Hypertensive crises

Hypertensive crises refer to acute increases in blood pressure (generally defined as ≥ 180/120 mm Hg) that cause or increase the risk of end-organ damage, i.e., damage to the brain (e.g., encephalopathy, stroke), eyes (e.g., retinopathy), cardiovascular system (e.g., ACS, pulmonary edema, aortic dissection), and/or kidneys (e.g., acute kidney injury). They can be due to primary hypertension or precipitated by underlying conditions (e.g., pheochromocytoma, pre-eclampsia, drug toxicity). Management consists of rapidly identifying end-organ damage with patient history, physical examination, and focused testing, and determining whether the rapid lowering of the blood pressure with IV antihypertensives is required. The ideal IV antihypertensive agent is determined by the underlying disorder, end-organ systems affected, and other patient factors. In the absence of end-organ damage, hypertensive crises should be managed with rapid follow-up and oral antihypertensives, as the prognosis is poor if they are left untreated. See also hypertension.

• Preferred terminology
  • Hypertensive crisis (acute severe hypertension): systolic blood pressure ≥ 180 mm Hg and/or diastolic blood pressure ≥ 120 mm Hg ^[1]
  • Hypertensive urgency: hypertensive crisis that is either asymptomatic or associated with isolated nonspecific symptoms (e.g., headache, dizziness, or epistaxis) without signs of acute organ damage ^[2][3]
  • Hypertensive emergency: hypertensive crisis with signs of acute end-organ damage, mainly in the cardiovascular, central nervous, and renal systems (see “Clinical features” below)
• Historical terminology
  • Accelerated hypertension: identical to hypertensive emergency
  • Malignant hypertension: severe hypertension that occurs with retinopathy (flame hemorrhages, papilledema) ^[4]

• Drug-related
  • Nonadherence to antihypertensives
  • Drugs that may exacerbate hypertension (e.g., MAO inhibitors, TCAs, NSAIDS, cocaine, amphetamines, ecstasy, stimulant diet pills)
  • Consumption of foods rich in tyramine (e.g., wine, chocolate, aged cheese, cured meat) during therapeutic use of MAOIs
  • Combination or overlap (e.g., due to incorrect washout periods) of MAOIs with other drugs that increase the monoamine concentration (e.g., SSRIs)
• Pheochromocytoma, hyperthyroidism
• Acute and rapidly progressive renal disorders
• Collagen vascular diseases (e.g., SLE)
• Eclampsia/Pre-eclampsia
• Head trauma, spinal cord disorders

Clinical features of hypertensive urgency

• Asymptomatic or isolated, nonspecific symptoms (e.g., headache, dizziness, or epistaxis) ^[5][6]

Clinical features of hypertensive emergency

Signs and symptoms of end-organ dysfunction

• Cardiac
  • Heart failure exacerbation, de novo heart failure, flash pulmonary edema: dyspnea, crackles on examination
  • Myocardial infarction: chest pain, diaphoresis
  • Aortic dissection: chest pain, asymmetric pulses
• Neurological ^[7]
  • Hypertensive encephalopathy
    • Pathophysiology: severe hypertension → failure of CNS blood flow autoregulation → vasodilation and hyperperfusion → cerebral edema
    • Symptoms: headache, vomiting, confusion, seizure, blurry vision, papilledema
  • Ischemic or hemorrhagic stroke: focal neurological deficits, altered mental status
  • Posterior reversible encephalopathy syndrome: seizures, headache, visual changes, altered mental status
• Renal: Acute hypertensive nephrosclerosis (formerly malignant nephrosclerosis)
  • Acute kidney injury (azotemia and/or oliguria, edema) and microhematuria
  • Pathophysiology: severe hypertension → acute thrombotic microangiopathy → thrombosis of glomerular capillaries and red blood cell extravasation and fragmentation as well as luminal thrombosis of arterioles → infarction and necrosis of endothelial and mesangial cells → decreased glomerular blood flow → acute kidney damage
  • Biopsy: petechial subcapsular hemorrhages, renal infarction, and segmental capillary loop necrosis with crescent formation
• Ophthalmic
  • Acute hypertensive retinopathy: blurry vision, decrease in visual acuity, retinal flame hemorrhages, papilledema, Elschnig spots
• Other
  • Microangiopathic hemolytic anemia: fatigue, pallor

Suspect hypertensive encephalopathy in a patient presenting with diffuse neurological symptoms, severe hypertension, and nonspecific or normal neuroimaging. ^[7]

Red flags for hypertensive emergency

The following symptoms in a patient with severe hypertension should raise suspicion for a hypertensive emergency:

• Dyspnea
• Chest pain
• Altered mental status
• Focal neurological symptoms

Additional clinical features that may be present

• Signs of sympathomimetic toxicity
• In pregnant patients (in the second or third trimester ): signs of preeclampsia or eclampsia (see “Clinical features of hypertensive pregnancy disorders”)
• Signs of catecholamine-secreting tumors (see “Clinical features of pheochromocytoma”)

All patients

• Confirm blood pressure manually and on bilateral upper extremities.
• Determine if there are signs of acute end-organ damage.
  • Focused history/physical to identify clinical features of hypertensive emergencies
  • Targeted diagnostics for hypertensive crisis
• Evaluate and treat underlying disorders.

Hypertensive urgency

• Initiate, reinstitute, or modify oral antihypertensive therapy.
• Refer for evaluation of newly diagnosed hypertension and assessment for secondary hypertension.
• Arrange follow-up, monitoring, and counseling.

Hypertensive emergency

• ABCDE approach
• Admit patients to ICU.
• Give IV antihypertensives and aim for targets based on the affected end-organs.

Patients without symptoms of a hypertensive emergency can usually be managed as outpatients and do not require emergency department evaluation. ^[8]

Evaluate for evidence of end-organ damage ^[6][8][9]

Testing should be targeted based on clinical suspicion (e.g., presence of red flags for hypertensive emergencies). ^[2][10]

• Laboratory studies
  • CBC: signs of microangiopathic hemolytic anemia
  • BMP: altered electrolytes and/or elevated creatinine and urea, which suggest kidney failure
  • BNP: elevated in heart failure
  • Troponin: elevated in myocardial ischemia
  • Urinalysis: signs of glomerular injury (e.g., proteinuria, hematuria)
• ECG: signs of cardiac ischemia or acute heart failure, e.g.:
  • ECG findings of STEMI
  • ECG findings of NSTEMI
  • ECG findings of AHF
  • ECG findings of LVH
• Chest x-ray: cardiomegaly, pulmonary edema

In patients with asymptomatic severe hypertension, routine testing may not be required in the acute setting; follow local guidelines and protocols.

Additional evaluation to consider

• Urine pregnancy test
• Urine toxicology screen
• CTA chest, abdomen, and pelvis if chest pain is concerning for aortic dissection (see also “Diagnostics for aortic dissection”)
• POCUS for suspected acute heart failure
• CT head if neurological symptoms are present

Consider a urine pregnancy test to rule out preeclampsia in women of childbearing age.

Approach ^[1][6]

Hypertensive urgency

• Usually, no immediate intervention is required for asymptomatic patients.
• Consider oral antihypertensive agents and monitoring if nonspecific symptoms are present.
• See “Management of hypertensive urgency” for details.

Hypertensive emergencies

See “Management of hypertensive emergencies” for further information.

• General therapeutic goals
  • First hour: Reduce BP by max. 25% to prevent coronary insufficiency and to ensure adequate cerebral perfusion pressure.
  • Subsequent 2–6 hours: Reduce BP to ∼ 160/100–110 mm Hg.
  • Next 24–48 hours: Reduce BP to patients baseline.
• Special cases: i.e., conditions with unique therapeutic strategies
  • Stroke: targets vary based on multiple factors
    • See “Antihypertensives in ischemic stroke” for details.
    • See “Antihypertensives in ICH” for details.
  • Aortic dissection: first-hour lowering to SBP < 120 mm Hg (See “Management of aortic dissection” for details.) ^[1]
  • Severe preeclampsia, eclampsia, and pheochromocytoma: first-hour lowering to SBP < 140 mm Hg ^[1]
    • See “Management of urgent hypertensive pregnancy disorders” for details.
    • See “Treatment of pheochromocytoma” for details.
  • Scleroderma renal crisis (SRC): oral ACEIs are the mainstay of therapy (see “Management of SRC” for details).

Most patients with hypertensive emergency require immediate IV antihypertensives and critical care.

Avoid lowering MAP by more than 25% within the first hour, except in special cases, as this can lead to hypoperfusion and ischemia in certain organs (e.g., brain, kidney, heart).

Management of hypertensive urgency ^[1][6]

Initial management

• Asymptomatic patients: No immediate intervention is required. ^[2][6]
• Nonspecific symptoms (e.g., isolated headache, nonspecific dizziness, epistaxis)
  • Move the patient to a quiet room for 30 minutes followed by repeat BP measurement. ^[6]
  • If symptoms persist and are attributable to high BP: Consider a rapid-acting oral antihypertensive agent. ^[2];
    • Clonidine
    • Captopril
    • Labetalol
    • Prazosin
  • Monitor the patient for a few hours to ensure BP and symptoms improve.

Subsequent management and disposition

• Newly diagnosed hypertension
  • Refer for outpatient management.
  • Consider evaluation for secondary hypertension.
  • If unable to ensure outpatient follow-up, consider prescription of oral antihypertensives.
• Known hypertension: Reinstitute or increase the dosage of existing oral antihypertensive therapy.
• All patients
  • Ensure outpatient follow-up within 1 week.
  • Provide drug adherence counseling and educate patients on lifestyle modifications for hypertension.
  • See “Management of hypertension” for long-term treatment goals.

Most patients with asymptomatic severe hypertension have chronic poorly controlled hypertension. Acute lowering of blood pressure is usually not indicated in these patients and may be harmful. ^[2][10]

Management of hypertensive emergencies ^[1][6]

Initial management

• ICU admission and immediate initiation of intravenous antihypertensive therapy (indicated in most patients)
• Continuous cardiac monitoring
• Consider intraarterial blood pressure monitoring.
• Identify and treat any contributing comorbidities (e.g., chronic renal failure).
• Monitor BMP every 6 hours.

Mean arterial pressure should not be lowered by more than 25% within the first hour, except in special cases. Reducing the blood pressure too rapidly can lead to hypoperfusion and ischemia in certain organs (e.g., brain, kidney, heart).

Intravenous antihypertensives ^[1]

Choice of agent depends on BP-lowering rate and targets, end-organ affected, underlying disorder, and patient comorbidities.

Agents by class

• Calcium channel blockers
  • Nicardipine
  • Clevidipine
• Nitric-oxide dependent vasodilators
  • Sodium nitroprusside
  • Nitroglycerin
• Direct arterial vasodilators: hydralazine
• Antiadrenergic drugs
  • Selective beta-1 antagonist: esmolol
  • Nonselective beta blocker with alpha-1 antagonism: labetalol
  • Nonselective alpha antagonist: phentolamine
• D1 agonist: fenoldopam
• ACE inhibitor: enalaprilat

The response to and duration of action of IV hydralazine can be unpredictable. It should, therefore, be used with caution.

Because prolonged use of sodium nitroprusside carries a risk of cyanide toxicity, it should be limited in dose and duration of use.

Agents by underlying condition ^[1][6][8]

The drugs most commonly used to treat hypertensive emergencies are nitroprusside, labetalol, and nicardipine.

All patients

• Confirm blood pressure manually and on bilateral upper and lower extremities.
• Assess for end-organ damage: BMP, BNP, troponin, urinalysis, ECG, CXR (see “Diagnostics”)
• Identify and treat the underlying cause (e.g., medication nonadherence, pain, missed hemodialysis session).

Hypertensive urgency

• Restart oral antihypertensive medication, if applicable (see “Antihypertensive therapy”).
• Discharge home with close follow-up (within a week).

Hypertensive emergency

• Continuous cardiac monitoring
• Consider intraarterial blood pressure monitoring.
• Treat any contributing comorbidities (e.g., chronic kidney disease).
• Consider CT head.
• Consider CTA chest, abdomen, and pelvis if aortic dissection is suspected.
• Start IV antihypertensive treatment based on patient comorbidities and end-organ involved (see “Treatment”).
  • First hour: goal of reduction in mean arterial pressure by no more than 25%
  • Over the next 2–6 hours: Reduce to 160/100–110 mm Hg.
  • Once at goal (typically < 160/110 mm Hg): Transition to PO medications.
• Trend BMP every 6 hours.
• Admit to the ICU.

• If left untreated, hypertensive emergencies are associated with a 1-year mortality rate of > 80% and a median survival of 10–11 months. ^[1]