Hypertensive emergency is severely elevated blood pressure (BP) associated with new or progressive target organ dysfunction.
If the clinical suspicion is high, treatment should be initiated immediately without waiting for further tests.
BP must be lowered over minutes to hours with parenteral medications in an intensive care setting.
The initial goal of therapy is to reduce mean arterial BP by no more than 25% (within minutes to 1 hour). If the patient remains stable, further reduce the BP to 160 mmHg systolic and 100-110 mmHg diastolic within the next 2 to 6 hours. Normal BP may be targeted over the next 24 to 48 hours.
Excessive falls in pressure may precipitate renal, cerebral, or coronary ischaemia and so should be avoided.
Exceptions to this general rule are patients with aortic dissection, phaeochromocytoma crisis, and severe pre-eclampsia or eclampsia, in whom systolic BP should be reduced to 140 mmHg within the first hour (120 mmHg in the first 20 minutes in aortic dissection).
With appropriate treatment, prognosis is good.
Hypertensive emergency is defined as severely elevated blood pressure (BP) associated with new or progressive target organ dysfunction. Although the absolute value of the BP is not as important as the presence of end-organ damage, the systolic BP is usually >180 mmHg and/or the diastolic BP is >120 mmHg.
History and exam
Key diagnostic factors
- blood pressure (BP) >180/120 mmHg
- presence of risk factors
Other diagnostic factors
- neurological symptoms
- cardiac symptoms
- abnormal cardiopulmonary examination
- oliguria or polyuria
- abnormal fundoscopic examination
- abnormal neurological examination
- inadequately treated hypertension
- chronic kidney disease (CKD)
- renal artery stenosis
- renal transplant
- endocrine disorders with known hypertensive effects
- older age
- black ethnicity
- male sex
- use of sympathomimetic drugs
- pharmacotherapy with known hypertensive effect
- obstructive sleep apnoea
- vasculitis and connective tissue diseases
1st investigations to order
- blood chemistry
- FBC with smear
- urinalysis with microscopy
- chest x-ray
Investigations to consider
- thyroid function tests
- cardiac enzymes
- brain natriuretic peptide (BNP)
- urine toxicology screen
- thoracic CT scan with contrast
- transoesophageal echocardiography
- renal ultrasound with Doppler
- head CT without contrast
- head MRI
- plasma renin activity and aldosterone level
- spot urine or plasma metadrenaline (metanephrine)
- 24-hour urine free cortisol
- sleep study
accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage
acute ischaemic stroke
left ventricular failure and/or pulmonary oedema
acute kidney injury
severe hypertension in pregnancy (pre-eclampsia and eclampsia)
M. Lee Sanders, PhD, MD
Clinical Assistant Professor
Division of Nephrology
University of Iowa
MLS is an author of a reference cited in this topic.
Manish Suneja, MD, FASN, FACP
Division of Nephrology
University of Iowa
MS is an author of a reference cited in this topic.
Dr M. Lee Sanders and Dr Manish Suneja would like to gratefully acknowledge Dr Hector Ventura and Dr Madhavi T. Reddy, previous contributors to this topic.
HV declares that he has no competing interests. MTR is employed by Merck and owns stocks in Merck, and Johnson & Johnson.
Aparna Sundaram, DO, MBA, MPH
AS declares that she has no competing interests.
Ethan Cumbler, MD
Department of Internal Medicine
University of Colorado Health Sciences Center
EC declares that he has no competing interests.
Michael Schachter, MB, BSc, FRCP
Department of Clinical Pharmacology
St Mary’s Hospital
MS declares that he has no competing interests.
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