Summary

Defined as elevated BP (usually systolic BP >210 mmHg and diastolic BP >130 mmHg) with rapid decompensation of vital organ function. 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. Oral medications should be given shortly thereafter to permit weaning from parenteral agents. The initial goal of therapy is to reduce mean arterial BP by no more than 25% (within minutes to 1 hour), then, if stable, to 160/110 to 100 mmHg within the next 2 to 6 hours. Exceptions to this general rule are patients with intracranial pathology and patients with aortic dissection. Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischaemia should be avoided. With appropriate treatment, prognosis is good.

Other related conditions

Essential hypertension Gestational hypertension Subarachnoid haemorrhage Non-ST-elevation myocardial infarction ST-elevation myocardial infarction Acute renal failure Pre-eclampsia Aortic dissection Polycystic kidney disease
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Fundus photograph of the right eye with multiple dot-blot haemorrhages typical of hypertensive retinopathy

Courtesy Angie Wen MD, Columbia University College of Physicians and Surgeons, New York

Fundus photograph of the left eye with multiple cotton-wool spots typical of hypertensive retinopathy Courtesy Angie Wen MD, Columbia University College of Physicians and Surgeons, New York

Fundus photograph of the right eye centred on the optic nerve, showing multiple cotton-wool spots and macular exudates in a radiating star configuration around the fovea Courtesy Angie Wen MD, Columbia University College of Physicians and Surgeons, New York

Definition
Hypertensive emergency is elevated BP (usually systolic BP >210 mmHg and diastolic BP >130 mmHg) with rapid deterioration of vital organ function, resulting in symptoms such as encephalopathy, retinopathy, myocardial ischaemia, or renal failure. The absolute value of the BP is not as vital as the presence of acute end-organ damage.

Epidemiology
The worldwide prevalence of hypertension is around 26%, totalling 1 billion people. [1] Of these, 1% to 2% will suffer a hypertensive crisis in their lifetime. [2] [3] Men may be more likely than women to suffer a hypertensive emergency. Hypertensive emergency is also more common in older patients and in black people. [4] [5] [6] In the US, 30% of people suffer from hypertension; [7] [8] lack of insurance or a primary care doctor and non-adherence to treatment all predispose toward development of hypertensive emergency. [9] [10] As populations age globally, the prevalence of hypertension and therefore hypertensive emergency is expected to increase. [1]

Aetiology
There are many causes of hypertensive emergency. By far the most common cause is essential hypertension that is either undiagnosed or inadequately treated. [4] The next most common cause is secondary to renal disease, such as renal artery stenosis, acute glomerulonephritis, collagen-vascular diseases, or kidney transplantation. [11] [12]Pregnancy-related eclampsia is also an important cause of hypertensive emergency. Other rarer causes include hyperaldosteronism and conditions leading to excess circulating catecholamines (e.g., phaeochromocytoma, sympathomimetic drug intake, autonomic dysfunction after spinal cord injury, or inadvertent drug or food interactions with monoamine oxidase inhibitors). [13]

Pathophysiology
The factors that lead to the development of hypertensive emergency are poorly understood. A rise in systemic vascular resistance initiates the cycle. The subsequent increase in BP generates mechanical stress and endothelial injury leading to increased permeability, activation of the coagulation cascade and platelets, and deposition of fibrin. These processes result in ischaemia and the release of additional vasoactive mediators, generating ongoing injury. Volume depletion caused by pressure natriuresis and activation of the reninangiotensin system often leads to further vasoconstriction. Systemic vasoconstriction leads to decreased blood flow to vital organs and the subsequent organ injury that is the hallmark of hypertensive emergency. Neurological injury may manifest as retinopathy, papilloedema, encephalopathy, cerebrovascular accidents, seizures, or coma. Cardiac injury may manifest as chest pains or SOB, signifying impending or actual MI, aortic

dissection, or left ventricular failure with pulmonary oedema. Renal failure may manifest as oliguria and azotaemia. [6] [13] [14] [15]

Primary prevention
The mainstay of primary prevention is appropriate screening and treatment of essential hypertension.

Secondary prevention
Major lifestyle modifications shown to lower BP include the Dietary Approaches to Stop Hypertension (DASH) eating plan, dietary sodium reduction, weight reduction in overweight patients, physical activity, and moderation of alcohol consumption. [46] [47]

History & examination

Key diagnostic factorshide all
BP above 210/130 mmHg (common) BP is usually above 210/130 mmHg in hypertensive emergencies. presence of risk factors (common)

Risk factors include: inadequately treated hypertension, older age, black ethnicity, male gender,

use of sympathomimetic drugs, and use of monoamine oxidase inhibitors. Other diagnostic factorshide all neurological symptoms (common)

Neurological abnormalities such as dizziness, headaches, mental status changes, and loss of sensation or motor strength are symptoms often associated with hypertensive emergency. [6]

cardiac symptoms (common)

Cardiac abnormalities (e.g., chest pain or pressure, SOB, oedema) are frequently associated with hypertensive emergency. [6]

abnormal cardiopulmonary examination (common)

The presence of new murmurs, S3, jugular venous distension, rales, or lower extremity oedema may be found.

oliguria or polyuria (common) Any changes in renal output can be indicative of renal damage. [11] abnormal fundoscopic examination (common)

The following signs are indicative of hypertensive retinopathy: arteriolar spasm, retinal oedema, retinal haemorrhages, retinal exudates, papilloedema, engorged retinal veins. [16]

abnormal neurological examination (common)

Abnormal findings in cranial nerve function, motor strength, gross sensory function, and gait can frequently result from hypertensive crisis.

Risk factorshide all

Strong inadequately treated hypertension

A history of inadequately treated hypertension is commonly seen. [5] [9] [10]

In the US, lack of medical insurance or access to a primary care doctor have been shown to predispose to hypertensive emergency. [10]

Weak older age Older age predisposes to hypertensive emergency. [4][5] [6] black ethnicity Black people are predisposed to hypertensive emergency, compared with white people. [4] [5] [6] male gender Men may be more likely than women to suffer a hypertensive emergency. [4] [5] [6] use of sympathomimetic drugs

Use of sympathomimetic street drugs (e.g., cocaine, LSD, amphetamines, ecstasy) predisposes to hypertensive emergency.

use of monoamine oxidase inhibitors (MAOIs)

Inadvertent ingestion of food containing tyramine in patients taking MAOIs can precipitate a hypertensive emergency.

Diagnostic tests
1st tests to orderhide all
Test

FBC with smear of developing acute renal failure. [17]

Microangiopathic haemolytic anaemia (MAHA) may occur in patients with hypertensive emergency and increase

blood chemistry Renal failure as manifested by elevated creatinine may be the only sign of hypertensive emergency. urinalysis with microscopy Renal failure as manifested by haematuria and proteinuria may be the only sign of hypertensive emergency. electrocardiogram If ECG is abnormal, troponin levels are tested to rule out ongoing ischaemia or infarction. If ECG is normal, aortic dissection should be considered as an explanation for chest pain. CXR CXR is useful to assess for pulmonary oedema, LVH, and aortic dissection.

Note, however, that a CXR has low sensitivity in detection of aortic dissection (56% in type B and 63% in type A)

aortic dissection is suspected, an urgent CT scan with contrast should be ordered.

head CT without contrast acute ischaemic stroke, it is usually ordered to exclude or confirm haemorrhage.

Indicated if neurological complications are suspected. Although the non-contrast CT scan (NCCT) is of low sensi

MRI, although more sensitive than NCCT, may not be widely available in a timely fashion and should be ordered Dopplers) should be considered if initial tests indicate ischaemia or infarct. [22] head MRI More sensitive than non-contrast CT scan, but may not be available as first-line investigation in all centres. spot urine or plasma metanephrine

up to a NCCT. Further neuroimaging (e.g., CT-angiography, magnetic resonance angiography, carotid and verte

May be useful before initiation of drug therapy to rule out phaeochromocytoma. However, needs to be interpreted

carefully, with consideration for possible confounding factors such as drugs (e.g., tricyclic antidepressants, cloza

phenoxybenzamine, beta-blockers, sympathomimetics, buspirone) or major physiological or psychological stress

Tests to considerhide all

Test

thoracic CT scan with contrast especially in the presence of possible underlying renal abnormality. The sensitivity and specificity of standard CT for the diagnosis of aortic dissection is around 90% and 95%, respectively. Newer imaging techniques such as helical CT approach 100% sensitivity and specificity. [19] [20] CT. [20] [21] CT scan may be recommended as the initial test of choice but this is institutionally variable and TEE may be substituted if available in a timely fashion. transoesophageal echocardiography (TEE) May be substituted for CT if available in a timely fashion. More sensitive than standard CT and comparable with helical CT. [20] [21] plasma renin activity and aldosterone level

This test should be ordered only if aortic dissection is suspected, given the risk of contrast-induced nephropathy,

Transoesophageal echocardiogram (TEE) and MRI are comparable to helical CT and more sensitive than standa

This test is an indirect measure of the activity of renin through measurement of the rate of production of angioten

I, which increases as a result of renin stimulation. Aldosterone levels are usually measured at the same time. Hig catheterisation and so needs formal consent from the patient.

plasma renin activity suggests hypertension from the vasoconstrictive effects of angiotensin. Requires renal vein

single-dose captopril challenge May be useful where renovascular hypertension is suspected, particularly in patients who have not received previous medical therapy.

Baseline plasma renin activity is measured and the patient is then given 25 to 50 mg of captopril; measurement o plasma renin activity is repeated 60 minutes later.

Test sensitivity is excellent but specificity is poor. Further testing with renal arterial Doppler ultrasonography, rena magnetic resonance angiography, or contrast angiography may be necessary to confirm diagnosis.

Differential diagnosis
Condition Hypertensive urgency Differentiating signs/symptoms Differentiating tests

Symptomatic elevated BP

History, physical examination, laboratory tests, and imaging sh organ damage.

Hypertension

Asymptomatic elevated BP

History, physical examination, laboratory tests, and imaging sh organ damage.

Step-by-step diagnostic approach

The key to diagnosis of hypertensive emergency is a rapid but thorough evaluation. If hypertensive emergency is suspected, initiation of treatment should not be delayed while conducting a full diagnostic appraisal.

History
Any prior history of hypertension and previous treatment should be identified. Clinical features that may identify specific organ compromise include: Neurological compromise; for example, blurry vision, dizziness, loss of sensation, or loss of movement Cardiac compromise; for example, chest pain or pressure, SOB, orthopnoea, paroxysmal nocturnal dyspnoea, or oedema

Renal compromise; for example, decrease in urine output. When appropriate, use of street drugs, particularly sympathomimetics (cocaine, amphetamines, phenylpropanolamine, phencyclidine, ecstasy, LSD) should be investigated.

Physical examination
An appropriately sized cuff should be used for BP readings. The cuff bladder should encircle at least 80% of the upper arm. The arm should also be supported at heart level during recordings. Using too large a cuff results in an underestimation of BP; conversely, too small a cuff will lead to overestimation. BP readings should be taken from both arms and readings repeated after 5 minutes to confirm. If there is a more than 20 mmHg pressure difference between arms, aortic dissection should be considered. A fundoscopic examination should be performed, looking for the presence of arteriolar spasm, retinal oedema, retinal haemorrhages, retinal exudates, papilloedema, or engorged retinal veins. View imageView imageView image A rapid bedside neurological examination is also required, including testing cranial nerve function, motor strength, gross sensory function, and gait. Cardiopulmonary status should be assessed, examining in particular for the presence of new murmurs, additional heart sounds, jugular venous distension, rales, and lower extremity oedema.

Laboratory evaluation
Baseline blood and urine samples must be collected prior to administration of treatment. Laboratory evaluation should include the following: FBC, including peripheral blood smear Blood chemistry panel, including creatinine and electrolytes Urinalysis with microscopy. In some circumstances, the following may also be indicated: Plasma renin activity and aldosterone levels, if primary aldosteronism is suspected (e.g., in patients with diastolic hypertension with persistent hypokalaemia and metabolic alkalosis) Plasma renin activity before and 1 hour after 25-mg captopril is administered if renovascular hypertension is suspected. Renovascular hypertension should be suspected in patients with severe hypertension who have abdominal bruits and/or unexplained renal deterioration with angiotensin-converting enzyme (ACE) inhibitor treatment, although the clinical presentation is variable

Spot urine or plasma-free metanephrine levels if phaeochromocytoma is suspected (e.g., in patients with hypertension and palpitations, headaches and/or diaphoresis although clinical presentation is very variable).

Further investigation
CXR and ECG are obtained. If aortic dissection is considered, an urgent thoracic CT scan with contrast or a transoesophageal echocardiogram should also be obtained. If ischaemic stroke or intracranial haemorrhage is suspected (e.g., in patients with focal neurological defects) urgent non-contrast CT scan (NCCT) of the head and/or an MRI are done, depending on local availability.
Click to view diagnostic guideline references.

Diagnostic criteria
Clinical criteria
Elevated BP in the presence of acute or rapidly deteriorating end-organ damage (e.g., neurological, cardiac, or renal compromise) based on historical or clinical criteria (physical examination, laboratory tests, or imaging), posing an immediate threat to life, is sufficient for diagnosis of hypertensive emergency. [3]

Case history
A 50-year-old black man with a history of untreated hypertension presents to the emergency department with substernal chest pressure. His symptoms started 1 day prior. The pain was initially intermittent in nature but has become constant and radiates to his jaw and left shoulder. He also complains of dizziness and some SOB. Apart from a history of hypertension diagnosed 1 year ago, the patient denies any past medical history. He is not taking any antihypertensive medications. The patient denies smoking, or alcohol or drug use. Family history is unremarkable. His BP is 230/130 mmHg with otherwise normal vital signs and no other significant findings. ECG shows diffuse Twave inversion and ST depression in lateral leads. Laboratory testing is significant for elevated troponin, signalling MI.

Other presentations
Other ways in which hypertensive emergency can present include neurological symptoms (e.g., cerebrovascular accidents, encephalopathy), chest pain signifying cardiac conditions other than infarction or ischaemia (e.g., aortic dissection, pulmonary oedema), or nephrological symptoms (e.g., decreased or absent urine output).

Treatment Options
Treatment Patient group accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage increased intracranial pressure or renal disease 1st line Treatmenthide all

labetalol

Labetalol is drug of choice in situations characterised by markedly elevated intracranial pressure.

Onset of action: 5 to 10 minutes. Duration of action: 3 to 8 hours. In cases of intracranial haemorrhage, goal mean arterial pressure (MAP) is 130 mmHg and goal cerebral perfusion pressure is above 70 mmHg. MAP should not be dropped below 110 mmHg.

Encephalopathy should improve once BP is lowered. If there is no improvement despite a decrease in BP, an alternative diagnosis should be considered.

Dose should be adjusted to maintain BP in desired range and is continued until BP controlled on oral agents. Primary Options labetalol : 20 mg intravenously every 10 minutes according to response, maximum 300 mg total dose; or 0.5 to 2 mg/minute intravenous infusion

2nd

nicardipine

Nicardipine is a second-generation dihydropyridine derivative calcium-channel blocker with high vascular selectivity and strong cerebral and coronary vasodilatory activity. The onset of action of IV nicardipine is from 5 to 15 minutes, with a duration of action of 4 to 6 hours.

Treatment Patient group accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage line Treatmenthide all

Nicardipine is especially useful in the presence of cardiac disease due to coronary vasodilatory effects. Primary Options nicardipine : 5 mg/hour intravenously initially, increase by 2.5 mg/hour increments every 15 minutes according to response, maximum 15 mg/hour

3rd

fenoldopam

Fenoldopam is especially useful in renal insufficiency, where the use of nitroprusside is restricted because of the risk of thiocyanate poisoning.

It acts as a selective peripheral dopamine-1receptor agonist with arterial vasodilator effects. Its haemodynamic effects are a decrease in afterload and an increase in renal perfusion.

Onset of action: 5 minutes. Duration of action: 30 minutes. In cases of intracranial haemorrhage, goal mean arterial pressure (MAP) is 130 mmHg and goal cerebral perfusion pressure is above 70 mmHg. MAP should not be dropped to below 110 mmHg.

Encephalopathy should improve once BP is lowered. If there is no improvement despite a decrease in BP, an alternative diagnosis should be considered.

Continue until BP controlled on oral agents Primary Options

Treatment Patient group accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage line Treatmenthide all

fenoldopam : 0.1 to 0.3 micrograms/kg/minute intravenously initially, increase by 0.05 to 0.1 micrograms/kg/minute increments every 15 minutes according to response, maximum 1.6 micrograms/kg/minute
normal intracranial pressure and renal function 1st

labetalol

Onset of action: 5 to 10 minutes. Duration of action: 3 to 8 hours. In cases of intracranial haemorrhage, goal mean arterial pressure (MAP) is 130 mmHg and goal cerebral perfusion pressure is above 70 mmHg. MAP should not be dropped below 110 mmHg.

Encephalopathy should improve once BP is lowered. If there is no improvement despite a decrease in BP, an alternative diagnosis should be considered.

Dose should be adjusted to maintain BP in desired range and is continued until BP controlled on oral agents. Primary Options labetalol : 20 mg intravenously every 10 minutes according to response, maximum 300 mg total dose; or 0.5 to 2 mg/minute intravenous infusion

2nd

nitroprusside or nicardipine

Sodium nitroprusside acts as a potent arterial and venous vasodilator, thereby reducing afterload and preload. Its haemodynamic effects are to decrease mean arterial pressure (MAP), with a modest increase or no change in cardiac output. Onset of

Treatment Patient group accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage line Treatmenthide all

action: immediate. Duration of action: 3 to 5 minutes.

Patients should be monitored by drawing thiocyanate levels after 48 hours of therapy (levels kept at <2064 micromol/L (<12 mg/dL or 120 mg/L)). Maximum dose should be delivered for less than 10 minutes to decrease chance of cyanide toxicity.

Nicardipine is a second-generation dihydropyridine derivative calcium-channel blocker with high vascular selectivity and strong cerebral and coronary vasodilatory activity. The onset of action of IV nicardipine is from 5 to 15 minutes, with a duration of action of 4 to 6 hours. It is especially useful in the presence of cardiac disease due to coronary vasodilatory effects.

In cases of intracranial haemorrhage, goal MAP is 130 mmHg and goal cerebral perfusion pressure is above 70 mmHg. MAP should not be dropped to below 110 mmHg. Encephalopathy should improve once BP is lowered. If there is no improvement despite a decrease in BP, an alternative diagnosis should be considered.

Continue until BP controlled on oral agents. Primary Options nitroprusside : 0.3 to 0.5 micrograms/kg/minute intravenously initially, increase by 0.5 micrograms/kg/minute increments according to response, maximum 10 micrograms/kg/minute OR

Treatment Patient group accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage line Treatmenthide all

nicardipine : 5 mg/hour intravenously initially, increase by 2.5 mg/hour increments every 15 minutes according to response, maximum 15 mg/hour
3rd

fenoldopam

Fenoldopam acts as a selective peripheral dopamine-1-receptor agonist with arterial vasodilator effects. Its haemodynamic effects are a decrease in afterload and an increase in renal perfusion.

Onset of action: 5 minutes. Duration of action: 30 minutes. In cases of intracranial haemorrhage, goal mean arterial pressure (MAP) is 130 mmHg and goal cerebral perfusion pressure is above 70 mmHg. MAP should not be dropped to below 110 mmHg.

Encephalopathy should improve once BP is lowered. If there is no improvement despite a decrease in BP, an alternative diagnosis should be considered.

Continue until BP controlled on oral agents Primary Options fenoldopam : 0.1 to 0.3 micrograms/kg/minute intravenously initially, increase by 0.05 to 0.1 micrograms/kg/minute increments every 15 minutes according to response, maximum 1.6 micrograms/kg/minute

acute ischaemic stroke

Treatment Patient group accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage SBP 220 mmHg and DBP 120 mmHg 1st line Treatmenthide all

close observation BP reduction

Treatment of a hypertensive emergency with an associated acute ischaemic stroke warrants greater caution in reducing BP than with other types of hypertensive emergency. Overly rapid or too great a reduction of mean arterial pressure (MAP) may decrease cerebral perfusion pressure to a level that could theoretically worsen brain injury. The following may be used as guidance:

If the systolic BP is below 220 mmHg and the diastolic BP is below 120 mmHg, there is no evidence of end organ involvement or intracranial haemorrhage and thrombolytic treatment is not proposed, then it is reasonable to maintain close observation without direct intervention to reduce BP.

If there is other end-organ involvement such as aortic dissection, renal failure, or acute MI, or the patient is to receive thrombolytics, the target systolic BP is below 185 mmHg and diastolic BP is below 110 mmHg.

If there is intracranial haemorrhage, the target systolic BP is 140 to 160 mmHg and/or a mean arterial pressure (MAP) of 130 mmHg and a cerebral perfusion pressure maintained above 70 mmHg.

MAP should not be dropped below 110 mmHg. The choice of agent to reduce blood pressure depends on the associated end-organ involvement.

SBP >220 mmHg or DBP 121 to 140 mmHg

1st

labetalol

If the systolic BP is above 220 mmHg or the

Treatment Patient group accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage line Treatmenthide all

diastolic BP is between 121 and 140 mmHg, then labetalol [13] [14] [15] [C Evidence] or nicardipine [13] [14][15] [33] [C Evidence] should be used to achieve a 10% to 15% reduction in 24 hours.

Labetalol acts as an alpha-1-blocker and nonselective beta-blocker, and its haemodynamic effects include decreasing systemic vascular resistance, MAP, and heart rate, accompanied by a slight decrease or minimal change in cardiac output.

Onset of action: 5 to 10 minutes. Duration of action: 3 to 8 hours. Continue until BP controlled on oral agents. Primary Options labetalol : 20 mg intravenously every 10 minutes according to response, maximum 300 mg total dose; or 0.5 to 2 mg/minute intravenous infusion

2nd

nicardipine

If systolic BP is above 220 mmHg or diastolic BP is between 121 and 140 mmHg, then labetalol [13] [14] [15] [C Evidence] or nicardipine [13] [14] [15][33] [C Evidence] should be used to achieve a 10% to 15% reduction in 24 hours.

Nicardipine is a dihydropyridine calcium-channel blocker, which increases stroke volume and has strong cerebral and coronary vasodilatory activity.

Onset of action: 5 to 10 minutes. Duration of action: 2 to 4 hours.

Treatment Patient group accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage line Treatmenthide all

Continue until BP controlled on oral agents. Primary Options nicardipine : 5 mg/hour intravenously initially, increase by 2.5 mg/hour increments every 15 minutes according to response, maximum 15 mg/hour

DBP >140 mmHg

1st

nitroprusside

If diastolic BP is above 140 mmHg, then nitroprusside [13] [14] [C Evidence]may be used to achieve a 10% to 15% reduction over 24 hours.

It acts as a potent arterial and venous vasodilator thereby reducing afterload and preload. Its haemodynamic effects are to decrease MAP, with a modest increase or no change in cardiac output.

Onset of action: immediate. Duration of action: 3 to 5 minutes. Patients should be monitored by drawing thiocyanate levels after 48 hours of therapy (levels maintained <2064 micromol/L (<12 mg/dL or 120 mg/L)). Maximum dose should be delivered for less than 10 minutes to decrease chance of cyanide toxicity.

Continue until BP controlled on oral agents. Primary Options nitroprusside : 0.3 to 0.5 micrograms/kg/minute intravenously initially, increase by 0.5 micrograms/kg/minute increments according to response, maximum 10 micrograms/kg/minute

Treatment Patient group accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage 1st line Treatmenthide all

myocardial ischaemia/infarction

esmolol and glyceryl trinitrate

Esmolol onset of action: 1 to 5 minutes. Duration of action: 5 minutes. Glyceryl trinitrate acts as a peripheral vasodilator, with greater action on the venous vessels than on arterial vessels. It causes a decrease in preload and cardiac output and increases coronary blood flow. Onset of action: immediate. Duration of action: 3 to 5 minutes.

Continue until BP controlled on oral agents. Primary Options esmolol : 50-100 micrograms/kg/minute intravenously and glyceryl trinitrate : 5-100 micrograms/minute intravenously

2nd

labetalol and glyceryl trinitrate

Labetalol is an alpha-1-blocker and non-selective beta-blocker that decreases systemic vascular resistance, mean arterial pressure (MAP) and heart rate, and causes a decrease or no change in cardiac output. Onset of action: 5 to 10 minutes. Duration of action: 3 to 8 hours.

Glyceryl trinitrate acts as a peripheral vasodilator, with greater action on the venous vessels than on arterial vessels. It causes a decrease in preload and cardiac output and increases coronary blood flow. Onset of action: immediate. Duration of action: 3 to 5 minutes.

Treatment Patient group accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage line Treatmenthide all

Continue until BP controlled on oral agents. Primary Options glyceryl trinitrate : 5-100 micrograms/minute intravenously

3rd

nitroprusside

Sodium nitroprusside acts as a potent arterial and venous vasodilator thereby reducing afterload and preload. Its haemodynamic effects are to decrease mean arterial pressure, with a modest increase or no change in cardiac output.

Onset of action: immediate. Duration of action: 3 to 5 minutes. Patients should be monitored by drawing thiocyanate levels after 48 hours of therapy (levels maintained <2064 micromol/L (<12 mg/dL or 120 mg/L)). Maximum dose should be delivered for less than 10 minutes to decrease chance of cyanide toxicity.

Continue until BP controlled on oral agents. Primary Options nitroprusside : 0.3 to 0.5 micrograms/kg/minute intravenously initially, increase by 0.5 micrograms/kg/minute increments according to response, maximum 10 micrograms/kg/minute

left ventricular failure and/or pulmonary oedema

1st

glyceryl trinitrate + furosemide

Glyceryl trinitrate acts as a peripheral vasodilator, with greater action on the venous vessels than on

Treatment Patient group accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage line Treatmenthide all

arterial vessels.

It causes a decrease in preload and cardiac output and increases coronary blood flow. Onset of action: immediate. Duration of action: 3 to 5 minutes. Continue until BP controlled on oral agents. If patient is not already on one, a loop diuretic should be started (e.g., furosemide). Primary Options glyceryl trinitrate : 5-100 micrograms/minute intravenously and furosemide : 40-80 mg intravenously initially, increase according to response

2nd

nitroprusside + furosemide

Sodium nitroprusside acts as a potent arterial and venous vasodilator thereby reducing afterload and preload. Its haemodynamic effects are to decrease mean arterial pressure, with a modest increase or no change in cardiac output.

Patients should be monitored by drawing thiocyanate levels after 48 hours of therapy (levels maintained <2064 micromol/L (<12 mg/dL or 120 mg/L)). Maximum dose should be delivered for less than 10 minutes to decrease chance of cyanide toxicity.

Continue until BP controlled on oral agents.

Treatment Patient group accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage line Treatmenthide all

Primary Options nitroprusside : 0.3 to 0.5 micrograms/kg/minute intravenously initially, increase by 0.5 micrograms/kg/minute increments according to response, maximum 10 micrograms/kg/minute and furosemide : 40-80 mg intravenously initially, increase according to response

aortic dissection

1st

labetalol or esmolol

Medical therapy of aortic dissection involves lowering the BP and decreasing the velocity of left ventricular contraction, which decreases aortic shear stress and minimises the tendency for propagation of the dissection.

Systolic BP should be reduced to 100 to 120 mmHg in the first 20 minutes or as tolerated by the patient.

Labetalol is an alpha-1-blocker and non-selective beta-blocker that decreases systemic vascular resistance, mean arterial pressure, and heart rate, and causes a decrease or no change in cardiac output. Onset of action: 5 to 10 minutes. Duration of action: 3 to 8 hours.

The mechanism of action of esmolol is as a selective beta-blocker, producing a decrease in heart rate. Onset of action: 1 to 5 minutes. Duration of action: 5 minutes.

Dose adjusted to maintain BP in desired range;

Treatment Patient group accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage line Treatmenthide all

continue until patient has undergone surgical repair/evaluation and is stable on oral therapy. Primary Options labetalol : 20 mg intravenously every 10 minutes according to response, maximum 300 mg total dose; or 0.5 to 2 mg/minute intravenous infusion OR esmolol : 50-100 micrograms/kg/minute intravenously
2nd

nitroprusside

Medical therapy of aortic dissection involves lowering the BP and decreasing the velocity of left ventricular contraction, both of which will decrease aortic shear stress and minimise the tendency for propagation of the dissection.

Systolic BP should be reduced to 100 to 120 mmHg in the first 20 minutes or as tolerated by patient.

Sodium nitroprusside must be administered with a beta-blocker as nitroprusside-induced vasodilation would otherwise induce a compensatory tachycardia and worsen shear stress.

Nitroprusside acts as a potent arterial and venous vasodilator thereby reducing afterload and preload. Its haemodynamic effects are to decrease mean arterial pressure (MAP), with a modest increase or no change in cardiac output. Onset of action: immediate. Duration of action: 3 to 5 minutes.

Patients should be monitored by drawing

Treatment Patient group accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage line Treatmenthide all

thiocyanate levels after 48 hours of therapy (levels maintained <2064 micromol/L (<12 mg/dL or 120 mg/L)). Maximum dose should be delivered for less than 10 minutes to decrease chance of cyanide toxicity. Primary Options nitroprusside : 0.3 to 0.5 micrograms/kg/minute intravenously initially, increase by 0.5 micrograms/kg/minute increments according to response, maximum 10 micrograms/kg/minute plus [?] labetalol or esmolol

Labetalol is an alpha-1-blocker and non-selective beta-blocker that decreases systemic vascular resistance, MAP and heart rate, and causes a decrease or no change in cardiac output. Onset of action: 5 to 10 minutes. Duration of action: 3 to 8 hours.

The mechanism of action of esmolol is as a selective beta-blocker, producing a decrease in heart rate. Onset of action: 1 to 5 minutes. Duration of action: 5 minutes.

Dose adjusted to maintain BP in desired range; continue until patient has undergone surgical repair/evaluation and is stable on oral therapy Primary Options labetalol : 20 mg intravenously every 10 minutes according to response, maximum 300 mg total dose; or 0.5 to 2 mg/minute intravenous infusion

Treatment Patient group accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage line Treatmenthide all

OR esmolol : 50-100 micrograms/kg/minute intravenously

acute renal failure

1st

fenoldopam

Fenoldopam is useful in renal insufficiency because it causes an increase in blood flow to the kidneys.

It acts as a selective peripheral dopamine-1receptor agonist with arterial vasodilator effects. Its haemodynamic effects are a decrease in afterload and an increase in renal perfusion. Primary Options fenoldopam : 0.1 to 0.3 micrograms/kg/minute intravenously initially, increase by 0.05 to 0.1 micrograms/kg/minute increments every 15 minutes according to response, maximum 1.6 micrograms/kg/minute

2nd

nicardipine

Nicardipine is a dihydropyridine calcium-channel blocker that increases stroke volume and has strong cerebral and coronary vasodilatory activity.

Onset of action: 5 to 10 minutes. Duration of action: 2 to 4 hours. Primary Options nicardipine : 5 mg/hour intravenously initially,

Treatment Patient group accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage line Treatmenthide all

increase by 2.5 mg/hour increments every 15 minutes according to response, maximum 15 mg/hour

hyperadrenergic state sympathomimetic drug use 1st

benzodiazepines

Sympathomimetic drug use includes cocaine, amphetamines, phenylpropanolamine, phencyclidine, or the combination of a monoamine oxidase inhibitor with foods rich in tyramine.

If the patient is agitated, benzodiazepines can be given first. Lorazepam should be used with caution in patients with renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease. Excess CNS or respiratory depression can occur with higher doses and should be watched for.

Anti-hypertensive agents can be given if the blood pressure response to benzodiazepines is inadequate. Primary Options lorazepam : 1 mg intravenous bolus initially, repeated every 10-15 minutes according to response, maximum 8 mg OR diazepam : 5 mg intravenous bolus initially, repeated every 5-10 minutes according to

Treatment Patient group accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage line Treatmenthide all

response, maximum 50 mg
2nd

phentolamine

Phentolamine acts to block alpha-adrenoceptors. Its main haemodynamic effects are to increase heart rate and contractility.

Onset of action: 1 to 2 minutes. Duration of action: 3 to 10 minutes. Primary Options phentolamine : 2-5 mg intravenous bolus

3rd

labetalol and nitroprusside

Labetalol is an alpha-1-blocker and non-selective beta-blocker that decreases systemic vascular resistance, mean arterial pressure (MAP), and heart rate, and causes a decrease or no change in cardiac output. Onset of action: 5 to 10 minutes. Duration of action: 3 to 8 hours.

Sodium nitroprusside must be administered with a beta-blocker as nitroprusside-induced vasodilation would otherwise induce a compensatory tachycardia and worsen shear stress.

Nitroprusside acts as a potent arterial and venous vasodilator thereby reducing afterload and preload. Its haemodynamic effects are to decrease MAP, with a modest increase or no change in cardiac output. Onset of action: immediate. Duration of action: 3 to 5 minutes.

Patients should be monitored by drawing thiocyanate levels after 48 hours of therapy (levels maintained <2064 micromol/L (<12 mg/dL or 120

Treatment Patient group accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage line Treatmenthide all

mg/L)). Maximum dose should be delivered for less than 10 minutes to decrease chance of cyanide toxicity.

Continue until BP controlled on oral agents. Primary Options labetalol : 20 mg intravenously every 10 minutes according to response, maximum 300 mg total dose; or 0.5 to 2 mg/minute intravenous infusion and nitroprusside : 0.3 to 0.5 micrograms/kg/minute intravenously initially, increase by 0.5 micrograms/kg/minute increments according to response, maximum 10 micrograms/kg/minute

no sympathomimetic drug use

1st

phentolamine

Causes of hyperadrenergic states include phaeochromocytoma and abrupt discontinuation of a short-acting sympathetic blocker.

Phentolamine acts to block alpha-adrenoceptors. Its main haemodynamic effects are to increase heart rate and contractility.

Onset of action: 1 to 2 minutes. Duration of action: 3 to 10 minutes. Primary Options phentolamine : 2-5 mg intravenous bolus

2nd

labetalol and nitroprusside

Labetalol is an alpha-1-blocker and non-selective beta-blocker that decreases systemic vascular

Treatment Patient group accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage line Treatmenthide all

resistance, mean arterial pressure (MAP), and heart rate, and causes a decrease or no change in cardiac output. Onset of action: 5 to 10 minutes. Duration of action: 3 to 8 hours.

Sodium nitroprusside must be administered with a beta-blocker as nitroprusside-induced vasodilation would otherwise induce a compensatory tachycardia and worsen shear stress.

Nitroprusside acts as a potent arterial and venous vasodilator thereby reducing afterload and preload. Its haemodynamic effects are to decrease MAP, with a modest increase or no change in cardiac output. Onset of action: immediate. Duration of action: 3 to 5 minutes.

Patients should be monitored by drawing thiocyanate levels after 48 hours of therapy (levels maintained <2064 micromol/L (<12 mg/dL or 120 mg/L)). Maximum dose should be delivered for less than 10 minutes to decrease chance of cyanide toxicity.

Continue until BP controlled on oral agents. Primary Options labetalol : 20 mg intravenously every 10 minutes according to response, maximum 300 mg total dose; or 0.5 to 2 mg/minute intravenous infusion and nitroprusside : 0.3 to 0.5 micrograms/kg/minute intravenously initially, increase by 0.5 micrograms/kg/minute increments according to

Treatment Patient group accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage line Treatmenthide all

response, maximum 10 micrograms/kg/minute

eclampsia

1st

hydralazine, labetalol, or nicardipine

A guide target in these patients is to maintain a systolic BP of 130 to 150 mmHg and a diastolic BP of 80 to 100 mmHg. However, it should be noted that there are no trials supporting these suggested thresholds, and treatments should be tailored to individual patient circumstances.

Hydralazine, labetalol, or nicardipine can be used first-line. Hydralazine is an arterial vasodilator with minimal effects on the fetus. Onset of action: 10 to 20 minutes. Duration of action: 3 to 8 hours. Its main haemodynamic effects are a decrease in systemic vascular resistance, an increase in heart rate and an increase in intracranial pressure.

Labetalol acts as an alpha-1-blocker and nonselective beta-blocker and its haemodynamic effects include decreasing systemic vascular resistance, mean arterial pressure, and heart rate, accompanied by a slight decrease or minimal change in cardiac output. Onset of action: 5 to 10 minutes. Duration of action: 3 to 8 hours.

Nicardipine is a dihydropyridine calcium-channel blocker that increases stroke volume and has strong cerebral and coronary vasodilatory activity. Onset of action: 5 to 10 minutes. Duration of action: 2 to 4 hours.

Therapy should be continued until the fetus has

Treatment Patient group accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage line Treatmenthide all

been delivered and the patient is stable on oral therapy. Primary Options hydralazine : 5-10 mg intravenously every 30 minutes according to response OR labetalol : 20 mg intravenously every 10 minutes according to response, maximum 300 mg total dose; or 0.5 to 2 mg/minute intravenous infusion OR nicardipine : 5 mg/hour intravenously initially, increase by 2.5 mg/hour increments every 15 minutes according to response, maximum 15 mg/hour adjunct [?] magnesium

There is no consensus on the optimal magnesium regimen, when it should be started and terminated, or route of administration.

Usually initiated at the onset of labour. Therapeutic levels: 2.0 to 3.5 mmol/L (4.8 to 8.4 mg/dL). Continued for 24 hours after delivery. Discontinue if patellar reflex absent, respiratory rate below 12/minute, or urine output above 25 mL/hour. Primary Options magnesium sulphate : 6 g intravenously over 20

Treatment Patient group accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial haemorrhage line Treatmenthide all

minutes as a loading dose at onset of labour, followed by 2 mg/hour infusion

Acute

Treatment approach
If hypertensive emergency is suspected, treatment should not be delayed while conducting a full diagnostic evaluation.

Appropriate facilities
Patients with hypertensive emergencies should be admitted to an ICU for continuous monitoring of BP and parenteral administration of appropriate therapeutic agent(s). [23] Other supportive measures that may be required include intracranial pressure monitoring (in rare cases of increased intracranial pressure), intubation (in case of respiratory distress), or dialysis (in case of renal failure).

Choice of agents and route of administration

The specific parenteral agents used for treating a hypertensive emergency should be dictated by the end-organ systems that have been damaged, patient comorbidities, and overall clinical condition. Oral therapy should begin as soon as possible so that parenteral therapy can be weaned. There are very few randomised controlled trials studying different parenteral agents in hypertensive emergency. Published guidelines are therefore based on common clinical experience and practice.

Rate of BP reduction
The seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure [23] states the initial goal of therapy in hypertensive emergencies is to reduce mean arterial BP by no

more than 25% (within minutes to 1 hour), then, if stable, to 160/100 to 110 mmHg within the next 2 to 6 hours. Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischaemia should be avoided. For this reason, short-acting nifedipine is no longer considered acceptable in the initial treatment of hypertensive emergencies or urgency. If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradual reductions towards a normal BP can be implemented over the next 24 to 48 hours. Exceptions to the above recommendation include:
Patients with an ischaemic stroke, as there is no clear evidence from clinical trials to support the use of immediate antihypertensive treatment Patients with aortic dissection, who should have their systolic BP lowered to less than 100 mmHg if tolerated Patients in whom BP needs to be lowered to enable the use of thrombolytic agents, in which case the target systolic BP is under 185 mmHg and diastolic BP under 110 mmHg.

Accelerated (malignant) hypertension, hypertensive encephalopathy or intracranial haemorrhage

Accelerated hypertension (also known as malignant hypertension) is severe hypertension occurring with retinopathy of grade III (flame haemorrhages, dot and blot haemorrhages, hard and soft exudates) or grade IV (papilloedema). Hypertensive encephalopathy encompasses the transient neurological symptoms that occur with malignant hypertension, which are usually reversed by prompt treatment and lowering of BP. In the management of intracerebral haemorrhage, the ideal level of a patient's BP should be based on individual factors including: baseline BP, presumed cause of haemorrhage, age, elevated intracranial pressure, and interval since onset. While elevated BP could in theory increase the risk of ongoing bleeding from ruptured small arteries and arterioles, the relationship between BP,

intracranial pressure, and volume of haemorrhage is complex and not yet fully understood. The rationale for lowering BP is to minimise further haemorrhage - for example, from a ruptured aneurysm or arteriovenous malformation. However, in primary intracerebral haemorrhage, when a specific vasculopathy is not apparent, the risk from a mildly elevated BP may be lower, so aggressive reduction of BP must be balanced against the possible risk of inducing cerebral ischaemia in other brain areas. [24] [25] In cases of intracranial haemorrhage, target mean arterial pressure (MAP) is 130 mmHg, with a goal of maintaining a cerebral perfusion pressure (CPP) above 70 mmHg. Avoid BP dropping to below 110 mmHg. The first-line treatment is labetalol. [13] [14] [15] [C Evidence] If patients do not have evidence of raised intracranial pressure, a second-line treatment choice is nitroprusside. [13] [14] [C Evidence] However, if raised intracranial pressure is present or suspected, nitroprusside is contraindicated and another agent should be used. Nitroprusside decreases cerebral blood flow while increasing intracranial pressure, effects that are particularly disadvantageous in patients with hypertensive encephalopathy or following a cerebrovascular accident. [26] [27][28] It should also be avoided in patients with renal or hepatic insufficiency. Nicardipine is another second-line agent which can be used. One RCT found that intravenous nicardipine significantly increased the proportion of people who reached physician-specified target range systolic BP within 30 minutes compared with intravenous labetalol. [29] Nicardipine is especially useful in the presence of cardiac disease due to coronary vasodilatory effects. The third-line treatment choice is fenoldopam, a selective peripheral dopamine-1-receptor agonist with arterial vasodilator effects. [13] [14] [15] [30] [31] [C Evidence] This drug is particularly useful in patients with renal insufficiency, where the use of nitroprusside is restricted due to the risk of thiocyanate poisoning.

Acute ischaemic stroke

Treating a hypertensive emergency with an associated acute ischaemic stroke warrants greater caution in reducing BP than in other types of hypertensive emergency. Overly rapid or too great a reduction of MAP may decrease CPP to a level that could theoretically worsen brain injury. The following may be used as guidance.

If systolic BP is below 220 mmHg and diastolic BP below 120 mmHg, then it is reasonable to maintain close observation without direct intervention to reduce BP, [32] unless:
There is other end-organ involvement such as aortic dissection, renal failure, or acute MI The patient is to receive thrombolytics, in which case the target systolic BP is below 185 mmHg and diastolic BP below 110 mmHg There is concurrent intracranial haemorrhage, in which case the goals are a systolic BP of between 140 and 160 mmHg and/or a mean arterial pressure (MAP) of 130 mmHg with the CPP maintained above 70 mmHg. Additionally, MAP should not be dropped to below 110 mmHg.

If systolic BP is above 220 mmHg or diastolic BP is between 121 to 140 mmHg, then labetalol[13] [14] [15] [C Evidence] or nicardipine [13] [14] [15] [33] [C Evidence] should be used to achieve a 10% to 15% reduction in 24 hours. If diastolic BP is above 140 mmHg, then nitroprusside [13] [14] is used to achieve a 10% to 15% reduction over 24 hours. [13] [14] [34] [C Evidence]

Suspected aortic dissection

If aortic dissection is suspected in a hypertensive emergency, the BP should be lowered quite aggressively, typically with a target of reducing systolic BP to between 100 and 120 mmHg within 20 minutes. Medical therapy aims to both lower the BP and decrease the velocity of left ventricular contraction, so decreasing aortic shear stress and minimising the tendency for propagation of the dissection. First-line treatment choice is beta-blockers, either labetalol or esmolol, administered intravenously. [13] [14] [15] [35] [C Evidence] Second-line treatment choice would be the combination of nitroprusside and beta-blockers.[13] [14] [15] [35] [C Evidence] Nitroprusside must be administered with a beta-blocker, as nitroprusside-induced vasodilation would otherwise induce a compensatory tachycardia and worsen shear stress on the intimal flap.

Myocardial ischaemia/infarction
First-line treatment of hypertensive emergency complicated by myocardial ischaemia or infarction is the combination of esmolol (a selective beta-

blocker) plus glyceryl trinitrate (a peripheral vasodilator, which affects venous vessels more than arterial). [13] [14] [15] [34][36] [C Evidence] Esmolol acts to reduce heart rate and glyceryl trinitrate acts to decrease preload and cardiac output and increases coronary blood flow. Second-line treatment choice would be labetalol plus glyceryl trinitrate. [13] [14] [15] [34] [36][C Evidence] The third-line treatment choice would be nitroprusside. [13] [14] [34] [C Evidence]

Left ventricular failure and/or pulmonary oedema

First-line treatment of hypertensive emergency with left ventricular failure and/or pulmonary oedema is glyceryl trinitrate. [13] [14] [15] [36] [C Evidence] Nitroprusside (a potent arterial and venous vasodilator that decreases afterload and preload) is the second-line treatment choice in this situation. [13] [14] [34] [C Evidence] If patient is not already on one, a loop diuretic should be started (e.g., furosemide).

Acute renal failure

Fenoldopam is the first-line treatment choice of hypertensive emergency complicated by acute renal failure. [13] [14] [15] [30] [31] [C Evidence] This drug (a selective peripheral dopamine-1-receptor agonist with arterial vasodilator effects) is particularly useful in renal insufficiency because it acts to both decrease afterload and increase renal perfusion. Second-line treatment choice is nicardipine, a dihydropyridine calcium-channel blocker, which increases stroke volume and has strong cerebral and coronary vasodilatory activity. [13] [14] [15] [33] [C Evidence]

Hyperadrenergic states
Hyperadrenergic states include:
Phaeochromocytoma Sympathomimetic drug use - for example, cocaine, amphetamines, phenylpropanolamine, phencyclidine, or the combination of monoamine oxidase inhibitors with foods rich in tyramine Following abrupt discontinuation of a short-acting sympathetic blocker.

If the hyperadrenergic state is due to sympathomimetic drug use, the first-line agents are benzodiazepines, and anti-hypertensive medications are given only if the blood pressure response is inadequate. In all other clinical situations, the first-line treatment choice is phentolamine (which acts by blocking alpha-adrenoceptors). [13] [14] [15] [C Evidence] The second-line treatment choice is the combination of labetalol[C Evidence] plus nitroprusside.[13] [14] [15] [C Evidence] Administration of a beta-blocker alone is contraindicated, since inhibition of beta-adrenoceptor-induced vasodilation results in unopposed alpha-adrenergic vasoconstriction and a further rise in BP.

Eclampsia
The first-line treatment choices in this situation are hydralazine, [13] [14] [15] [37] [38] [39] [C Evidence] labetalol, [13] [14] [15] [37] [39] [40] [C Evidence] or nicardipine. [13] [14] [15][37] [40] [41] [C Evidence] In pregnancy, angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) are avoided due to potential teratogenic effects, and nitroprusside is avoided due to its potential for fetal cyanide poisoning. A guide target in these patients is to maintain a systolic BP of 130 to 150 mmHg and a diastolic BP of 80 to 100 mmHg. It should be noted, however, that there are no trials supporting these suggested thresholds, and treatments should be tailored to individual patient circumstances. In addition to the first-line treatments mentioned, it has been proposed that magnesium may be useful as an adjunctive therapy, [13] [14] [15] [37] [42] [B Evidence] although there is no consensus on the optimal regimen, when it should be started and terminated, or the optimal route of administration. The drug is usually initiated at the onset of labour.

Emerging treatments
Clevidipine Clevidipine is a third-generation dihydropyridine calcium-channel blocker that appears promising for the treatment of hypertensive emergency. [43] It is a potent and short-acting selective arteriolar vasodilator. It has been shown to be effective in postoperative hypertension but has not been studied in hypertensive emergency.

Monitoring
The patient should return for a follow-up visit and BP check within 1 week of discharge. During the follow-up visit, BP should be checked by a medical professional in both arms and with the appropriate cuff size. The goal BP is below 140/90 mmHg. In patients with hypertension and diabetes or renal disease, the BP goal is below 130/80 mmHg. Patients should return for follow-up visits once a month until goal BP is achieved. Once goal BP is achieved, patient should be monitored every 3 to 6 months (or more frequently based on comorbidities). Serum potassium and creatinine should be measured twice a year.

Patient Instructions
Patients should be reminded of the importance of taking medications as directed and not missing doses. Patients are advised to call their doctor or an ambulance immediately if they experience any dizziness, loss of sensation or mobility, blurred vision, chest pain, SOB, or any other relevant symptoms.

Complications
Complicationhide all

cardiac impairment Myocardial damage and subsequent heart failure is a frequent complication and cause of death in hypertensive emergency. [44] [45] neurological deficit see our comprehensive coverage of Overview of stroke Permanent neurological compromise may occur after cerebrovascular accident, haemorrhage, or hypertensive encephalopathy and is a frequent cause of death. [44] [45] renal impairment Renal insufficiency and failure is both a frequent cause and complication of hypertensive emergency. [44] [45]

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Prognosis
Without therapy, the prognosis of hypertensive emergencies is grim, with 1-year survival rates of 10% to 20%. However, current antihypertensive therapy has greatly improved survival, with 5-year survival rates around 70% in patients who receive appropriate treatment. The presence of renal failure on diagnosis of hypertensive emergency increases mortality rate. [44] [45]