Author: Jason M Kendall / Editors: Martin Dore, Tajek B Hassan / Reviewer: Emma Everitt, Rafeeq Ahmed Sulaiman / Codes: ACCS LO 2, CC9, CP1, CP2, ResP1, SLO1, SLO3Published: 24/08/2023

A hypertensive emergency is defined as the clinical situation in which there is a marked elevation of blood pressure (BP) associated with acute or progressive end organ damage, e.g. cardiovascular, renal or neurological dysfunction.

It is a life-threatening condition that requires aggressive lowering of the blood pressure to limit end organ damage and prevent an adverse outcome [1].

Conditions defining hypertensive emergencies when associated with acute elevation of blood pressure are:

  • Hypertensive encephalopathy
  • Intracranial haemorrhage
  • Acute myocardial ischaemia or infarction
  • Acute left ventricular failure
  • Dissecting aneurysm
  • Eclampsia


There are a number of aetiologies that have been implicated in the development of hypertension.

The commonest form of hypertension is essential hypertension in which no specific cause can be identified but with which various risk factors are associated. For example:

  • Age
  • Family history
  • Obesity
  • Salt ingestion

There are, however, various specific causes of hypertension (secondary hypertension) which can be identified in about 10% of hypertensive patients

Causes of Hypertensive Emergencies

Most hypertensive emergencies occur in patients with known hypertension and are the result of inadequate treatment or poor compliance [1].

Whatever the aetiology of the underlying hypertension, hypertensive emergencies are thought to be triggered by abrupt rises in systemic vascular resistance and failure of normal autoregulatory mechanisms.

Hypertensive emergencies result in:

  • Microvascular injury
  • Arteriolar fibrinoid necrosis
  • Local mediator release
  • Platelet activation and aggregation and ischaemic injury
  • Further autoregulatory dysfunction and a continued cycle leading to organ damage

Effects on Organs and Systems

Learn more about the effects of hypertensive emergencies.


Chronic hypertension activates the renin-angiotensin-aldosterone system resulting in systemic vasoconstriction and increased systemic vascular resistance. This in turn leads to left ventricular hypertrophy and reduced diastolic myocardial coronary perfusion. Further critical rises in BP, occurring in the context of a hypertensive emergency, will result in myocardial ischaemia and/or the left ventricle failing to overcome systemic vascular resistance with resultant pulmonary oedema.


Normal cerebral autoregulation results in constant cerebral blood flow in the presence of a fluctuating systemic BP. This process, however, has limits and if these are exceeded cerebral endovascular damage occurs, leading to cerebral oedema and microhaemorrhage. The clinical manifestation of autoregulatory breakdown and cerebral vascular damage is hypertensive encephalopathy which, untreated, leads to further macroscopic cerebral haemorrhage and death.


Chronic hypertension also results in impaired renal autoregulation as a consequence of pathological changes within renal arteries. Similar to the brain, when autoregulation fails in the kidney, it is no longer protected from critical changes in systemic BP resulting in:

  • Endovascular damage
  • Fibrinoid necrosis
  • Acute renal ischaemia


The uterine pathology associated with the hypertensive emergency eclampsia is similar to that seen in the kidney, brain and heart. Fibrinoid necrosis, platelet aggregation and thrombus formation occurs within the spiral and basal arteries which supply the placental intervillous space and the uterine decidua. This leads to reduction in placental blood flow and placental infarction and failure.

Identifying a Hypertensive Emergency

The emergency physician must be able to differentiate a true hypertensive emergency from other conditions presenting with an elevated BP (hypertensive urgencies), so that appropriate decisions about BP control can be made.

In particular, the need to rapidly control elevated BP must be balanced by the potential to compromise organ perfusion.

Once significant elevation of BP is confirmed, the clinical assessment is primarily directed at establishing whether there is evidence of acute or progressive end organ damage, with emphasis on the cardiovascular, renal and central neurological systems.


The history of presenting complaint should be directed towards identifying symptoms reflecting acute or progressive end organ involvement.

This table outlines the features which indicate potential end organ damage.

Organ system Symptoms Underlying pathology
Cardiovascular Chest pain


Myocardial ischaemia

Myocardial infarction

Thoracic aortic dissection

Left ventricular failure

Pulmonary oedema

Central Neurological Headache


Visual disturbance



Cerebral encephalopathy +/- cerebral Haemorrhage
Renal Oliguria


Renal impairment


Information for Patient History

The following information should be sought when a history is taken:

Duration of pre-existing hypertension

Determine the duration of pre-existing hypertension and related issues, such as medication compliance and previous emergency presentations.

Predisposing illnesses or conditions

Check whether there are any other illnesses or conditions which may predispose the patient to hypertension. For example:

  • Connective tissue diseases
  • Renal disease
  • Cushing disease
  • Pregnancy for risk of eclampsia

Related illnesses

Establish whether the patient has any other illnesses which may be related to hypertension. For example:

  • Previous stroke
  • Ischaemic heart disease

Drug history

The drug history should focus both on relevant antihypertensive medication and drugs with hypertensive side effects, such as sympathomimetic agents, which might be implicated in a hypertensive emergency.

The patient should be specifically questioned about use of drugs of abuse such as cocaine, particularly when there are no clear risk factors, or a past history of hypertension.

Physical Examination

After confirming that the BP is elevated, the physical examination is primarily directed to identifying any end organ damage, which will define a hypertensive emergency in this context.

The physical examination may also help determine (if its not already known) the underlying cause of hypertension, e.g. markedly reduced femoral pulses in coarctation.

It is important to accurately determine the BP so that trends over time and in response to therapy can be gauged. BP should be assessed (with an appropriately sized cuff) in both upper limbs, evaluating whether there is any discrepancy between the limbs. A thorough cardiovascular and neurological examination is essential if end organ dysfunction is to be identified.

This table outlines the physical examination required to determine end organ damage.

Organ system Examination finding Underlying pathology
Cardiovascular Differential pulses

Differential blood pressures

Diastolic murmur (aortic regurgitation)

Elevated jugular venous pressure

Third heart sound

Pulmonary crepitations

Thoracic dissection

Cardiac failure+/-

Cardiac ischaemia



Reduced level of consciousness

Focal neurological deficit

Retinal haemorrhages/papillodema

Cerebral encephalopathy+/-

Cerebral haemorrhage

Initial investigations

Initial investigations for potential hypertensive emergencies can be organised rapidly within the emergency department.

These investigations will supplement clinical assessment in evaluating end organ dysfunction and hence define whether the presentation is a true hypertensive emergency.

Some studies will be determined by the type of presentation (e.g. CT mediastinum if aortic dissection is suspected or CT head if encephalopathy is present).

However, many initial investigations will be common to any hypertensive emergency (e.g. renal function, ECG).

Essential Initial Investigations

Appropriate initial investigations for patients presenting with a possible hypertensive emergency are as follows:


  • Renal function: to evaluate possible renal impairment
  • Electrolyte panel: electrolyte abnormalities may precipitate arrhythmias in cardiac ischaemia, and may also occur in renal impairment


  • Haematuria, proteinuria or casts may indicate primary renal parenchymal disease or secondary renal impairment
  • Pregnancy test


  • To assess for myocardial ischaemia/infarction or evidence of left ventricular hypertrophy/strain
  • The image shows a markedly ischaemic ECG

Chest x-ray:

  • To assess for evidence of left ventricular failure (pulmonary oedema, left ventricular enlargement)
  • To assess for widening of the mediastinum (aortic dissection)
  • The CXR shows cardiac enlargement and marked failure

CT medisatinum/aortogram:

  • If thoracic aortic dissection is suspected following clinical examination
  • The CT shows true and false lumens associated with a thoracic dissection

CT Head:

  • When there is evidence of neurological dysfunction and cerebral encephalopathy, haemorrhage or infarction is suspected
  • The CT shows a left middle cerebral artery sign in a patient who presented with a cerebral infarction and elevated blood pressure

Hypertensive Urgencies

Most patients presenting to the ED with significantly elevated BP will not demonstrate acute progressive target organ damage and will not, therefore, fulfil criteria for the diagnosis of a hypertensive emergency.

Should BP be aggressively lowered for these patients?

There is no indication for urgent pharmacological intervention. It may cause harm by precipitating acute organ hypoperfusion (i.e. cause end organ dysfunction where it was not previously present).

Treatment Options

Patients presenting with such hypertensive urgencies may benefit from a moderate increase in the antihypertensive drugs that they are already taking. Compliance with antihypertensive medication should be ensured.

Only occasionally will commencement of new oral antihypertensive therapy be indicated in the emergency department [3]. These patients can usually be managed as an outpatient.

Appropriate follow-up should be arranged, normally through their primary care practitioner.


It is a common misconception that patients should never be discharged from the emergency department with an elevated BP.

Hypertensive Emergencies

If the initial clinical examination or investigations have identified target organ impairment in the presence of significantly elevated BP, then the diagnosis of a hypertensive emergency is established and expedient, controlled and progressive lowering of the blood pressure is indicated.

Should BP be lowered to normal levels for these patients?

The goal is not to immediately reduce BP to normal levels. Sudden large drops in blood pressure may compromise blood flow to vital organs in which autoregulatory mechanisms (which would normally preserve blood flows) are damaged.

Hypertensive Emergencies – Mean Arterial Pressure

For hypertensive emergencies, the aim is to reduce Mean Arterial Pressure (MAP*) by up to 25% in the first hour of treatment. If the patient remains stable with no evidence of organ hypoperfusion, further reductions in the BP towards normal are indicated over the ensuing 24 hours.

Learning Bite

A progressive lowering of BP is indicated in hypertensive emergencies, aiming for an initial reduction in MAP* of ~25% over an hour.

Controlled, progressive reductions in BP are generally achieved with a titratable, intravenous, short-acting antihypertensive agent. This will need to occur in an environment where continuous observation and monitoring of the patient is feasible. These patients will all require admission, ideally to a high dependency unit.
MAP* can be calculated from systolic pressure and diastolic pressure.


MAP* = [(2 x diastolic pressure) + systolic pressure] / 3

Hypertensive Encephalopathy

Hypertensive encephalopathy is acute in onset and presents with headache, confusion and drowsiness. With expedient treatment it is reversible, but, without appropriate intervention, it can progress to:

  • Seizures
  • Focal neurological deficits
  • Coma
  • Death

In the early stages, CT scan is usually normal, but in the later stages haemorrhages may be present.

CT must be ordered prior to treatment to differentiate from intracranial haemorrhage. BP reduction in this instance could be detrimental.

Expedient and controlled reduction of blood pressure is essential. The agent of choice is Labetalol as it provides a steady consistent drop in blood pressure without compromising CBF. An initial reduction of MAP of approximately 25% over an hour should be the aim, followed by further controlled MAP reduction over the ensuing 24 hours.

Nicardipine can be considered in those intolerant of Beta blockers.

Learning Bite

Labetalol is the agent of choice in hypertensive encephalopathy.

Focal Neurological Deficit

Focal neurological deficit (stroke syndromes) is the exception to the general rule of expedient reduction of MAP in hypertensive emergencies.

The CT scan shows an acute ischaemic stroke with left middle cerebral artery sign.

Why is it the exception?

Elevated BP, in the context of acute stroke, is often a physiological response rather than an underlying cause.

The majority of strokes (>80%) are either embolic or thrombotic (i.e. not haemorrhagic). Consequently any attempts to reduce MAP may, because of damaged autoregulatory mechanisms, compromise blood flow causing further ischaemia and worsening of the neurological deficit.

Focal Neurological Deficit: ICP

Patients with primary intracerebral haemorrhage may also have raised intracranial pressure (ICP) as a consequence of mass effect of the haemorrhage.

Evidence of benefit associated with reduction in BP in these patients is lacking and this may be because cerebral perfusion pressure (CPP) is critically dependant on MAP and will be further compromised by rises in ICP.

Cerebral perfusion pressure (CPP)

Furthermore, cerebral blood flow is related to CPP by autoregulatory mechanisms and this relationship will be compromised in a hypertensive emergency.

Vasodilators, such as nitrates and nitroprusside, may theoretically increase ICP and are therefore not indicated.


CPP Cerebral Perfusion Pressure

MAP Mean Arterial Pressure

ICP Intracranial Pressure

Focal Neurological Deficit: Thrombolysis

In patients being considered for thrombolysis therapy blood pressure is important. Significant elevations in BP (>185/110) is a contra-indication to this therapy [5].

In exceptional circumstances, if the BP is slightly elevated above this limit, and thrombolysis is clinically indicated, there is some evidence for controlling BP prior to administering thrombolysis.

Intravenous labetalol is the agent of choice. Careful BP control, following administration of thrombolysis, is important to prevent secondary intracranial haemorrhage.

Learning Bite 

If BP control is to be attempted in the setting of stroke, then intravenous labetalol is the agent of choice.

Cardiac Ischaemia

Patients presenting with a hypertensive emergency with evidence of cardiac ischaemia require rapid control of their BP to prevent progression to myocardial infarction, or to prevent further myonecrosis if evidence of infarction has already occurred. Intravenous nitrates which reduce preload on the heart and are also coronary vasodilators are generally used in this setting.

Intravenous nitrates are also used for symptom control in patients with ischaemic chest pain. BP reduction is often only modest with nitrates. Intravenous beta blockers are an ideal adjunctive therapy in this situation since they are known to be cardioprotective in the setting of acute coronary syndromes (even without hypertension).

Commonly used agents in the UK include intravenous atenolol or metoprolol.

Cardiac Ischaemia: Controlling BP

BP control is particularly important where thrombolysis is to be used as the primary reperfusion therapy for a patient with acute myocardial infarction.

A more aggressive approach to blood pressure reduction can be taken with myocardial infarction than with stroke, since the evidence of benefit for aggressive reperfusion is stronger even in the setting of elevated BP.

Intravenous beta blockers are the agents of choice.

Intravenous nitrates and beta blockers are the agents of choice in the setting of acute cardiac ischaemia.

Pulmonary Oedema

Patients presenting with left ventricular failure and pulmonary oedema often have some degree of elevated BP.

What is the cause of this elevated BP?

Elevated BP is a consequence of chronically increased peripheral vascular resistance and activation of the renin-aldosterone system.

A minority of patients will have a marked acute elevation of BP which has precipitated acute left ventricular failure. Expedient control of BP is indicated in these patients to allow normal functioning of the left ventricle. The drugs used to treat pulmonary oedema will all encourage a fall in BP (i.e. intravenous opiates, intravenous nitrates and intravenous diuretics).

These interventions may be adequate to gain control of the BP. However, if further reduction is required, intravenous nitroprusside can be used since it reduces preload and afterload on the failing heart.

Learning Bite

Standard treatments for pulmonary oedema will reduce elevated BP.

Other Hypertensive Emergencies

Other hypertensive emergencies include:

Acute renal impairment

Acute renal dysfunction, associated with severe elevations in BP, mandate urgent control of hypertension in order to prevent progression to acute renal failure.

In patients with renal failure, accumulation of the metabolite thiocyanate can produce toxicity over a period of days. Expert advice should be rapidly sought when a hypertensive emergency presents with renal impairment.

Aortic dissection

The main priority in the initial management of aortic dissection associated with elevated BP is prevention of extension of the dissection. Ideally the aim is to reduce systemic vascular resistance by vasodilation without causing a reflex increase in cardiac output.

Intravenous labetalol (with its mixed alpha and beta antagonist properties) is a useful drug in this context. A nitrate infusion can be added if needed or alternatively, a nitrate infusion with a more selective beta-blocker (e.g. atenolol) is suitable.

A further alternative is the combination of nitroprusside with a beta blocker. The goal is to reduce the systolic BP to 110-120 mmHg or lower.


Eclampsia is characterised by convulsions and coma associated with hypertension during pregnancy or soon after delivery. The treatment of this hypertensive emergency involves magnesium sulphate (4g parentally) to control seizures, reduction of blood pressure and immediate obstetric consultation.

Intravenous hydralazine has historically been used for BP control in eclampsia, but more recently intravenous labetalol or nicardipine have been shown to be the agents of choice. Nitroprusside should be avoided in pregnancy because of its potential toxicity to the foetus.


Phaeochromocytomas are catecholamine-secreting tumours predominantly of the adrenal glands. Confirmation of the diagnosis requires demonstration of increased levels of urinary or plasma catecholamines.

Hypertensive emergencies associated with phaeochromocytomas should be treated with predominantly alpha or mixed alpha and beta adrenergic blocking agents: intravenous phentolamine or labetalol are suitable.

The Evidence or Lack of It

Robust outcome data from Randomised Controlled Trials (RCTs) to support the use of specific drugs in specific hypertensive emergencies are lacking.

A recent Cochrane Collaboration Review addressing this issue found that there was no:

  • RCT evidence to support the hypothesis that antihypertensive therapy reduces mortality or morbidity in hypertensive emergencies
  • Robust RCT evidence to recommend the use of one specific antihypertensive agent over another in the treatment of hypertensive emergencies [6]

There is an acknowledgement that, despite the lack of evidence, it is not hard to accept the necessity of reducing BP in hypertensive emergencies where progressive end organ damage is occurring and, therefore, that placebo controlled trials would be unethical.

It also appears that, with respect to the relative benefits of specific agents, it is a lack of evidence rather than evidence of no benefit due to trials being too small or poorly designed. There is a clear need for further research in this area.

Key drugs

Historical precedent and current experience would suggest that various parenteral antihypertensive agents are theoretically/potentially suited to specific hypertensive emergencies. These are:

Sodium nitroprusside

It is rapid in onset, rapid in offset, titratable, and it works! It is a potent vasodilator causing a reduction in preload and afterload and can often result in improvement of cardiac output when there is impairment of left ventricular function. It can, however, also cause cerebral vasodilation and exacerbate raised intracranial pressure. The metabolites of nitroprusside (thiocyanate and cyanide) are excreted by the kidney and may accumulate with prolonged usage or in patients with significant renal impairment.

Nitroprusside is light sensitive and the delivery device should therefore be covered in opaque material. Because of its potency, rapid onset and offset, nitroprusside must be administered with regular monitoring in an appropriate environment (e.g. high dependency unit). Extravasation may result in local necrosis. Nitroprusside should not be used in pregnancy due to the potential for foetal poisoning with metabolites.

Learning Bite

Labetolol is the agent of choice for most hypertensive emergencies. It is predictable, titratable and it works!


Labetalol is a mixed alpha and beta blocker and lowers BP by vasodilation (vascular smooth muscle receptor blockade) and by reducing cardiac contractility (cardiac receptor blockade). Labetolol does not produce the reflex tachycardia seen with other vasodilators (e.g. nitrates and nitroprusside). It is not associated with reduced cerebral blood flow and is the agent of choice when used for hypertensive stroke syndromes. Because labetolol has a component of alpha -blockade, it can be used as in hypertensive crises that result primarily from stimulation (e.g. phaeochromocytoma) where pure beta -blockers would be contraindicated.


Intravenous nitrates cause vasodilation of capacitance vessels which reduces preload on the heart and left ventricular end diastolic pressure.

It is also a coronary vasodilator. It is, therefore, particularly useful in the setting of hypertension associated with myocardial ischaemia and in left ventricular failure with pulmonary oedema.

Response of the BP to nitrates is often unpredictable and tolerance occurs within 24 hours of commencing the infusion.


Hydralazine has historically been used in hypertensive emergencies of pregnancy (i.e. eclampsia) because of its theoretical positive effects on uterine blood flow.

More recently, other agents (e.g. nicardipine and labetalol) have been found to be superior.

Hydralazine causes a marked reflex tachycardia and is associated with raised intracranial pressure and so should be avoided in patients with cardiac or cerebral disease.


Nicardipine is a calcium channel blocker and acts predominantly as a vasodilator. It has a fairly rapid onset of action and is therefore titratable, dosing is not dependant on body weight, it appears to be safe in pregnancy, and it reduces cerebral and coronary ischaemia.

Like all calcium antagonists, it should be used with caution in patients with impaired left ventricular function because of its negative inotropic effects. It is gaining popularity in some countries as an alternative to nitroprusside but a parenteral form is not yet available in the UK.


Phentolamine is an lpha blocking agent which is used exclusively for hypertensive emergencies related to excess catecholamine release (e.g. phaeochromocytoma, cocaine overdose).

It is (like hydralazine) rarely used today since other agents are effective and have a more predictable response (e.g. nitroprusside and labetalol).

Essentially, all hypertensive emergencies can be treated with one of (or a combination of) three key drugs: nitroprusside, labetalol, or nitrates.

Learning Bite

Nitroprusside, nitrates and labetalol are the three key drugs used in all hypertensive emergencies.

Indications and Administration Details

This table summarises the indications and administration details of parenteral agents used in hypertensive emergencies.







Sodium Nitroprusside Initially 0.5-1.5mcg/kg/min.

Titrate up in increments of 0.5 mcg/kg/minMax up to 8 mcg/kg/min

Hypertensive encephalopathy

Cardiac ischaemia

Cardiac failure/pulmonary oedema

Aortic dissection (+ beta blocker)

Labetalol Initial 20-50mg over at least 1 minute. Can be repeated every 5 minutes to a maximum of 200mg OR titrate infusion starting at 2mg/min.

Then infusion 2mg/min, titrated as required

Stroke syndromes

Hypertensive encephalopathy

Aortic dissection



Nitrates Isosorbide dinitrate 2-10mg/hr max 20mg/hr

Glyceryl trinitrate 10-20 mcg/min max 200 mcg/min

Cardiac ischaemia

Cardiac failure/pulmonary oedema

Hydralazine Initial 5-10mg slow bolus.

Then repeat boluses or infusion 50-100 mcg/min

Eclampsia (second line treatment)
Nicardipine Infusion of 2.5-5mg/hr.

Increase according to response by 0.5 1mg every 15 minutes to a maximum of 15mg/hr


Hypertensive encephalopathy

Phentolamine 2-5mg bolus doses, repeated as necessary Phaeochromocytoma
  1. Vaughan CJ, Delanty N. Hypertensive emergencies. Lancet. 2000 Jul 29;356(9227):411-7.
  2. Zampaglione, B., Pascale, C., Marchisio, M., et al. (2003) Hypertensive urgencies and emergencies. Prevalence and clinical presentation. Hypertension, 42(6), pp. 1206-52.
  3. Gallagher EJ. Hypertensive urgencies: treating the mercury? Ann Emerg Med. 2003 Apr;41(4):530-1.
  4. Wardlaw JM, Murray V, Berge E, del Zoppo GJ. Thrombolysis for acute ischaemic stroke. Cochrane Database Syst Rev. 2014 Jul 29;2014(7):CD000213.
  5. National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med. 1995 Dec 14;333(24):1581-7.
  6. Perez MI, Musini VM. Pharmacological interventions for hypertensive emergencies: a Cochrane systematic review. J Hum Hypertens. 2008 Sep;22(9):596-607.