Hypertensive Crises: Challenges and Management

1 DOI 2007;131;1949-1962 Chest Paul E. Marik and Joseph Varon ManagementHypertensive Crises: Challenges and services can be found online on the World Wide Web at: The online version of this article, along with updated information). ISSN: 0012-3692. (of the copyright holder may be reproduced or distributed without the prior written permission Northbrook IL 60062. All rights reserved. No part of this article or PDFby the American College of Chest Physicians, 3300 Dundee Road, 2007 Physicians. It has been published monthly since 1935. Copyright CHEST is the official journal of the American College of ChestCopyright 2007 by American College of Chest Physicians on June 12, 2007 from Hypertensive Crises* Challenges and ManagementPaul E. Marik, MD, FCCP; and Joseph Varon, MD, FCCPH ypertension affects>65 million people in the United States and is one of the leading causes ofdeath.

2 One to two percent of patients with hypertension have acute elevations of BP that requireurgent medical treatment. Depending on the degree of BP elevation and presence of end-organdamage, severe hypertension can be defined as either a Hypertensive emergency or a hyperten-sive urgency. A Hypertensive emergency is associated with acute end-organ damage and requiresimmediate treatment with a titratable short-acting IV antihypertensive agent. Severe hyperten-sion without acute end-organ damage is referred to as ahypertensive urgencyand is usuallytreated with oral antihypertensive agents. This article reviews definitions, current concepts,common misconceptions, and pitfalls in the diagnosis and Management of patients with acutelyelevated BP as well as special clinical situations in which BP must be controlled.(CHEST 2007; 131:1949 1962)Key words:aortic dissection; -blockers; calcium-channel blockers; clevidipine; eclampsia; fenoldopam; hypertension; Hypertensive crises; Hypertensive encephalopathy; labetalol; nicardipine; nitroprusside; pre-eclampsia; pregnancyAbbreviations:ACE angiotensin-converting enzyme; APH acute postoperative hypertension; DBP diastolicBP; FDA Food and Drug Administration; JNC Joint National Committee; MAP mean arterial pressure;SBP systolic BPHypertension is one of the most common chronicmedical conditions in the United States, affect-ing close to 30% of the population 20 years chronic hypertension is an established riskfactor for cardiovascular, cerebrovascular, and renaldisease, acute elevations in BP can result in acuteend-organ damage with significant morbidity.

3 Hy-pertensive emergencies and Hypertensive urgencies(see definitions below) are commonly encounteredby a wide variety of clinicians. Prompt recognition,evaluation, and appropriate treatment of these con-ditions are crucial to prevent permanent end-organdamage. This article reviews our current understand-ing of Hypertensive crises, the common misconcep-tions and pitfalls in its diagnosis and Management , aswell as pharmacotherapy and special situations thatclinicians may classification and approach to hypertensionundergoes periodic review by the Joint NationalCommittee (JNC) on Prevention, Detection, Evalu-ation, and Treatment of High Blood Pressure, withthe most recent report (JNC 7) having been releasedin 2003 (Table 1).2 Although not specifically ad-dressed in the JNC 7 report, patients with a systolicBP (SBP) 179 mm Hg or a diastolic BP (DBP) 109 mm Hg are usually considered to be having a Hypertensive crisis.

4 The 1993 report3of the JNCproposed an operational classification of hyperten-sive crisis as either Hypertensive emergencies or Hypertensive urgencies. This classification remainsuseful today. Severe elevations in BP were classified*From the Department of Pulmonary and Critical Care ( ), Thomas Jefferson University, Philadelphia, PA; andDepartment of Acute and Continuing Care (Dr. Varon), TheUniversity of Texas Health Science Center at Houston, Houston, authors have no conflicts of interest to received October 11, 2006; revision accepted January23, of this article is prohibited without written permissionfrom the American College of Chest Physicians ( ).Correspondence to: Paul E. Marik, MD, FCCP, 834 Walnut St,Suite 650, Philadelphia, PA 19107; e-mail: Education CornerCONTEMPORARY REVIEWS IN CRITICAL CARE / 131/6/JUNE, 20071949 Copyright 2007 by American College of Chest Physicians on June 12, 2007 from as Hypertensive emergencies in the presence of acuteend-organ damage, or as Hypertensive urgencies inthe absence of acute target-organ involvement.

5 Dis-tinguishing Hypertensive urgencies from emergen-cies is important in formulating a therapeutic with Hypertensive urgency should have theirBP reduced within 24 to 48 h, whereas patients withhypertensive emergency should have their BP low-ered immediately, although not to normal termmalignant hypertensionhas been used todescribe a syndrome characterized by elevated BPaccompanied by encephalopathy or acute term, however, has been removed fromNational and International Blood Pressure Controlguidelines and is best referred to as emergencies were first described byVolhard and Fahr5in 1914, who saw patients withsevere hypertension accompanied by signs of vascu-lar injury to the heart, brain, retina, and kidney. Thissyndrome had a rapidly fatal course, ending in heartattack, renal failure, or stroke. It was not, however,until 1939 when the first large study6of the naturalhistory of Hypertensive emergencies was results of this seminal article by Keith andcolleagues6revealed that untreated hypertensiveemergencies had a 1-year mortality rate of 79%, witha median survival of months.

6 Prior to theintroduction of antihypertensive medications, ap-proximately 7% of Hypertensive patients had a hy-pertensive , it is estimatedthat 1 to 2% of patients with hypertension will havea Hypertensive emergency at some time in ,9In the United States, Hypertensive emergenciescontinue to be quite common, and the epidemiologyof this disorder parallels the distribution of essentialhypertension, being higher among the elderly andAfrican Americans, with men being affected twotimes more frequently than ,11 Despite thedevelopment of increasingly effective antihyperten-sive treatments over the past 4 decades, the inci-dence of Hypertensive emergencies has vast majority of patients presenting with ahypertensive emergency to an emergency depart-ment have a previous diagnosis of hypertension andhave been prescribed antihypertensive ,13 However, in many of these patients BP control priorto presentation was lack of aprimary care physician, as well as the failure toadhere to prescribed antihypertensive regimens havebeen associated with the development of a hyperten-sive ,15In some studies,15 50% ofpatients presenting to an emergency departmentwith a Hypertensive emergency were not adherentwith their antihypertensive medication regimen inthe preceding week.

7 In both major metropolitanareas and smaller communities, illicit drug use hasbeen reported14to be a major risk factor for thedevelopment of Hypertensive severe hypertension can developde novoorcan complicate underlying essential or secondaryhypertension. The factors leading to the severe andrapid elevation of BP in patients with hypertensivecrises are poorly understood. The rapidity of onsetsuggests a triggering factor superimposed on preex-isting hypertension. Hypertensive crisis is thought tobe initiated by an abrupt increase in systemic vascu-lar resistance likely related to humoral ,17 The subsequent increase in BP generatesmechanical stress and endothelial injury leading toincreased permeability, activation of the coagulationcascade and platelets, and deposition of fibrin. Withsevere elevations of BP, endothelial injury and fi-brinoid necrosis of the arterioles ,17 Thisprocess results in ischemia and the release of addi-tional vasoactive mediators generating a vicious cycleof ongoing injury.

8 The renin-angiotensin system isoften activated, leading to further vasoconstrictionand the production of proinflammatory cytokinessuch as ,19 The volume depletion thatresults from pressure natriuresis further simulatesthe release of vasoconstrictor substances from thekidney. These collective mechanisms can culminatein end-organ hypoperfusion, ischemia and dysfunc-tion that manifests as a Hypertensive PresentationMost patients have persistent BP elevation foryears before they manifest a Hypertensive emer-gency. The clinical manifestations of hypertensiveemergency are directly related to the particularend-organ dysfunction that has occurred (Table 2).Table 1 JNC 7 BP Categorization*BP ClassSBP, mm HgDBP, mm HgNormal 120 80 Prehypertension121 13980 89 Stage I140 15990 99 Stage II 160 100*From Chobanian et Education CornerCopyright 2007 by American College of Chest Physicians on June 12, 2007 from The signs and symptoms therefore vary from patientto patient.

9 Zampaglione and colleagues20reportedthat the most frequent presenting signs in patientswith Hypertensive emergencies were chest pain(27%), dyspnea (22%), and neurologic deficits(21%). No particular BP threshold has been associ-ated with the development of a Hypertensive emer-gency. However, organ dysfunction is uncommonwith a DBP 130 mm Hg (except in children andpregnancy).21 The absolute level of BP may not be asimportant as the rate of increase. For example, inpatients with long-standing hypertension, a SBP of200 mm Hg or a DBP up to 150 mm Hg may be welltolerated without the development of hypertensiveencephalopathy; whereas in children and pregnantwomen, encephalopathy may develop with a DBP ofonly 100 mm EvaluationPatients with Hypertensive emergency usuallypresent for evaluation as a result of a new symptomcomplex related to their elevated BP.

10 Patient triageand physician evaluation should proceed expedi-tiously to prevent ongoing end-organ damage. Afocused medical history that includes the use of anyprescribed or over-the-counter medications shouldbe obtained. If the patient is known to have hyper-tension, their Hypertensive history, previous control,current antihypertensive medications with dosing,adherence with their medication regimen, and thetime from last dose are important facts to acquireprior to initiating treatment. Inquiry into the use ofrecreational drugs (amphetamines, cocaine, phen-cyclidine) or monoamine oxidase inhibitors shouldbe made. Confirmation of the BP should be obtainedby a physician in both arms using an appropriate-sizeBP cuff. The appropriate-size cuff is particularlyimportant because the use of a cuff too small for thearm has been shown to artificially elevate BP read-ings in obese ,24 The physical examination should attempt to iden-tify evidence of end-organ damage by assessingpulses in all extremities, auscultating the lungs forevidence of pulmonary edema, the heart for mur-murs or gallops, the renal arteries for bruits, andperforming a focused neurologic and fundoscopicexamination.