This document discusses hypertensive emergencies. It defines hypertensive emergency as acute end-organ damage from severely high blood pressure that requires rapid control. Over 500,000 Americans experience this each year. Treatment involves quickly starting intravenous drugs to lower blood pressure 20% within 60 minutes to prevent further damage, while oral medications are initiated. Conditions like stroke, aortic dissection and eclampsia may require specific approaches. Rapid diagnosis and management of hypertensive emergencies is critical to reducing mortality rates that can be as high as 90%.

1. Hypertensive Emergency
Daniel J. McFarlane M.D.
Division of Hospital Medicine
January 2011

2. Outline
 Epidemiology
 Definitions
 Pathophysiology
 Diagnosis and Recognition
 Treatment
 Special Circumstances

3. Epidemiology
 Why should we care about hypertension?
 One of the most common chronic medical
concerns in the US
 Affects >30% of the population > age 20
 Risk factor for
 Cardiovascular disease and mortality
 Cerebrovascular disease and mortality
 End stage renal disease
 Other end organ damage

4. Epidemiology
 Why should we care about hypertension?
 30% of the population is unaware they have
hypertension
 Control rates for known cases is about 50%
(we don’t do a great job at controlling BP)
 Risk Factors
 If >50, systolic BP > 140 is a more concerning
risk factor for cardiovascular disease than
diastolic BP.
 The risk of cardiovascular disease doubles for
every increase in BP of 20/10 over 115/75.

5. Epidemiology
 Hypertensive Emergency
 Estimates are that about 1% of those
with hypertension will present with
hypertensive emergency each year
 That is >500,000 Americans per year
 Correct and quick diagnosis and
management is critical
 Mortality rate of up to 90%

6. Definitions
 Hypertension (according to JNC VII)
 Normal BP <120/<80
 Prehypertension 121-139/80-89
 Stage I HTN 140-159/90-99
 Stage II HTN >160/>100
 (Severe HTN >180/>110)
 Severe HTN is not a JNC VII defined entity

7. Definitions
 Hypertensive Emergency
 Acute, rapidly evolving end-organ damage
associated with HTN (usu. DBP > 120)
 BP should be controlled within hours and
requires admission to a critical care setting
 Hypertensive Urgency
 DBP > 120 that requires control in BP over
24 to 48 hours
 No end organ damage
 Malignant Hypertension is no longer used

8. Definitions
 End-Organ Damage (% of cases)
 Cerebral infarction…………………………………… 24%
 Hypertensive encephalopathy……………………16%
 Intracranial hemorrhage……………………………4.5%
 Acute aortic dissection………………………………2%
 Acute coronary syndrome/myocardial infarction…12%
 Pulmonary edema with respiratory failure…………22%
 Severe eclampsia/HELLP syndrome………………2%
 Acute congestive heart failure……………………14%
 Acute renal failure……………………………………9%

9. Pathophysiology
 Hypertensive Emergency
 Failure of normal autoregulatory function
 Leads to a sharp increase in systemic
vascular resistance
 Endovascular injury with arteriole necrosis
 Ischemia, platelet deposition and release of
vasoactive substances
 Further loss of autoregulatory mechanism
 Exposes organs to increased pressure

10. Diagnosis and Recognition
 Presentation
 Always present with a new onset
symptom
 Take a good history
 History of HTN and previous control
 Medications with dosage and compliance
 Illicit drug use, OTC drugs

11. Diagnosis and Recognition
 Physical
 Confirm BP in more than one extremity
 Ensure appropriate cuff size
 Pulses in all extremities
 Lung exam—look for pulmonary edema
 Cardiac—murmurs or gallops, angina, EKG
 Renal—renal artery bruit, hematuria
 Neurologic—focal deficits, HA, altered MS
 Fundoscopic exam—retinopathy, hemorrhage

12. Diagnosis and Recognition
 Laboratory/Radiologic evaluations
 Basic Metabolic Panel (BUN, Cr)
 CBC with smear (hemolytic anemia)
 Urinalysis (proteinuria, hematuria)
 EKG to look for ischemia
 CXR to look for pulmonary edema if dyspnea
 Head CT for hemorrhage if HA or altered MS
 MRI chest if unequal pulses and wide
mediastinum to look for aortic dissection

13. Treatment
 Hypertensive Urgency
 No end-organ damage—NOT emergent
 Look for reactive HTN and treat this first
 Drugs, pain, anxiety, cocaine, withdrawal
 Use oral medications to lower BP gradually
over 24-48 hours, likely 2 agents needed
 May be chronic, decrease BP slowly to avoid
hypoperfusion of organs
 Avoid sublingual and IM administration due to
unpredictable absorption

14. Treatment
 Hypertensive Urgency
 Appropriate follow up for asymptomatic
patients with no end-organ damage
BP range Action Plan
 140-159/90-99 Observe, confirm BP 2mos
 160-179/100-109 Confirm, treat within 1mo
 180-209/110-119 Confirm, treat within 1wk
 210+/120+ Confirm, treat now, close f/u

15. Medications
 Oral drug choices often based on
comorbid conditions
 Heart failure—TH, BB, ACEI, ARB, ALDO
 Post MI—BB, ACEI, ALDO
 High CVD risk—TH, BB, ACEI, CCB
 Diabetes—TH, BB, ACEI, ARB, CCB
 Chronic Renal Failure—ACEI, ARB
 Recurrent stroke prevention—TH, ACEI
 KEY: ACEI, angiotensin converting enzyme inhibitor; ALDO, aldosterone antagonist; ARB,
angiotensin receptor blocker; BB, b blocker; CCB, calcium channel blocker; TH, thiazide.

16. Treatment
 Hypertensive Emergency
 Act Quickly
 Start IV goal directed pharmacologic therapy
 Continuous infusion: short acting titratable meds
 Initiate critical care monitoring
 Intraortic BP monitoring may be necessary
 Start SLOW: Limit initial lowering of BP to 20% below
pretreatment level
 Due to increased threshold of hypoperfusion of
the organs from abnormal autoregulation
 Goal: Lower DBP by 10-15% in 30-60 min
 Initiate oral therapy and titrate IV medications down

17. Medications
 IV, short acting, titratable.
 Arterial Vasodilators
 Hydralazine, fenoldepam, nicardipine, enalapril
 Venous Vasodilators
 Nitroglycerine
 Mixed Arterial and Venous Vasodilators
 Sodium nitroprusside
 Negative Inotrope/Chronotrope
 Labetolol (also vasodilates), Esmolol
 Alpha blockers (inc. sympathetic activity)
 Phentolamine

18. Medications
 Preferred agents by usage
 Labetolol>Esmolol>Nicardipine>Fenoldopam (esp in
pheochromocytoma)
 Preferred agents by end organ damage
 Pulmonary Edema (systolic)—Nicardipine
 Pulmonary Edema (diastolic)—Esmolol
 Acute MI—Labetolol or Esmolol
 Hypertensive Encephalopathy—Labetolol
 Acute Aortic Dissection—Labetolol
 Eclampsia—Labetolol or Nicardipine
 Acute Renal Failure—Fenoldopam
 Sympathetic Crisis/Cocaine—Verapamil or Diltiazem

19. Special Circumstances
 Acute Aortic Dissection
 Start IV meds STAT to lower pulsitile load and
aortic stress to lessen the dissection
 Vasodilators alone may  reflex tachycardia
 Use beta blocker AND vasodilator
 Esmolol and Nitroprusside
 Surgical evaluation
 Type A all go to surgery
 Type B only if rupture/leak. Treat with
aggressive BP control

20. Special Circumstances
 Stroke
 Number one cause of permanent disability
 HTN is a protective physiologic effect to maintain
blood flow to brain
 One study showed better outcome if hypertensive
upon presentation of stroke
 Treat HTN “rarely and cautiously”
 Lower BP 10-15% in first 24 hours (not >20%)
 Hemorrhagic stroke
 Treat if >200/>110, but still with modest lowering
of BP because still worse outcome with low BP

21. Special Circumstances
 Eclampsia
 Vasoconstricted and hemoconcentrated
 Volume expand, magnesium sulfate, and
aggressive BP control.
 Delivery is only definitive treatment
 Labetolol or Nicardipine are drugs of choice.
 Hydralazine was first line but slow onset and
unpredictable so may lead to hypotension

22. Special Circumstances
 Sympathetic Crisis
 Cocaine use, rarely pheochromocytoma
 AVOID beta blockers—leads to uninhibited
alpha stimulation and increased BP
 Labetolol has alpha and beta blockade, but
experimental studies show poor outcomes
 Nicardipine, fenoldopam or verapamil (with a
benzodiazepine) are drugs of choice

23. References
 Haas, A. and Marik, P. “Current Diagnosis
and Management of Hypertensive
Emergency.” Seminars in Dialysis. Vol
19, No 6. (2006) pp. 502-512.
 Flanigan, J. and Vitberg, D.
“Hypertensive Emergency and Severe
Hypertension: What to Treat, Who to
Treat, and How to Treat.” The Medical
Clinics of North America. Vol 90 (2006)
pp. 439-451.