EM@3AM: Hypertensive Emergency
- Nov 11th, 2017
- Brit Long
Author: Brit Long, MD (@long_brit, EM Attending Physician, San Antonio, TX) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)
Welcome to EM@3AM, an emDocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.
A 63-year-old female presents with nausea, vomiting, and altered mental status. Initial VS include BP 225/121, HR 88, 98% RA, T 98F, RR 18. Her husband is with her, who states she is markedly confused, and her normal BP approaches 140-150/70-80. She has not taken her antihypertensive medications for the last week.
What’s the diagnosis, and what’s your next step in evaluation and treatment?
Answer: Hypertensive Emergency
Defined by hypertension with end-organ dysfunction. Hypertensive urgency, or severely elevated hypertension without symptoms, does not require treatment in the ED.
End-organ involvement: 1. Head (encephalopathy, CVA, central retinal occlusion), 2. Chest (ACS, heart failure, dissection) 3. Abdomen (eclampsia, acute renal failure, microangiopathic hemolytic anemia).
Epidemiology: Affects over 65 million people in the U.S. annually.
Pathophysiology: Acute rise in blood pressure can result in vascular mechanical stress and endothelial injury, leading to fibrinoid necrosis. Pressure natriuresis results in decreased effective blood flow (meaning these patients are actually intravascularly dehydrated).
Symptoms include dyspnea, chest pain, headache, altered mental staus, focal deficit. Headache alone is not sufficient for diagnosis of HTN emergency. Evaluate medication use and compliance, substance abuse, and symptoms involved for underlying cause (night sweats, weight loss, fevers).
Evaluation: ABCs, thorough H&P, followed by laboratory studies/imaging (EKG, CXR, UA, BMP, Troponin, CT and/or MRI) and BP reduction as dictated by the clinical scenario and involved organ system.
Treatment: Goal is to decrease MAP by 20-25%, except for eclampsia and aortic dissection, where goal is SBP 100-120, HR 60s. Provide analgesia and IV fluids, as many patients are actually dehydrated.
Avoid nitroprusside (unpredictable, risk of cyanide toxicity), hydralazine (except in select cases below; may cause precipitous drop, half life approaches 12 hours), and oral medications.
Neurologic: Ischemic stroke (tPA candidate) + BP >185/110 mmHg => Medication options: labetalol (10-20mg IV over 1-2 mins, may repeat x1) or nicardipine (5mg/hr IV, increased by 2.5mg q 5-15 mins; max 15mg/hr). Ischemic stroke (not a tPA candidate): treat if BP ≥ 220/120 mmHg or evidence of active ischemic coronary disease, heart failure, aortic dissection, hypertensive encephalopathy, acute renal failure, or pre-eclampsia/eclampsia. Recommendation: BP reduction by 15-25% over the first 24 hours status post stroke. Hemorrhagic stroke: weigh risks (reducing cerebral perfusion) vs. benefits (limiting intracranial bleeding). Consider use of labetalol or nicardipine in consultation with a specialist if signs/symptoms of increased ICP. Hypertensive encephalopathy (pathognomonic neurologic improvement s/p BP reduction): reduce BP 10-20% during the first hour of treatment and subsequently by ≤ 25% over the first 24 hrs of treatment (nicardipine or labetalol).
Cardiac: Acute heart failure (LV dysfunction + pulm edema) => BiPAP + preload/afterload reduction (nitroglycerin); avoid B-blockers (decreases contractility) and hydralazine (increases myocardial oxygen demand). ACS: IV nitroglycerin, clevidipine, nicardipine, or esmolol are first line; ensure preservation of CPP.
Vascular: Aortic dissection => SBP to goal of 100-120 mmHg within 20 minutes of diagnosis; IV B-blocker (esmolol (#1), labetalol, propranolol, metoprolol) first to reduce HR to 60 bpm + vasodilator after HR control (nicardipine).
Renal: AKI/ARF => antihypertensive therapy often leads to worsening renal function. May consider fenoldopam / labetalol / nicardipine.
Pre-eclampsia: Hypertension + proteinuria/edema/other organ injury, reduce BP by ≤ 20% with labetalol (first choice) or hydralazine; magnesium load (4-6g), then drip (1-2g/hr).
Pediatrics: Often present with HA or blurred vision. Common etiologies: renovascular lesions or pheochromocytoma. Treat if BP exceeds previous measurements by 30% or SBP >95th percentile for age. Acutely symptomatic => 25% BP reduction within 1 hr with labetalol or nicardipine (phentolamine for pheochromocytoma).
Marik PE, Rivera R. Hypertensive emergencies: an update. Current Opinion in Critical Care 2011;17(6):569-80.
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