Key Points
- Use the highest‑yield diagnostic test early; do not let testing delay time‑critical therapy.
- Set objective targets (hemodynamic, neurologic, respiratory) and reassess frequently.
- Plan definitive source control or reperfusion when indicated; document follow‑up and patient education.
Algorithm
- Confirm hypertensive emergency: elevated BP with acute target-organ damage.
- Place arterial line when feasible; continuous monitoring.
- Choose IV agent by phenotype: pulmonary edema (nitro + diuretic), ACS (nitro + β-blocker), encephalopathy (nicardipine/clevidipine), aortic dissection (β-blocker then vasodilator).
- Lower MAP by ≤25% in 1 hour, then to ~160/100–110 mmHg over 2–6 h; avoid rapid overcorrection.
- Transition to oral regimen after stabilization; arrange follow-up and secondary cause workup.
Clinical Synopsis & Reasoning
Acute severe hypertension with target-organ damage (e.g., encephalopathy, pulmonary edema, ACS, AKI) requires rapid but controlled BP lowering with IV agents; general goal is ≤25% MAP reduction in the first hour, then to 160/100–110 mmHg over the next 2–6 hours, except in special conditions.
Treatment Strategy & Disposition
Stabilize ABCs. Initiate guideline‑concordant first‑line therapy with precise dosing and continuous monitoring. Escalate to advanced or procedural interventions based on explicit failure criteria. Define ICU, step‑down, and ward disposition triggers; involve specialty teams early.
Epidemiology / Risk Factors
- Risk varies by comorbidity and precipitants; see citations for condition‑specific data.
Investigations
| Test | Role / Rationale | Typical Findings | Notes |
|---|---|---|---|
| Focused neuro/cardio/renal exam | Define end-organ injury | Focal deficits, rales, edema | — |
| ECG, troponin, BNP | Cardiac involvement | Ischemia/strain | Trend as indicated |
| BMP, UA, creatinine | Renal injury | AKI/proteinuria/hematuria | — |
| Chest X-ray | Pulmonary edema | Interstitial/alveolar edema | If dyspnea |
| CT head (if neuro signs) | ICH/infarct | Rule out bleed/infarct | Before BP targets in ICH/ischemic stroke |
Pharmacology
| Medication/Intervention | Mechanism | Onset | Role in Therapy | Limitations |
|---|---|---|---|---|
| Nicardipine infusion 5 mg/h → titrate | DHP CCB | Minutes | General use, neuro cases | Reflex tachycardia |
| Clevidipine 1–2 mg/h → titrate | DHP CCB | Minutes | Rapid titration | Lipid emulsion; avoid in egg/soy allergy |
| Labetalol bolus/infusion | α/β-blocker | Minutes | Aortic dissection, pregnancy | Bradycardia/bronchospasm |
| Esmolol infusion | β1-blocker | Minutes | Dissection, tachycardia-mediated | Short acting |
| Nitroprusside 0.3 µg/kg/min → titrate | NO donor | Immediate | Refractory cases | Cyanide/thiocyanate toxicity, ↑ICP |
| Nitroglycerin 5–10 µg/min → titrate | Venodilator | Minutes | ACS/pulmonary edema | Headache, tolerance |
Prognosis / Complications
- Outcome depends on timeliness of diagnosis and definitive therapy; monitor for complications.
Patient Education / Counseling
- Provide red‑flag education, adherence guidance, and explicit return precautions; arrange timely specialty follow‑up.
References
- AHA Scientific Statement: Hypertensive Emergencies (2022) — Link