Treatment algorithm

Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer

ACUTE

accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial hemorrhage

1st line – labetalol

Back
ACUTE
|
accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial hemorrhage
|
increased intracranial pressure or renal disease
1st line – 

labetalol

Labetalol is the drug of choice in situations characterized by markedly elevated intracranial pressure.[18][39][41][42]

Onset of action: 5-10 minutes. Duration of action: 3-8 hours.

The American College of Cardiology/American Heart Association Task Force on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure states that the initial goal of therapy in hypertensive emergencies is to reduce mean arterial blood pressure (BP) by no more than 25% (within minutes to 1 hour), then, if stable, to 160 mmHg systolic and 100-110 mmHg diastolic within the next 2-6 hours.[1] 

Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided.[1][57]​ 

If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented over the next 24-48 hours.

Encephalopathy is usually reversed by prompt treatment and lowering of BP.[18][54]​ 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.

In the management of intracerebral hemorrhage (ICH), the patient's ideal BP should be based on individual factors, including baseline BP, presumed cause of hemorrhage, age, elevated intracranial pressure, and interval since onset. In cases of large or severe ICH, or an initial systolic BP (SBP) ≥220 mmHg, cautious BP lowering should be pursued.[76] In patients with initial SBP ≥220 mmHg, early intensive BP reduction, compared with standard BP lowering, was associated with higher rates of renal adverse events in one post-hoc analysis of a large randomized clinical trial.​​[76][77]​​​​

For the management of patients with spontaneous ICH, the American Heart Association and American Stroke Association (AHA/ASA) recommend careful titration in patients requiring acute BP lowering, to ensure continuous smooth and sustained control of BP, avoiding peaks and large variability in SBP. This can be beneficial for improving functional outcomes.[76]​ Initiating treatment within 2 hours of ICH onset, and reaching target within 1 hour, can be beneficial to reduce the risk of hematoma expansion and improve functional outcome.[76]​ In patients with spontaneous ICH of mild to moderate severity presenting with SBP between 150 and 220 mmHg, acute lowering of SBP to a target of 140 mmHg, with the goal of maintaining it within the range of 130-150 mmHg, is safe and may be reasonable for improving functional outcomes.[76]​ In patients with spontaneous ICH presenting with large or severe ICH, SBP >220 mmHg, more than 6 hours after symptom onset, or in those requiring surgical decompression, the safety and efficacy of intensive BP lowering is not well established.[76]

These recommendations from the AHA/ASA are based on two of the largest trials for early intensive BP lowering after ICH (INTERACT2, ATACH-2), meta-analyses, and several post-hoc analyses of these two trials.[76][78][79]

See Hemorrhagic stroke (Management approach).

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][7]​​[74]​ Arterial lines are preferred for the use of intravenous antihypertensive medications.[7]​

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 line – nicardipine

Back
ACUTE
|
accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial hemorrhage
|
increased intracranial pressure or renal disease
2nd line – 

nicardipine

Nicardipine is a second-generation dihydropyridine derivative calcium-channel blocker with high vascular selectivity and strong cerebral and coronary vasodilatory activity.[18]​ The onset of action of intravenous nicardipine is from 5-15 minutes, with a duration of action of 4-6 hours.

Nicardipine is especially useful in the presence of cardiac disease due to coronary vasodilatory effects.[82][83]

The American College of Cardiology/American Heart Association Task Force on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure states that the initial goal of therapy in hypertensive emergencies is to reduce mean arterial blood pressure (BP) by no more than 25% (within minutes to 1 hour), then, if stable, to 160 mmHg systolic and 100-110 mmHg diastolic within the next 2-6 hours.[1] 

Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided.[1][57]​ 

If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented over the next 24-48 hours.

In the management of intracerebral hemorrhage (ICH), the patient's ideal BP should be based on individual factors, including baseline BP, presumed cause of hemorrhage, age, elevated intracranial pressure, and interval since onset. In cases of large or severe ICH, or an initial SBP ≥220 mmHg, cautious BP lowering should be pursued.[76] In patients with initial SBP ≥220 mmHg, early intensive BP reduction, compared with standard BP lowering, was associated with higher rates of renal adverse events in one post-hoc analysis of a large randomized clinical trial.​​[76][77]​​​​

For the management of patients with spontaneous ICH, the AHA/ASA recommend careful titration in patients requiring acute BP lowering, to ensure continuous smooth and sustained control of BP, avoiding peaks and large variability in SBP. This can be beneficial for improving functional outcomes.[76]​ Initiating treatment within 2 hours of ICH onset, and reaching target within 1 hour, can be beneficial to reduce the risk of hematoma expansion and improve functional outcome.[76]​ In patients with spontaneous ICH of mild to moderate severity presenting with SBP between 150 and 220 mmHg, acute lowering of SBP to a target of 140 mmHg, with the goal of maintaining it within the range of 130-150 mmHg, is safe and may be reasonable for improving functional outcomes.[76]​ In patients with spontaneous ICH presenting with large or severe ICH, SBP >220 mmHg, more than 6 hours after symptom onset, or in those requiring surgical decompression, the safety and efficacy of intensive BP lowering is not well established.

These recommendations from the AHA/ASA are based on two of the largest trials for early intensive BP lowering after ICH (INTERACT2, ATACH-2), meta-analyses, and several post-hoc analyses of these two trials.[76][78][79]

See Hemorrhagic stroke (Management approach).

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][7]​​[74]​ Arterial lines are preferred for the use of intravenous antihypertensive medications.[7]​

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 line – fenoldopam

Back
ACUTE
|
accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial hemorrhage
|
increased intracranial pressure or renal disease
3rd line – 

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-1-receptor agonist with arterial vasodilator effects. Its hemodynamic effects are a decrease in afterload and an increase in renal perfusion.

Onset of action: 5 minutes. Duration of action: 30 minutes.

The American College of Cardiology/American Heart Association Task Force on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure states that the initial goal of therapy in hypertensive emergencies is to reduce mean arterial blood pressure (BP) by no more than 25% (within minutes to 1 hour), then, if stable, to 160 mmHg systolic and 100-110 mmHg diastolic within the next 2-6 hours.[1] 

Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided.[1][57]​ 

If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented over the next 24-48 hours.

Encephalopathy is usually reversed by prompt treatment and lowering of BP.[18][54]​ If there is no improvement despite a decrease in BP, an alternative diagnosis should be considered.

Continue until the BP is controlled on oral agents.

For the management of patients with spontaneous ICH, the AHA/ASA recommend careful titration in patients requiring acute BP lowering, to ensure continuous smooth and sustained control of BP, avoiding peaks and large variability in SBP. This can be beneficial for improving functional outcomes.[76]​ Initiating treatment within 2 hours of ICH onset, and reaching target within 1 hour, can be beneficial to reduce the risk of hematoma expansion and improve functional outcome.[76]​ In patients with spontaneous ICH of mild to moderate severity presenting with SBP between 150 and 220 mmHg, acute lowering of SBP to a target of 140 mmHg, with the goal of maintaining it within the range of 130-150 mmHg, is safe and may be reasonable for improving functional outcomes.[76]​ In patients with spontaneous ICH presenting with large or severe ICH, SBP >220 mmHg, more than 6 hours after symptom onset, or in those requiring surgical decompression, the safety and efficacy of intensive BP lowering is not well established.[76]​

These recommendations from the AHA/ASA are based on two of the largest trials for early intensive BP lowering after ICH (INTERACT2, ATACH-2), meta-analyses, and several post-hoc analyses of these two trials.[76][78][79]

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][74]

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

1st line – labetalol

Back
ACUTE
|
accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial hemorrhage
|
normal intracranial pressure and renal function
1st line – 

labetalol

Labetalol is the drug of choice.

Onset of action: 5-10 minutes. Duration of action: 3-8 hours.

In cases of intracranial hemorrhage, treatment should commence if the initial SBP is above 220 mmHg. The American College of Cardiology/American Heart Association Task Force on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure states that the initial goal of therapy in hypertensive emergencies is to reduce mean arterial blood pressure (BP) by no more than 25% (within minutes to 1 hour), then, if stable, to 160 mmHg systolic and 100-110 mmHg diastolic within the next 2-6 hours.[1] 

Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided.[1][57] 

If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented over the next 24-48 hours.

Encephalopathy is usually reversed by prompt treatment and lowering of BP.[18][54]​​ 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.

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][7]​​[74]​ Arterial lines are preferred for the use of intravenous antihypertensive medications.[7]​

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 line – nitroprusside or nicardipine

Back
ACUTE
|
accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial hemorrhage
|
normal intracranial pressure and renal function
2nd line – 

nitroprusside or nicardipine

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

Patients should be monitored by drawing thiocyanate levels after 48 hours of therapy (levels kept at <12 mg/dL). The maximum dose should be delivered for less than 10 minutes to decrease the 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 intravenous nicardipine is from 5-15 minutes, with a duration of action of 4-6 hours. It is especially useful in the presence of cardiac disease due to coronary vasodilatory effects.[82][83]

In cases of intracranial hemorrhage, treatment should commence if the initial SBP is above 220 mmHg. The American College of Cardiology/American Heart Association Task Force on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure states that the initial goal of therapy in hypertensive emergencies is to reduce mean arterial blood pressure (BP) by no more than 25% (within minutes to 1 hour), then, if stable, to 160 mmHg systolic and 100-110 mmHg diastolic within the next 2-6 hours.[1] 

Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided.[1][57] 

If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented over the next 24-48 hours.

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

Continue until the BP is controlled on oral agents.

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][74]

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

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

3rd line – fenoldopam

Back
ACUTE
|
accelerated (malignant) hypertension or hypertensive encephalopathy or intracranial hemorrhage
|
normal intracranial pressure and renal function
3rd line – 

fenoldopam

Fenoldopam acts as a selective peripheral dopamine-1-receptor agonist with arterial vasodilator effects. Its hemodynamic 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 hemorrhage, treatment should commence if the initial SBP is above 220 mmHg. The American College of Cardiology/American Heart Association Task Force on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure states that the initial goal of therapy in hypertensive emergencies is to reduce mean arterial blood pressure (BP) by no more than 25% (within minutes to 1 hour), then, if stable, to 160 mmHg systolic and 100-110 mmHg diastolic within the next 2-6 hours.[1] 

Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided.[1][57] 

If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented over the next 24-48 hours.

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

Continue until the BP is controlled on oral agents.

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][7]​​[74]​ Arterial lines are preferred for the use of intravenous antihypertensive medications.[7]​

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 ischemic stroke

1st line – close observation ± blood pressure reduction

Back
ACUTE
|
acute ischemic stroke
|
SBP ≤220 mmHg and DBP ≤120 mmHg
1st line – 

close observation ± blood pressure reduction

Treatment of hypertension with an associated acute ischemic stroke warrants greater caution in reducing blood pressure (BP) than with other types of hypertensive emergency. Overly rapid or too great a reduction of mean arterial pressure may decrease cerebral perfusion pressure to a level that could theoretically worsen brain injury (e.g., through watershed infarcts). However, American Heart Association/American Stroke Association guidelines recommend early treatment of hypertension when required by comorbid conditions, including preeclampsia/eclampsia.[69]

If the systolic BP (SBP) is below 220 mmHg and the diastolic BP is below 120 mmHg, there is no evidence of end organ involvement or intracranial hemorrhage 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, acute kidney injury, or acute myocardial infarction, or the patient is to receive thrombolysis, the target SBP should be below 185 mmHg and diastolic BP should be below 110 mmHg. The BP should be maintained below 185/105 mmHg for at least 24 hours after initiating intravenous thrombolysis.

The choice of agent to reduce BP depends on the associated end-organ involvement.

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][74]

1st line – labetalol

Back
ACUTE
|
acute ischemic stroke
|
SBP >220 mmHg or DBP 121-140 mmHg
1st line – 

labetalol

If the SBP is above 220 mmHg or the diastolic BP is between 121-140 mmHg, labetalol can be used to achieve a 10% to 15% reduction in BP within 24 hours.[39][41][42]

Labetalol acts as an alpha-1-blocker and nonselective beta-blocker and its hemodynamic 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: 5-10 minutes. Duration of action: 3-8 hours.

Continue until the BP is controlled on oral agents.

If there is other end-organ involvement such as aortic dissection, acute kidney injury, or acute myocardial infarction, or the patient is to receive thrombolysis, the target SBP should be below 185 mmHg and diastolic BP should be below 110 mmHg. The BP should be maintained below 185/105 mmHg for at least 24 hours after initiating intravenous thrombolysis.

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][7]​​[74]​ Arterial lines are preferred for the use of intravenous antihypertensive medications.[7]​

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

1st line – nicardipine or clevidipine

Back
ACUTE
|
acute ischemic stroke
|
SBP >220 mmHg or DBP 121-140 mmHg
1st line – 

nicardipine or clevidipine

If the SBP is above 220 mmHg or the diastolic BP is between 121-140 mmHg, nicardipine or clevidipine can be used to achieve a 10% to 15% reduction in BP within 24 hours.[39][41][42][93][94]

Nicardipine and clevidipine are dihydropyridine calcium-channel blockers, which increase stroke volume and have strong cerebral and coronary vasodilatory activity.

Nicardipine onset of action: 5-10 minutes. Duration of action: 2-4 hours.

Clevidipine onset of action: 2-4 minutes. Duration of action: 5-15 minutes.

Continue until the BP is controlled on oral agents.

If there is other end-organ involvement such as aortic dissection, acute kidney injury, or acute myocardial infarction, or the patient is to receive thrombolysis, the target SBP should be below 185 mmHg and diastolic BP should be below 110 mmHg. The BP should be maintained below 185/105 mmHg for at least 24 hours after initiating intravenous thrombolysis.

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][74]

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

OR

clevidipine: 1-2 mg/hour intravenously initially, dose may be doubled every 90 seconds initially until blood pressure reaches target, usual dose 4-6 mg/hour, maximum 32 mg/hour (maximum duration 72 hours)

1st line – nitroprusside

Back
ACUTE
|
acute ischemic stroke
|
DBP >140 mmHg
1st line – 

nitroprusside

If the diastolic BP is above 140 mmHg, nitroprusside may be used to achieve a 10% to 15% reduction over 24 hours.[39][41][95]​ 

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

Onset of action: immediate. Duration of action: 3-5 minutes.

Patients should be monitored by drawing thiocyanate levels after 48 hours of therapy (levels maintained <12 mg/dL). The maximum dose should be delivered for less than 10 minutes to decrease the chance of cyanide toxicity.

Continue until the BP is controlled on oral agents.

If there is other end-organ involvement such as aortic dissection, acute kidney injury, or acute myocardial infarction, or the patient is to receive thrombolysis, the target SBP should be below 185 mmHg and diastolic BP should be below 110 mmHg. The BP should be maintained below 185/105 mmHg for at least 24 hours after initiating intravenous thrombolysis.

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][7]​​[74]​ Arterial lines are preferred for the use of intravenous antihypertensive medications.[7]​

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

myocardial ischemia/infarction

1st line – esmolol and nitroglycerin

Back
ACUTE
|
myocardial ischemia/infarction
1st line – 

esmolol and nitroglycerin

Esmolol is a selective beta-blocker that acts to reduce the heart rate.

Contraindications to beta-blockers include moderate-to-severe left ventricular failure with pulmonary edema, bradycardia, hypotension, poor peripheral perfusion, second- or third-degree heart block, and reactive airway disease.[1]

Esmolol onset of action: 1-5 minutes. Duration of action: 5 minutes.

Nitroglycerin 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: 3-5 minutes.

The American College of Cardiology/American Heart Association Task Force on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure states that 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 mmHg systolic and 100-110 mmHg diastolic within the next 2-6 hours.[1]

Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided.[1][57] 

If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented over the next 24-48 hours.

Continue until the BP is controlled on oral agents.

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][74]

Primary options

esmolol: 50-100 micrograms/kg/minute intravenously

and

nitroglycerin: 5-100 micrograms/minute intravenously

2nd line – labetalol and nitroglycerin

Back
ACUTE
|
myocardial ischemia/infarction
2nd line – 

labetalol and nitroglycerin

Labetalol is an alpha-1-blocker and nonselective beta-blocker, which decreases systemic vascular resistance, mean arterial pressure, and heart rate, and causes a decrease or no change in cardiac output. Contraindications to beta-blockers include moderate-to-severe left ventricular failure with pulmonary edema, bradycardia, hypotension, poor peripheral perfusion, second-or third-degree heart block, and reactive airway disease.[1]

Onset of action: 5-10 minutes. Duration of action: 3-8 hours.

Nitroglycerin 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: 3-5 minutes.

The American College of Cardiology/American Heart Association Task Force on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure states that 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 mmHg systolic and 100-110 mmHg diastolic within the next 2-6 hours.[1]

Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided.[1][57] 

If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented over the next 24-48 hours.

Continue until the BP is controlled on oral agents.

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][7]​[74]​ Arterial lines are preferred for the use of intravenous antihypertensive medications.[7]​

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

nitroglycerin: 5-100 micrograms/minute intravenously

3rd line – nitroprusside

Back
ACUTE
|
myocardial ischemia/infarction
3rd line – 

nitroprusside

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

Onset of action: immediate. Duration of action: 3-5 minutes.

Patients should be monitored by drawing thiocyanate levels after 48 hours of therapy (levels maintained <12 mg/dL). The maximum dose should be delivered for less than 10 minutes to decrease the chance of cyanide toxicity.

The American College of Cardiology/American Heart Association Task Force on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure states that 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 mmHg systolic and 100-110 mmHg diastolic within the next 2-6 hours.[1]

Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided.[1][57] 

If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented over the next 24-48 hours.

Continue until the BP is controlled on oral agents.

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][74]

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 edema

1st line – nitroglycerin + furosemide

Back
ACUTE
|
left ventricular failure and/or pulmonary edema
1st line – 

nitroglycerin + furosemide

Nitroglycerin 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: 3-5 minutes.

Continue until the blood pressure (BP) is controlled on oral agents.

If the patient is not already on a loop diuretic, one should be started (e.g., furosemide).

The American College of Cardiology/American Heart Association Task Force on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure states that 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 mmHg systolic and 100-110 mmHg diastolic within the next 2-6 hours.[1]

Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided.[1][57] 

If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented over the next 24-48 hours.

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][7]​​[74]​ Arterial lines are preferred for the use of intravenous antihypertensive medications.[7]​

Primary options

nitroglycerin: 5-100 micrograms/minute intravenously

and

furosemide: 40-80 mg intravenously initially, increase according to response

1st line – clevidipine + furosemide

Back
ACUTE
|
left ventricular failure and/or pulmonary edema
1st line – 

clevidipine + furosemide

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

Onset of action: 2-4 minutes. Duration of action: 5-15 minutes.

The American College of Cardiology/American Heart Association Task Force on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure states that the initial goal of therapy in hypertensive emergencies is to reduce mean arterial blood pressure (BP) by no more than 25% (within minutes to 1 hour), then, if stable, to 160 mmHg systolic and 100-110 mmHg diastolic within the next 2-6 hours.[1]

Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided.[1][57] 

If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented over the next 24-48 hours.

Continue until the BP is controlled on oral agents.

If the patient is not already on a loop diuretic, one should be started (e.g., furosemide).

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][74]

Primary options

clevidipine: 1-2 mg/hour intravenously initially, dose may be doubled every 90 seconds initially until blood pressure reaches target, usual dose 4-6 mg/hour, maximum 32 mg/hour (maximum duration 72 hours)

and

furosemide: 40-80 mg intravenously initially, increase according to response

2nd line – nitroprusside + furosemide

Back
ACUTE
|
left ventricular failure and/or pulmonary edema
2nd line – 

nitroprusside + furosemide

Nitroprusside acts as a potent arterial and venous vasodilator, thereby reducing afterload and preload. Its hemodynamic 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 <12 mg/dL). The maximum dose should be delivered for less than 10 minutes to decrease the chance of cyanide toxicity.

The American College of Cardiology/American Heart Association Task Force on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure states that the initial goal of therapy in hypertensive emergencies is to reduce mean arterial blood pressure (BP) by no more than 25% (within minutes to 1 hour), then, if stable, to 160 mmHg systolic and 100-110 mmHg diastolic within the next 2-6 hours.[1]

Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided.[1][57] 

If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented over the next 24-48 hours.

Continue until the BP is controlled on oral agents.

If the patient is not already on a loop diuretic, one should be started (e.g., furosemide).

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][7]​​[74]​ Arterial lines are preferred for the use of intravenous antihypertensive medications.[7]​

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 line – labetalol or esmolol

Back
ACUTE
|
aortic dissection
1st line – 

labetalol or esmolol

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

SBP should be reduced to <120 mmHg in the first 20 minutes or as tolerated by the patient.[1][75]

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

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

The dose should be adjusted to maintain the BP in the desired range. This should be continued until the patient has undergone surgical repair/evaluation and is stable on oral therapy.

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][74]

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

Consider – nitroprusside or nicardipine

Back
ACUTE
|
aortic dissection
Consider – 

nitroprusside or nicardipine

Treatment recommended for SOME patients in selected patient group

If there is no significant improvement with beta-blocker monotherapy, nitroprusside or nicardipine can be added to the beta-blocker.[39][41][42][97]

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

Nitroprusside onset of action: immediate. Duration of action: 3-5 minutes.

Patients should be monitored by drawing thiocyanate levels after 48 hours of therapy (levels maintained <12 mg/dL). The maximum dose should be delivered for less than 10 minutes to decrease the chance of cyanide toxicity.

Alternatively, nicardipine can be used.[1] Nicardipine is a dihydropyridine calcium-channel blocker, which increases stroke volume and has strong cerebral and coronary vasodilatory activity.

Nicardipine onset of action: 5-10 minutes. Nicardipine duration of action: 2-4 hours.

Nitroprusside or nicardipine must be administered after a beta-blocker, as nitroprusside-induced or calcium-channel blocker-induced vasodilation would otherwise induce a compensatory tachycardia and worsen shear stress.[1]

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][7]​​[74]​ Arterial lines are preferred for the use of intravenous antihypertensive medications.[7]​

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

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

acute kidney injury

1st line – fenoldopam

Back
ACUTE
|
acute kidney injury
1st line – 

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-1-receptor agonist with arterial vasodilator effects. Its hemodynamic effects are a decrease in afterload and an increase in renal perfusion.

The American College of Cardiology/American Heart Association Task Force on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure states that the initial goal of therapy in hypertensive emergencies is to reduce mean arterial blood pressure (BP) by no more than 25% (within minutes to 1 hour), then, if stable, to 160 mmHg systolic and 100-110 mmHg diastolic within the next 2-6 hours.[1]

Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided.[1][57] 

If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented over the next 24-48 hours.

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][74]

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

1st line – nicardipine or clevidipine

Back
ACUTE
|
acute kidney injury
1st line – 

nicardipine or clevidipine

Nicardipine and clevidipine are dihydropyridine calcium-channel blockers, which increase stroke volume and have strong cerebral and coronary vasodilatory activity.

Nicardipine onset of action: 5-10 minutes. Duration of action: 2-4 hours.

Clevidipine onset of action: 2-4 minutes. Duration of action: 5-15 minutes.

The American College of Cardiology/American Heart Association Task Force on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure states that the initial goal of therapy in hypertensive emergencies is to reduce mean arterial blood pressure (BP) by no more than 25% (within minutes to 1 hour), then, if stable, to 160 mmHg systolic and 100-110 mmHg diastolic within the next 2-6 hours.[1]

Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided.[1][57] 

If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented over the next 24-48 hours.

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][7]​​[74]​ Arterial lines are preferred for the use of intravenous antihypertensive medications.[7]​

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

OR

clevidipine: 1-2 mg/hour intravenously initially, dose may be doubled every 90 seconds initially until blood pressure reaches target, usual dose 4-6 mg/hour, maximum 32 mg/hour (maximum duration 72 hours)

hyperadrenergic state

1st line – benzodiazepine

Back
ACUTE
|
hyperadrenergic state
|
sympathomimetic drug use
1st line – 

benzodiazepine

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.[18][54]​ Benzodiazepines reduce agitation and prevent neurologic complications such as seizures by their action on gamma-aminobutyric acid receptors.[18]

Lorazepam should be used with caution in patients with renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease. Excess central nervous system or respiratory depression can occur with higher doses, and should be watched for.

Antihypertensive agents can be given if the blood pressure (BP) response to benzodiazepines is inadequate.

The American College of Cardiology/American Heart Association Task Force on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure states that 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 mmHg systolic and 100-110 mmHg diastolic within the next 2-6 hours.[1]

Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided.[1][57] 

If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented over the next 24-48 hours.

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][74]

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 response, maximum 50 mg

2nd line – phentolamine

Back
ACUTE
|
hyperadrenergic state
|
sympathomimetic drug use
2nd line – 

phentolamine

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

Onset of action: 1-2 minutes. Duration of action: 3-10 minutes.

The American College of Cardiology/American Heart Association Task Force on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure states that the initial goal of therapy in hypertensive emergencies is to reduce mean arterial blood pressure (BP) by no more than 25% (within minutes to 1 hour), then, if stable, to 160 mmHg systolic and 100-110 mmHg diastolic within the next 2-6 hours.[1]

Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided.[1][57] 

If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented over the next 24-48 hours.

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][7]​​[74]​ Arterial lines are preferred for the use of intravenous antihypertensive medications.[7]​

Primary options

phentolamine: 5-15 mg intravenous bolus

2nd line – nicardipine or clevidipine

Back
ACUTE
|
hyperadrenergic state
|
sympathomimetic drug use
2nd line – 

nicardipine or clevidipine

Nicardipine and clevidipine are dihydropyridine calcium-channel blockers, which increase stroke volume and have strong cerebral and coronary vasodilatory activity.

Nicardipine onset of action: 5-10 minutes. Duration of action: 2-4 hours.

Clevidipine onset of action: 2-4 minutes. Duration of action: 5-15 minutes.

The American College of Cardiology/American Heart Association Task Force on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure states that the initial goal of therapy in hypertensive emergencies is to reduce mean arterial blood pressure (BP) by no more than 25% (within minutes to 1 hour), then, if stable, to 160 mmHg systolic and 100-110 mmHg diastolic within the next 2-6 hours.[1]

Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided.[1][57] 

If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented over the next 24-48 hours.

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][74]

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

OR

clevidipine: 1-2 mg/hour intravenously initially, dose may be doubled every 90 seconds initially until blood pressure reaches target, usual dose 4-6 mg/hour, maximum 32 mg/hour (maximum duration 72 hours)

1st line – phentolamine

Back
ACUTE
|
hyperadrenergic state
|
no sympathomimetic drug use
1st line – 

phentolamine

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

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

Onset of action: 1-2 minutes. Duration of action: 3-10 minutes.

The American College of Cardiology/American Heart Association Task Force on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure states that the initial goal of therapy in hypertensive emergencies is to reduce mean arterial blood pressure (BP) by no more than 25% (within minutes to 1 hour), then, if stable, to 160 mmHg systolic and 100-110 mmHg diastolic within the next 2-6 hours.[1]

Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided.[1][57] 

If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented over the next 24-48 hours. In patients with pheochromocytoma crisis, SBP should be reduced to <140 mmHg in the first hour.[1]

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][7]​​[74]​ Arterial lines are preferred for the use of intravenous antihypertensive medications.[7]​

Primary options

phentolamine: 5-15 mg intravenous bolus

Consider – labetalol

Back
ACUTE
|
hyperadrenergic state
|
no sympathomimetic drug use
Consider – 

labetalol

Treatment recommended for SOME patients in selected patient group

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

The 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.

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

1st line – nicardipine or clevidipine

Back
ACUTE
|
hyperadrenergic state
|
no sympathomimetic drug use
1st line – 

nicardipine or clevidipine

Nicardipine and clevidipine are dihydropyridine calcium-channel blockers, which increase stroke volume and have strong cerebral and coronary vasodilatory activity.

Nicardipine onset of action: 5-10 minutes. Duration of action: 2-4 hours.

Clevidipine onset of action: 2-4 minutes. Duration of action: 5-15 minutes.

The American College of Cardiology/American Heart Association Task Force on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure states that the initial goal of therapy in hypertensive emergencies is to reduce mean arterial blood pressure (BP) by no more than 25% (within minutes to 1 hour), then, if stable, to 160 mmHg systolic and 100-110 mmHg diastolic within the next 2-6 hours.[1]

Excessive falls in pressure that may precipitate renal, cerebral, or coronary ischemia should be avoided.[1][57] 

If the initial level of reduced BP is well tolerated and the patient is clinically stable, further gradual reductions toward a normal BP can be implemented over the next 24-48 hours.

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

OR

clevidipine: 1-2 mg/hour intravenously initially, dose may be doubled every 90 seconds initially until blood pressure reaches target, usual dose 4-6 mg/hour, maximum 32 mg/hour (maximum duration 72 hours)

severe hypertension in pregnancy (preeclampsia and eclampsia)

1st line – labetalol or hydralazine or nifedipine

Back
ACUTE
|
severe hypertension in pregnancy (preeclampsia and eclampsia)
1st line – 

labetalol or hydralazine or nifedipine

The American College of Obstetricians and Gynecologists (ACOG) recommends antihypertensive therapy for women with preeclampsia and a sustained systolic BP ≥160 mmHg or diastolic BP ≥110 mmHg.[48]​ However, thresholds for treatment vary internationally, with lower thresholds recommended by a number of societies.[100]​ The UK National Institute for Health and Care Excellence recommends treatment if BP remains above 140/90 mmHg.[61]​​

Although some of the available literature suggests that antihypertensive agents should be administered within 30-60 minutes, it is recommended that antihypertensive therapy begin as soon as reasonably possible after the criteria for acute onset severe hypertension are met.[48] It should be noted, however, that there are no trials supporting these suggested thresholds, and treatments should be tailored to individual patient circumstances. Specialist advice should be sought.

For acute-onset, severe hypertension managed in a critical care setting, intravenous labetalol, intravenous hydralazine, or oral nifedipine can be used first line.

Labetalol is usually considered the antihypertensive of choice, and is effective as monotherapy in 80% of pregnant women.[48][61]​​[98]​​​​​[99]​ It seems to be safe and effective in pregnant women for the management of preeclampsia; however, it should be avoided in women with asthma or any other contraindication to its use.[48]​​​

Labetalol acts as an alpha-1-blocker and nonselective beta-blocker and its hemodynamic 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: 5-10 minutes. Duration of action: 3-8 hours.

Hydralazine is an arterial vasodilator with minimal effects on the fetus. Onset of action: 10-20 minutes. Duration of action: 3-8 hours. Its main hemodynamic effects are a decrease in systemic vascular resistance, an increase in heart rate, and an increase in intracranial pressure. Although intravenous hydralazine is still widely used, particularly in North America, it can produce an acute fall in BP. The consequences of this are mostly related to maternal hypotension, including a greater risk of cesarean section, more frequent placental abruption, more maternal oliguria, and fetal tachycardia, suggesting the need for close monitoring of maternal BP and fetal wellbeing during its use.[63]​ UK guidelines recommend to consider volume expansion with crystalloid fluid before or at the same time as the first dose of intravenous hydralazine in the prenatal period.[61]

Immediate-release oral nifedipine may also be considered first-line therapy, particularly when intravenous access is not available.[48]​​ Nifedipine is a dihydropyridine calcium-channel blocker, which increases stroke volume and has strong cerebral and coronary vasodilatory activity. Onset of action: 30-45 minutes. Duration of action: 4-6 hours.

Therapy should be continued until the fetus has been delivered and the patient is stable on oral therapy.

Patients with hypertensive emergencies should be admitted to an intensive care unit for continuous monitoring of blood pressure and target organ damage and for parenteral administration of appropriate therapeutic agent(s).[1][74]​ See Preeclampsia (Management approach).

Primary options

labetalol: 10-20 mg intravenously initially, followed by 20-80 mg every 10-30 minutes according to response, maximum 300 mg/total dose; or 1-2 mg/minute intravenous infusion

OR

nifedipine: 10-20 mg orally (immediate-release) initially, repeat in 20 minutes if needed, followed by 10-20 mg every 2-6 hours according to response, maximum 180 mg/day

OR

hydralazine: 5 mg intravenously initially, followed by 5-10 mg every 20-40 minutes according to response, maximum 20 mg/total dose; or 0.5 to 10 mg/hour intravenous infusion

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