What is the recommended management for a hypertensive crisis?

Management of Hypertensive Crisis

The management of hypertensive crisis depends critically on whether acute target organ damage is present: hypertensive emergencies require immediate ICU admission with IV antihypertensive therapy, while hypertensive urgencies can be managed with oral medications and outpatient follow-up. 1

Initial Assessment: Emergency vs. Urgency

Distinguish between hypertensive emergency and urgency immediately:

• Hypertensive emergency: BP >180/120 mmHg WITH acute target organ damage (hypertensive encephalopathy, intracranial hemorrhage, acute MI, acute left ventricular failure with pulmonary edema, aortic dissection, acute renal failure, eclampsia, or advanced retinopathy with papilledema) 1
• Hypertensive urgency: Severe BP elevation (>180/120 mmHg) WITHOUT acute or impending target organ damage 1
• The actual BP level may be less important than the rate of BP rise; patients with chronic hypertension often tolerate higher pressures than previously normotensive individuals 1

Critical pitfall: Do not treat the BP number alone—many patients with acute pain or distress have transiently elevated BP that normalizes when the underlying condition is treated 2

Management of Hypertensive Emergency

Immediate Actions

Admit to ICU for continuous BP monitoring and parenteral therapy (Class I, Level B-NR recommendation): 1

• Establish continuous intraarterial BP monitoring to prevent "overshoot" hypotension 1
• Obtain essential laboratory tests: hemoglobin, platelets, creatinine, sodium, potassium, LDH, haptoglobin, urinalysis for protein and sediment, troponins if chest pain present 2
• Perform ECG and assess for specific target organ damage 2

BP Reduction Targets

The rate and extent of BP reduction depends on the specific clinical scenario:

For compelling conditions (Class I, Level C-EO): 1

• Aortic dissection: Reduce SBP to <120 mmHg within the first hour 1
• Severe preeclampsia/eclampsia: Reduce SBP to <140 mmHg within the first hour 1
• Pheochromocytoma crisis: Reduce SBP to <140 mmHg within the first hour 1

For patients WITHOUT compelling conditions (Class I, Level C-EO): 1

• Reduce SBP by no more than 25% within the first hour 1
• Then, if stable, reduce to 160/100 mmHg within the next 2-6 hours 1
• Then cautiously reduce to normal during the following 24-48 hours 1

Critical warning: Avoid excessive acute drops in SBP (>70 mmHg) as this may precipitate acute renal injury, cerebral ischemia, or coronary ischemia in patients with altered autoregulation from chronic hypertension 1, 2

First-Line IV Medications

Nicardipine (preferred for most situations): 1, 3

• Initial dose: 5 mg/hr IV infusion 1
• Titrate by 2.5 mg/hr every 5 minutes (for gradual reduction) or every 5 minutes (for rapid reduction) 1, 3
• Maximum dose: 15 mg/hr 1
• Advantages: Predictable, titratable, no cyanide toxicity risk 1
• Contraindications: Advanced aortic stenosis 1
• Change infusion site every 12 hours if using peripheral vein 3

Clevidipine: 1

• Initial dose: 1-2 mg/hr IV, doubling every 90 seconds until BP approaches target 1
• Then increase by less than double every 5-10 minutes 1
• Maximum dose: 32 mg/hr; maximum duration 72 hours 1
• Contraindications: Soybean/egg allergy, defective lipid metabolism 1

Labetalol (excellent for renal involvement and cerebrovascular events): 1, 2

• Dose: 0.25-0.5 mg/kg IV bolus, followed by 2-4 mg/min continuous infusion, then 5-20 mg/hr 1
• Onset: 5-10 minutes; duration: 3-6 hours 1
• Contraindications: 2nd/3rd degree AV block, systolic heart failure, asthma, bradycardia 1
• Do not use in cocaine/amphetamine intoxication or pheochromocytoma (can paradoxically worsen hypertension) 1

Sodium nitroprusside (use with extreme caution): 1, 4

• Initial dose: 0.3-0.5 mcg/kg/min; increase by 0.5 mcg/kg/min increments 1
• Maximum dose: 10 mcg/kg/min; duration as short as possible 1
• Major toxicity concern: Cyanide toxicity with prolonged use (>30 minutes at high doses) can cause irreversible neurological changes and cardiac arrest 1
• For infusion rates ≥4-10 mcg/kg/min or duration >30 minutes, coadminister thiosulfate 1
• Requires intraarterial BP monitoring 1

Condition-Specific Medication Selection

Acute coronary syndrome/acute pulmonary edema: 1

• Nitroglycerin: Initial 5 mcg/min, increase by 5 mcg/min every 3-5 minutes to maximum 20 mcg/min 1
• Do not use in volume-depleted patients 1

Acute ischemic stroke: 1, 2

• Avoid BP reduction within first 5-7 days unless BP >220/120 mmHg 1, 2
• If BP ≥220/110 mmHg and not receiving reperfusion: Reduce by approximately 15% during first 24 hours 1
• If eligible for reperfusion therapy: Maintain BP <180/105 mmHg for at least 24 hours after treatment 1

Acute intracerebral hemorrhage: 1, 2

• Immediate BP lowering (within 6 hours) to SBP 140-160 mmHg if presenting SBP ≥220 mmHg 1, 2
• Goal: Prevent hematoma expansion 1

Cocaine/amphetamine intoxication: 1

• Initiate benzodiazepines FIRST 1
• If additional BP lowering needed: Phentolamine, nicardipine, or nitroprusside 1
• Avoid beta-blockers (including labetalol): Ineffective for coronary vasoconstriction 1

Eclampsia/preeclampsia: 1

• Hydralazine: 10 mg slow IV (maximum initial dose 20 mg), repeat every 4-6 hours 1
• Alternative: Labetalol or nicardipine 1

Management of Hypertensive Urgency

Do NOT admit to hospital or use IV medications: 5, 2

• These patients are stable without acute target organ damage and do not require emergency department referral 1
• Many result from medication noncompliance or withdrawal 1

Oral Medication Options

First-line oral agents (per European Society of Cardiology): 5, 2

Captopril (ACE inhibitor): 5

• Must start at very low doses due to risk of sudden BP drops in volume-depleted patients (from pressure natriuresis) 5
• Unpredictable response due to variable renin-angiotensin system activation 2

Labetalol (combined alpha/beta-blocker): 5

• Dual mechanism of action 5
• Effective for most hypertensive urgencies 5

Extended-release nifedipine (calcium channel blocker): 5

• NEVER use short-acting nifedipine: Can cause stroke and death from uncontrolled BP falls 5, 2
• Only use extended-release formulation 5

Monitoring and Follow-up

• Observe for at least 2 hours to evaluate BP-lowering efficacy and safety 5
• Target: Reduce SBP by no more than 25% within first hour, then aim for <160/100 mmHg over next 2-6 hours 5
• Schedule frequent follow-up visits (at least monthly) until target BP reached 5
• Address medication adherence issues 5

Critical pitfall: Up to one-third of patients with diastolic BP >95 mmHg normalize before follow-up; rapid BP lowering may be harmful 2

Post-Stabilization Management

Screen for secondary hypertension causes (found in 20-40% of malignant hypertension cases): 1, 2

• Renal artery stenosis 2
• Pheochromocytoma 2
• Primary aldosteronism 2

Transition to oral therapy: 2

• Combination of RAS blockers, calcium channel blockers, and diuretics 2
• Target SBP 120-129 mmHg for most adults 2
• Consider fixed-dose single-pill combination treatment 2

Long-term prognosis: 1

• Without treatment, 1-year mortality >79% with median survival 10.4 months 1
• Even with treatment, patients remain at increased risk of cardiovascular and renal disease compared to hypertensive patients without prior emergency 1
• Elevated troponin-I and renal impairment at presentation are prognostic factors for major adverse events 1

Medications to AVOID

Never use these agents: 5, 6, 7

• Short-acting nifedipine: Unpredictable precipitous BP drops, reflex tachycardia, stroke, death 5, 6, 7
• Hydralazine (except eclampsia): Unpredictable response, prolonged duration of action 1
• Clonidine: Significant CNS adverse effects (sedation, cognitive impairment), especially in elderly; rebound hypertension with abrupt discontinuation 5

Use sodium nitroprusside only when absolutely necessary due to cyanide toxicity risk 1, 6, 7