Hypertensive emergency

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.