Chapter 57: Systemic Hypertension

Hypertension affects approximately 30% of the U.S. population, and 1% to 6% of all ED patients will present with severe hypertension.^1,2,3,4,5 Of the latter, between a third and one half will have end-organ damage.^2,3,4,5 Risk factors for the development of hypertensive crisis include obesity, cigarette smoking, and older age.⁶

Chronic hypertension is categorized into three classifications: prehypertension, stage 1 hypertension, and stage 2 hypertension⁷ (Table 57-1).

Hypertensive emergency is an acute elevation of blood pressure (≥180/120 mm Hg) associated with end-organ damage; the targeted end organs include the brain, heart, aorta, kidneys, or eyes⁷ (Table 57-2). Acute hypertensive emergencies are more common in chronic hypertensive patients who fail to adhere to their antihypertensive therapy regimens and those who are unable to access outpatient health care.⁶

Hypertensive urgency is a term for profound elevations in blood pressure without acute target organ dysfunction.⁷ An arbitrary blood pressure of ≥180/120 mm Hg is often cited as an urgency and an indication for rapid pharmacologic intervention (often parenteral) to reduce blood pressure within hours; however, no clear clinical benefit of such treatment exists, and risk can occur from precipitous drops in blood pressure.^8,9 Hypertensive urgency is better seen as another form of severe hypertension where prompt therapy with oral agent(s) is the best path, seeking reduction in blood pressure over days to weeks.

At baseline, chronic hypertensive patients have biochemical and structural changes in the arterial walls that shift the vascular autoregulatory curve, requiring higher arterial pressures to maintain end-organ blood flow, notably in the brain.^10,11,12 Eventually, the ability to adapt is passed. The resultant mechanical wall stress and endothelial injury lead to increased permeability, and excessive perfusion of the cerebral, cardiac, and renal vascular beds results. This can be followed by activation of the coagulation cascade and platelets, and deposition of fibrin results in fibrinoid necrosis of the arterioles. Clinically, this is manifested by hematuria (involvement of the renal vasculature) or arterial hemorrhages or exudates on funduscopic examination. Further contributing to the damage are prostaglandins, free radicals, cytokines, and mitogenic, chemoattractant, and proliferation factors, which result in endothelial damage, smooth muscle proliferation, and thrombosis.^10,12 The renin-angiotensin system may also be activated, which leads to vasoconstriction. Pressure natriuresis occurs, leading to volume depletion, prompting additional release of vasoconstrictors from the kidney. These combined effects produce hypoperfusion, ischemia, and dysfunction of end organs. Endothelial dysfunction from such crises can persist for years after the acute event.¹³

Measure blood pressure in both arms quickly and consecutively, while the patient is quietly resting. Check blood pressure several times before starting antihypertensive therapy. Blood pressure differences can result from aortic dissection, coarctation, peripheral vascular disease, and some unilateral neurologic and musculoskeletal abnormalities. However, interarm blood pressure differences are also reported in "normal" individuals. The most important factor in blood pressure difference is increasing age, with the thought that loss of vascular elasticity or asymmetrical atheromatous narrowing of subclavian or brachial arteries might be causative. Although there are no guidelines or standards for determining the significance of blood pressure measurement disparities, a between-arm difference >10 to 20 mm Hg is suggested as meaningful,^14,15 and each 10-mm Hg difference carries an increasing mortality hazard. When a blood pressure difference is detected, treat the higher blood pressure and make sure that subsequent measurements are made on the same arm.¹⁵ Blood pressure measurements with wrist oscillometric devices give lower readings than arm measurements, so arm measurements are preferred.¹⁶ Use the same device for repeat blood pressure measurements.

After careful blood pressure measurement, the next question in a patient with severely elevated blood pressure is whether this constitutes a hypertensive crisis. Although a modest drop (4 to 12 mm Hg) in systolic and diastolic blood pressures can be expected in patients presenting with elevated blood pressures,^17,18,19 do not discount a diagnosis of hypertensive emergency simply because the patient has no prior history of hypertension. Up to 16% of patients presenting with hypertensive emergency have no known history of hypertension.⁴ The key is to seek acute end-organ involvement.

Table 57-3 lists the proportion of patients who present with elevated blood pressure by stroke subtypes, aortic dissection subtypes, heart failure, and acute coronary syndrome. Although elevations in blood pressure accompany the majority of these presentations, note that severe elevations of blood pressure are far less common in presentations typically labeled as hypertensive emergencies (Table 57-2).

CHEST PAIN AND SEVERE HYPERTENSION

Rapid diagnosis and treatment of acute aortic dissection are critical because delays increase mortality. Differentiating the relatively uncommon aortic dissection from the more common acute coronary syndromes is important because blood pressure management is different in these two disorders, and anticoagulation can prove catastrophic in a patient with acute aortic dissection.²⁷

Acute aortic dissection presents with abrupt, sudden onset of pain, usually in the chest, often described as tearing or ripping, and radiating to the interscapular region^23,28 (see chapter 59, "Aortic Dissection and Related Aortic Syndromes"). Less than a quarter of patients with acute aortic dissection have a neurologic deficit or pulse deficits based on blood pressure differentials ≥20 mm Hg, and only about a third have a diastolic murmur. Chest radiograph is abnormal in most but usually nonspecific, and only 25% of radiographs demonstrate the classic widened mediastinum,²⁴ so CT of the chest is needed for the diagnosis. ECG changes are nonspecific, but <10% demonstrate findings consistent with a myocardial infarction.²⁴ D-Dimer testing cannot be used in isolation to exclude the diagnosis, but elevated D-dimer and C-reactive protein levels are associated with higher in-hospital mortality.^29,30

ACUTE NEUROLOGIC SYMPTOMS AND SEVERE HYPERTENSION

Elevated blood pressure, headache, and focal neurologic deficits are associated with either ischemic or hemorrhagic strokes. Acute ischemic strokes may be diagnosed with MRI, and cerebral hemorrhage is identified on head CT (see chapter 167, "Stroke Syndromes") (Figure 57-2).

Hypertensive encephalopathy is a clinical diagnosis after excluding focal ischemia or bleeding. It is characterized by altered mental status, headache, vomiting, seizures, or visual disturbances, and most patients will have papilledema. When MRI findings demonstrate reversible edema that is primarily focused posteriorly (occipital vs frontal regions), this is referred to as posterior reversible encephalopathy syndrome (Figure 57-3).

ACUTE RENAL FAILURE, PERIPHERAL EDEMA, AND SEVERE HYPERTENSION

Patients with new-onset renal failure may have peripheral edema, oliguria, loss of appetite, nausea and vomiting, orthostatic changes, or confusion. However, some patients have few or no specific symptoms (see chapter 88, "Acute Kidney Injury"). Elevated serum creatinine confirms the diagnosis, and urinary sediment is also abnormal.

Pre-eclampsia is associated with hypertension, peripheral edema, and proteinuria. These patients may also develop hemolysis, elevated liver enzyme levels, and low platelet counts (HELLP syndrome) (see chapter 100, "Maternal Emergencies after 20 Weeks of Pregnancy and in the Postpartum Period").

SYMPATHETIC CRISIS AND SEVERE HYPERTENSION

There are four settings in which an excess of catecholamines can result in a hypertensive emergency. An acute catecholaminergic syndrome may occur with abrupt discontinuation of oral or transdermal clonidine. The withdrawal syndrome is potentiated by concomitant β-blocker therapy due to unopposed α-mediated vasoconstriction.

Pheochromocytoma is rare, and between 5% and 20% of tumors are malignant. Patients may experience life-threatening hypertension.³¹ Signs of pheochromocytoma include headache, alternating periods of normal and elevated blood pressure, tachycardia, and flushed skin, punctuated by asymptomatic periods.

Sympathomimetic drugs such as cocaine, amphetamines, phencyclidine hydrochloride (PCP), and lysergic acid diethylamide (LSD), can precipitate a hypertensive emergency, with tachycardia, diaphoresis, chest pain, and, depending on the agent, mental status changes.³² Patients receiving monoamine oxidase inhibitor therapy who consume tyramine-containing foods may develop a hyperadrenergic state.³³ Autonomic dysfunction due to spinal cord or severe head injury or abnormalities such as spina bifida may also present as a hypertensive emergency, with the diagnosis made clinically based on the existing injury.

ASYMPTOMATIC PATIENTS WITH SEVERE HYPERTENSION

Formal recommendations for the evaluation of an ED patient presenting with asymptomatic but severe hypertension do not exist.⁹ Commonly ordered tests include basic metabolic panel (73%), ECG (53%), chest radiograph (46%), and urinalysis (43%).³ In a prospective study of over 100 ED patients with asymptomatic severe hypertension, clinically meaningful results existed in only 6% of patients, with only 5% of patients thought to have abnormal results attributable to acute hypertensive target organ injury.³⁴ Until more data are available, base ED evaluation on the patient complaint, history, and review of systems, and perform selected testing.

Table 57-4 lists agents for the management of hypertensive emergencies categorized by diagnosis. Hypertensive emergencies in pregnancy are discussed in chapter 100. In selecting therapy, be familiar with the use of the selected agent, and establish a target range for blood pressure reduction. The goal is to minimize end-organ damage by initial blood pressure reduction while avoiding hypoperfusion of cerebral, coronary, and renovascular beds. Acute aortic dissection is the exception, because the risk of morbidity and mortality due to inadequate blood pressure and heart rate control outweighs the risk of hypoperfusion syndromes.

AORTIC DISSECTION

The therapeutic goal in acute aortic dissection is a systolic blood pressure between 100 and 140 mm Hg and a heart rate ≤60 beats/min.^23,35,36,37 The resultant reduction in tachycardia decreases the shearing forces and aortic wall stress, limiting the progression of the dissection.³⁷ Pain control with opioids helps to decrease sympathetic tone.

ACUTE HYPERTENSIVE PULMONARY EDEMA

The treatment of hypertensive pulmonary edema is tailored to the underlying pathophysiology, which could be due to transient left ventricular systolic or diastolic dysfunction, acute dyssynchrony, or ischemic mitral regurgitation. Occasionally, the left ventricular ejection fraction may be normal during the acute episode with only a decrease in systolic function and increased diastolic stiffness and filling pressures, suggesting decreased myocardial capacity to adapt to changes in loading.^39,67 For these reasons, there are no clear evidence-based guidelines for the single best treatment of hypertensive pulmonary edema.

The mainstay of therapy is vasodilators and intravenous diuretics.³⁹ Intravenous, sublingual, and topical nitrates reduce blood pressure, decrease myocardial oxygen consumption, and improve coronary blood flow.^39,40,68 Diuretics improve symptoms within 6 hours of administration but may not ultimately affect mortality. Be careful using loop diuretics in combination with nesiritide, or to a lesser degree nitroglycerin, because together these might worsen renal function.^40,69 In patients with systolic dysfunction, intravenous nicardipine is an option that increases both stroke volume and coronary blood flow, a potential benefit.⁷⁰ When hypertensive pulmonary edema is a result of acute coronary syndrome or atrial fibrillation with rapid ventricular response, β-blockers are an appropriate choice.⁷¹

ACUTE MYOCARDIAL INFARCTION

Patients presenting with severely elevated blood pressure and ischemic changes on ECG should be treated with sublingual or intravenous nitrates.^42,43,44 Routine intravenous β-blockade has fallen out of favor due to conflicting reports of mortality benefits. Currently, intravenous β-blockade is only recommended for patients presenting with severe hypertension. Oral β-blockade in patients presenting with ST-segment elevation myocardial infarctions and non–ST-segment elevation myocardial infarctions remains part of early care, but this route may not provide sufficient or rapid enough blood pressure control in a hypertensive emergency.^42,44

ACUTE SYMPATHETIC CRISIS

Patients in acute sympathetic crisis due to either cocaine or amphetamines should initially be managed with an IV benzodiazepine, such as lorazepam or diazepam, to decrease adrenergic stimulation.^32,45 Monitor for respiratory depression and sedation. If benzodiazepines are not effective, nitroglycerin or phentolamine may be used next. A calcium channel blocker can serve as a third-line agent.^42,45,72 β-Blockers can result in unopposed α-blockade, which then can worsen coronary vasoconstriction and increase blood pressure.⁴⁵ If a β-blocker is used, labetalol is the adrenergic blocking agent in conjunction with a vasodilator.⁴²

In patients with pheochromocytoma and a hypertensive emergency, intravenous phentolamine is recommended (intramuscular if venous access is impaired).^73,74 In the preoperative setting, patients who are hypertensive but not in crisis may be managed and prepared for resection with oral phenoxybenzamine, a long-acting adrenergic α-receptor blocker. Another option before resection is urapidil, a selective α₁-receptor antagonist and 5-HT_1a receptor agonist that is available in Europe but is not yet approved by the U.S. Food and Drug Administration.⁷⁵

Patients with monoamine oxidase inhibitor toxicity often respond to an intravenous benzodiazepine; if more therapy is needed, use phentolamine, nitroglycerin, or nitroprusside. Nitroglycerin is indicated for associated chest pain or cardiac ischemia. Monitor closely after reaching a targeted blood pressure, because the hypertensive phase is often followed by a hypotensive phase.

ACUTE RENAL FAILURE

Fenoldopam, nicardipine, and clevidipine are all suitable for acute hypertension-induced renal failure, because they reduce systemic vascular resistance while preserving renal blood flow.⁴⁶ Nitroprusside is an alternative, although cyanide toxicity with high or prolonged use dampens enthusiasm in practice. Fenoldopam is considered by some to be a first-line agent because it improves natriuresis and creatinine clearance in patients with elevated blood pressure and impaired renal function.⁴⁶

ECLAMPSIA AND PRE-ECLAMPSIA

Obstetrical hypertensive emergencies can occur well below the blood pressure threshold for other hypertensive emergencies. Treatment is discussed in detail in Section 11, "Obstetrics and Gynecology," in chapter 100, "Maternal Emergencies after 20 Weeks of Pregnancy and in the Postpartum Period."

NEUROLOGIC EMERGENCIES

Hypertensive encephalopathy (defined as a change in sensorium or seizure from the blood pressure elevation) is a clear indication for rapid blood pressure reduction, once other neurologic emergencies, notably ischemic or hemorrhagic stroke, are excluded.^47,76

Appropriate agents for the management of hypertensive encephalopathy include intravenous nicardipine, labetalol, fenoldopam, and clevidipine.^49,50,51,77 Do not use nitroglycerin because it dilates cerebral arteries and alters both global and regional blood flow, which may worsen the autoregulation failure.⁴⁸

The ideal targets for blood pressure control in subarachnoid hemorrhage and ischemic stroke are not clear and should be balanced to avoid worsening ischemia or rebleeding. For subarachnoid hemorrhage,⁷⁸ recommended agents include intravenous nicardipine, labetalol, and clevidipine^54,55,56 without one superior agent to date.⁵² Oral nimodipine is a good choice for those with modest blood pressure elevations because it lowers blood pressure and reduces vasospasm and subsequent cerebral infarction rates, improving neurologic outcomes.^52,79,80 Clazosentan can also decrease the incidence of vasospasm-related delayed ischemic neurologic deficits and has similar blood pressure–lowering effects as nimodipine.⁵³ If an anticonvulsant is used and an agent that may further reduce blood pressure is selected, such as intravenous phenytoin (rate dependent) or a benzodiazepine, caution must be exercised with additional blood pressure reduction attempts.

The treatment of hypertension in patients with intracerebral hemorrhage includes labetalol, nicardipine, and esmolol.^{56,57,61,62,63,64} Enalaprilat may also be used, but due to concerns of precipitous blood pressure drop, start with a smaller test dose (0.625 mg).⁶⁴ Lowering systolic blood pressures from >180 mm Hg to 120 to 160 mm Hg may improve clinical outcomes.^58,59,60

In ischemic stroke, moderately elevated blood pressure may be beneficial in preserving cerebral perfusion of ischemic areas. Conversely, it may also worsen edema and contribute to hemorrhagic transformation. It is likely that ideal blood pressure ranges exist for ischemic stroke subtypes, but at this time, such ranges have not yet been determined. For the treatment of ischemic stroke, labetalol and nicardipine are the recommended agents; however, the route and degree of blood pressure reduction depend on whether the patient is a candidate for reperfusion therapy (Table 57-4).⁶⁵ Fibrinolytic therapy is contraindicated in patients who maintain a blood pressure >185/110 mm Hg after antihypertensive therapy. In patients who maintain blood pressures ≤185/110 mm Hg (with or without antihypertensive therapy) and undergo fibrinolytic therapy, blood pressure goal is at or below 180/105 mm Hg. Blood pressure should be monitored every 15 minutes for 2 hours from the start of recombinant tissue plasminogen activator therapy, then every 30 minutes for 6 hours, and then every hour for 16 hours. Specific antihypertensive agents and blood pressure recommendations for severely hypertensive patients presenting with ischemic stroke are presented in Table 57-4.

Parenteral agents used for hypertensive emergencies, including dosage, mechanisms, and warnings, are listed in Table 57-5. Refer to Table 57-4 for indications. Other considerations for drug choice include ability to monitor the patient and comorbidities, including respiratory and vascular disease.

β-BLOCKERS

Labetalol is unique among commonly used β-blockers because it also has modest selective α₁-inhibitory effects, with an α- to β-blocking ratio of 1:7.⁸² It recommended for nearly all hypertensive emergencies with the exception of cocaine intoxication and systolic dysfunction in association with decompensated heart failure. In the latter, nicardipine is preferred when nitroglycerin fails. Oral metoprolol is indicated in the majority of patients presenting with acute coronary syndromes: Oral β-blockers have a clear benefit in terms of survival, whereas mortality data are conflicting with intravenous formulations.^42,44 However, if blood pressure control is needed in a patient with acute coronary syndrome, the intravenous formulation should be used. Esmolol has a short duration of action and is titrable, an advantage in patients at risk for the adverse effects of β-blockers, such as those with severe asthma and chronic obstructive pulmonary disease.

CALCIUM CHANNEL BLOCKERS

Clevidipine is a third-generation dihydropyridine calcium channel blocker with ultra-short-acting selective arteriolar vasodilator properties.⁸² It has been studied in the perioperative setting and in patients with renal dysfunction.^83,84,85 Its advantage is its ability to be titrated with a half-life less than a minute. Nicardipine has an onset of action of 5 to 15 minutes and can be titrated at 15-minute intervals. It has been found to be safe and effective in neurologic hypertensive emergencies and has a favorable effect on myocardial oxygen balance increasing both stroke index and coronary blood flow. When compared to labetalol, patients were more likely to reach physician-specified target blood pressure goal in the initial 30 minutes of therapy.⁸¹ Nifedipine use (10 milligrams PO) is discouraged in hypertensive emergencies except in peripartum patients.^86,87

VASODILATORS

Nitroglycerin is a potent venodilator, showing arterial dilatation only at very high doses. Use may cause hypotension and reflex tachycardia, both worsened by the volume depletion characteristic of hypertensive emergencies. Nitroglycerin is recommended as a first-line agent only in the treatment of heart failure and acute coronary syndromes due to its favorable effects on coronary blood flow and cardiac workload. Its hypotensive effects are due to its reduction of preload and cardiac output, which makes it a poor choice in other hypertensive emergencies.

Sodium nitroprusside is best used when other agents fail. It requires more titration than nicardipine in hypertensive neurosurgical patients⁸⁸ and has higher mortality rates in cardiac surgery patients when compared to clevidipine.⁸⁹ Concerns about cyanide toxicity, heightened in patients with renal or hepatic insufficiency, and the need for invasive monitoring further curtail its use.⁹⁰ Combination therapy is the most common current use, as in aortic dissection patients who also receive esmolol to achieve blood pressure targets at lower doses.

OTHER AGENTS

Fenoldopam is a unique peripheral dopaminergic-1 receptor agonist, and due to its ability to promote diuresis, natriuresis, and creatinine clearance, its primary application is in renal hypertensive emergencies.⁸² Phentolamine is used successfully in cocaine-, amphetamine-, and pheochromocytoma-related hypertensive emergencies.^73,74,82 Enalaprilat, the only available IV angiotensin-converting enzyme inhibitor, has special application in patients with heart failure or acute coronary syndrome, but caution should be exercised because of common first-dose hypotension.⁶⁴

Clonidine, a central α₂-agonist, generally does not have a role in the treatment of patients with hypertensive emergencies with the exception of those who have recently stopped taking the drug. An abrupt cessation of clonidine can induce a rebound hypertension, which may be difficult to control with other agents. It can be given orally, at 0.2 to 0.3 milligram initially, with blood pressure reduction starting within 30 to 60 minutes and peaking at 2 to 4 hours.⁸² In patients who are unable to take oral medications, a clonidine patch for dermal delivery may be used. However, the onset action may be delayed by 2 to 3 days, and titration is challenging. For maximum absorption, apply the patch to the chest or upper arm.^82,91 Although abrupt cessation of either clonidine or a β-blocker may result in rebound hypertension, clonidine withdrawal tends to be more severe and often will not respond to therapy without reinstitution.

Acute treatment of asymptomatic severe hypertension does not prevent or reduce short-term patient morbidity or mortality.⁸ Nevertheless, a small study demonstrated increased risk of cardiovascular events within 4 years of ED presentation in hypertensive urgency patients (systolic blood pressure >220 mm Hg and/or diastolic blood pressure >120 mm Hg) compared to control patients with systolic blood pressures between 135 and 180 mm Hg and diastolic blood pressures between 85 and 110 mm Hg.⁹² These data, combined with the evidence that uncontrolled blood pressure is a major risk factor for cardiovascular disease, renal failure, and cerebrovascular accidents, are reasons to initiate outpatient blood pressure reduction regimens prior to discharge. Table 57-6 lists oral agents commonly used for hypertension. The drugs listed are chosen for their relatively rapid onset of action and their potential use for ongoing control of chronic hypertension. Choosing an agent that can be used once daily and is inexpensive is often an ideal plan (e.g., generic lisinopril, started at 10 milligrams daily). If choosing an angiotensin-converting enzyme inhibitor or angiotensin II receptor antagonist, check the creatinine and potassium first.

Table 57-7 provides consensus-based and the newer, focused Eighth Report of the Joint National Committee recommendations.^9,93,94,95 Many ED patients who present with elevated blood pressure have a reduction after approximately 90 minutes; however, patients whose blood pressures remain persistently elevated (systolic blood pressure >140 mm Hg or diastolic blood pressure >90 mm Hg, age <60 years, no medical problems or systolic blood pressure >150 mm Hg or diastolic blood pressure >90 mm Hg, age ≥60 years or a history of diabetes or chronic kidney disease) should have clear follow-up and can benefit from starting oral therapy, because only 6% have normal blood pressure values later.⁹³ Reinforce the need for outpatient follow-up, with or without ED-initiated oral therapy, even if elevated blood pressure was not part of the chief complaint.⁹⁵

Initial therapy recommendations for nonblack individuals are a thiazide diuretic (e.g., hydrochlorothiazide, 25 milligrams daily), an angiotensin-converting enzyme inhibitor (e.g., lisinopril, 10 milligrams daily), or a calcium channel blocker. In blacks, initiate a thiazide diuretic or a calcium channel blocker, alone or in combination.⁹⁵ In patients with chronic kidney disease, with or without diabetes, initiate an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker.^7,93,95 Table 57-8 lists indications for recommended oral antihypertensive classes based on trial data, as put forward in the Seventh and Eighth Reports of Joint National Committee.^7,95

Consider and teach patients about potential adverse effects when prescribing an antihypertensive medication to a patient at discharge. A list of the most common side effects stratified by drug class appears in Table 57-9.

The epidemiology, presentation, and management of hypertensive emergencies in children is less well documented than in adults. A formal definition of hypertension crisis does not exist for children.⁹⁶ Hypertension in children is defined as systolic and/or diastolic blood pressure measurement that exceeds the 95th percentile for that child's age, sex, and weight on three or more occasions, and this determination can be made using the pediatric nomograms found at http://www.nhlbi.nih.gov/health-pro/guidelines/current/hypertension-pediatric-jnc-4/blood-pressure-tables; a single elevated blood pressure in the ED is insufficient to diagnose hypertension. Severe blood pressure elevation can be considered any blood pressure that exceeds the 95th to 99th percentile for that child's age, sex, and weight by an additional 20 mm Hg or more.⁹⁷ As in adults, hypertensive emergencies in children refer to severely elevated blood pressures accompanied by target organ damage. Neonates may present with apnea, cyanosis, irritability, and poor feeding, whereas older children may have symptoms that more closely approximate adult presentations, such as headache, confusion or encephalopathy, focal neurologic deficits, vision changes, shortness of breath, peripheral edema, and decreased renal output.⁹⁶

In children who are noted to have severely elevated blood pressures but no evidence of target organ damage, consult the child's pediatrician for outpatient follow-up or initiation of an antihypertensive agent prior to discharge. In children who present with a hypertensive emergency, immediate blood pressure control is needed, along with consultation with the pediatric intensivist or nephrologist, with admission to the pediatric intensive care unit. Blood pressure control should be initiated in the ED, with the primary aim of therapy to reduce the blood pressure to <95th percentile and to <90th percentile in the presence of comorbid conditions like diabetes or cardiac or renal disease. The mean arterial blood pressure should be lowered no more than ≤25% of the initial value in the first hour, with normalization of blood pressure gradually over the next 24 to 48 hours. Preferred first-line medications for hypertensive emergencies in children include labetalol, 0.2 to 1.0 milligram/kg per dose up to 40 milligrams/dose, or an infusion of 0.25 to 3.0 mg/kg/h; or nicardipine, 0.5 to 3 microgram/kg/min infusion. Second-line agents include hydralazine, 0.2 to 0.6 milligram/kg administered as a bolus to a maximum of 20 milligrams; esmolol administered as a 100 to 500 microgram/kg loading dose followed by an infusion of 50 to 150 micrograms/kg/min to a maximum of 1000 micrograms/kg/min; and clevidipine 0.5 to 3.5 micrograms/kg/min infusion; if prior drugs fail, use IV nitroprusside, 0.5 to 10.0 microgram/kg/min.^96,98,99 Phentolamine, 0.1 milligram/kg to a maximum of 5 milligrams, is the drug of choice for conditions associated with high circulating catecholamines, such as cocaine or pseudoephedrine overdose.

The American College of Emergency Physicians policy document titled "Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients in the Emergency Department with Asymptomatic Elevated Blood Pressure" can be found at http://www.acep.org/Content.aspx?id=30060.

The full 2003 Seventh Report of the Joint National Committee can be found at http://www.nhlbi.nih.gov/guidelines/hypertension/jnc7full.htm. The 2013 update, the Eighth Report of the Joint National Committee, focuses primarily on blood pressure goals and initial therapies.⁹⁵

Acknowledgments: The author gratefully acknowledges the contributions of David M. Cline, the author of this chapter in the previous edition.