Hypertension Journal

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Hypertensive Emergencies and Urgencies
Hypertensive Emergencies and Urgencies
Satyendra Tewari, Roopali Khanna, Nikunj Kotecha
Department of Cardiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
Address for correspondence: Satyendra Tewari, Professor, Department of Cardiology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow - 226014,Uttar Pradesh, India
Tel.: +91(0)9415012127. Fax.: +91(0) 522 2668573.
E-mail: stewari_sgpgi@yahoo.com
Received: 10-11-2017; Accepted: 17-12-2017
Hypertension is leading cause of death related to cardiovascular cause. Hypertensive emergencies are life threating conditions andneed urgent treatment. This review emphasizes the importance of timely diagnosis and implication of correct treatment in differentclinical situations. Hypertensive urgencies can be treated on out patients basis and hypertensive emergencies require treatment withrapid onset and shorter duration intravenous anti hypertensive drugs. Optimal management of hypertensive emergencies will leadto lesser target organ damage and eventually less incidence of stroke, myocardial infarction and congestive heart failure.
Keywords: Hypertensive emergencies, hypertensive urgencies, hypertension management
How to cite this article: Tewari S, Khanna R, Kotecha N.Hypertensive emergencies and urgencies. Hypertens2018;4(1): 36-40.
Source of support: Nil
Conflict of interest: None


Hypertension is a major traditional risk factor for cardiovasculardisease such as coronary artery disease and cerebrovasculardisease and is also associated with major target organ damagesuch as kidney and retina. It is one of the leading causes of deathrelated to cardiovascular cause.[1] Incidence and prevalence ofhypertension vary according to age, sex, race, and geographicarea, and it is increased with age. Most patients with markedlyincreased blood pressure (BP) (systolic pressure ≥180 and/ordiastolic pressure ≥120 mmHg) are usually asymptomatic, butif increased BP associated with acute target organ damage, it is alife-threatening condition and needs urgent intervention. Thesehypertensive emergencies though uncommon if not treatedin a timely fashion can be life threatening and therefore need athorough evaluation with appropriate treatment. Hypertensiveemergencies can be seen in patients with or without pre-existinghypertension.

According to the 2017 American College of Cardiology(ACC) guideline for prevention, detection, evaluation, andmanagement of hypertension, hypertensive crisis includeshypertensive emergencies and urgencies. Hypertensiveemergency is defined as severe elevation of BP (systolic BP[SBP] >180 and/or diastolic BP [DBP] >120 mmHg) associatedwith acute or worsening of target organ damage. In contrast, hypertensive urgencies have been defined as a severe elevationof BP in otherwise stable patients without acute or impendingchange in target organ damage or dysfunction.[2] Various otherterminologies such as malignant or accelerated hypertensionwere previously used in literature commonly but not usednowadays. Malignant hypertension was first described by Keithand Wagener in 1928 which is characterized by marked elevationof BP and widespread target organ damage, particularly Grades 3and 4 hypertensive retinopathy.[3]

Earlier in the absence of effective antihypertensive treatment,the prognosis of significantly elevated BP was similar topatients with cancer, and therefore, it was labeled as malignanthypertension. However, with the introduction of effectiveantihypertensive treatment, the prognosis of these patients hassignificantly improved, and therefore, this term is no longer used.

Hypertensive emergencies include patients who have acuteaortic dissection, acute pulmonary edema, acute myocardialinfarction, acute pulmonary edema, acute intracranial bleedor acute ischemic stroke, hypertensive disorder of pregnancy,catecholamine crisis, perioperative hypertension, andsympathetic hypertensive crisis. It is not level of BP, but rapiditywith which BP gets elevated is important. Early identificationand immediate treatment with parenteral antihypertensive arean essential component in the management of hypertensiveemergencies to prevent further target organ damage. In a follow-up study of 89 patients with hypertensive emergencies,1-year death rate associated with hypertensive emergencieswas 79% and median survival was 10.4 months if hypertensiveemergencies were left untreated.[4]

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Contrast to hypertensive emergencies which merit earlydiagnosis and prompt treatment, hypertensive urgencies werecharacterized by severe elevation of BP without acute targetorgan damage or dysfunction. Most of these patients had a historyof noncompliant with prescribed drugs or change in dietarypattern (high salt intake). These patients do not have clinicalor laboratory parameter suggestive of target organ damage andthey do not require immediate reduction of BP s instead thesepatients usually require intensification or restarting of previousantihypertensive medication. Despite severe elevation of BP,these patients are at low risk of developing cardiovascular events.At first, veteran's administration cooperative trial in which70 patients with DBP between 115 and 129 were randomized toplacebo had zero major adverse cardiovascular events or adverseevents.[5] The BP should be lowered over a period of hours ordays, and the rapid fall of BP within minutes is contraindicated.If the BP is lowered too rapidly, then there is an increased risk ofadverse effects (cerebrovascular accident, myocardial infarction,and acute renal failure) due to the tissue hypoperfusion.

Pathophysiology of Hypertensive Crisis

Autoregulation is the ability of blood vessel to dilate or constrictto maintain normal perfusion. In normotensive individual,normal arteries maintain normal blood flow over a wide rangeof BP. Primary abnormality in patients with hypertensiveemergency is severe, and a rapid elevation of BP results in alteredautoregulatory mechanism, particularly, in cerebral and renalarteries which can lead to ischemia or even infarct. In Abruptelevation of systemic vascular resistance due to vasoconstrictioncaused by amplification of renin angiotensin system leadsvascular injury, tissue ischemia and further production of renin.Most of the patients who are presented with hypertensiveemergency are euvolemic, and hence, diuretics are not the drugof choice.

Clinical Evaluation

Clinical evaluation of hypertensive crisis includes focusedhistory, targeted physical examination, and limited numberof laboratory investigations for immediate identification ofhypertensive crisis and to differentiate between hypertensiveemergencies and urgencies.

Clinical features of hypertensive emergencies were easilyidentified by target organ involved. Most common clinicalfeatures are cerebral infarction (20-25%), pulmonary edema(14-21%), hypertensive encephalopathy (0-16%), acutecoronary syndrome (12-25%), and intracerebral hemorrhage orsubarachnoid hemorrhage (4-15%).[6] A focused clinical historyshould include regarding acute onset change in mental status,headache, seizure, decreased in urine output, chest discomfort, acute severe back pain, acute onset shortness of breath, andintake of sympathomimetic drugs. History of antihypertensivemedications and compliance to antihypertensive medicationshould be included in the history.

A targeted physical examination should done. Accuratemeasurement of BP by sphygmomanometer of both upperlimbs and lower limb with appropriate size is crucial for thediagnosis of hypertensive crisis. Fundus examination has to bedone to look for papilledema and exudates. A cardiovascularexamination including peripheral pulses should be done to ruleout any aortic dissection. A thorough neurological examinationshould be conducted. The focused physical examination shouldinclude renal bruit (renovascular hypertension), discrepanciesin upper and lower limb BP (aortic dissection), and abdominallump (polycystic kidney or pheochromocytoma). Laboratoryexamination should include blood investigation such as completehemogram, kidney function (blood urea and serum creatinine),serum electrolyte, and urine analysis to look for proteins,red blood cells, and red blood cell cast which is indicativeof acute tubular necrosis and acute glomerulonephritis. Anelectrocardiogram is to be done rule out acute myocardialinfarction and left ventricular hypertrophy. Chest X-ray wasdone for the evaluation of pulmonary edema and cardiac sizeestimation. Computed tomography (CT) scan or magneticresonance imaging of the brain should be done in patients whopresented with neurological symptoms.[6]

Treatment depends on organ that is involved in hypertensiveemergency. The drug of choice and rate of BP reduction dependon the specific hypertensive emergency. Patients presented withhypertensive emergencies require Intensive Care Unit (ICU)admission for the measurement of continuous BP and initiationof parenteral antihypertensive drugs for immediate reduction ofBP, to prevent ongoing target organ damage. Ideally parenteralantihypertensive drug with rapid onset of action and shorterin half-life which can be easily titrated should be used. Exceptin setting of acute aortic dissection, the BP should be reducedslowly: 20-25% reduction in 1st h, < 160/100 mmHg in next2-6 h, and then gradually to normal over 24-48 h.[2] Rapidreduction of BP can lead to ischemic changes in vascular bedwhich are habituated to increase BP. In the setting of acute aorticdissection, SBP should be brought down to 120 mmHg within20 min of diagnosis.[2]

Specific Hypertensive Emergencies [Table 1]

Acute Coronary Syndrome

Antihypertensive medication with vasodilatory property whichdilates coronary artery and improves myocardial perfusion isthe drug of choice in the setting of acute coronary syndrome.Intravenous nitroglycerin is considered as first-line therapy.Short-acting beta-blocker such as esmolol and calcium channelblocker (CCB) with vasodilatory properties such as nicardipineare safe alternative. Drug which produces reflex tachycardiashould be avoided. Patients with acute coronary syndrome who are presented with acute left ventricular failure nitroglycerinshould be the drug of choice. Patients who are presented withacute coronary syndrome and BP with more than 140/90 mmHgshould be treated with IV antihypertensive medication; it willreduce after load and hence improve perfusion in myocardium.Target BP in such patients is < 140/90 mmHg. Table 2 summarizes the dose and contraindication of antihypertensivedrugs.

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Acute Aortic DissectionAcute aortic dissection is hypertensive emergencies in whichrapid reduction of BP is utmost important. Initial BP reduction should be done within 20 min, and SBP should be reduced to< 120 mmHg.[2] The aim of medical treatment of a patient withaortic dissection is not only to reduce BP but also to reduceshear stress.[6] Short-acting beta-blocker such as esmolol is thefirst line of treatment. Vasodilator therapy alone can cause reflextachycardia increase risk of aortic dissection propagation. Invasodilatory therapy, sodium nitroprusside is the drug of choice.In case of type A aortic dissection involving ascending aorta,immediate surgical consultation has to be done.[6]

Table 1: Various hypertensive emergencies and drug of choice
Hypertensive Emergencies and Urgencies
SBP: Systolic blood pressure, AV: Atrioventricular, ACE: Angiotensin-converting enzyme, ARB: Angiotensin receptor blocker, DBP: Diastolic blood pressure

Table 2: Commonly used drugs for hypertensive emergencies, its doses and side effects
Hypertensive Emergencies and Urgencies
BP: Blood pressure, CCB: Calcium channel blocker, AV: Atrioventricular
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Acute Intracranial Bleed

Stroke is one of the leading causes of disability globally. ElevatedBP is associated with increased mortality, poor neurologicaloutcome, and worsening size of hematoma. According to the2017 guideline, patients presented with acute intracranialbleed and SBP of more than 220 mmHg should be treated withintravenous antihypertensive drug, and close monitoring of BPis vital for maintaining cerebral autoregulation. First-line drugfor this condition is CCB such as nicardipine and clevidipine.Immediate reduction of BP to < 140 mmHg in case of thosewho presented with spontaneous IC bleed within 6 h of eventand has SBP between 150 and 220 mmHg is harmful and doesnot associated with a reduction of death or disability.[2] Variousresolution CTs evaluating the effect of lowering of SBP in acutesetting do not meet the primary endpoint of reduction of deathand disability at 3 months.[7,8]

Acute Ischemic Stroke

Elevation of BP is common during acute ischemic stroke.[7]Elevated BP is considered as an adaptive mechanism to maintainblood flow in affected area. According to the 2017 ACCguideline for BP, patients with acute ischemic stroke who areeligible for intravenous tissue plasminogen activator should haveBP lowered to < 185/110 mmHg and BP should be maintainedbelow 180/105 mmHg for at least first 24 h after initiating drugtherapy.[2] In patients with acute ischemic stroke who are noteligible for tissue plasminogen activator and SBP of more than220 mmHg and DBP of more than 110 mmHg, the benefit ofinitiating and reinitiating antihypertensive medication in first48-72 h has uncertain. It is not associated with a reductionof death and disability. First-line drug for this condition isdihydropyridine CCB such as nicardipine and clevidipine.It might be reasonable to reduced BP to 15% in the first 24 h.Patients who are previously hypertensive, who developedstroke or transient ischemic attack, or whose BP is more than140/90 mmHg should be started on antihypertensive therapyafter 1st few days of index events for the prevention of recurrenceof stroke or vascular events.

Perioperative Hypertension

Hypertension during perioperative period is associated with anincreased risk of bleeding, cardiovascular, and cerebrovascularevents. Elevation of BP is due to increased sympathetic stimulation due to surgical stress, anxiety, and increase inintravascular volume. Approximately one-fourth of patientsundergoing non-cardiac surgery and 80% of patients undergoingcardiac surgery are associated with hypertension.[2] Patientsundergoing surgery should continue their antihypertensivemedication except angiotensin-converting enzyme (ACE)inhibitor. In patients who had planned surgical procedure, SBPmore than 180 mmHg and DBP more than 110 mmHg shouldbe deferred. Intraoperative hypertension should be managed byintravenous antihypertensive medication until patients consumeoral drug.[2]

Hypertension During Pregnancy

Preeclampsia affects 7% of pregnancies.[9] It is associatedwith increased risk of pre-term delivery, intrauterine growthretardation, and perinatal mortality. The aim of treatment inpreeclampsia is to reduce BP to such an extent that it preventsmaternal complication and maintains uteroplacental flow. Thecutoff level for lowering BP is still conflicting. An aggressiveapproach to lower BP in pregnancy may have a detrimentaleffect on the fetal growth due to excessive lower BP or due toharmful effects of drugs. According to the American College ofObstetrician and Gynecologist persistent (lasting for more than15 min), acute severe hypertension that is SBP >160 mmHg orDBP >110 mmHg in setting of preeclampsia or eclampsia shouldbe treated.[10] According to the ACC guidelines, patients withsevere eclampsia SBP should be brought < 140 mmHg within 1 h.Methyldopa has been widely used antihypertensive in pregnancyand is considered safe. Drawback with methyldopa is its sloweronset of action and mild antihypertensive effect. Beta-blockershave also been shown safe during pregnancy, and labetalol (bothalpha and beta blockers) is preferred among other beta-blockers.It has faster onset of action as compared to methyldopa and morepotent. Nifedipine can also be given safely during pregnancy.Drug such as ACE inhibitor and angiotensin receptor blockerare contraindicated due to their teratogenic effect.[2] The useof mineralocorticoid receptor blockers is to be avoided duringpregnancy.

Catecholamine Crisis

Pheochromocytoma is rare of this crisis. It is best managedwith IV antihypertensive drug with alpha-blocker propertiessuch as phentolamine. In patients with pheochromocytomacrisis, SBP should be reduced to < 140 mmHg during 1st h.[2] Abeta-blocker can be added if necessary. The use of bet-blockerwithout prior alpha blockade results in dangerous rise in BP.[6]Although labetalol considers as ideal drug for this situation dueto both alpha and beta blockades, studies do not support its usein clinical setting.[11]

Pediatric Hypertensive Emergencies

Hypertensive emergencies are rare in children and usuallydue to secondary cause. Pediatric hypertension was defined as SBP and/or DBP more than or equal to 95 percentile forsex, age, and height percentile on three separate occasions.Etiology of hypertensive crisis varies according to age suchas, in newborn, it is usually due to renal vascular, urological,or coarctation of the aorta. From infancy to up to 12 yearsof age, renal parenchymal disease is the main cause, andafter 12 years of age, primary hypertension is the main causeof hypertension emergency. As in adult patients, focusedclinical history and targeted clinical examination shouldbe done. The current recommendation is to reduce SBPnot more than 25% in first 8 h followed by gradual returnto BP over 24-36 h.[12] Antihypertensive medication for thetreatment of hypertensive emergencies is the same as adultpatients.

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Hypertensive Urgencies

Unlike hypertensive emergencies, patients with markedlyelevated BP do not require ICU admission and immediatereduction of BP instead of that reinitiating or intensificationof pre-existing medication is sufficient. Serial BPmeasurement should be done as BP often falls spontaneously.Approximately 32% of such patients had a satisfactoryresponse to 30 min of rest. Patients with hypertensiveurgencies should be treated with oral antihypertensivetreatment, and BP should be decreased over 24-48 h.A rapid reduction of BP in this setting is detrimental as itmight precipitate stroke or myocardial infarction. Thereis no difference across various classes of antihypertensivemedication but ACE inhibitor is slightly better tolerated ascompared to CCB. Follow-up is very essential in patientswho are treated for hypertensive urgencies as long term andadequate controlled of BP.


Hypertensive emergencies is life- and organ-threateningcondition require prompt identification and urgent treatmentbecause if left untreated it carries high mortality. Treatment withrapid onset and shorter duration intravenous antihypertensivedrug has to be done, and initial BP reduction should not be morethan 25% of baseline to maintain adequate perfusion to vitalorgan. Patients with hypertensive urgencies should be treatedon outpatient basis. Main difference between emergencies andurgencies is acute target organ damage and not the level of BP.

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