By Rafael Ortega, MD, NREMT-P; Meredith Williamson, MD; and Daniel Migliaccio, MD
EXECUTIVE SUMMARY
- Hypertension is defined as a blood pressure (BP) > 130/80 mmHg.
- Markedly elevated BP is defined as BP > 180/110-120 mmHg.
- Hypertensive emergency is defined as a markedly elevated BP PLUS new or worsening end-organ injury.
- The five major organ systems that should be assessed for the presence of end-organ damage are the brain, heart, vasculature, kidneys, and retina.
- In general, reduction of the systolic blood pressure (SBP) in a hypertensive emergency should be by no more than 25% within the first hour of treatment, and if clinically stable without worsening end-organ injury, efforts can continue to carefully lower SBP to 160/100 mmHg over the next two to six hours.
- The three hypertensive emergencies where emergency reduction in BP with intravenous medications exceeds this general recommendation are acute aortic dissection, severe preeclampsia or eclampsia, and pheochromocytoma crisis.
- There is no proven benefit, and even indications of harm, with intravenous antihypertensive treatment in asymptomatic patients with markedly elevated BP.
- Initiation of treatment for a newly identified patient with hypertension in the emergency department generally should be the exception, not the rule.
- When initiating treatment for hypertension, thiazide-type diuretics are superior in preventing one or more major forms of cardiovascular disease, are less expensive, and generally should be used as the first-line antihypertensive treatment.
Definition
Hypertension, which has been redefined frequently over the past decades, is one of the most common complaints among adult patients presenting to the emergency department (ED). In 2017, Hypertension Clinical Practice Guidelines redefined inpatient hypertension as blood pressure (BP) ≥ 130 mmHg systolic BP (SBP) or ≥ 80 mmHg diastolic BP (DBP).1 In acute care, hypertension has been categorized broadly as either asymptomatic or symptomatic with evidence of end-organ damage (hypertensive emergency). While the standard of care is to aggressively treat hypertensive emergencies with pharmacotherapy, the management of less severe hypertension is vague with fewer current recommendations.
The American Heart Association (AHA) issues periodic guidelines and recommendations for the management of hypertension.1 These statements have reshaped our understanding and treatment of hypertension over the past decades. More relevant to emergency physicians, this article will focus on the recent AHA scientific statement on the management of hypertension in the acute care setting.2
Epidemiology
The management of hypertension is crucial because of its significant effect on morbidity and mortality of several devastating conditions, including cardiovascular disease (CVD), stroke, and renal failure. In all these chronic diseases, hypertension has been found to be a leading modifiable risk factor, and effective outpatient and possible emergency department initiation of treatment could have the potential to substantially lower the incidence of these adverse health outcomes. A meta-analysis performed in 2002 concluded that at ages 40-69 years, each difference of 20 mmHg SBP was associated with both a greater than twofold difference in stroke death rate and a twofold increase in the rate of death from ischemic heart disease and other vascular causes.3 Hypertension can have devastating effects on public health, especially in minority communities where both severity and onset are higher and earlier than in white communities.4
Etiology
Essential, Primary, or Idiopathic Hypertension
Essential, primary, and idiopathic hypertension all are synonymous. More than 95% of patients who present with hypertension are diagnosed with primary hypertension. There is emerging evidence that points to a complex interplay between genetics (inherited) and modifiable factors as contributors to primary hypertension.5 Several papers have discussed the discovery of specific familial gene mutations responsible for “inherited hypertension,” including ectopic expression of aldosterone, mutations in sodium channels, and variation at the angiotensinogen locus, among others.6 Of the numerous modifiable risk factors, the following have been identified as primary contributors: obesity, insulin resistance, elevated alcohol intake, high salt intake, age (recognize this is not modifiable), sedentary lifestyle, stress, and low electrolyte intake.7
While these modifiable risk factors are chronic in nature, we can address them in the emergency department and provide patients with concrete evidence of the effect on their blood pressure. In 1973, the Framingham study concluded that on average, every 10% weight gain is associated with a 6.5 mmHg increase in systolic blood pressure.8 With the rise in obesity, sedentary lifestyles, increasingly processed foods, and stress, a concordant rise can be expected in these contributing factors to primary hypertension. Providing objective data and helping form actionable specific, measurable, achievable, relevant, and time bound (SMART) goals with patients could be the only intervention needed to correct essential hypertension in those with the risk factors mentioned earlier.
While relatively uncommon, 5% to 10% of patients presenting with hypertension have an identifiable pathologic cause for their elevated blood pressures. This should be considered in individuals with an onset of hypertension before the age of 30 years, abrupt onset with no previous history, severe elevations (considered > 220 mmHg SBP), resistant to multiple antihypertensives of differing classes, unprovoked hypokalemia, diastolic hypertension in patients older than 65 years of age, and disproportionate end-organ damage for degree of hypertension. Following is a sampling of these possible etiologies of hypertension presented in order of prevalence.
Obstructive Sleep Apnea
Obstructive sleep apnea (OSA) is a comorbid condition with hypertension, occurring at rates ranging from 6% to 17%, and up to 49% in advanced age groups.9 It is characterized as recurrent episodes of nocturnal upper airway collapse, episodes of hypo/apnea, hypercarbia, and hypoxemia. The effects on the cardiovascular system are widely known, including increasing the rates of hypertension, accelerated coronary artery disease, heart failure (HF), increased rates of atrial fibrillation, increased daytime fatigue, and overall greater morbidity and mortality.
Data published in 2022 concluded that 89% of patients aged 18-35 years with secondary hypertension have underlying OSA.10 There are many complex underlying causes for this phenomenon, but the most accepted mechanism is the effect of episodic obstruction causing recurrent hypoxia and hypercapnia, leading to sympathetic overactivity and, ultimately, increases in systemic pressure. Mainstays of treatment include weight loss, referral to a primary care physician to refer for sleep study/initiation of continuous positive airway pressure (CPAP), and initiation of diuretics. Using CPAP has been shown to reduce arterial stiffness and hypertension, and improve vascular inflammation in those with OSA.11 Emergency providers are well suited to potentially recognize this easily treatable comorbidity.
Renovascular Disease
More than 90% of renal artery stenosis is caused by atherosclerosis, compared to the less than 10% caused by fibromuscular dysplasia.12 The typical prevalence is approximately 10% to 15% in those older than age 50 years and up to 50% to 60% in the older adult population. Finally, vasculitis is an extremely rare cause of renovascular secondary hypertension (comprising less than 1% of cases).12
The first-line intervention for hypertension due to renal artery stenosis is with an angiotensin-converting enzyme inhibitor (ACE-I) or angiotensin receptor blocker (ARB). Direct interventions include percutaneous intervention and surgical revascularization, such as aortorenal bypass.12 Although these latter advanced therapies are well outside the scope of the emergency department, it is clear initiation of an ACE-I or ARB is a simple first-line intervention followed by referral to nephrology for further interventional considerations.
Primary Aldosteronism
Primary aldosteronism results from excessive production of aldosterone independent of renin and angiotensin II, leading to increased sodium retention, potassium excretion, and overall increase in intravascular volume. Several studies have determined that, although once thought to be more rare, the prevalence of primary aldosteronism ranges from 5% to 15%, interestingly with many patients being normokalemic.13 In approximately half of these patients, primary aldosteronism is caused by unilateral excessive production from either an adenoma or adrenal hyperplasia. The other half is the result of idiopathic bilateral adrenal hyperplasia.1
Standard first-line medical management involves initiation of a mineralocorticoid receptor antagonist, such as spironolactone or eplerenone. Those with unilateral pathology, such as adrenal-producing adenoma or adrenal hyperplasia, can be considered for unilateral laparoscopic adrenalectomy with excellent results.14
Drug or Alcohol Induced
Thought to contribute up to 2% to 4% of cases of secondary hypertension, drugs and alcohol have been implicated and largely are a preventable and reversible etiology. While not an exhaustive list, frequently used offending medications and substances include alcohol, caffeine, nonsteroidal anti-inflammatory drugs (NSAIDs), systemic corticosteroids, oral contraceptives, antipsychotics, antidepressants, and various illicit drugs, including but not limited to amphetamines, cocaine, etc.
According to the 2023 National Survey on Drug Use and Health, 79% of respondents aged 12 years and older endorsed ingestion of alcohol at some point in their lifetime. More concerning, 23% reported binge drinking, defined as at least four to five standard drinks in less than two hours, at least once in the previous month, and 6% reported heavy alcohol use the previous month, defined as greater than four or more standard drinks per day for females and five or more standard drinks per day for males.15 Recent meta-analyses have confirmed the findings of experimental studies that demonstrate the direct effect of chronic alcohol consumption on hypertension, although the mechanism is yet to be known.16
Others
Although much less common than the previously mentioned etiologies, many other rare diagnoses contribute to the development of secondary hypertension. Examples include pheochromocytoma, Cushing’s syndrome, thyroid dysfunction, aortic coarctation, congenital adrenal hyperplasia, and acromegaly, among others.
Hypertensive Emergency
A hypertensive emergency is defined as an acute increase in blood pressure associated with severe, potentially life-threatening target organ damage.2 There is a general consensus that an SBP of > 180 mmHg or DBP > 120 mmHg warrants consideration of hypertensive emergency.17 Although it is more common for hypertensive emergencies to be associated with severe elevations in SBP and DBP, they still can be present in individuals with a history of normotension presenting with moderate elevations (for example, SBP 170s mmHg) due to a component of acuity of the abrupt rise contributing to the development of organ damage.
Because of the severe consequences of untreated hypertensive emergencies, it is important for the emergency physician (EP) to recognize this rather rare diagnosis and initiate treatment expeditiously to prevent further injury. There generally are five major organ systems that should be assessed for the presence of end-organ damage: brain, heart, vasculature, kidney, and retina.
Pathophysiology
A basic understanding of the hemodynamic components of blood pressure will help guide the management of hypertension, especially when discussing hypertensive emergencies. The standard formula for mean arterial blood pressure (MAP) is MAP = cardiac output (CO) × systemic vascular resistance (SVR). Based on this equation, an increase in MAP must be caused by an increase in either CO or SVR, with SVR being the primary driver of prolonged hypertension. Intravascular arterial blood volume and its balance between peripheral venous system/runoff also is a contributor of hypertension because of their inverse correlation.
A third contributor to the development of hypertension is atherosclerosis. As one ages, the burden of atherosclerotic disease increases and causes decreased elasticity and compliance of the arterial vessels. This decreased compliance and “stiffness” causes a greater increase in SBP during systole.18 Finally, the arterial system has mechanisms to autoregulate blood pressure, which has important protective effects on the most sensitive organs, such as the central nervous system, heart, and kidneys. In normotensive individuals, the cerebral vasculature can dilate and constrict to maintain MAPs between 60 mmHg and 120 mmHg. However, in chronic hypertension, the cerebral vasculature experiences chronically elevated pressures, causing a protective hypertrophy while at the same time causing a lower capacity to dilate. It is important to consider that these patients now have a reduced ability to maintain blood flow when systemic pressures decrease and form the basis for the treatment target blood pressure.
Discussed in detail later, it is recommended that MAPs should be lowered cautiously and no more than 25% over 24 hours.19 There have been many studies aimed at elucidating the mechanism of the transition from asymptomatic severe hypertension to hypertensive emergency with organ damage. It is thought that a combined acute increase in humoral vasoconstrictors along with the failure of the vasculature autoregulatory mechanisms are the main contributors. This sudden increase in systemic vascular resistance causes elevated shearing forces and mechanical damage to the endothelial layer of the vasculature, leading to an inflammatory sequence of events. These events include platelet activation, release of inflammatory cytokines, initiation of the coagulation cascade, deposition of fibrin, and oxidative stress.20 These mechanisms induce downstream tissue ischemia and further propagation of this dangerous cycle.
Evaluation and Diagnostic Studies
In the ED, evaluation of a patient presenting with elevated pressures and concern for hypertensive emergency should include a blood pressure measurement of both arms while the patient is at rest. Interarm differences in blood pressure greater than 10 mmHg to 20 mmHg can be indicative of pathologies such as aortic dissection, coarctation, stenosis, or musculoskeletal conditions. This phenomenon also can be seen in patients, particularly the older adults, which can correlate with advanced atherosclerosis, narrowing of vessels, or loss of elasticity and compliance.21
The EP then should perform a standard history and targeted physical exam, with particular attention on the neurologic, cardiovascular, and renal systems. In patients for whom the differential includes hypertensive emergency, the standard laboratory and imaging workup includes: complete blood count (can assess for microangiopathic hemolytic anemia), basic metabolic panel (assess for renal failure), urinalysis with urine pregnancy in females of child-bearing age (assess for renal failure, glomerulonephritis, preeclampsia), electrocardiogram (assess for presence of left ventricular hypertrophy [LVH], and chest X-ray (assess for pulmonary edema seen with heart failure).22
Neurologic End-Organ Damage
Severe hypertension associated with acute neurologic involvement often is difficult to identify given various patient presentations. Pertinent history includes questioning the patient regarding a history of stroke or known cerebral aneurysms. The EP also should perform a focused review of systems, including identifying any ongoing headaches, visual changes, nausea, emesis, seizures, or focal neurologic deficits. The physical exam should include an examination of the cranium to assess for any trauma as well as a full neurologic exam searching for any focal motor or sensory deficits. Patients presenting with visual complaints should have a fundoscopic exam performed to assess for papilledema, hemorrhages, or cotton-wool spots, which would suggest ocular end-organ damage.
Patients with concerning symptoms and exam findings should be considered for neuroimaging, usually first with computed tomography (CT)/CT angiography to assess for intracranial hemorrhages (ICHs) or large ischemic strokes. In patients who have persistent neurologic deficits in the setting of severe-range hypertension, the clinical diagnosis of hypertensive encephalopathy should be considered. If available, magnetic resonance imaging (MRI) can be considered to evaluate for posterior reversible encephalopathy syndrome (PRES), a rare neurologic condition characterized by acute neurologic deficits caused by vasogenic edema in the posterior brain. This condition carries a poor prognosis and can have lasting neurologic sequelae.23
Cardiac End-Organ Damage
Severe hypertension also can cause numerous cardiac emergencies with deadly outcomes, including acute heart failure, aortic dissection, and acute coronary syndrome, among others. Obtaining a prompt history, exam, and initial diagnostics is key to initiating expeditious treatment, since many of the pathologies mentioned earlier are treated in vastly different ways, and if mistaken can cause severe morbidity and mortality.
The EP should inquire regarding a history of heart failure, coronary artery disease, aneurysms, and prior intrathoracic surgeries. A review of systems should encompass assessing for chest pain, referred pain, dyspnea, weakness, palpitations/arrhythmias, syncope, nausea/emesis, and chest/abdominal pain radiating to the back, among others. A focused physical exam should assess the pulmonary system (auscultate for the presence of rales), cardiac exam (auscultating for new murmurs, gallops, or rhythm abnormalities), abdominal exam (assessing for ascites, pulsatile mass), and a lower extremity exam (assessing for symmetric distal pulses or anasarca).
In addition to the previously mentioned standard hypertensive emergency diagnostic workup, concerns for cardiac ischemia should prompt analysis of the patient’s troponin levels and brain natriuretic peptide. If aortic dissection is suspected, rapid identification can be obtained using point-of-care ultrasound (POCUS), with excellent sensitivity (93%) and specificity (90%) in one multicenter study, along with the benefit of timely diagnosis.24 In patients who are stable without definitive findings of an aortic dissection on POCUS or when confirmation of aortic dissection is desired, a CT angiogram of the chest and abdomen should be obtained to further determine the presence or absence of an aortic dissection.
Renal End-Organ Damage
Renal damage from severe hypertension can present with symptoms, such as acute oliguria, or other typical nonspecific findings associated with renal failure, such as altered mental status, nausea with emesis, anorexia, or peripheral edema. The standard workup, including basic metabolic panel and urinalysis, will confirm the diagnosis with elevated creatinine from baseline and urinary sediment.25
Management
General Management of Acute Hypertensive Emergencies
Once a patient has been identified as experiencing severe hypertension with acute end-organ damage, immediate therapy with intravenous agents is critical. (See Tables 1-4.) These are preferred because they are short-acting and easily titratable. In an absence of the aforementioned conditions, the American College of Cardiology (ACA) and the AHA Task Force in their 2017 guidelines recommend reduction of the SBP by no more than 25% within the first hour of treatment.26 If clinically stable without worsening end-organ injury, efforts can continue to carefully lower SBP to 160/100 mmHg over the next two to six hours, then cautiously to normal over the next 24-48 hours.
Table 1. IV Agents for Acute Hypertension: Beta-Blockers |
Labetalol
Esmolol
|
IV: intravenous Adapted from: Cline DM, Ma OJ, Meckler GD, et al. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill Education; 2020. |
Table 2. IV Agents for Acute Hypertension: Calcium Channel Blockers |
Nicardipine
Clevidipine
|
BP: blood pressure; IV: intravenous Adapted from: Cline DM, Ma OJ, Meckler GD, et al. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill Education; 2020. |
Table 3. IV Agents for Acute Hypertension: Vasodilators |
Hydralazine
Nitroglycerin
Nitroprusside
|
IV: intravenous; BP: blood pressure; ICP: intracranial pressure Adapted from: Cline DM, Ma OJ, Meckler GD, et al. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill Education; 2020. |
Table 4. IV Agents for Acute Hypertension: Other Agents |
Phentolamine
|
IV: intravenous Adapted from: Cline DM, Ma OJ, Meckler GD, et al. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill Education; 2020. |
Once the pathologic cycle of vasoconstriction and hypoperfusion is terminated, treatment can transition from intravenous agents to oral medication. (See Tables 5-7.) Although there are several effective antihypertensive medication classes, the choice of agent should be guided by the primary type of end-organ damage, drug pharmacokinetics, and the patient’s comorbidities.
Table 5.Oral Medications for Hypertension: Alpha-1 and Beta-Adrenergic Blockers |
Carvedilol
Labetalol
|
PO: orally; COPD: chronic obstructive pulmonary disease Adapted from: Cline DM, Ma OJ, Meckler GD, et al. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill Education; 2020. |
Table 6.Oral Medications for Hypertension: Beta-Adrenergic Blocker |
Metoprolol
|
PO: orally; COPD: chronic obstructive pulmonary disease Adapted from: Cline DM, Ma OJ, Meckler GD, et al. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill Education; 2020. |
Table 7. Oral Medications for Hypertension: Other Agents |
Lisinopril (Angiotensin-converting enzyme inhibitor)
Losartan (Angiotensin II antagonist)
Hydrochlorothiazide (Thiazide diuretic)
Nifedipine (Calcium channel blocker)
Clonidine (Central alpha-2 agonist)
|
PO: orally; CHF: congestive heart failure Adapted from: Cline DM, Ma OJ, Meckler GD, et al. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. McGraw-Hill Education; 2020. |
Conditions Warranting Special Attention
The AHA Task Force 2017 recommendations highlighted three specific pathologies that deviate from the goal to decrease SBP by no greater than 25% over an hour. The three mentioned conditions are acute aortic dissection, severe preeclampsia or eclampsia, and pheochromocytoma crisis.26 In addition, there are unique considerations in the management of acute ICH and ischemic stroke regarding hypertension that will be reviewed.
Aortic Dissection
Aortic dissection occurs when the intima layer becomes compromised and allows blood to enter the media, causing dissection between the intimal and adventitial layers.27 The primary tear sites in an ascending aortic dissection (Stanford type A dissection) occur at the sinotubular junction at the start of the ascending aorta and just beyond the left subclavian (Stanford type B dissection). In addition, dissections can extend in a retrograde fashion involving the coronary ostia, causing further complications, including acute myocardial ischemia and hemorrhagic pericardial effusion, with tamponade leading to the majority of deaths.27
Per the ACA 2017 guidelines, the two preferred titratable pharmacologic agents are the two beta-blocker agents to achieve impulse control, esmolol and labetalol. In patients with relative contraindications to beta-blockades, such as asthma or severe heart failure, esmolol has been found to be the agent of choice since it has a short half-life and can be paused quickly. The goal SBP within 20 minutes should be less than 120 mmHg, although other sources quote a primary goal heart rate of less than 60 beats per minute, since this has been shown to reduce the frequency of shear force on the active dissecting region.26 In patients with severe refractory hypertension, vasodilators such as nicardipine or nitroprusside can be added. This should be done cautiously because vasodilators can increase the force of the left ventricular ejection, causing an undesired increase in aortic wall stress.28
Pheochromocytoma
Pheochromocytoma is one of the rarest tumors but one that can cause hypertensive emergencies and warrants special consideration. The incidence is approximately 0.05% in those with diastolic hypertension and occurs most commonly in the fourth and fifth decades of life.29 Although rare, it is estimated that approximately 75% of deaths caused by pheochromocytomas were missed.30
Pheochromocytomas are catecholamine-secreting tumors that primarily secrete norepinephrine, although they have been documented to also secrete epinephrine and dopamine. These tumors can secrete catecholamines persistently or episodically, causing paroxysmal symptoms and severe hypertension, often making the diagnosis even more challenging. The symptoms most often described include headaches, generalized hyperhidrosis, palpitations, and anxiety.29
Beyond the positive laboratory findings associated with hypertensive emergency, a nonspecific common finding is hyperglycemia. Severe hypertension with end-organ damage should be treated with prompt alpha blockade, with the most common agent being phentolamine.29 Second-line agents include nitroprusside and nicardipine infusions. In the acute setting, beta-blockade should be avoided because this can prompt unopposed alpha activity potentially worsening the effects of severe range hypertension.
Severe Preeclampsia/Eclampsia
Hypertensive disorders are a common occurrence in the peri-partum period, which can put both the mother and fetus at risk for severe morbidity and mortality. Of the disorders associated with hypertension, preeclampsia and eclampsia are pathologies mentioned by the 2017 AHA guidelines that also require a unique treatment approach. These conditions can occur between 20 weeks of pregnancy up to and even past the delivery of the fetus, with sources noting manifestations up to six weeks postpartum.31
Preeclampsia affects 5% to 7% of all pregnant women but is responsible for more than 70,000 maternal deaths and 500,000 fetal deaths worldwide annually.32 Common sequelae include intrauterine growth restriction, premature labor, low birth weight, placental abruption, and higher likelihood of maternal CVD.
Preeclampsia is defined as the presence of hypertension (> 140 mmHg SBP or > 90 mmHg DBP) after 20 weeks’ gestation in a previously normotensive patient with proteinuria or other end-organ dysfunction. Eclampsia is the development of seizure superimposed on a diagnosis of preeclampsia. The top three risk factors for the development of preeclampsia are a history of preeclampsia (relative risk [RR], 8.4), chronic hypertension (RR, 5.1), and gestational diabetes mellitus (RR, 3.7).32 The inclusion criteria of proteinuria are either a dipstick reading of 1+, protein/creatinine ratio of greater than or equal to 0.30, or greater than 300 mg/24 hour protein urine collection.
End-organ damage or preeclampsia with “severe features” includes SBP > 160 mmHg or DBP > 110 mmHg on two separate occasions four hours apart, thrombocytopenia with platelets less than 100,000 PLT/mL, impaired liver function with liver enzymes greater than two times normal range, severe medication-refractory right upper quadrant pain not due to another diagnosis, acute doubling of creatinine or > 1.1 mg/dL, pulmonary edema, or new onset cerebral and visual symptoms.
The pathogenesis of preeclampsia has not been fully elucidated, although there are several theories with strong evidence. It is believed that the development occurs in two phases: first trimester abnormal placentation, followed by late second and third trimester excess maternal antigenic factors.32 In stage one, during normal implantation, the fetal-maternal interface is formed when fetal cytotrophoblasts migrate into the maternal spiral arteries. During normal pregnancy, the connection appears to penetrate deep into the myometrium, developing high-flowing healthy arterioles.
This remodeling appears to differ in placentas bound for preeclampsia. In this case, fetal cytotrophoblasts appear to not fully develop into the invasive endothelial subtype, causing incomplete remodeling of the maternal spiral arteries, with subsequent narrowing of arterioles and placental insufficiency.33 This poor placental perfusion has been hypothesized to lead to the creation of reactive oxygen species, free radicals, and inflammatory cytokines that are thought to contribute to the end-organ damage seen in preeclampsia.
Management of early preeclampsia involves perinatal blood pressure monitoring, prenatal aspirin in high-risk pregnancies, and parental magnesium. The only definitive treatment for both preeclampsia and eclampsia is delivery of the fetus and placenta. The American College of Obstetricians and Gynecologists 2020 practice bulletin states that women with evidence of preeclampsia without severe features can be expectantly managed until 37 weeks. Those presenting with severe features beyond 34 weeks should be considered for induction of delivery, whereas before 34 weeks expectant management can be considered by the obstetric team.34
In addition to appropriate management of delivery, the two main goals are seizure prophylaxis and control of hypertension. The landmark MAGPIE randomized controlled trial of 10,110 females concluded that patients presenting with preeclampsia with severe features have a reduction of seizures by approximately 50% if administered magnesium sulfate.35
The objective of treating severe hypertension is prevention of end-organ damage. Acute onset severe hypertension (SBP > 160 mmHg or > 110 mmHg DBP) should receive antihypertensive agents within 30-60 minutes. The three recommended agents with similar efficacy and safety are intravenous labetalol, hydralazine, and oral nifedipine.34 It is important to consult with the obstetric team regarding patient disposition and further management.
Acute Intracranial Hemorrhage and Ischemic Stroke
ICH and ischemic stroke contribute as the leading causes of mortality, morbidity, and disability. The treatment objectives and strategies differ greatly depending on the underlying cause.
Acute ICH is classified as any bleeding that occurs within the intracranial vault, including the brain parenchyma and surrounding meningeal spaces.36 Studies have found the general incidence of spontaneous ICH to be approximately 24.6 per 100,000 people. This is a devastating insult with one-month median case fatality rates of 40% and extremely low rates of functional independence.37 Many non-modifiable risk factors contribute to the development of spontaneous ICH, such as gender (male), age (older adult), race (Hispanic and African American), and socioeconomic status (lower income). Some clinical and modifiable risk factors include hypertension, cerebral amyloid angiopathy, alcohol use, hypertriglyceridemia, illicit drug use, and anticoagulation status.36
There are two general mechanisms that contribute to the endpoint of spontaneous ICH. First, it is believed that chronic uncontrolled hypertension leads to the development of hypertensive vasculopathy where small- and medium-sized penetrating vessels undergo microscopic degenerative changes, increasing the risk for spontaneous rupture. Second, the deposition of amyloid peptide in the walls of small leptomeningeal and cortical vessels further destabilizes the vessel walls, leading to loss of smooth muscle cells, wall thickening, luminal narrowing, and continued microhemorrhages.36
Following initial rupture, the lack of blood supply and mechanical injury of expanding hematoma to the specific region of the brain causes the development of acute neurologic deficits seen on physical exam. This cortical damage extends past the initial insult with development of perihematomal edema within three hours, followed by the secondary reactions as a result of free blood in the cranium, including activation of the coagulation cascade, release of inflammatory reactants, and iron deposition from hemoglobin breakdown.
Studies have shown that greater than 75% of patients presenting with an acute ICH have an SBP greater than 140 mmHg.38 To date, there have been many ongoing debates regarding the acute blood pressure management in ICH. Advocates for acute rapid control of hypertension argue that data show a direct relationship with blood pressure and hematoma expansion, with the INTERACT I trial demonstrating every 1 mL increase in hematoma size increasing the risk of death and dependency by 5%.39 In contrast, some have hypothesized that the perihematomal region experiences mechanical compression of small arteries, leading to decreased cerebral perfusion, and that by aggressively decreasing systemic blood pressure, we potentially can be increasing the degree of perihematomal ischemia.
Until the results of ongoing trials are published, the 2017 AHA guidelines recommend prompt continuous antihypertensive intravenous infusion and close blood pressure monitoring in those presenting with an SBP > 220 mmHg, with a goal of an immediate reduction in MAP of 15%.1,2 They also conclude that immediate lowering of blood pressure to less than 140 mmHg within six hours of the acute event is not recommended and likely harmful. The gray zone of anti-hypertensive initiation with 140-220 mmHg SBP should be guided by consultation with the appropriate neurosurgical team.
Ischemic stroke encompasses approximately two-thirds of cerebrovascular disease and, like acute ICH, is a leading cause of mortality and long-term disability. It commonly occurs from progressive cerebral atherosclerosis, cardiac embolism, or thrombosis of cerebral vessels.40 With inadequate blood to cerebral tissue, there is first a reversible loss of tissue function, followed by infarction of neuronal cells. Acute treatment of ischemic stroke is directed at early perfusion of at-risk tissue with intravenous thrombolysis and/or endovascular thrombectomy with optimization of the patient’s hemodynamic status.41 Similar to acute ICH, hypertension is present in approximately 80% of acute ischemic strokes, especially if the patient has a history of chronic hypertension.
The therapeutic goal of blood pressure management is to maintain cerebral perfusion of the ischemic tissue while minimizing the exacerbation of brain edema and hemorrhagic transformation. Studies have shown patients with acute ischemic stroke have higher rates of mortality at the extremes of blood pressure.42 Interestingly, data published in 2018 from the RIGHT 2 trial showed prehospital treatment of hypertension in patients with presumed stroke and concurrent hypertension did not improve functional outcomes.43
Based on published data, the AHA 2017 guidelines recommend early initiation or resumption of antihypertensive treatment in acute ischemic stroke only in two conditions: patients treated with tissue-type plasminogen activator (tPA) and patients with severe-range hypertension, defined as an SBP > 220 mmHg or DBP > 110 mmHg. In patients where tPA is clinically indicated, recommendations are to slowly lower the blood pressure to a goal of < 185 mmHg SBP and < 110 mmHg DBP before drug administration. In addition, over the next 24 hours, blood pressure should be maintained at a goal of < 180 mmHg SBP and < 105 mmHg DBP.
In patients who were not candidates for tPA or endovascular intervention and presenting with a BP > 220/110 mmHg, cautious reduction of BP by approximately 15% during the first 24 hours may be reasonable, although there is a lack of data that shows a mortality or dependency benefit. For patients with preexisting hypertension and, again, who are not candidates for intervention presenting with BP < 220/110 mmHg, the AHA guidelines recommend resumption of antihypertensive regimen following clinical neurological stability.1
Nonemergent Hypertension
As mentioned earlier, the role of the EP is to identify the rare patient presenting with hypertensive emergency and intervene according to the guidelines discussed earlier. When end-organ damage is ruled out, physicians and patients are left wondering what the next step should be, leading to a wide variation in practice patterns. With the aging baby boomer generation, there has been an increase in the amount of ED visits related to hypertension annually, with estimates of approximately 27 million in 2012.44 In addition, lack of primary care access, insurance, transportation, and many other factors leaves patients presenting to the ED for many primary care-related complaints, which may represent valuable opportunities to intervene on chronic hypertension early to prevent the disastrous secondary related outcomes.2
The new 2017 and 2024 AHA guidelines provide a workflow for the management of asymptomatic hypertension that can be applied to the ED setting.1,2 The novel guidance incorporates not only absolute blood pressure measurements but also includes absolute CVD risk to provide more efficient, tailored, and cost-effective management.45
Although there are many CVD risk calculators to date, the AHA recommends using the ACC/AHA Pooled Cohort Equations (http://tools.acc.org/ASCVD-Risk-Estimator/) to estimate the 10-year risk of atherosclerotic CVD to guide blood pressure treatment. Several studies have confirmed the importance of using CVD risk combined with blood pressure monitoring to guide drug therapy.46 Barriers to implementing this in the ED are the incorporation of cholesterol laboratory values into the calculations, which are not routinely acquired in the emergency setting.
The AHA guidelines first stratify patients based on the blood pressure levels corresponding with their classifications of either normal (< 120/80 mmHg), elevated (< 129/80 mmHg), stage 1 hypertension (130-139/80-89 mmHg), and stage 2 hypertension (> 140/90 mmHg). Patients in the normal category are encouraged to undergo/continue healthy lifestyle habits. Patients in the elevated category should undergo nonpharmacologic interventions and coaching, including weight loss, Dietary Approaches to Stop Hypertension (DASH) dietary pattern, reduced sodium intake, increased potassium intake, engaging in aerobic and anaerobic physical activity, and reduction in alcohol consumption.
These patients also should have their blood pressure reassessed in three to six months with their primary care physician. Patients in the stage 1 hypertension category are those where clinical atherosclerotic cardiovascular disease (ASCVD) score is incorporated. Those with a 10-year > 10% CVD risk should begin both nonpharmacologic interventions as mentioned earlier and initiation of an antihypertensive. They also should have expedited reassessment in one month with their primary care physician. Lastly, patients in the stage 2 hypertension category should automatically be started on both nonpharmacological and an antihypertensive regimen along with expedited one-month follow-up with their primary care physician.
Pharmacologic Agents
There are several oral antihypertensive drug classes to choose from when blood pressure control is indicated. (See Tables 5-7.) Similar to the primary care setting, the choice should be guided based on several factors, including medication benefits, medication adherence, dosing requirements, side effects, and patient cost, among others. The 2017 AHA guidelines recommend choosing from four classes of medications as first-line agents: thiazide diuretics, ACE inhibitors, ARBs, and calcium channel blockers.
The ALLHAT trial in 2002 randomized patients to a thiazide diuretic (chlorthalidone), calcium channel blocker (amlodipine), and lisinopril. The primary outcome was combined fatal coronary heart disease or nonfatal myocardial infarction, with secondary outcomes of all-cause mortality, stroke, combined coronary heart disease, and combined cardiovascular disease. Results showed thiazide-type diuretics were superior in preventing one or more major forms of cardiovascular disease, were less expensive, and generally should be used as the first-line antihypertensive treatment. Additionally, ACE inhibitors were less effective than thiazide diuretics and calcium channel blockers at lowering blood pressure and stroke prevention.47 Calcium channel blockers have been found to be an effective alternative for thiazide diuretics because they also reduce all CVD events other than heart failure when a patient cannot tolerate the side effects of diuretics.
Specific Populations
Certain comorbidities may affect which class of medications to choose from based on their profile. The 2017 AHA guidelines mention several common comorbid conditions that may have specific recommendations from the broader asymptomatic antihypertensive management strategy as discussed earlier.
Stable Ischemic Heart Disease (SIDH)
It is well documented that hypertension is one of the main risk factors for the development of ischemic heart disease. A randomized trial of 9,361 patients in 2015 evaluated a systolic goal BP of 120 mmHg vs. 140 mmHg and found that the more intensive BP control resulted in lower rates of fatal and nonfatal major cardiovascular events and death from any cause.48 In patients with SIDH and hypertension, the AHA recommendation is to reduce blood pressure to < 130/80 mmHg with goal-directed medical therapy (GDMT) beta-blockers (metoprolol, carvedilol, propranolol, nadolol, bisoprolol, or timolol), an ACE inhibitor, or an ARB. Patients with persistent hypertension and anginal episodes also should be started on a calcium channel blocker (CCB) or CCB vs. thiazide type diuretic vs. mineralocorticoid receptor antagonist if no angina is present.
Heart Failure Prevention
Patients presenting with chronic HF have been found to have hypertension in up to 75% of cases preceding the development of HF.49 There is a continuous positive association between SBP and HF in older adults, with an adjusted incidence of 1.6, 2.2, and 2.6 in those with SBPs within 120-139 mmHg, 140-159 mmHg, and > 160 mmHg, respectively.50 There are no randomized controlled trials to date comparing the efficacy in HF prevention with specific drug regimens; therefore, the blanket goal AHA recommendation is to maintain an optimal blood pressure of less than 130 mmHg with the general medication guidelines discussed earlier.
Heart Failure with Reduced Ejection Fraction
Approximately 50% of cases of chronic HF associated with myocardial infarction or hypertension have a reduced left ventricular ejection fraction.51 The 2017 AHA guidelines are similar to the HF prevention strategy, with a goal BP < 130/80 mmHg and the use of goal-directed medical therapy. The important caveat is to avoid the use of nondihydropyridine calcium channel blockers (diltiazem, verapamil, etc.) in this subset of patients. The inherent myocardial depressant side effect of calcium channel blockers is the primary reason for this recommendation, along with data demonstrating an increase in late-onset chronic HF and earlier reduction in ejection fraction.52
Heart Failure with Preserved Ejection Fraction
Conversely, 50% of patients with HF have a preserved ejection fraction. HF with reduced ejection fraction (HFrEF) vs. preserved ejection fraction (HFpEF) represent two different entities with very different pathophysiology. Although GDMT as mentioned earlier is the mainstay of HFrEF treatment, there are fewer data demonstrating improvement in mortality and morbidity in HFpEF. The 2017 AHA guidelines recommend initiation of diuretics in patients with HFpEF and symptoms of fluid overload, such as peripheral edema, pulmonary edema, etc. In addition, those with persistent hypertension despite management of hypervolemia should be started on a beta-blocker or ACE/ARB since data have shown a small reduction in mortality rate.53
Chronic Kidney Disease
It is estimated that the prevalence of hypertension in patients with chronic kidney disease (CKD) approaches approximately 86%, with a direct correlation to progressive renal disease.54 It is thought that hypertension is problematic on two fronts. First, uncontrolled hypertension leads to chronically elevated glomerular capillary pressures, resulting in damage and sclerosis. In addition, hypertension activates the renin-angiotensin-aldosterone system (RAAS), which further exacerbates renal damage by promoting inflammation, fibrosis, and oxidative stress.
The development of CKD also contributes to further hypertension via several mechanisms. CKD leads to reduced nephron mass, which impairs the kidneys’ ability to excrete sodium, resulting in sodium retention and extracellular volume expansion, causing elevated blood pressures. CKD also is associated with overactivation of the sympathetic nervous system. As discussed earlier, CKD also further activates the RAAS, leading to vasoconstriction and sodium retention. The AHA class 1 recommendation is to aim for a goal BP of < 130/80 mmHg. In the presence of albuminuria, an ACE or ARB is recommended as the first-line treatment, followed by the other agents highlighted in this section.
Disposition
Patients with evidence of hypertensive emergency should be admitted to a critical care unit for close observation and careful titration of their antihypertensives. Those presenting with isolated asymptomatic hypertension generally are safe for discharge with the recommendation to begin an antihypertensive regimen as described earlier and expedited outpatient follow-up for reassessment.2
Summary
As ED visits continue to rise and a significant number of patients present with elevated BP, the responsibility for recognizing and managing not only hypertensive emergencies but largely asymptomatic hypertension is expanding beyond outpatient care and becoming an integral part of emergency medicine. To seize these opportunities, EPs must be well-versed in the definitions of hypertension, the distinction between nonemergent hypertension and hypertensive emergencies, and the appropriate treatment for all levels of BP elevation. The ED can play a vital role in broader, system-wide efforts to reduce hypertension-related morbidity, particularly in underserved communities.
Rafael Ortega, MD, NREMT-P, is PGY-2 Emergency Medicine, University of North Carolina Hospitals, Chapel Hill.
Meredith Williamson, MD, is Clinical Assistant Professor of Emergency Medicine, University of North Carolina at Chapel Hill.
Daniel Migliaccio, MD, FPD, FAAEM, is Clinical Associate Professor, Division Director of Emergency Ultrasound, Ultrasound Fellowship Director, Department of Emergency Medicine, University of North Carolina at Chapel Hill.
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Hypertension is one of the most common complaints among adult patients presenting to the emergency department. The American Heart Association (AHA) issues periodic guidelines and recommendations for the management of hypertension. This article will focus on the recent AHA scientific statement on the management of hypertension in the acute care setting.
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