Authors: Lisa Freeman Grossheim, MD, FACEP, Assistant Professor, Department of Emergency Medicine, University of Texas Medical School at Houston; Monica Carvajal, MD, Resident Physician, Department of Emergency Medicine, University of Texas Medical School at Houston; and Heidi Knowles-Ely, MD, Resident Physician, Department of Emergency Medicine, University of Texas Medical School at Houston.
Peer Reviewers: Charles Emerman, MD, Professor and Chairman of Emergency Medicine, Case Western Reserve University, Cleveland, OH; and Richard O. Gray, MD, Assistant Professor of Emergency Medicine, Hennepin County Medical Center, Minneapolis, MN.
Hypertension affects 25% of all adults and 60% of all people older than 60 years in the United States.1 Emergency physicians routinely evaluate and treat elevated blood pressure in a variety of settings, ranging from the asymptomatic patient with increased blood pressure noted on an unexpected emergency department (ED) visit, to the seriously ill patient with elevated blood pressure and end-organ damage.2 Almost 30% of ED patients have elevated blood pressure during their ED evaluations. Most patients (68%) had a previous history of hypertension.3
Hypertension is the most widely recognized modifiable risk factor for stroke, myocardial infarction, peripheral vascular disease, heart failure, and end-stage renal disease.4 The role of the emergency physician is to stabilize acute disease and to assess the potential for deterioration, initiate appropriate treatment when indicated, and determine proper patient disposition.
This issue of Emergency Medicine Reports reviews urgent and emergent hypertension syndromes encountered in the ED and approaches to patient assessment and pharmacologic management. Part I will cover the clinical evaluation of hypertensive patients and hypertension syndromes. Part II will discuss antihypertensive medications and the management of hypertension in specific disease processes.—The Editor
The definition of hypertension is somewhat indiscriminate and usually is defined as the level of blood pressure linked with a doubled increased long-term risk for adverse events. It also could be thought of as the level at which the benefits of action exceed the risks and costs of inaction.5 According to the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC7), the diagnosis and classification is based on an average of two or more properly measured seated blood pressure readings on two or more office visits.4 (See Table 1.) This definition does not apply to the ED setting, since the diagnosis of hypertension requires blood pressure measurements taken on more than one occasion, but it still can be used in a general discussion about the proper diagnosis of hypertension.
Table 1. Classification of Blood Pressure4
More than 90% of patients with hypertension have idiopathic or essential hypertension. The exact cause of essential hypertension is unknown, but it is thought to be multifactorial, with several contributing factors such as age, race, obesity, dietary salt intake, and heredity.6 Secondary hypertension occurs when an etiology is identified. The most common causes of hypertension are listed in Table 2.
Table 2. Causes of Hypertension1,2,4
Initially, increased ED blood pressures frequently decrease spontaneously by the time a second reading is obtained. Most of the time this is not the result of reduced stress but of a regression to the mean, a property of all extreme observations.2,7
Clinical Evaluation of the Hypertensive Patient
There are three goals in the evaluation of a patient with hypertension in the ED. First, assess presence of acute or rapidly progressive target organ damage. Second, reveal identifiable causes of hypertension. Third, assess the patient’s lifestyle and identify other cardiovascular risk factors for concomitant disorders that may affect prognosis and guide therapy.4
It is important to ascertain the duration and severity of pre-existing hypertension and the degree of previous success with blood pressure control. In some cases the patient has never been diagnosed with high blood pressure. Identification of the presence of target end-organ damage is key to the determining the urgency of the hypertension. Symptoms of end-organ involvement may include symptoms consistent with acute coronary syndrome or congestive heart failure (cardiovascular); paresthesias, weakness, headache, or altered mental status (cerebrovascular); and oliguria or hematuria (renovascular).4,8 Inquire about medication use and compliance, dosage adjustments, use of over-the-counter drugs as well as illicit drug use and alcohol use. Past medical history should focus on illnesses associated with potential end organ damage as noted above. Family history should include questions about renal or cardiac disease or major vessel aneurysms.
Often, an elevated blood pressure is the only abnormal finding on examination in patients with hypertension. Blood pressure should be verified by appropriate measurement of blood pressure in both arms. The accurate measurement of blood pressure is key, as treatment decisions are based in large part on this reading. The mercury sphygmomanometer always has been the gold standard device for the measurement of blood pressure. The customary location for blood pressure measurement is the brachial artery.9 Newer home models that measure pressure at the wrist and fingers are inaccurate, often producing falsely elevated readings. The auscultatory method (manual) utilizes the Korotkoff technique for measuring blood pressure. The American Heart Association recommends using Korotkoff Phase I (clear sounds) to record systolic blood pressure, while using Korotkoff Phase V to record diastolic pressure (sound disappears). In children, Korotkoff Phase IV (muffling) is suggested to record diastolic pressure. Korotkoff sounds gives systolic values that are lower than intraarterial blood pressure and diastolic ones that are higher. The oscillometric (electronic) method currently is used throughout ambulatory clinics, hospitals, and as home monitors. These devices use algorithms to calculate the blood pressure, as the point of maximal oscillation corresponds to the mean arterial pressure. Its advantages are that it is less susceptible to noise, easily placed on/off by patients, and an exact cuff placement is not required.9 For accurate readings, the most important concept is cuff size. The cuff size is critical to an accurate measurement of blood pressure. Cuffs that are too small tend to overestimate blood pressure and vice-versa. Bladder widths should be two-thirds the width of the arm. The bladder within the cuff should encircle approximately 80% of the circumference of the arm.
The mean arterial pressure (MAP) often is used as a target value in the treatment of hemodynamic instability. It is calculated by the following formula: MAP = systolic blood pressure + (2 x diastolic blood pressure)/3. A seated blood pressure reading after five minutes of rest is recommended, even though this is not always possible in ED patients. Postural changes in blood pressure should be assessed by taking readings seated and two minutes after the patient stands.5
Theoretically, patients should refrain from caffeine for 30-60 minutes, smoking for 15-30 minutes, and/or exogenous stimulants such as phenylephrine, nasal decongestants, or eye drops prior to blood pressure monitoring to eliminate potential secondary causes of hypertension.1 (See Tables 3 and 4.)
Table 3. Causes of Resistant Hypertension4
Table 4. Causes of Isolated
Invasive Blood Pressure Monitoring
Invasive blood pressure monitoring via an arterial catheter connected to a transducer is indicated in some clinical circumstances. These include patients who have very high or very low blood pressures, patients who require continuous infusions of antihypertensive medications or pressors, or those in whom accurate blood pressures may not able to be obtained, such as obese patients.10
The physical examination should be directed toward identifying signs of end-organ damage. (See Table 5.)
Table 5. Physical Examination Clues
of Hypertensive End-Organ Damage
Laboratory and Radiographic Evaluation
Patients with severe, symptomatic hypertension should have a diagnostic evaluation targeted to their symptoms, such as electrocardiogram (ECG), chest x-ray, cardiac enzymes, or computed tomography (CT) of the brain. Few studies have assessed the prognostic value of abnormal laboratory findings in patients with severe asymptomatic hypertension.2 Measurement of blood urea nitrogen (BUN), creatinine, and a urinalysis are reasonable since renal failure often is asymptomatic. An ECG is indicated in a patient with chest pain, but no studies demonstrate benefit of obtaining an ECG in an asymptomatic patient.2 A baseline chest radiograph is of low yield as well in the asymptomatic patient.11,12 A urine drug screen can be useful for patients in whom drug use is suspected as a cause of hypertension. More specialized tests are indicated to diagnose causes of secondary hypertension. (See Table 6.)
Table 6. Diagnosis of Causes
of Secondary Hypertension
These diagnostic studies are not meant to be used as decision tools in the ED patient, as the results are not usually available in a timely manner. It is reasonable, however, to initiate the diagnostic evaluation in the ED when a secondary cause of hypertension is suspected.
Hypertension syndromes span a clinical spectrum of diseases that differ in the swiftness and aggressiveness of their management. The definitions of the various syndromes differ between authors, and the boundaries separating the syndromes often are blurred. The presence or risk of progressive end-organ damage determines the urgency with which severely increased blood pressure needs to be lowered.2
Hypertensive Emergency. Hypertensive emergency (also known as hypertensive crisis) includes a spectrum of clinical entities that share the common requirement of elevated blood pressure and rapid, progressive damage to end-organs. The most severely affected end-organs include the heart, brain, kidneys, and large arteries. It is important to keep in mind that the diagnosis of hypertensive emergency is not only dependent on an absolute blood pressure measurement, but is based on the clinical manifestations at the time of presentation. A hypertensive emergency requires immediate blood pressure reduction within 1-2 hours to prevent or limit target organ damage. Immediate blood pressure reduction to a normal range is not indicated, as this may decrease cerebral blood flow in a patient who is chronically hypertensive who likely has impaired cerebral autoregulation.
Clinical Presentation. Patients may present with symptoms of headache, vomiting, altered mental status, cardiac ischemia, acute left ventricular failure with pulmonary edema, dissecting aortic aneurysm, or preeclampsia/eclampsia as a manifestation of their hypertensive emergency. Hypertensive emergencies also can present as a product of catecholamine excess such as occurs with drug intoxication such as cocaine, pheochromocytoma, or monoamine oxidase inhibitor crisis. A thorough history, including medications/drugs used, sometimes can be the only clue as to a secondary etiology.
Physical exam findings vary, depending on what organ system is affected. There may be fundoscopic evidence of papilledema, new hemorrhages or exudates, neurologic manifestations of acute stroke (i.e., focal weakness), rales, or a gallop, indicating cardiac involvement.
Treatment. Treatment includes reduction the blood pressure by 10% in the first hour, with an additional 15% reduction gradually over the next 2-3 hours. Hypertension associated with aortic dissection is the exception to this rule, as immediate blood pressure reduction is important in limiting the extent of the dissection. An easily titratable parenteral agent must be used in the treatment of hypertensive emergencies. Oral agents can result in a harmful, precipitous decrease in blood pressure that often is difficult to reverse. Nitroprusside (Nipride) is the cornerstone of treatment of hypertensive emergencies. It does require a continuous infusion and does have risk of cyanide toxicity. Other choices include esmolol (Brevibloc), labetalol (Trandate, Normodyne), fenoldopam (Corlopam), and nicardapine (Cardene).
Hypertensive Encephalopathy. Hypertensive encephalopathy is an uncommon, potentially reversible constellation of neurologic symptoms associated with an abrupt rise in blood pressure. The clinical presentation is thought to be due the increased MAP overwhelming the brain’s ability to autoregulate cerebral blood flow. Significant vasospasm may occur, leading to increased intracranial pressure secondary to a transient decrease in the blood-brain barrier integrity, with a resultant cerebral edema. With persistently elevated systemic pressure, arteriolar damage and necrosis occur, leading to cerebral hemorrhage and death.
Clinical Presentation. The patient with hypertensive encephalopathy may present with symptoms ranging from vomiting, headache, or visual changes to seizures or altered mental status. Focal neurologic deficits can occur but usually do not follow an anatomic distribution. Papilledema often is found as well. CT of the head is warranted to exclude other conditions such as hemorrhage or mass. CT often is normal, but may show white-matter edema of the occipital lobes and other posterior structures.13 It is important to keep in mind that hypertensive encephalopathy should be a diagnosis of exclusion; the emergency physician must exclude other potentially life-threatening causes of the patient’s symptoms. The diagnosis can confirmed if the patient’s symptoms improve with lowering of the blood pressure.2
Treatment. An easily titratable parenteral agent should be used in the treatment of hypertensive encephalopathy. The rapid, controlled reduction of blood pressure over a few hours can be lifesaving. The most commonly used agent for this is IV nitroprusside. The MAP should be reduced by 25% over an hour, with a minimum diastolic pressure of 110 mmHg.14 Excessive reduction of blood pressure must be avoided to prevent the increased cerebral ischemia and potential for stroke that results if the pressure falls below the lower level of cerebral autoregulation. In non-hypertensive individuals, this is at about a MAP of 60, but in chronically hypertensive patients, the MAP below which cerebral ischemia will occur is much higher.14 Admission to the intensive care unit (ICU) is necessary for close monitoring and titration of parenteral anti-hypertensive medications.
Hypertensive Urgency. Hypertensive urgency is the presence of an elevated blood pressure, generally recognized as a systolic blood pressure greater than 180 or diastolic blood pressure greater than 110, accompanied by non-specific symptoms in the absence of acute, severe target organ damage but where the patient is at high risk for such an event. The above parameters are arbitrary numbers and are not absolute cutoffs for the diagnosis of urgency. The clinical scenario mandates the level at which the physician becomes concerned and may wish to contemplate giving antihypertensive drug therapy.15 Many factors need to be considered when determining the need to urgently treat significantly elevated blood pressure in the absence of end-organ damage. The risk of an acute complication of elevated blood pressure is related to the patient’s age, chronicity of the disease, the rapidity of the blood pressure increase, and the nature of any previous end-organ damage. Patients with a higher risk of a temporally related adverse event include those with prior end-organ disease such as stroke, coronary artery disease, or renal insufficiency.2 Despite the common practice of treating severely increased blood pressure in the asymptomatic ED patient, there is little evidence to support this approach.2,16 In most patients with a greatly elevated blood pressure but no symptoms referable to the blood pressure have little risk of developing an adverse event such as a stroke or myocardial infarction in the near term.2,17
Clinical Presentation. Does the asymptomatic little old lady strapped to the back board after her fender bender accident who has the isolated systolic blood pressure of 210 really need urgent treatment of that blood pressure? The most common clinical presentations are asymptomatic patients who have severe elevations in blood pressure without any target organ damage presenting to an acute medical setting for a complaint unrelated to hypertension.15 The absence of an acute stroke in evolution, subarachnoid hemorrhage, hypertensive encephalopathy, myocardial ischemia, acute left ventricular failure, pulmonary edema, aortic dissection, pheochromocytoma, drug-related, catecholamine-excess state, and preeclampsia or eclampsia imparts a diagnosis of hypertensive urgency. If the aforementioned symptomatology is present, aggressive treatment within minutes for hypertensive emergency is indicated. Otherwise, asymptomatic individuals who have a normal physical exam and clinical evaluation do not require emergent treatment. Hypertension associated with chest pain or headache are common ED presentations. It may be difficult to determine if the symptoms are due to the elevated blood pressure or the blood pressure is elevated secondary to the pain. Often this determination is not made until retrospect.
Treatment. To manage hypertensive urgency, two issues must be addressed. First, the physician must believe that there is a high short-term risk of complications should the blood pressure rise acutely.18 Second, the patient must be at high risk for cardiovascular or renal complications in the near future such that acutely lowering the blood pressure might improve the prognosis.15 A significant consideration in the decision to treat hypertensive urgency is the local medical standard of care predetermined by tort law and legal precedents set by personal injury lawsuits. These cases are based on arbitrary blood pressure readings that do not consider individual patient presentations. EDs and urgent care centers have formulated standard policies not to discharge patients if the blood pressure is above the arbitrary threshold. However, to date no outcome data corroborate that acutely lowering blood pressure other than in a hypertensive emergency improves short-term prognosis.15 Essentially this is a judgement call, and most likely a consensus panel of experts would disagree with each other. Secondly, the physician must decide that the benefits of treatment are likely to outweigh the risks.18 If both answers are yes, the process to reduce blood pressure safely over a few hours can be started.15 These patients should have a treatment strategy initiated from the ED, but the blood pressure does not necessarily need to be decreased to normal prior to discharge.2 The choice of oral agents is discussed in a subsequent section.
Accelerated Malignant Hypertension. Accelerated malignant hypertension is an uncommon entity, affecting only 1-5% of all patients with hypertension. Young black men are particularly prone to this condition, which is caused most often by underlying renal or renovascular disease.19 Patients often present with a long-standing history of hypertension associated with acutely elevated blood pressure and with eye findings such as papilledema, flame-shaped hemorrhages, or soft exudates.2 Patients may present with headache, blurred vision, nocturia, scotomata, and weakness. Renal insufficiency and proteinuria often are seen on laboratory evaluation. Accelerated malignant hypertension is associated with a massive over-secretion of rennin and aldosterone.19,20 Treatment should be started urgently, as in the case of hypertensive emergencies and hypertensive encephalopathy. Nitroprusside or fenoldopam can be used, except in marked renal failure, in which case the renal vasculature no longer may respond to vasodilators. A beta-blocker such as labetalol is another reasonable choice.21 Drugs that interrupt the renin-angiotensin system (such as propanolol [Inderal] or captopril [Capoten]) can normalize and maintain blood pressure in patients with malignant hypertension even during a hypertensive crisis.21
Transient Hypertension. Transient hypertension is elevated blood pressure in the presence of no prior history. It cannot be distinguished from other forms of hypertension based on one visit. However, transient hypertension typically does not produce severely elevated blood pressures. The most common causes include pain, anxiety, hypoxia, alcohol withdrawal, bladder distention, and drugs (e.g., oral contraceptives, steroids, NSAIDs, nasal decongestants, cold remedies, appetite suppressants, and antidepressants). Before treatment is initiated with antihypertensive medications, it is prudent to obtain a thorough history to identify any possible reversible causes of the high blood pressure. Treatment of the primary underlying process or discontinuation of the offending agent generally results in resolution of the elevated blood pressure. End-organ damage is highly unlikely, and the blood pressure rarely requires specific intervention. All patients should be referred for a follow-up blood pressure measurement after the acute process has resolved.
1. Victor R. Arterial Hypertension. In: Goldman L, Ausiello D, eds. Cecil Textbook of Medicine, 22nd ed; St. Louis: WB Saunders; 2004.
2. Shayne PH, Pitts SR. Severely elevated blood pressure in the emergency department. Ann Emerg Med 2003;41:513-529.
3. Karras DJ, Wald DA, Harrigan RA, et al. Elevated blood pressure in an urban emergency department: Prevalence and patient characteristics. Acad Emerg Med 2001;8:559 (abstract).
4. Chobanian AV, Bakris GL, Black HR, et al. The 7th report of the joint national committee on prevention, detection, evaluation and treatment of high blood pressure: The JNC 7 Report. JAMA 2003; 289(19)L2560-2571.
5. Braunwald E, Zipes DP, Libby P, eds. Heart Disease: A Textbook of Cardiovascular Medicine, 6th ed; Philadelphia: WB Saunders; 2001:941,968,972-992.
6. Kornitzer M, Dramaix M, DeBacker G. Epidemiology of risk factors for hypertension: implications for prevention and therapy. Drugs 1999;57: 695-712.
7. Pitts SR, Heilpern K, Peters HL. Emergency department patients with very severe hypertension. Poster presented at the annual meeting of the Southeast chapter of the Society of Academic Emergency Medicine, 1998; Atlanta, GA.
8. Gray RO, Matthews JJ. Hypertension. In: Marx JA, Hockberger RS, Walls RM, et al, eds. Rosen’s Emergency Medicine, 5th ed. Mosby: St. Louis; 2002: 1158-1171.
9. Pickering TG. Principles and techniques of blood pressure measurement. Cardiology Clinics 2002;20;207-223.
10. Bander JJ, Guzman JA, Araght A. Arterial blood pressure monitoring in overweight critically ill patients: invasive or non-invasive? Chest 2004;126:746S (Abstract).
11. Bartha GW, Nugent CA. Routine chest rotengenograms and electrocardiograms: usefulness in the hypertension workup. Arch Int Med 1978; 138:1211-1213.
12. Dimmitt SB, West JN, Littler WA. Limited value of chest radiography in uncomplicated hypertension. Lancet 1989;2:104.
13. Mak W, Chan KH, Cheung RTF, et al. Hypertensive encephalopathy: BP lowering complicated by posterior circulation ischemic stroke. Neurology 2004;63:1131-1132.
14. First International Study of Infarct Survival Collaborative Group. Randomised trial of intravenous atenolol among 16,027 cases of suspected acute myocardial infarction: ISIS-1. Lancet 1986;2:57-66.
15. Bakris GL, Mensah GA. Pathogenesis and clinical physiology of hypertension. Cardiol Clin 2002;20:195-206.
16. Quan AP. Insufficient reliable evidence about treating hypertensive emergencies. Evidence-based Cardiovascular Medicine 2003;7: 150-152.
17. Veterans Administration Cooperative Study Group on Antihypertensive Agents. Effects of treatment on morbidity in hypertension. Results in patients with diastolic blood pressures averaging 115 through 129 mm Hg. JAMA 1967;202:1028-1034.
18. Thach AM, Shultz PJ. Nonemergent hypertension: New perspectives for emergency physicians. Emerg Med Clin 1005;13: 1009-1035.
19. Kumar V, Abbas AK, Fausto N, eds. Robbins and Cotran: Pathologic Basis of Disease, 7th ed; St. Louis: WB Saunders; 2005: 1007-1008.
20. Lip GY, Beevers M, Potter JF, et al. Complications and survival of 315 patients with malignant-phase hypertension. J Hypertens 1995; 13:915-924.
21. Brenner BM, ed. Brenner and Rectors The Kidney,7th ed; St. Louis: WB Saunders; 2004:2109-2129.