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VCU HEALTH SYSTEM
EMERGENCY DEPARTMENT
GUIDELINE
SUBJECT: Hypertension ED Algorithm Guidance
FILE SECTION: VCUHS/ED Section: H
Please note: Clinical Practice Guideline– Evidence-based interventions related to a patient’s diagnosis or condition that provides the basis for
patient care. Clinical Practice Guidelines may be general or specialty-specific e.g. as generated by specialty organizations.
REVIEWED/REVISED (HISTORICAL):
Original date: 01/2016
Last Date Reviewed/Revised:
PURPOSE and BACKGROUND:
In 1993, the Joint National committee (JNC) on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure created a classification for hypertensive
crises in their JNC VII publication.1 Hypertensive urgency was defined as patients with marked elevation in blood pressure without acute target-organ damage.
Hypertensive emergency was defined as patients with marked blood pressure elevation and acute target-organ damage requiring hospitalization and parenteral
drug therapy. Examples of end organ damage included encephalopathy, myocardial infarction, pulmonary edema, eclampsia, ischemic or hemorrhagic stroke, and
aortic dissection. Current classification of hypertensive urgency or emergency affects patient therapeutic goals, medication selection, and eventual disposition.
This guidance was developed to help facilitate appropriate therapy and disposition of hypertensive patients presenting to the emergency department (ED).
Pertinent Abbreviations:
HTN: Hypertension
BP: Blood pressure
SBP: Systolic blood pressure
DBP: Diastolic blood pressure
MAP: Mean arterial pressure
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WHO CAN PERFORM: Physicians, Residents, Nurse Practitioner and Physician Assistants.
Target Organ Damage?
GUIDELINE:
-
SBP >180
DBP > 110
-
Acute coronary syndrome, unstable
angina, myocardial infarction
Dissecting aortic aneurysm
Pulmonary edema with respiratory
compromise
Encephalopathy
Ischemic or hemorrhagic stroke
Pre-eclampsia, eclampsia, HELLP
YES
NO
Hypertensive Urgency
-
Therapy:
VCUHS/PoPC.PS.010
Panic Values and Critical
Oral medications
o Restart/adjust patient’s home BP medication
Goal:
o Patient education and facilitate follow up to
gradually decrease blood pressure
Disposition:
o Home with follow-up if no other indication for
admission
o CDU, medicine: Further observation and follow up
Hypertensive Emergency
-
-
Therapy:
o Parenteral medications
Goal:
o Decrease MAP by no more than 25% within 60
minutes.
o If stable, decrease to 160/100 within the next 2-6
hours
o Exceptions:
 Aortic dissection
 Ischemic and hemorrhagic stroke
 Pre-eclampsia, eclampsia, gestational HTN,
HELLP
Disposition:
o Medicine, step down, intensive care unit
Hypertensive Urgency
Most patients who present to the ED with severe HTN will present as hypertensive urgency with no signs or symptoms of end organ damage. These patients may
be managed with oral anti-hypertensive medications to gradually lower their BP over 24-48 hrs.i Patients may be re-started on their home BP medications or be
prescribed other oral antihypertensives, based on patient specific factors and disease states, with appropriate inpatient or outpatient follow up. Rapid reduction in
BP may cause ischemia and infarction due to the rightward shift of the cerebral, coronary, and renal auto-regulation curves in the chronic hypertensive patient and
should be avoided. According to the American College of Emergency Physicians (ACEP) Clinical Policy on Asymptomatic Hypertension in the ED, treatment of
asymptomatic HTN is unnecessary if the patient has appropriate follow up. ii Minimal evidence exists to show that acute treatment of patients with markedly
elevated blood pressure reduces morbidity or mortality.iii If ED treatment is initiated to gradually lower blood pressure, BP normalization during the patient’s ED
visit should not be expected.3
Hypertensive Emergency
Hypertensive emergency is differentiated from urgency based on the presence of organ damage. The most common presentations of hypertensive emergencies to
the ED are cerebral infarction (24.5%), pulmonary edema (22.5%), hypertensive encephalopathy (16.3%) and congestive heart failure (12%).2 Other clinically
significant presentations include aortic dissection, intracranial hemorrhage, sympathetic crises (cocaine toxicity/pheochromocytoma), eclampsia, and myocardial
infarction. Patients with hypertensive emergency require immediate treatment to prevent further organ damage. Due to altered autoregulation, excessive
decreases in BP should be avoided to prevent hypoperfusion injury. Parenteral antihypertensive medications that are able to be titrated are preferred in this
setting.
Hypertensive Emergency Exceptions:
Aortic Dissection
Rapid HR and BP management in aortic dissection is required to decrease aortic wall stress and minimize further damage. Per the 2010 AHA
recommendations, β-blockers (e.g. esmolol, labetalol) should be initiated first and titrated to a HR of <60 beats/minute to prevent reflex
tachycardia associated with other vasodilators that may increase aortic wall stress, propagating the dissection. iv If patients are unable to tolerate a
β-blockade, then a non-dihydropyridine Ca2+ blocker (e.g. diltiazem) may be initiated for rate control. Subsequently, if SBP remains >120 mmHg
then other vasodilators (e.g. nicardipine) should be administered to further reduce BP without compromising end-organ perfusion.
Acute Pulmonary Edema
Patients with acute cardiogenic pulmonary edema often present to the ED with significant shortness of breath due to leakage of fluid from the
pulmonary capillaries into the alveolar space, impairing gas exchange and resulting in hypoxia. Excessive catecholamine production results in
increased systemic vascular resistance and blood pressure, impairing cardiac output and further worsening pulmonary fluid buildup. Nitroglycerin
effectively dilates the inferior vena cava, directly reducing preload and myocardial oxygen demand and at higher doses dilates arteries, allowing
for better myocardial blood flow and decreased afterload. It has been shown to be effective for preload reduction and symptomatic improvement
and is available in multiple dosage forms. v,vi,vii Most patients should be started on a nitroglycerin drip at a minimum of 100-200 mcg/min, titrated by
50-100 mcg/min every 5 minutes to goal MAP reduction of 25% in the first hour, and BP goal of <160/90 over the subsequent 4-6 hours. Nitrates
should be avoided in patients with hemodynamic instability, aortic stenosis, or pulmonary hypertension due to their dependence on preload to
maintain adequate perfusion. Nitrates are contraindicated in patients on concomitant phosphodiesterase inhibitors.
Ischemic Stroke
In most patients with ischemic stroke, elevated BP is often a physiologic response to the injury. A rapid reduction in BP may actually compromise
cerebral blood flow resulting in increased ischemia and negative neurologic outcome. The Intravenous Nimodipine West European Trial (INWEST)
was terminated early due to a correlation between nimodipine induced reduction in BP and unfavorable outcomes. viii Consequently, unless the
patient is receiving thrombolytic therapy, ischemic stroke patients should be allowed to have permissive HTN up to BP of 220/120 mmHg.ix
Patients who present at higher BP should have their MAP lowered gradually over the next 24 hrs to minimize compromise to cerebral blood flow. If
thrombolytic therapy is indicated, BP should be treated to <185/110 mmHg and then sustained at <180/105 mmHg for the next 24 hours to
minimize the risk of hemorrhagic conversion. Minimal data exists to support one medication class over the other, and the AHA/ASA only makes
recommendations of “reasonable choices” based on a general consensus. 5 At VCU, labetalol IVP and nicardipine IV infusion are the preferred
agents due to their quick onset and ability to be titrated.
Hemorrhagic Stroke
In hemorrhagic stroke, the presence of an elevated BP may be both the causative force and physiologic response to the injury. While no studies
have defined absolute BP goals for hemorrhagic stroke, others have shown that elevated SBP is associated with greater hematoma expansion,
neurological deterioration, and death and that aggressive SBP lowering may reduce hematoma growth. x,xi,xii At VCU, hemorrhagic stroke BP goals
are set to <160 mmHg to minimize hypoperfusion and retard hemorrhagic expansion.
Pre-Eclampsia, Eclampsia, Gestational HTN, HELLP (hemolysis, elevated liver enzymes, low platelet count)
Acute-onset, severe systolic HTN (SBP >160 mmHg), sever diastolic HTN (DBP >110 mmHg), or both can occur during pregnancy and the
postpartum period. Acute-onset HTN persisting for >15 minutes is considered a hypertensive emergency and should be treated immediately to
prevent neurologic sequelae. Similar to other hypertensive emergency settings, the goal is not to achieve normalization, but instead a BP of 140150/90-100 mmHg. ACOG recommends that IV labetalol and hydralazine be used first line. xiii No significant changes in umbilical blood flow have
been observed with the use of either labetalol or hydralazine, and maternal and perinatal outcomes are similar for both drugs.xiv,xv,xvi Second line
therapies include labetalol and nicardipine continuous infusions.
Medications
Continuous Infusions:
Drug
MOA
Nicardipine
Ca2+ blocker
Arterial/Venous
Dilation
Arterial
Clevidipine
Ca2+ blocker
Arterial
2-4 min
5-15 min
1-2 mg/h
Sodium
nitroprusside
Nitrate
Arterial +
Venous
<1 min
1-2 min
0.05-0.3
mcg/kg/min
Nitroglycerin
Nitrate
Venous (arterial
at high doses)
2-5 min
10-20 min
5-15 mcg/min
Esmolol
β1 blocker
1 min
10-30 min
Labetalol
α, non-selective
β blocker
D1 agonist
Arterial via ↓ in
cardiac output
Arterial
2-5 min
(15 min)
5 min
(15 min)
2-18 hrs
25-50
mcg/kg/min
1-2 mg/min
30-60 min
0.1 mcg/kg/min
Arterial/Venous
Dilation
Arterial
Onset
(Peak)
2-5 min
(15 min)
Duration
Initial Dose
Titration (Max)
2-4 hrs
10-20 mg
6 hrs
1.25 mg
1-4 hrs
10-20 mg
3-6 hrs
1-5 mg
Repeat 40-80 mg
q10min
(300 mg in 24 hrs)
1.25 mg q6h
(5 mg q6h)
Repeat 10-20mg q4-6h
(40 mg)
Repeat q2-4h
(15 mg)
Fenoldapam
Intermittent IV Pushes
Drug
MOA
Arterial
Onset
(Peak)
5-15 min
Duration
Initial Dose
Titration (Max)
4-6 hrs
2.5-5 mg/h
2.5 mg/h q5 min
(15 mg/h)
Double dose q2-5 min
(16 mg/h)
0.1 mcg/kg/min q3-5
min
(10 mcg/kg/min)
5-10 mcg/min q5min
(300 mcg/min)
Labetalol
α, non-selective
β blocker
Enalaprilat
ACE inhibitor
Arterial
Hydralazine
Unknown
Arterial
15 min
(1-4 hrs)
10-20 min
Phentolamine
α blocker
Arterial
5-10 min
SUPPORTIVE DATA/REFERENCES:
Marik PE, Rivera R. Hypertensive emergencies: an update. Curr Opin Crit Care 2011;17:569-80.
25 mcg/kg/min q10 min
(300 mcg/kg/min)
0.25-2 mg q30min
(300 mg in 24 hrs)
0.05-0.1 mcg/kg/min
q15min
(1.6 mcg/kg/min)
Notes
Lipid emulsion
Cyanide,
thyocyanate toxicity
Start higher doses in
acute pulmonary
edema
May require boluses
for immediate onset
Notes
Avoid in AKI,
hyperkalemia
Prolonged + variable
effects
Pheochromocytoma,
cocaine and
amphetamine use
2
Decker WW, Goodwin SA, Hess EP, Lenamond CC, Jagoda AS. Clinical policy: Critical issues in the evaluation and management of adult patients with asymptomatic hypertension in the emergency department. Annals of
EmergMed 2006;47:237
3
Wolf SJ, Lo B, Shih RD, Smith MD, Fesmire FM. Clinical policy: critical issues in the evaluation and management of adult patients in the emergency department with asymptomatic elevated blood pressure. Ann Emerg Med
2013;62:59-68
⁴Zampaglione B, Pascale C, Marchisio M, Cavallo-Perin P. Hypertensive urgencies and emergencies. Prevalence and clinical presentation. Hypertension. 1996 Jan. 27(1):144-7.
5 Hiratzka LF, Bakris GL, Beckman JA et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the diagnosis and management of patients with thoracic and aortic disease. Circulation 2010;121:1544-79
6 Beltrame JF, Zeitz CJ, Unger SA, et al. Nitrate therapy is an alternative to furosemide/ morphine therapy in the management of acute cardiogenic pulmonary edema. J Card Fail 1998;4:271–9.
7
Hoffman JR, Reynolds S. Comparison of nitroglycerin, morphine and furosemide in treatment of presumed pre-hospital pulmonary edema. Chest 1988;92:586–93.
8 Levy, P., Compton, S., Welch, R., Delgado, G., Jennett, A., Penugonda, N., et al. (2007). Treatment of severe decompensated heart failure with high-dose intravenous nitroglycerin: A feasibility and outcome analysis.
⁹Wahlgren NG, MacMahon Dg, De Keyser J, Indredavik B, Ryman T, for the INWEST Study Group. The intravenous nimodipine West European Trial (INWEST) of nimodipine in the treatment of acute ischemic stroke.
Cerebrovasc Disc 1994;4:204-10.
10 Jauch EC, Saver JL, Adams HP, et al. Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke
Association. Stroke. 2013;44(3):870-947.
11 Rodriguez-Luna D, Piñeiro S, Rubiera M, et al. Impact of blood pressure changes and course on hematoma growth in acute intracerebral hemorrhage. Eur J Neurol. 2013;20:1277–1283
12
Sakamoto Y, Koga M, Yamagami H et al. Systolic blood pressure after intravenous antihypertensive treatment and clinical outcomes in hyperacute intracerebral hemorrhage: The Stroke Acute Management With Urgent
Risk Factor Assessment and Improvement-Intracerebral Hemorrhage Study. Stroke. 2013;44:1846–1851
13
Anderson CS, Huang Y, Wang JG, et al. Intensive blood pressure reduction in acute cerebral hemorrhage trial (INTERACT): a randomized pilot trial. Lancet Neurol. 2008;7(5):391-9.
14 Committee on Obstetric Practice American College of Obstetrics & Gynecology. ACOG committee opinion no. 623: Emergent therapy for acute-onset, severe hypertension during pregnancy and the postpartum period.
Obstet Gynecol 2015;125(2):521-5.
15 Duley L, Meher S, Jones L. Drugs for treatment of very high blood pressure during pregnancy. Cochrane Database of Systematic Reviews 2006;3:CD001449.
17
World Health Organization. (2011). WHO recommendations for prevention and treatment of pre-eclampsia and eclampsia. Geneva: World Health Organization.
GUIDELINE AUTHOR(S):
 Tammy T. Nguyen, PharmD, BCPS
Clinical Pharmacy Specialist, Emergency Medicine, VCU Medical Center
STAKEHOLDER REVIEWERS and APPROVAL: Authors, Chief of Emergency Medicine, Operations, Director of Emergency Nursing, and ED
Quality Committee.
RESPONSIBILITY: It is the responsibility of Authors, Stakeholders, QA Coordinator and Practice Council members, to implement, maintain,
evaluate, review and revise this policy.
SIGNATURES:
_________________________________
Chief of Emergency Medicine, Operations
___________
Date
___________________________________
Director of Emergency Nursing
___________
Date