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CE: Hypertensive Emergencies: A Review

Mathews, Essie P. DNP, APRN, ACNP-BC; Newton, Faith APRN, AGACNP-BC; Sharma, Kartavya MD

Author Information
AJN, American Journal of Nursing: October 2021 - Volume 121 - Issue 10 - p 24-35
doi: 10.1097/01.NAJ.0000794104.21262.86

A hypertensive emergency is a sharp rise in blood pressure to a level above 180/120 mmHg that is associated with target organ damage, often involving exigent neurologic, cardiovascular, or renal manifestations.1Hypertensive urgency is a term used to describe similarly high blood pressure values that neither produce nor worsen target organ damage.1 The term hypertensive crisis is sometimes used to describe the spectrum of severe uncontrolled hypertension, encompassing both hypertensive emergency and hypertensive urgency. The distinction between the latter two is important because the ongoing or imminent target organ damage that characterizes hypertensive emergency warrants immediate hospitalization for close hemodynamic monitoring and IV pharmacotherapy, whereas hypertensive urgency often produces no symptoms of target organ damage and can be managed without hospitalization by simply reinstituting or intensifying previously prescribed oral antihypertensive drug therapy; it does not require immediate blood pressure reduction.1 Despite these important distinctions, in all hypertensive crises, the goal of treatment is to reduce blood pressure safely without compromising organ perfusion.


An analysis of eight studies conducted in Thailand, France, Italy, and Brazil found that the combined prevalence of hypertensive emergency and hypertensive urgency in EDs was roughly 1.2%, with hypertensive urgency being significantly more common than hypertensive emergency, though prevalence varied across studies.2 The mean prevalence of hypertensive urgency in EDs was 0.94% and the mean prevalence of hypertensive emergency was 0.3%.

In the United States, although 18% of ED patients have severely elevated blood pressure at or above 180/110 mmHg upon presentation,3 far fewer have hypertensive emergency, as previously defined, which occurs in conjunction with acute or impending target organ damage. From 2006 through 2013, the estimated number of visits for hypertensive emergency more than doubled, but true hypertensive emergency accounted for only 0.2% of adult ED patients overall and 0.6% of adult ED patients with a diagnosis of hypertension. Mortality rates, however, were relatively high among patients with qualifying hypertensive emergency who presented to U.S. EDs, at 4.8% in 2006 and 4.5% in 2013, underscoring the need for prompt diagnosis and appropriate management of the condition.4

In view of the considerable morbidity associated with hypertensive emergency and the potential for preventing life-threatening deterioration with timely therapy, a thorough understanding of this condition will be of value to nurses in both hospital and ambulatory settings. This article provides an overview of the risk factors for hypertensive emergency; the pathophysiology, clinical manifestations, and management of hypertensive emergency; as well as a discussion of nursing considerations pertinent to the acute and preventive care of patients with this diagnosis.


A 2000 study of 350 patients in a West Birmingham hypertension database found that the majority (55.7%) of patients with hypertensive emergency had no previous diagnosis of hypertension.5 In patients with a history of chronic hypertension, however, risk factors for developing hypertensive crises include the following6:

  • female sex
  • obesity
  • hypertensive heart disease, such as coronary artery disease
  • nonadherence to prescribed medication
  • somatoform disorder
  • a greater number of prescribed antihypertensive drugs, which is significantly associated with both nonadherence to prescribed medication and somatoform disorder

In 20% to 40% of patients with blood pressure levels above 200/120 mmHg and advanced retinopathy, secondary causes such as renal parenchymal disease and renal artery stenosis, among others, can be identified.7 (See Conditions Associated with Hypertensive Emergency.1, 5, 7-10)

Box 1:
Conditions Associated with Hypertensive Emergency1, 5, 7-10

Sometimes the initiating event causing a rapid and severe rise in blood pressure can be clearly identified, for instance antihypertensive nonadherence, stress, hyperthyroidism, or the use of drugs such as cocaine, amphetamines, phencyclidine, or the prescribed use of monoamine oxidase inhibitors.6, 11 In most cases, however, the precise mechanisms that trigger an acute elevation in blood pressure aren't immediately clear.7


Activation of the renin–angiotensin–aldosterone system seems to play an important role in the development of severe hypertension. Renin secretion may increase in response to a variety of conditions, including reduced renal perfusion pressure, reduced sodium delivery, and β-adrenergic receptor stimulation, which together can trigger a series of reactions that convert angiotensin to angiotensin II, a potent vasoconstrictor that also induces proinflammatory cytokines.8

With increased systemic blood pressure, the kidneys may produce a diuretic response called pressure natriuresis, a maladaptive increase in renal sodium excretion, which may exacerbate hypovolemia and cause further activation of the renin–angiotensin system.7

Under normal circumstances, sudden elevation of blood pressure triggers a vascular myogenic response, which is the inherent property of vascular smooth muscle in small arteries to constrict, thereby limiting sudden increases in blood flow and protecting the capillary endothelium.8 However, when blood pressure surpasses a critical point, this response may be overwhelmed, resulting in endothelial damage from mechanical injury and proinflammatory molecular changes in the endothelium.8

Reduced production of endothelial vasodilators such as nitric oxide and prostacyclin further elevates blood pressure and exacerbates endothelial damage, a vicious cycle that culminates in enhanced vascular permeability, inhibition of fibrinolysis, platelet aggregation, inflammation, thrombosis, and finally end-organ ischemia.12, 13 (See Figure 1.8, 12-14)

Figure 1.:
Pathophysiology of Hypertensive Emergencies8,12-14


The initial evaluation of a patient with suspected hypertensive emergency consists of assessing the signs and symptoms of damage to such target organs as the brain; heart; kidneys; large blood vessels, including the aorta; and the microvasculature, including the retina.15

A survey developed by an Italian Society of Hypertension research working group and administered to members of several Italian emergency medical societies between December 22, 2017, and March 15, 2018, found that symptoms commonly reported by patients with hypertensive emergency included chest pain (89%), visual disturbances (89.8%), dyspnea (82.7%), and headache (82.1%).16 Less commonly reported symptoms included dizziness (52%), conjunctival hemorrhages (41.5%), tinnitus (38.2%), and epistaxis (34.4%).16

In U.S. EDs, a study of incidence trends for hypertensive emergencies found that heart failure, stroke, and myocardial infarction represented the most common hypertensive emergency diagnoses, trailed by intracranial hemorrhage and ruptured aneurysm or dissection.4 The occurrence of hypertensive emergency with advanced retinopathy was relatively low. Presentations vary with the specific target organ damage involved. (See Table 111, 17-21 for clinical findings associated with specific target organ damage, as well as recommended diagnostic tests.)

Table 1. - Target-Organ Damage and Associated Clinical Findings in Hypertensive Emergencies11, 17-21
Target Organ Dysfunction Associated Clinical Findings Recommended Diagnostic Tests
Acute heart failure with pulmonary edema Dyspnea, orthopnea, cough, fatigue, basilar lung crackles, third heart sound, jugular venous distension ECG, chest X-ray, BNP, echocardiogram (if aortic dissection is suspected)
ACS Crushing chest pain or pressure radiating to the jaw, shoulders, or epigastrium; new-onset murmur (for ACS caused by aortic dissection) 12-lead ECG, cardiac enzymes and cardiac troponin I (for ACS caused by ischemia or MI)
Acute aortic syndrome, including acute aortic dissection Syncope, neurologic deficit, limb ischemia, chest pain with or without radiating to the back, new onset murmur, aortic insufficiency, asymmetry of pulse and blood pressure between the arms (in aortic dissection) Chest X-ray, contrast-enhanced CT angiography of chest and abdomen, transesophageal echocardiography
Hypertensive encephalopathy Headache, visual disturbances, nausea, vomiting, altered mental status, seizures, visual field deficits, cortical blindness Contrast-enhanced CT or MRI of the brain
Ischemic or hemorrhagic stroke Altered sensorium, focal neurologic deficits CT or MRI of the brain
Preeclampsia/eclampsia Pregnant > 20 weeks, dyspnea, visual disturbances, headache, seizures Electrolytes, serum creatinine, urinalysis, liver function test
ACS = acute coronary syndrome; BNP = brain natriuretic peptide; CT = computed tomography; ECG = electrocardiogram; MI = myocardial infarction; MRI = magnetic resonance imaging.


Patients presenting with hypertensive emergency should be admitted to an ICU for close monitoring and care.1 The goals of care can be envisioned as follows:

  • Identify the cause and specific manifestation of the hypertensive emergency.
  • Initiate rapid life-preserving treatment of severely elevated blood pressure.
  • Monitor the patient for medication-related adverse effects as well as for symptoms of renal, coronary, or cerebral ischemia from excessive blood pressure lowering.
  • Provide preventive health education related to nutrition, medication adherence, and disease monitoring.

Blood pressure targets may vary based on the specific clinical findings. The goal is not to achieve a particular blood pressure value but to preserve organ perfusion and prevent hypertensive target organ damage.7 Close interdisciplinary collaboration between nurses and physicians is essential in stabilizing these critically ill patients. Target organ damage and medical comorbidities influence medical decisions concerning target blood pressure, the time frame for achieving blood pressure control, and the choice of pharmacologic agents to be administered. Initially, IV medications are preferred because of their rapid onset, ability to titrate, and relatively short half-life.7 (See Table 222 for IV medications commonly used in hypertensive emergency.)

Table 2. - Common IV Antihypertensive Medications Used in Hypertensive Emergencies22
Medication Onset of Action, min Duration of Action Contraindications Potential Adverse Effects
Clevidipine (Cleviprex) 2-4 5-15 min
  • Severe aortic stenosis

  • Defective lipid metabolism

  • Allergy to soy or eggs

  • Headache

  • Nausea and vomiting

  • Hypotension

  • Reflex tachycardia

Enalprilat (Vasotec) 15-30 6-≥ 12 hours
  • Renal insufficiency

  • Pregnancy (category D)

  • Headache

  • Hypotension

Esmolol (Brevibloc) 1-2 10-30 min
  • Severe sinus bradycardia

  • 1st or 2nd degree AV heart block

  • Decompensated heart failure

  • Cardiogenic shock

  • Current use of IV calcium channel antagonists

  • Pulmonary hypertension

  • Risk of hypotension

  • Bradycardia

  • Cardiac failure

  • Asthma exacerbation

  • Increases the effect of hypoglycemic agents in diabetes mellitus and masks hypoglycemic tachycardia

Fenoldopam (Corlopam) 5-10 30-60 min
  • No contraindications, but may increase intraocular pressure in patients with glaucoma or intraocular hypertension

  • Headache

  • Flushing

  • Nausea

  • Hypotension

Hydralazine 10-20, IV 20-30, IM 1-≥ 4 hours, iv 4-6 hours, IM
  • Coronary artery disease

  • Mitral valvular rheumatic heart disease

  • Tachycardia

  • Headache

  • Nausea and vomiting

  • Diarrhea

  • Palpitations

  • Angina

Labetalol 5-10 2-4 hours
  • Asthma

  • > 1st degree heart block

  • Cardiogenic shock

  • Severe bradycardia

  • Nausea

  • Dizziness

Nicardipine (Cardene) 5-15 1.5-≥ 4 hours
  • Aortic stenosis

  • Headache

  • Hypotension

  • Reflex tachycardia

Nitroglycerin 2-5 5-10 min
  • Intracranial hypertension

  • PDE-5 inhibitor use

  • Severe anemia

  • Circulatory failure and shock

  • Headache

  • Dizziness

  • Paresthesia

  • Methemoglobinemia

Nitroprusside (Nitropress, Nipride RTU) 0.5-1 1-10 min
  • Inadequate cerebral perfusion

  • Acute coronary syndrome

  • Recent PDE-5 inhibitor use

  • Cyanide toxicity

  • Hypotension

Phentolamine 1-2 10-30 min
  • Hypersensitivity to any ingredients

  • Arrhythmias

  • Cerebrovascular spasm

  • Myocardial infarction

  • Injection site pain

AV = atrioventricular; PDE-5 = phosphodiesterase-5.

Intraarterial blood pressure monitoring is used because it is the most accurate means of assessing blood pressure in real time, and accuracy is essential in preventing overly aggressive treatment that could result in complications. However, placement of an arterial line for monitoring should not delay the initiation of therapy. For most adults presenting with hypertensive emergency, systolic blood pressure should be reduced by no more than 25% within the first hour, followed by a more gradual reduction to 160/100 mmHg within the next two to six hours before being cautiously reduced to normal over the subsequent 24 to 48 hours.1 Some clinical conditions, such as aortic dissection, preeclampsia, or pheochromocytoma may require more rapid blood pressure reduction, while others, such as some cases of ischemic stroke, might warrant less aggressive approaches.

Once controlled, medications can be switched to oral formulations. Some clinical situations necessitate alternative management or special considerations, as discussed below.


Seen in up to 23% of ED visits for acute hypertension,4 acute congestive heart failure often occurs in patients with such preexisting cardiac pathologies as coronary artery disease or valve defects, which may predispose to the development of acute systolic or diastolic dysfunction.11 Even in the absence of previous heart disease or fluid excess, accelerated hypertension increases afterload and left ventricular strain, often culminating in cardiogenic pulmonary edema.11

Managing cardiogenic pulmonary edema involves gradually reducing blood pressure levels as low as tolerated without producing signs of hypotension or hypoperfusion.11 Nitroglycerin and nitroprusside are the preferred IV agents owing to their favorable effects on both preload and afterload reduction.7 Avoid administering medications that increase cardiac work, such as hydralazine, or reduce cardiac contractility, such as β-blockers.11 Although diuretics are not typically used to treat hypertensive emergencies, in the case of acute pulmonary edema, concomitant administration of loop diuretics can further lower blood pressure by reducing volume overload.11 Noninvasive positive-pressure ventilation can also help manage pulmonary edema by reducing venous return.7


During hypertensive emergency, endothelial injury activates the coagulation cascade in the coronary arteries, triggering platelet aggregation, which, in conjunction with the release of vasoactive mediators, can compromise myocardial blood flow.11 Immediate recognition and proper diagnosis of myocardial infarction depend on a careful history, an electrocardiogram (ECG), and laboratory studies including measuring cardiac enzyme levels. A retrospective data analysis of 236 patients who had presented with hypertensive crisis found that patients with elevated cardiac troponin I levels had nearly three times the risk of major adverse cardiovascular or cerebrovascular events at two years' follow-up than patients whose cardiac troponin I levels were normal.23

Since blood pressure fluctuation is common in the early phase of acute coronary syndrome (ACS) often due to pain or anxiety, these factors should be addressed before targeting blood pressure with antihypertensive therapy.24 While blood pressure targets for ACS patients have not been established, the American Heart Association recommends a slow blood pressure reduction that maintains diastolic pressure at or above 60 mmHg so as not to compromise coronary perfusion.24

To prevent reflex tachycardia and a subsequent increase in myocardial oxygen demand, preferred agents include11, 24

  • nitroglycerin, a vasodilator that reduces cardiac preload.
  • labetalol, which reduces systemic vascular resistance while maintaining cardiac output and without producing reflex tachycardia.
  • esmolol, for patients who do not have contraindications to β-blockers.


The annual incidence of all acute aortic syndromes, including aortic dissection, is relatively low in the general population, ranging from four to six per 100,000 person-years, though it rises to 30 or more per 100,000 person-years in people over age 65.25 The mortality rate is high for both type A dissections, which involve the ascending aorta, and type B dissections, which involve only the descending aorta.

Surgery is the recommended treatment for type A aortic dissection, whereas type B is generally treated medically in the absence of other life-threatening complications. According to data from the International Registry of Acute Aortic Dissection study, which were reported in 2000, even with surgery, 26% of patients with type A dissection do not survive, and if treated nonsurgically because of age or comorbidities, this figure rises to 58%.25, 26 Since hypertension is identified as a risk factor in up to 80% of aortic dissections,25 it should be on the clinician's radar for patients presenting to the ED with acute chest pain and elevated blood pressure.

Medical management involves effective pain control and rapid lowering of systolic blood pressure to 100 to 120 mmHg with a simultaneous reduction of heart rate to 60 beats per minute, referred to as “anti-impulse therapy.”20, 27 The purpose of anti-impulse therapy is to reduce left ventricular force and aortic wall stress, thereby limiting tearing and preventing rupture. This should not, however, compromise cerebral perfusion.

Labetalol is typically the drug of choice for rapid blood pressure reduction because of its α- and β-adrenergic blocking effects.7, 22

Alternative treatments include esmolol, which has a shorter half-life and may be used in patients with relative contraindications to β-blockers.11 Nitroprusside can be added if targets are not reached with a β-blocker alone.7

For patients with significant contraindications to β-blockade, calcium channel blockers may be used.28


Normally, with a rise in systemic blood pressure, cerebral arterioles constrict in order to maintain a constant rate of blood flow to the brain, a phenomenon called cerebral autoregulation.19 But when blood pressure rises very rapidly, the autoregulatory response may be insufficient to prevent cerebral hyperperfusion; a weakening of the blood–brain barrier; and fluid extravasation into brain tissue, particularly tissue in the posterior regions.19 In the absence of ischemia or hemorrhage, clinical and radiologic findings gradually resolve with the control of blood pressure. The syndrome is often referred to as posterior reversible encephalopathy syndrome.19

Controlled blood pressure reduction is the mainstay of treatment for hypertensive encephalopathy. A 20% to 25% reduction in initial mean arterial blood pressure is recommended in recent European Society of Cardiology guidelines.7 Reducing mean arterial blood pressure further could increase risk of cerebral hypoperfusion. After an initial gradual blood pressure reduction over at least 24 hours, further measures may be pursued; however, there is no clear guidance as to the optimal time over which to reduce blood pressure or to escalate treatment to normalize blood pressure. Medications that can be infused continuously, such as nicardipine or labetalol, are preferred to avoid blood pressure fluctuations, which can disrupt cerebral blood flow in the setting of impaired autoregulation.9 Nitroprusside should be avoided in hypertensive encephalopathy because it has vasodilatory effects and the potential to worsen cerebral edema and increase intracranial pressure.29


Sudden onset of a focal neurologic deficit, such as facial or limb weakness, ataxia, aphasia, dysarthria, or visual field loss, often indicate acute ischemic stroke (AIS) or transient ischemic attack.30 According to the 2003 International Society of Hypertension statement on management of blood pressure in acute stroke, blood pressure is elevated in about 75% of patients soon after ischemic stroke and in more than 80% of patients following intracerebral hemorrhage.31, 32 Managing hypertension in AIS can be challenging because elevated blood pressure may be a compensatory physiological response to inadequate cerebral perfusion pressure (CPP).33 CPP is calculated as the difference between mean arterial pressure and intracranial pressure. Reducing mean arterial pressure, and consequently CPP, could lead to additional infarction by further reducing perfusion to ischemic tissues.21 Higher blood pressure targets are thus permissible in this setting.

IV thrombolysis and mechanical thrombectomy. Patients with suspected ischemic stroke should be rapidly evaluated for IV thrombolysis and thrombectomy. Patients eligible for thrombolysis should have blood pressure quickly lowered to less than 185/110 mmHg and maintained at pressures below 180/105 mmHg for at least 24 hours following treatment in order to reduce risk of intracranial hemorrhage.21 IV labetalol, clevidipine, and nicardipine are recommended as initial agents in recent stroke guidelines.21

Sodium nitroprusside may be considered for patients with AIS if other agents fail to control blood pressure or if diastolic blood pressure is greater than 140 mmHg.21

Blood pressure management following recanalization in patients with AIS remains an area of study. To promote cerebral perfusion, common practice is to allow blood pressure as high as 180/105 mmHg for the first 24 to 48 hours following IV thrombolysis with tissue plasminogen activator.34 However, higher blood pressure following thrombectomy is associated with worse outcomes, hemorrhage, and reperfusion injury.34

Current literature suggests better outcomes with systolic blood pressure goals of less than 160 mmHg, or even less than 140 mmHg, following successful mechanical thrombectomy.35 Precise goals may be contingent on the degree of successful recanalization, so all members of the health care team should know the precise goals of the intervention.

For patients with transient ischemic attack and those ineligible for thrombolysis or thrombectomy, initial blood pressure as high as 220/120 mmHg can be considered in order to maintain perfusion to tissue with potentially reversible ischemia, followed by a gradual blood pressure reduction over the next 24 to 48 hours.30 In some patients, blood pressure reduction may exacerbate ischemic symptoms, in which case the time frame for reduction should be extended.


Patients with intracranial hemorrhage (ICH), like those with AIS, often present with extremely elevated blood pressure accompanied by focal neurologic abnormalities of sudden onset, including headache and reduced level of consciousness, though the latter occurs more often in ICH than in AIS and is frequently progressive in nature. Noncontrast computed tomography (CT) is both sensitive and specific for acute parenchymal hemorrhage, which in hypertensive ICH is frequently located in the basal ganglia, thalamus, pons, and cerebellum. However, in patients who have underlying vascular malformation, have cerebral amyloid angiopathy, or use anticoagulants, ICH may also occur in the cerebral hemispheres.18, 36 Since blood pressure and coagulopathy management for ICH and AIS are quite different, ICH-specific measures should only be started after the diagnosis is confirmed.

Results from recent large randomized controlled trials have been unable to clarify broadly applicable blood pressure targets for patients with spontaneous ICH.37, 38

INTERACT-2 (the second Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial), which enrolled patients within six hours of symptom onset, showed that reducing systolic blood pressure to less than 140 mmHg was as safe as reducing it to less than 180 mmHg.37 While aggressive blood pressure lowering did not reduce the primary outcome of death or severe disability, functional outcomes were slightly but statistically significantly better in the aggressive treatment group.

ATACH-2 (the Antihypertensive Treatment of Acute Cerebral Hemorrhage II trial), by contrast, compared the same target systolic blood pressure levels (less than 140 mmHg versus the standard of less than 180 mmHg) in treating patients with ICH, but with the aim of achieving the targets more rapidly (within 4.5 hours of symptom onset). Results of the trial showed no difference in mortality or functional outcome between the two treatment groups, though the intensive treatment group had a significantly higher rate of renal dysfunction at seven days than the standard treatment group.38 The risk–benefit of aggressive systolic blood pressure reduction to less than 140 mmHg in ICH thus remains unresolved.

Systolic blood pressure below 130 mmHg. A secondary analysis of INTERACT-2 found that achieved systolic blood pressure below 130 mmHg (the level at which the INTERACT-2 protocol called for cessation of IV antihypertensive treatment) was associated with increased risk of physical dysfunction compared with systolic blood pressure between 130 mmHg and 140 mmHg.39 It is thus reasonable to conclude that overly intensive blood pressure reduction in the first few hours after symptom onset is inadvisable.

Patients presenting with sustained systolic blood pressure above 220 mmHg, those with severe ICH, and those requiring surgical decompression are poorly represented in the data, so optimal blood pressure targets have not been established for these groups. General principles of blood pressure lowering using IV infusions while avoiding sudden drops in blood pressure are still applicable.1


Marked hyperadrenergic states can result from ingestion of sympathomimetic medications (cocaine, methamphetamine, phencyclidine, lysergic acid diethylamide, and monoamine oxidase inhibitors with ingestion of food-containing tyramine), withdrawal of short-acting antihypertensive agents (clonidine and β-blockers), and endocrine disorders such as pheochromocytoma. Altered mental status, agitation, chest pain, palpitations, and seizures are the usual presenting symptoms.

Hypertension from cocaine or amphetamine intoxication can be treated effectively with benzodiazepines to reduce the stimulant effects and with nitrates or calcium channel blockers to control blood pressure.11, 40 With the use of β-blockers in sympathomimetic drug overdose, there has historically been a concern for exacerbating coronary ischemia; this view however has come into question recently since supportive data seem to be weak.40


Pheochromocytomas are neuroendocrine catecholamine-producing tumors originating from chromaffin cells of the adrenal medulla or extraadrenal paraganglia, which produce varying amounts of epinephrine, norepinephrine, or dopamine.41

The clinical presentation is highly variable and often appears as a mimic for stress-related disorders. Symptoms of catecholamine excess can include headache, diaphoresis, palpitations, and panic attacks in addition to severe hypertension.42 Both plasma and urine tests for free normetanephrine, a major metabolite of norepinephrine, and metanephrine, a major metabolite of epinephrine, are commonly used for screening of this condition.41 Both plasma and urine tests for free metabolites have negative predictive values greater than 99% and specificities of 94%, though false positives may occur in critically ill patients.41

Imaging studies like contrast-enhanced CT or magnetic resonance imaging instead of or in addition to biochemical testing can improve sensitivity and specificity of diagnosis.41

Definitive therapy for pheochromocytoma is the surgical removal of the tumor, but presurgical administration of α-adrenergic receptor blockers is considered a first-choice treatment to prevent hypertensive crisis in the perioperative period from a massive release of catecholamines during tumor removal.41 Frequently prescribed α-blockers include phenoxybenzamine and doxazosin.41 Labetalol should not be used without prior adequate α-blockade in patients with hyperadrenergic states, such as pheochromocytoma, because α-adrenergic activity can increase blood pressure if β-blockade is not complete.22

Hypertension in primary hyperaldosteronism can also result in vascular target organ damage to the heart, kidney, and arterial walls.43 This results not only from high blood pressure but also from aldosterone-induced endothelial dysfunction, microvascular inflammation, and fibrosis.

Cushing syndrome during pregnancy is both rare and associated with high maternal and fetal mortality rates.44 Its symptoms, however, can mimic those of a normal pregnancy and its occurrence during pregnancy with uncontrolled hypertension can be misdiagnosed as preeclampsia.44


Preeclampsia refers to the onset of hypertension (sustained systolic blood pressure of 140 mmHg or above or diastolic blood pressure of 90 mmHg or above) after 20 weeks' gestation in a previously normotensive woman, in conjunction with one or more of the following17:

  • proteinuria
  • thrombocytopenia
  • renal insufficiency
  • impaired liver function
  • pulmonary edema
  • neurologic symptoms, such as intractable headache, visual scotomata, convulsions, altered mental status, blindness, stroke, or clonus

Eclampsia is the occurrence of generalized seizures not attributable to other causes in a patient with preeclampsia.

In pregnant women with preexisting chronic hypertension, acute exacerbation of hypertension can occur due to inadequate medical treatment or from superimposed preeclampsia.17 Regardless of nomenclature, acute-onset severe systolic hypertension (160 mmHg or above), severe diastolic hypertension (110 mmHg or above), or both, occurring during pregnancy is a hypertensive emergency.17 It's inadvisable to adhere too strictly to blood pressure thresholds, because target organ damage can occur with milder hypertension in preeclampsia, and the condition of patients with preeclampsia can deteriorate rapidly without warning.17

Management involves lowering blood pressure to a systolic range of 140 to 150 mmHg and a diastolic range of 90 to 100 mmHg.45 Preferred agents include IV labetalol, IV hydralazine, or immediate-release oral nifedipine.45 IV magnesium sulfate should be administered concurrently to reduce the risk of seizures.45 Additional considerations are monitoring of fetal heart rate for bradycardia with β-blocker use and evaluation for delivery.


Thrombotic microangiopathy (TMA) can result from hypertensive endothelial injury, involving platelet aggregation, coagulation activation, and inhibition of fibrinolysis.7 In hypertensive emergency, very high blood pressure can cause progressive vascular injury, acute renal failure, and TMA.7 It's important to distinguish hypertension-induced TMA and renal failure from thrombotic thrombocytopenic purpura (TTP) and acute renal failure from hemolytic uremic syndrome (HUS) because, while antihypertensive treatment will usually improve TMA and associated renal failure in hypertensive emergency, other treatments may be required for TTP and HUS.


Perioperative hypertensive emergencies can result from adrenergic stimulation from the surgical event, changes in intravascular volume, postoperative pain, or anxiety. If untreated, perioperative hypertension can result in new target organ damage, increased risk of bleeding, and myocardial infarction.46 To identify possible risk factors for hypertensive emergencies in preoperative patients with hypertension, a careful preoperative assessment is essential. When blood pressure is above 180/110 mmHg, urgent treatment or postponement of surgery should be considered on a case-by-case basis to avoid the risk of hypertensive emergencies in the perioperative or postoperative period.46 For each patient, comorbidities and specific blood pressure goals should be discussed with the surgeon, considering the patient's type of hypertension.


Initial evaluation. A thorough history should incorporate details of the duration and severity of preexisting hypertension and the presence of previous end-organ damage, especially renal, cardiac, and cerebrovascular disease. It should also include details of antihypertensive medications; level of blood pressure control; intake of over-the-counter drugs, such as sympathomimetic agents; and any use of illicit drugs. Document all information about ongoing or impending end-organ compromise, including but not limited to such symptoms as chest pain (associated with ACS and acute aortic dissection); back pain (as can occur with aortic dissection); dyspnea (a potential sign of pulmonary edema or congestive heart failure); and neurologic symptoms, such as seizures, altered consciousness, or hypertensive encephalopathy.

The physical examination should focus on identifying signs of target organ damage. If possible, blood pressure should be measured when the patient is in both supine and standing positions, so as to assess for volume depletion due to pressure natriuresis, which can sustain a cycle of renal ischemia, vasoconstriction, and progressively increasing hypertension.47 Blood pressure measurement in both arms, if found to be significantly different, can raise suspicion of aortic dissection. A fundoscopic assessment can reveal such signs of severe hypertension as retinal hemorrhages, exudates, or papilledema.

The cardiovascular assessment should focus on evaluating the patient for signs of heart failure or ACS, such as raised jugular venous pressure, crackles, third heart sound, or gallop.

The neurologic examination should assess the level of consciousness, signs of meningeal irritation like photophobia and neck stiffness, and note the presence of visual field defects, localized weakness or numbness, uncoordinated limb movements, dysarthria, and language deficits.48

Initial diagnostic tests may include renal function, electrolytes, complete blood count (including peripheral smear for signs of hemolysis), ECG, chest X-ray, and urine analysis, depending on patient presentation. Of note, during hypertensive emergency, abnormalities seen on ECG may result not only from ACS but also from acute neurologic conditions associated with a reversible myocardial dysfunction termed “neurogenic stunned myocardium.”49

Therapeutic considerations and safety monitoring. Adequate IV access should be established for medication administration and volume infusion. Preparation for intraarterial blood pressure monitoring may be necessary for medication adjustment. Nurses should document any precipitous drop in blood pressure as this may aggravate cerebral, myocardial, or renal ischemia. If there is evidence of volume depletion, IV saline may be administered to restore perfusion in advance of antihypertensive treatment.47 In the case of pregnancy-related hypertensive emergency, fetal monitoring may be necessary.

When transitioning patients from IV infusions to oral medications, allow sufficient overlap to reduce the risk of rebound hypertension. The specific time frame required will depend on the pharmacodynamics of the drug being titrated downward and the drug being initiated. Continuous ECG monitoring is necessary to detect arrhythmias and cardiac ischemia. Document any changes in the patient's level of consciousness, mood, or orientation; patient reports of headache or visual changes; any vomiting; and all intake and output measurements, which can signal both cardiac and renal complications. Unrelieved pain should be promptly addressed, as it may not only exacerbate hypertension but also indicate target organ damage. Similarly, treating anxiety in patients with acute hypertension has been shown to significantly reduce blood pressure in those without target organ damage, though the safety of such therapy has not been studied in patients with hypertensive emergency.50


Patient education. When preparing patients for discharge, nurses should emphasize preventive measures in patient teaching. The Dietary Approaches to Stop Hypertension (DASH) trial has shown that a low-sodium diet combined with the “DASH” diet, which is rich in fruits, vegetables, legumes, and low-fat dairy products and low in sweets, saturated fat, and total fat, can substantially aid in lowering blood pressure.51 This approach is recommended in the 2020 International Society of Hypertension Global Hypertension Practice Guidelines.52 Dietary advice should take into account comorbid conditions that may require additional modifications, such as diabetes or kidney disease. Recommended lifestyle modifications include smoking cessation, regular physical activity, and weight reduction when appropriate.52

Discharge planning should include information concerning the impact of long-term hypertension on various organ systems, as well as the importance of blood pressure control, adherence to the prescribed medication regimen, and regular follow-up with an established provider. For patients who lack requisite resources, consider social work consultation to find financial support, low-cost drug programs, and generic medication substitutions.48 Although data on long-term functional outcomes following discharge of patients after hypertensive emergency are sparse, specific rehabilitative and equipment needs may be determined by the sequelae of target organ damage in clinical situations, such as stroke, heart failure, and renal failure. Coordination of care between the nurse, hospitalist, specialist services, therapy services, and social work is essential for safe hospital discharge and appropriate follow-up.53


1. Whelton PK, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA guideline for the prevention, detection, evaluation, and management of high blood pressure in adults: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation 2018;138(17):e484–e594.
2. Astarita A, et al. Hypertensive emergencies and urgencies in emergency departments: a systematic review and meta-analysis. J Hypertens 2020;38(7):1203–10.
3. Adhikari S, Mathiasen R. Epidemiology of elevated blood pressure in the ED. Am J Emerg Med 2014;32(11):1370–2.
4. Janke AT, et al. Trends in the incidence of hypertensive emergencies in US emergency departments from 2006 to 2013. J Am Heart Assoc 2016;5(12).
5. Lip GY, et al. Do patients with de novo hypertension differ from patients with previously known hypertension when malignant phase hypertension occurs. Am J Hypertens 2000;13(8):934–9.
6. Saguner AM, et al. Risk factors promoting hypertensive crises: evidence from a longitudinal study. Am J Hypertens 2010;23(7):775–80.
7. van den Born BH, et al. ESC council on hypertension position document on the management of hypertensive emergencies. Eur Heart J Cardiovasc Pharmacother 2019;5(1):37–46.
8. Brathwaite L, Reif M. Hypertensive emergencies: a review of common presentations and treatment options. Cardiol Clin 2019;37(3):275–86.
9. Miller JB, et al. New developments in hypertensive encephalopathy. Curr Hypertens Rep 2018;20(2):13.
10. Suneja M, Sanders ML. Hypertensive emergency. Med Clin North Am 2017;101(3):465–78.
11. Papadopoulos DP, et al. Cardiovascular hypertensive emergencies. Curr Hypertens Rep 2015;17(2):5.
12. Vaughan CJ, Delanty N. Hypertensive emergencies. Lancet 2000;356(9227):411–7.
13. Derhaschnig U, et al. Hypertensive emergencies are associated with elevated markers of inflammation, coagulation, platelet activation and fibrinolysis. J Hum Hypertens 2013;27(6):368–73.
14. Makó K, et al. An updated review of hypertensive emergencies and urgencies. Journal of Cardiovascular Emergencies 2018;4(2):73–83.
15. Peixoto AJ. Acute severe hypertension. N Engl J Med 2019;381(19):1843–52.
16. Saladini F, et al. Diagnosis and treatment of hypertensive emergencies and urgencies among Italian emergency and intensive care departments. Results from an Italian survey: Progetto GEAR (Gestione dell'Emergenza e urgenza in ARea critica). Eur J Intern Med 2020;71:50–6.
17. Brown MA, et al. Hypertensive disorders of pregnancy: ISSHP classification, diagnosis, and management recommendations for international practice. Hypertension 2018;72(1):24–43.
18. Claude Hemphill J 3rd, Lam A. Emergency neurological life support: intracerebral hemorrhage. Neurocrit Care 2017;27(Suppl 1):89–101.
19. Fugate JE, Rabinstein AA. Posterior reversible encephalopathy syndrome: clinical and radiological manifestations, pathophysiology, and outstanding questions. Lancet Neurol 2015;14(9):914–25.
20. Morello F, et al. Diagnosis and management of acute aortic syndromes in the emergency department. Intern Emerg Med 2021;16(1):171–81.
21. Powers WJ, et al. Guidelines for the early management of patients with acute ischemic stroke: 2019 update to the 2018 guidelines for the early management of acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2019;50(12):e344–e418.
22. Elliott WJ, Varon J. Drugs used for the treatment of hypertensive emergencies. UpToDate 2019.
23. Pattanshetty DJ, et al. Elevated troponin predicts long-term adverse cardiovascular outcomes in hypertensive crisis: a retrospective study. J Hypertens 2012;30(12):2410–5.
24. Rosendorff C, et al. Treatment of hypertension in patients with coronary artery disease: a scientific statement from the American Heart Association, American College of Cardiology, and American Society of Hypertension. Hypertension 2015;65(6):1372–407.
25. Gawinecka J, et al. Acute aortic dissection: pathogenesis, risk factors and diagnosis. Swiss Med Wkly 2017;147:w14489.
26. Hagan PG, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA 2000;283(7):897–903.
27. Hiratzka LF, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease. A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine. J Am Coll Cardiol 2010;55(14):e27–e129.
28. Suzuki T, et al. Type-selective benefits of medications in treatment of acute aortic dissection (from the International Registry of Acute Aortic Dissection [IRAD]). Am J Cardiol 2012;109(1):1228–7.
29. Immink RV, et al. Cerebral hemodynamics during treatment with sodium nitroprusside versus labetalol in malignant hypertension. Hypertension 2008;52(2):236–40.
30. Gross H, Grose N. Emergency neurological life support: acute ischemic stroke. Neurocrit Care 2017;27(Suppl 1):102–15.
31. Qureshi AI. Acute hypertensive response in patients with stroke: pathophysiology and management. Circulation 2008;118(2):176–87.
32. Bath P, et al. International Society of Hypertension (ISH): statement on the management of blood pressure in acute stroke. J Hypertens 2003;21(4):665–72.
33. Bulwa Z, et al. Management of blood pressure after acute ischemic stroke. Curr Neurol Neurosci Rep 2019;19(6):29.
34. Mistry EA, et al. Systolic blood pressure within 24 hours after thrombectomy for acute ischemic stroke correlates with outcome. J Am Heart Assoc 2017;6(5).
35. Anadani M, et al. Blood pressure goals and clinical outcomes after successful endovascular therapy: a multicenter study. Ann Neurol 2020;87(6):830–9.
36. Morotti A, Goldstein JN. Anticoagulant-associated intracerebral hemorrhage. Brain Hemorrhages 2020;1(1):89–94.
37. Anderson CS, et al. Rapid blood-pressure lowering in patients with acute intracerebral hemorrhage. N Engl J Med 2013;368(25):2355–65.
38. Qureshi AI, et al. Intensive blood-pressure lowering in patients with acute cerebral hemorrhage. N Engl J Med 2016;375(11):1033–43.
39. Arima H, et al. Optimal achieved blood pressure in acute intracerebral hemorrhage: INTERACT2. Neurology 2015;84(5):464–71.
40. King A, et al. Sympathomimetic toxidromes and other pharmacological causes of acute hypertension. Curr Hypertens Rep 2018;20(1):8.
41. Lenders JWM, et al. Genetics, diagnosis, management and future directions of research of phaeochromocytoma and paraganglioma: a position statement and consensus of the Working Group on Endocrine Hypertension of the European Society of Hypertension. J Hypertens 2020;38(8):1443–56.
42. Kantorovich V, et al. Pheochromocytoma: an endocrine stress mimicking disorder. Ann N Y Acad Sci 2008;1148:462–8.
43. Born-Frontsberg E, et al. Cardiovascular and cerebrovascular comorbidities of hypokalemic and normokalemic primary aldosteronism: results of the German Conn's Registry. J Clin Endocrinol Metab 2009;94(4):1125–30.
44. Lim WH, et al. The medical management of Cushing's syndrome during pregnancy. Eur J Obstet Gynecol Reprod Biol 2013;168(1):1–6.
45. American College of Obstetricians and Gynecologists' Committee on Obstetric Practice. ACOG Committee Opinion No. 767: emergent therapy for acute-onset, severe hypertension during pregnancy and the postpartum period. Obstet Gynecol 2019;133(2):e174–e180.
46. Aronson S. Perioperative hypertensive emergencies. Curr Hypertens Rep 2014;16(7):448.
47. Marik PE, Rivera R. Hypertensive emergencies: an update. Curr Opin Crit Care 2011;17(6):569–80.
48. Alley WD, et al. Hypertensive emergency (nursing). In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing; 2020.
49. Kenigsberg BB, et al. Neurogenic stunned myocardium in severe neurological injury. Curr Neurol Neurosci Rep 2019;19(11):90.
50. Grossman E, et al. Antianxiety treatment in patients with excessive hypertension. Am J Hypertens 2005;18(9 Pt 1):1174–7.
51. Appel LJ, et al. A clinical trial of the effects of dietary patterns on blood pressure. DASH Collaborative Research Group. N Engl J Med 1997;336(16):1117–24.
52. Unger T, et al. 2020 International Society of Hypertension global hypertension practice guidelines. Hypertension 2020;75(6):1334–57.
53. Yeo TP, Burrell SA. Hypertensive crisis in an era of escalating health care changes. J Nurse Pract 2010;6(5):338–46.

hypertensive crisis; hypertensive emergency; hypertensive urgency; target organ damage

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