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 renal failure). 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): an acute increase in systolic blood pressure ≥ 180 mm Hg and/or diastolic blood pressure ≥ 120 mm Hg ^[1]
  • Hypertensive urgency: hypertensive crisis that is either asymptomatic or with isolated nonspecific symptoms (e.g., headache, dizziness, or epistaxis) without signs of organ damage
  • Hypertensive emergency: hypertensive crisis with signs of 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) ^[2]

• 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
• Pheochromocytoma, hyperthyroidism
• Acute and rapidly progressive renal disorders
• Collagen vascular diseases (e.g., SLE)
• Eclampsia/Pre-eclampsia
• Head trauma, spinal cord disorders

Hypertensive urgency

• Asymptomatic or isolated, nonspecific symptoms (e.g., headache, dizziness, or epistaxis)

Hypertensive emergency

• Signs and symptoms of end-organ dysfunction
  • Cardiac
    • Heart failure exacerbation, pulmonary edema: dyspnea, crackles on examination
    • Myocardial infarction: chest pain, diaphoresis
    • Aortic dissection: chest pain, asymmetric pulses
  • Neurologic
    • Hypertensive encephalopathy: headache, vomiting, confusion, seizure, blurry vision, papilledema
    • Ischemic or hemorrhagic stroke: focal neurological deficits, altered mental status
  • Renal
    • Acute renal failure: azotemia and/or oliguria, edema
  • Ophthalmic
    • Acute hypertensive retinopathy: blurry vision, decrease in visual acuity, retinal flame hemorrhages, papilledema
  • Other
    • Microangiopathic hemolytic anemia: fatigue, pallor

Additional clinical features that may be present

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

Approach to management

1. Confirm blood pressure manually and on bilateral upper extremities.
2. Determine if there are signs of end-organ damage.
   • Focused history/physical (see “Clinical features” below)
   • Select screening tests (see “Diagnostics” below)
3. For hypertensive emergencies
   • ABCDE approach
   • Admit patients (ideally to ICU).
   • Lower the blood pressure acutely using IV agents and aim for targets based on the affected end-organs (see "Treatment" below).
   • Evaluate and treat underlying disorders.
4. For hypertensive urgency
   • Select, reinstitute, or modify oral antihypertensive therapy.
   • In patients with a new diagnosis, evaluate for secondary causes of hypertension.
   • Arrange follow-up, monitoring, and counseling.

Red flags for hypertensive crisis

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

Evaluate for signs of end-organ damage ^[3][4]

• 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: left ventricular hypertrophy, signs of cardiac ischemia (e.g., ST depressions or elevations)
• Chest x-ray: cardiomegaly, pulmonary edema

Additional evaluation to consider

• Urine pregnancy test
• Toxicology screen
• CT chest with IV contrast if chest pain is concerning for aortic dissection (see also “Diagnostics” in aortic dissection)
• Consider TTE if clinical features suggest pulmonary edema (see also “Diagnostics” in congestive heart failure).
• Consider CT head if neurological symptoms are present.

Hypertensive urgency ^[1][5]

• Outpatient treatment is recommended.
• Move patient to a quiet room for 30 minutes.
• Reinstitute or increase the dosage of existing oral antihypertensive therapy.
• For patients with nonspecific symptoms that do not constitute end-organ damage (e.g., isolated headache, nonspecific dizziness, and epistaxis), consider a rapid-acting oral antihypertensive agent prior to discharge. ^[6]
  • Clonidine
  • Captopril
  • Labetalol
  • Prazosin
• Monitor the patient for a few hours to ensure BP is improving.
• For patients with a first diagnosis of hypertension, consider evaluation for secondary hypertension.
• Discharge and follow-up
  • Ensure close follow-up with an outpatient provider.
  • Long-term treatment goals: See “Treatment” of hypertension.
  • Sodium restriction diet

Hypertensive urgency is usually caused by nonadherence to antihypertensive therapy. Aggressive intravenous antihypertensive therapy is not required.

Hypertensive emergency ^[1][5]

• ICU admission and immediate initiation of intravenous antihypertensive therapy (see table below)
• Continuous cardiac monitoring
• Consider intra-arterial blood pressure monitoring.
• Identify and treat any contributing comorbidities (e.g., chronic renal failure).
• IV fluids if signs of volume depletion
• Monitor BMP every 6 hours.

Rate and target of blood pressure reduction

• General goal
  • Reduce BP by max. 25% within the first hour to prevent coronary insufficiency and to ensure adequate cerebral perfusion pressure.
  • Reduce BP to ∼ 160/100–110 mm Hg over the next 2–6 hours.
  • Reduce BP to patients baseline over 24–48 hours.
• Special cases
  • Indications for the rapid lowering of systolic BP (usually to < 140 mm Hg) in the first hour of treatment include severe pre-eclampsia or eclampsia, aortic dissection, and pheochromocytoma with hypertensive crisis. ^[1]
    • See “Treatment” in hypertensive pregnancy disorders.
    • See “Treatment” in aortic dissection.
    • See “Treatment” in pheochromocytoma.

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).

Choice of intravenous antihypertensive drugs

Intravenous antihypertensives ^[1]

• 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

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

Recommendations based on associated condition ^[1][4][5]

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 signs of end-organ damage: BMP, LFTs, troponin, urinalysis, ECG, CXR (see “Diagnostics” above).
  • Identify and treat the underlying cause (e.g., medication nonadherence, pain, missed hemodialysis session).
• Patients without end-organ damage
  • Restart oral antihypertensive medication, if applicable (see antihypertensive therapy).
  • Discharge home with close follow-up (within the next days, then monthly until BP is controlled).
• Patients with signs of end-organ damage
  • Continuous cardiac monitoring
  • Consider intra-arterial blood pressure monitoring.
  • Treat any contributing comorbidities (e.g., chronic renal failure).
  • Consider CT head with/without contrast.
  • Consider CT/MRI chest with contrast if aortic dissection is suspected.
  • Start IV antihypertensive treatment based on patient comorbidities and end-organ involved (see “Treatment” above).
    • 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 meds.
  • Consider IV fluids if there are signs of volume depletion.
  • Trend BMP every 6 hours.
  • Admit to the hospital.

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