Hypertensive emergency has no universally accepted definition. Actual numbers are often used to define hypertensive emergency, though strictly speaking a hypertensive emergency is any elevation in blood pressure in the presence of end-organ dysfunction.1,2,3
Aggressively treating severe asymptomatic hypertension (very high blood pressure without clear end organ damage) is not indicated, not supported by the literature and dangerous. First, do no harm.
No end-organ damage ≠ HTN emergency
Pathophys alert: the mechanism of HTN emergency is poorly understood but it generally results from an abrupt rise in systemic vascular resistance, direct endothelial injury, and a loss of the body’s ability to autoregulate flow in vital organs. This leads to a continued increase in BPs and end organ damage. 2,4,5 Furthermore extremes of pressure result in activation of the renin-angiotensin-aldosterone axis. This leads to further vasoconstrictor release and elevations in BP. Finally, many patients undergo a pressure-induced natriuresis. The resulting intravascular volume loss causes further mediator release that elevates BP.
Your patient may report (from most to least common) 6:
- Dyspnea (up to 30%)
- Chest pain
- Altered Mental Status
- Limb weakness or sensory changes
- Seizures (eclampsia)
You should ask about:
- History of hypertension
- Compliance with medication
- Illicit drug use
- Kidney disease
On physical examination you should look for:
- Changes in mental status
- Focal neurological abnormalities
- Asymmetric blood pressures between limbs
Is this really it?
If you patient has an elevated blood pressure in the setting of end organ dysfunction, then yes, it is.
If there are no clear signs of end organ damage, then no, it isn’t.
What tests does my patient need?
When evaluating your hypertensive patient it is imperative to make the distinction between a patient with symptomatic and asymptomatic hypertension. The recommendations below are for symptomatic patients only. Testing is mostly based on your patient’s presentation.
Labs: obtain a creatinine to assess for renal failure. A troponin and BNP are indicated if your patient has signs and symptoms consistent with cardiac ischemia or pulmonary edema.
Urine: perform a urinalysis to assess for proteinuria, indicating renal failure. If a pheochromocytoma is suspected obtain urine metanephrines. Obtain a toxicology screen if illicit drug use is suspected.
ECG: obtain if your patient has chest pain, shortness of breath, or signs and symptoms of pulmonary edema. Assess for ischemic changes.
Chest X-ray: indicated if pulmonary edema is suspected.
CT/MRI-scan: a CT-scan of the chest is indicated if an aortic dissection is suspected. CT scan of the brain should be obtained in a patient who has a history and/or physical examination consistent with an ischemic or hemorrhagic stroke. An MRI is more sensitive than a CT-scan for detecting changes consistent with hypertensive encephalopathy.
Is there a cure, doc?
For HTN emergencies, first, do no harm. Traditionally, a reduction of your patient’s mean arterial pressure (MAP) of no more than 20-25% in the first hour of treatment has been recommended. Several studies have indicated that we often do not do this well, and that we drop our patient’s blood pressure too rapidly in the emergency department. 7 Rapid lowering of the blood pressure poses your patient at risk of ischemic events (occurring in up to 5% of patients with rapid blood pressure reduction), and should be avoided at all cost. Aim for a reduction of 15-20% in the first hour, and no more than 25% in first 2 hours. It is important to monitor your patient’s blood pressure very closely. For that reason, an arterial line is highly recommended in HTN emergency. 6,9,10
What is the best route of drug administration?
A continuous, short acting, titratable intravenous agent is indicated for initial treatment. A continuous infusion is likely to achieve more predictable blood pressure control compared to repeated doses of antihypertensives. Oral and transdermal antihypertensives are not indicated in hypertensive emergency. These agents have a high failure rate and cannot easily be reversed.
Which agent should I use?
There are few studies with head to head comparison of agents in HTN emergency. One 2011 study suggested nicardipine, when compared to labetalol, may be superior in time to BP reduction, less adverse events and less need for use of additional agents. 11 Of note: most of the studies comparing nicardipine to labetolol are manufacturer sponsored. None of these studies report patient centered outcome differences (i.e. mortality benefit).
Consider the agents below depending on the specific end organ damage: 7,10,11
|Medication||End Organ Damage||Pearls|
Hemorrhagic or ischemic stroke
|If used in dissection, must give beta blocker first|
Hemorrhagic or ischemic stroke
|Fast onset and shorter half life than nicardipine makes, hence, very titratable but not available in many institutions|
Pre-eclampsia and eclampsia
Hemorrhagic or ischemic strokes
|Safe in pregnancy
Can be used as signal agent in aortic dissection
|Nitroglycerin||Acute Pulmonary Edema
Acute Coronary Syndrome
|May use sublingual or topical forms until IV access established|
|Esmolol||Aortic Dissection||Should be used before vasodilator in dissection
Bolus initially and then begin continuous infusion
|Phentolamine||Cocaine or amphetamine intoxication
|Secondary treatment with cocaine or amphetamines after trial of benzodiazepines|
|Fenoldopam||Acute Renal Failure|
|Furosemide||Acute Pulmonary Edema||Not a first line agent as patients are generally hypovolemic; furosemide is also slow to work so should be used as an adjunctive agent|
Additional Treatment Pearls:
- Aortic dissection: if your patient has aortic dissection, rapidly lower the heart rate to approximately 60 beats per minute to help prevent reflex tachycardia. Once the heart rate is controlled, rapidly lower the SBP to < 120 mm Hg. Aortic dissection is the one HTN emergency where the rule of a 15-20% reduction in MAP during the first hour does not apply.
- There is no clear data to prove that aggressive blood pressure lowering reduces hematoma expansion if your patient has a intracerebral hemorrhage, however, early high blood pressures are associated with mortality. 12 Therefore, aggressive blood pressure management should be considered, and recent data indicated that this may be safe. 13,14,15
- In stroke patients, blood pressure targets are guided by stroke subtype and presenting blood pressure. 12 Start with a MAP reduction of 15-20% in the first hour in the ED.
- Eclampsia: give intravenous magnesium sulfate combined with labetolol. Definitive treatment is delivery of fetus.
- A headache does not equal hypertensive encephalopathy. Hypertensive encephalopathy is diagnosed after a CT scan of the brain ruled out a bleed or stroke. 9
- Give IVF fluids – most patients with hypertensive emergency are intravascularly depleted. Providing IV fluids can help prevent dropped blood pressures after initiation of antihypertensives. 16,17
FOAM under pressure: blow of some steam with continued reading/listening
- Emergency Medicine Updates – Hypertension and the Emergency Physician
- Shortcoat in EM – Severely Elevated Blood Pressure in the ED
- EMCrit Practical Evidence 013 – ACEP Management of Asymptomatic Blood Pressure 2013
- EM Basic – Asymptomatic Hypertension
3. Wolfe SJ, Lo B, et al. Clinical policy: critical issues in the evaluation and management of adult patients in the emergency department with asymptomatic elevated blood pressure. Ann Em Med. 2013; 62: 59-64.
Written by: Phil Magidson, M.D., M.P.H. | Edited by: Maite Huis in ‘t Veld, M.D. | Peer reviewed by: Michael Winters | November 9th, 2014