19th June 2026

Hypertensive emergency

Background

Hypertensive emergency is defined as a significantly elevated blood pressure which usually results in end-organ damage. Generally, this is a systolic blood pressure greater than 180mmHg and a diastolic blood pressure of 120mmHg. End-organ damage may include acute kidney injury, ischaemic or haemorrhagic stroke, myocardial ischaemia or heart failure.

Epidemiology

1-2% of patients with hypertension will suffer from a hypertensive emergency in their lives.

Risk factors 

Hypertensive emergency occurs largely due to undiagnosed as well as poorly controlled essential hypertension. It may also be due to secondary hypertension caused by a systemic condition such as phaeochromocytoma or hyperaldosteronism. 

Poor lifestyle choices such as increased salt intake and obesity, as well as certain medications such as steroids, sympathomimetics and NSAIDs, may also predispose a hypertensive emergency.

Clinical features

A patient with hypertensive emergency may present with no symptoms and may incidentally find a very high blood pressure. Patients, however, may present with a variety of symptoms seen in the table below.

Diagnosis and investigations

Diagnosis is generally based on a systolic blood pressure >180mmHg and a diastolic pressure >120mmHg.

Investigations may include:

• CT head: This may reveal a hemorrhagic stroke, but will not rule out an ischaemic stroke
• Fundoscopy: to look for signs of papilloedema 
• Urine dipstick: to look for blood and protein in the urine
• Renal profile: deranged renal function may explain 
• ECG: to look for left ventricular hypertrophy and rule out ischaemia
• Cardiac enzymes: to rule out myocardial infarction
• Urine drug screen: illicit drugs
• Thyroid function tests
• Plasma renin and aldosterone levels may point towards hyperaldosteronism as a cause 
• Urine metanephrines for phaeochromocytoma
• 24-hour urinary cortisol for Cushing’s syndrome 
• CXR
• CT aortogram if aortic dissection is suspected.
• Renal ultrasound / MRA

Complications

• Heart failure
• Cerebral ischaemia, haemorrhage, encephalopathy
• Acute kidney injury

Management

Management of hypertensive emergencies should not be delayed whilst investigating end-organ damage and underlying cause. Patients are usually kept on a cardiac monitor and commenced on parenteral anti-hypertensive medication with the aim of gradual reduction in blood pressure to avoid renal, cerebral or cardiac ischaemia. This is with a few exceptions, as detailed below.

Generally, it is recommended to reduce blood pressure by no more than 25% in the first hour. A further reduction is done in the next 4-6 hours with an aim of reaching a normal blood pressure within 24-48 hours, and weaning parenteral infusion.

There are a few exceptions:

• Patients suffering from an ischaemic stroke should not have an aggressive reduction in blood pressure and may benefit from maintaining a very high blood pressure to maintain cerebral perfusion.
• On the other hand, patients with ischaemic stroke who are candidates for thrombolysis should have a gentle reduction in their blood pressure <185/110 before thrombolysis.
• Patients suffering from an aortic dissection should have aggressive reduction in blood pressure within the first hour to a systolic less than 120mmHg.
• Patients with pre-eclampsia, eclampsia or phaeochromocytoma crisis should have a reduction in their blood pressure within the first hour to a systolic <140mmHg.

Specific emergencies

Malignant hypertension

     Malignant hypertension is a subcategory of hypertensive emergency, which includes either grade III or IV retinopathy. Hypertensive encephalopathy refers to neurological symptoms caused by severely elevated blood pressure and typically improves with blood pressure correction. Intracranial haemorrhage may occur with malignant hypertension.

Management:

• 1st line – Labetalol infusion
• 2nd line – Nicardipine or nitroprusside if no evidence of raised intracranial pressure
• 3rd line – Fenoldopam

Aim to reduce mean arterial pressure by 20-25% within the first 2-4 hours, then to 160/100-110 mmHg within the next 2-6 hours [2].

Myocardial Ischaemia or Infarction

Management:

1. 1st line – Esmolol + GTN infusion
2. 2nd line – Labetalol + GTN infusion

Heart failure / pulmonary oedema

IV nitroglycerin or nitroprusside may be considered as an adjuvant to diuretic therapy. Due to the potential of significant hypotension, nitroprusside should be used with invasive haemodynamic monitoring, typically in the intensive care setting. 

Aortic Dissection

Aortic dissection requires particularly aggressive blood pressure management to reduce the risk of propagation of the dissection.

Aortic dissection is classified based on its location and duration:

1. Stanford Classification: 
   • Type A: Involves the ascending aorta, with or without the involvement of the aortic arch and descending aorta
   • Type B: Involves only the descending aorta
2. DeBakey Classification: 
   • Type I: Originates in ascending aorta, propagates at least to the aortic arch
   • Type II: Originates in and is confined to the ascending aorta
   • Type III: Originates in descending aorta, extends distally or proximally

Management:

1. 1st line – Combination of IV beta-blocker (e.g., labetalol or esmolol) and vasodilator (e.g., nicardipine or nitroprusside)
2. If using labetalol alone, higher doses may be required

Targets:

• Reduce systolic BP to <120 mmHg within the first hour of presentation
• Maintain systolic BP < 120 mmHg or to the lowest BP that maintains adequate end-organ perfusion
• Target heart rate of 60 to 80 bpm

Definitive treatment depends on the type of dissection: 

• Type A typically requires urgent surgical intervention
• Uncomplicated Type B can often be managed medically, with endovascular repair considered in certain cases

Remember, in all cases, the key principle is to lower blood pressure gradually to avoid organ hypoperfusion, while being mindful of the specific risks associated with each condition.