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

Hypertensive emergency

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Page 1: Hypertensive emergency

Hypertensive Emergency

Daniel J. McFarlane M.D.Division of Hospital MedicineJanuary 2011

Page 2: Hypertensive emergency

Outline

Epidemiology Definitions Pathophysiology Diagnosis and Recognition Treatment Special Circumstances

Page 3: Hypertensive emergency

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

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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.

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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%

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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

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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

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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%

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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

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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

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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

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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

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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

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Treatment

Hypertensive Urgency Appropriate follow up for asymptomatic

patients with no end-organ damageBP 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

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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.

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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

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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

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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

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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

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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

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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

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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

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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.