headache	Severe	Severe	Variable	Variable
Focal neurologic deficit	Unusual	Variable	Depends on location of hemorrhage	Depends on location of infarction
Retinopathy	Universal	Variable	Variable	Variable
Brain imaging	Typically normal	May show hemorrhage	Often demonstrates site and extent of hemorrhage	Frequently delineates site and extent of infarction
Lumbar puncture (if performed)	Typically normal—may have high opening pressure	Frank blood initially; xanthochromic later	Frank blood initially; xanthochromic later	Typically normal—may have high opening pressure
Acute treatment	ICU—vasodilator therapy	ICU—therapy with vasodilators; may require neurosurgical intervention	ICU—vasodilator therapy	ICU—cautious vasodilator therapy

ICU , intensive care unit.

Adapted from: Manning L, Robinson TG, Anderson CS. Control of blood pressure in hypertensive neurological emergencies. Curr Hypertens Rep . 2014;16:436.

Table 52-5

Recommended Vasodilator Management in Neurologic Hypertensive Emergencies

Hypertensive Emergency	Suitable Vasodilators	BP Goals	Comments
Hypertensive encephalopathy	Labetalol, clevidipine, nicardipine, sodium nitroprusside	25% decrease in mean arterial pressure over 4 to 8 hr	Consider anticonvulsants for control of seizures to tighten control of BP. Caution with sodium nitroprusside because it may increase intracranial pressure.
Acute cerebral infarction with BP > 220/120 mm Hg	Labetalol, clevidipine, nicardipine, sodium nitroprusside	15% decrease in mean arterial pressure over 1 to 2 hr	Monitor closely for neurologic deterioration.
Acute cerebral infarction with indication for thrombolytic therapy and BP > 185/110 mm Hg	Labetalol, clevidipine, nicardipine, sodium nitroprusside	15% decrease in mean arterial pressure over 1 to 2 hr	Monitor closely for neurologic deterioration.
Cerebral hemorrhage with normal intracranial pressure and systolic BP > 180 mm Hg or mean arterial pressure >130 mm Hg	Labetalol, clevidipine, nicardipine, sodium nitroprusside	Modest decrease in mean arterial pressure over 1 to 2 hr with a goal BP of ∼160/90 mm Hg, if tolerated clinically	Monitor closely for neurologic deterioration.
Cerebral hemorrhage with raised intracranial pressure and systolic BP > 180 mm Hg or mean arterial pressure >130 mm Hg	Labetalol, clevidipine, nicardipine, sodium nitroprusside	Modest decrease in mean arterial pressure over 1 to 2 hr with a goal BP of ∼160/90 mm Hg, if tolerated clinically	Monitor closely for neurologic deterioration. Consider monitoring of intracranial pressure and maintain cerebral perfusion pressure >60 mm Hg. Caution with sodium nitroprusside because it may increase intracranial pressure.
Subarachnoid hemorrhage	Labetalol, clevidipine, nicardipine	Modest decrease in mean arterial pressure over 1 to 2 hr with a goal BP of ∼140 to 160/90 mm Hg, if tolerated clinically	Caution with sodium nitroprusside because it may increase intracranial pressure. Maintain mean arterial pressure >90 mm Hg.
Hypertension after craniotomy	Labetalol, clevidipine, nicardipine, sodium nitroprusside	Modest decrease in mean arterial pressure over 1 to 2 hr with a goal BP of <160/90 mm Hg, if tolerated clinically	Monitor closely for neurologic deterioration.