hypertensive emergencies: diagnosis and treatment jamie johnston, md university of pittsburgh school...

Hypertensive Emergencies:Diagnosis and Treatment

Jamie Johnston, MD

University of Pittsburgh

School of Medicine

Today’s Road Map

• Case Presentations

• Definitions

• Evaluation

• Management

• Will not cover pre-eclampsia or pediatric hypertensive emergencies

Case 1

• 51 year old man admitted to an outside hospital

• CC: Sudden onset of left-sided weakness, severe headache, slurred speech and left facial droop– BP 260/172– Head CT Scan showed Right basal ganglia

hemorrhage with shift

• HPI: Transported by air ambulance to PUH.– Intubated en route due to declining mental status

Case 1

• PMH - Hypertension - according to wife, patient was non-adherent with prescribed medications– Out patient medications and allergies - not

available– Family History +for HTN/CVA

• Exam PUH - BP 196/130– Positive for Left dense hemiparesis

Case 1

• Hospital day 2– Dilated right pupil– Emergent right frontotemporal craniotomy

and evacuation of clot

• Subsequent Hospital Course– Difficult to control BP– Pneumonia

Case 1

• Renal MRI– Right kidney 8.1 cm with three renal

arteries– Left kidney 12.2 cm with two renal arteries

• Patient transferred to rehab at South Side Hospital on 7/19/07

Question 1

• What is the primary reason for hypertensive emergencies in the USA today?

1. Renovascular Disease2. Pheochromocytoma3. Non-adherence to anti-hypertensive

medication4. Hyperaldosteronism5. Erythropoeitin

What is the primary reason for hypertensive emergencies in the

USA today?

Ren

ovas

cula

r Dis

ease

Pheo

chro

mocy

tom

a

Non-a

dher

ence

to a

nt...

Hyp

eral

doster

onism

Ery

thro

poeitin

0% 0% 0%0%0%

1. Renovascular Disease

2. Pheochromocytoma

3. Non-adherence to anti-hypertensive medication

4. Hyperaldosteronism

5. Erythropoeitin

10

When you hear hoof beats…

Hypertensive Emergency

• According to the Joint National Committee on Hypertension Report

• Severely elevated blood pressure with signs and symptoms of acute end organ damage

• Requires hospitalization

• Requires parenteral medication

Hypertensive Urgency

• Severely elevated blood pressure without signs and symptoms of acute end organ damage

• Can be managed as an outpatient

• Can be managed with oral medications

Hypertensive Emergency

• Damage Heart - CHF, MI, angina

Kidneys - acute kidney injury, microscopic hematuria

CNS - encephalopathy, intracranial hemorrhage, Grade 3-4 retinopathy

Vasculature

Vasculature - aortic dissection, eclampsia

Epidemiology

• Hypertensive emergencies are common– Occur in 1-2% of the hypertensive population– But, 50 million hypertensive Americans– 500,000 hypertensive emergencies/year

• Parallels the distribution of primary hypertension

• Higher in the elderly and African Americans• Incidence in men 2 times higher than in

women

Epidemiology

• Common associations– Previous history of hypertension– Lack of a primary care physician– Non adherence to antihypertensive

regimen– Elicit drug use (cocaine)

PathophysiologySudden increase in Systemic Vascular Resistance

BP

Mechanical Stress with endothelial injury, increased permeability, Coag/Plt activation, fibrin deposition

1) Fibrinoid necrosis

2) Ischemia

3) Activation of RAA

4) Proinflammatory cytokines

Vaughan and Delanty Lancet 2000; 356:411

Underlying Etiology?

• Unclear, but some candidates

– ACE DD genotype

– Absence of the and subunit of ENaC

– Elevated adrenomedullin levels*

– Elevated natriuretic peptide level*

– Abnormalities in oxidative stress markers and endothelial dysfunction*

– *Correct after effective BP treatment

Question 2

• What is the most common complaint in hypertensive emergency?

1. Neurologic defect

2. Gross Hematuria

3. Chest pain

4. Headache

5. Epistaxis

What is the most common complaint in hypertensive emergency?

Neu

rolo

gic d

efec

t

Gro

ss H

emat

uria

Ches

t pai

n

Hea

dache

Epis

taxi

s

0% 0% 0%0%0%

1. Neurologic defect

2. Gross Hematuria

3. Chest pain

4. Headache

5. Epistaxis

Clinical Presentation

• Variable• Zampaglione et al (Hypertension 27:144, 1996)

– 14, 209 ER visits in one year period– 108 met definition of hypertensive

emergency (0.8%)– Mean Systolic BP 210 + 32– Mean Diastolic BP 130 + 15

Clinical Presentation

• Frequency of signs and symptoms– Chest Pain 27%– Dyspnea 22%– Neuro defect 21%– Interestingly….

• Headache was only 3% and epistaxis was 0% in this study

Question 3

• Hypertensive emergency is associated with a threshold BP of

1. Systolic > 225 mm Hg

2. Diastolic > 110 mm Hg

3. Systolic > 250 mm Hg

4. Diastolic > 120 mm Hg

5. All of the above

Hypertensive emergency is associated with a threshold BP of

Sys

tolic

> 2

25 m

m H

g

Dia

stol

ic >

110

mm

Hg

Sys

tolic

> 2

50 m

m H

g

Dia

stol

ic >

120

mm

Hg

All

of the

above

0% 0% 0%0%0%

1. Systolic > 225 mm Hg

2. Diastolic > 110 mm Hg

3. Systolic > 250 mm Hg

4. Diastolic > 120 mm Hg

5. All of the above

Threshold BP

• There is no specific BP where hypertensive emergencies occur

• But, organ dysfunction is rare with diastolic BPs < 130 mm Hg– Rate of increase may be more important– Hence, encephalopathy will occur at lower

BPs in pregnancy and in children

Initial Evaluation

• Focused history– History of hypertension?– How well is hypertension controlled?– What antihypertensives?– Adherence to antihypertensive regimen?– Last dose of antihypertensive?

Initial Evaluation

• Social History– Recreational Drugs

• Amphetamines• Cocaine• Phencyclidine

Initial Evaluation

• Confirm BP in both arms

• Use appropriate sized BP cuff

• Cuff that is too small– BP cuffs that are too small falsely elevate

BP measurements in obese patients

Initial Evaluation

• Assess for end-organ damage

• Vascular Disease– Assess pulses in all extremities– Auscultate over renal arteries for bruits

• Cardiopulmonary– Listen for rales (CHF)– Murmurs or gallops

Initial Evaluation

• Neurologic Exam– Hypertensive Encephalopathy - mental

status changes, nausea, vomiting, seizures– Lateralizing signs uncommon and suggest

cerebrovascular accident

• Retinal Exam– Lost art– Keith-Wagener-Barker Classification

Keith-Wagener-Barker Classification

• Grade 1– Mild narrowing of the arterioles– “Copper Wire”

• Grade 2– Moderate narrowing -

Copper wire and AV nicking

• Changes associated with long standing essential hypertension

Normal

Grade 1

Keith-Wagener-Barker Classification

• Grade 3– Severe Narrowing -

Silver wire changes, hemorrhage, cotton wool spots, hard exudates

• Grade 4– Grade 3 + Papilledema

• Grade 3 and 4 highly correlated with progression to end organ damage and decreased survival

Grade 3 KWB Retinopathy

Lab Testing

• ECG– LVH, look for signs of ischemia, injury, infarct

• Renal Function Tests (urine included)– Elevated BUN, Creatinine, proteinuria, hematuria

• CBC• CXR - pulmonary edema, aortic arch, cardiac

enlargement

Lab Testing

• Aortic Dissection?– Suspect with severe tearing chest pain,

unequal pulses, widened mediastinum– Contrast Chest CT Scan or MRI

• Pulmonary Edema/CHF– Transthoracic Echocardiogram – Differentiate between systolic dysfunction,

diastolic dysfunction, mitral regurgitation

Management

• Elevated BP without target organ damage

• Hypertensive urgency

• Oral meds

• Goal - gradual reduction of BP over 24 - 48 hours

Management

• Elevated BP with target organ damage

• Hypertensive emergency

• Parenteral meds

• Goal - Reduce diastolic BP by 10-15% or to 110 mm Hg over a period of 30 - 60 minutes

How Quickly?

• Cerebral Blood Flow Autoregulation– Cerebral Blood constant in normotensive

individuals over range of MAPs of 60 -120 mm Hg.

– In chronically hypertensive patients autoregulatory range is higher

– MAP Range 100-120 to 150-160 mm Hg

• Autoregulation also impaired in the elderly and those with cerebrovascular disease

How Quickly?

• General rule is to lower MAP by 20% in first hour

• Should always be done with close clinical observation

Management

• Where?– ICU with close monitoring– Severe requires intra-arterial BP

monitoring

• Which Parenteral meds?

• Depends on the situation

Question 4

• Which of the following drugs should not be used to treat hypertensive emergency?

1. Sublingual Nifedipine2. Labetolol3. ACE Inhibitors4. Nicardipine5. 1 and 3

Which of the following drugs should not be used to treat hypertensive

emergency?

Sublin

gual N

ifedi

pine

Lab

etolo

l

ACE In

hibito

rs

Nic

ardip

ine

1 a

nd 3

0% 0% 0%0%0%

1. Sublingual Nifedipine

2. Labetolol

3. ACE Inhibitors

4. Nicardipine

5. 1 and 3

Preferred Agents

• Beta blockers– Labetolol– Esmolol

• Calcium Entry blocker– Nicardipine

• Dopamine-1 receptor agonist– Fenoldapam

• Vasodilators - nitroprusside/nitroglucerin

Scenarios

• Our Case - Acute ischemic stroke/cerebrovascular bleed

• Agents– Fenoldopam– Labetolol– Nicardipine

CVA or Ischemic Stroke

• BP elevation after CVA or ischemic stroke can be protective to preserve cerebral perfusion

• Hold on aggressive lowering unless– Thrombolytic therapy anticipated or– BP excessively high ( SBP > 220 mm Hg or DBP

>120)

• BP Goal for thrombolytic therapy is to lower SBP if > 185 or DBP >110

Cardiac Conditions

• Acute Pulmonary Edema with systolic dysfunction– Nicardipine– Fenoldopam– Sodium nitroprusside– Nitroglycerin– Loop diuretic

Cardiac Conditions

• Acute Pulmonary Edema with diastolic dysfunction– Esmolol, metoprolol, labetolol– verapamil– Nitroglycerin– Loop diuretic

Cardiac Conditions

• Acute myocardial ischemia– Esmolol, labetolol– Nitroglycerin

Sympathetic Crisis

• Generally in association with recreational drugs such as cocaine, amphetamine or phencyclidine

• Sudden cessation of clonidine or Beta-adrenergic antagonist

• Pheochromocytoma - rare

Question 5

• Which of the following drugs should be avoided in sympathetic crises with hypertensive emergency?

1. Phentolamine2. Benzodiazepine3. Labetolol4. Nicardipine5. Fenoldopam

Which of the following drugs should be avoided in sympathetic crises with

hypertensive emergency?

Phen

tola

min

e

Ben

zodia

zepin

e

Lab

etolo

l

Nic

ardip

ine

Fen

oldopa

m

0% 0% 0%0%0%

1. Phentolamine

2. Benzodiazepine

3. Labetolol

4. Nicardipine

5. Fenoldopam

Sympathetic Crisis

• Beta-adrenergic antagonists will result in unopposed alpha-adrenergic stimulation

• In cocaine use, Beta blockers can– Increase blood pressure– Worsen coronary artery vasoconstriction– Decrease survival

• Avoid beta blockade (including non selective agents such as labetolol)

Sympathetic Crisis

• Recommended Drugs– Nicardipine– Fenoldopam– Verapamil– Benzodiazepine– If pheo suspected use phentolamine

Aortic Dissection

• Treatment is paramount– 75% of patients with ascending aortic

dissection die in 2 weeks of the acute episode without successful therapy

– 5 year survival is 75% with successful intervention

• Khan et al. Chest 2002, 122:311• Kouchoukos New Engl J Med 1997; 336:1876

Aortic Dissection

• Vasodilator alone?– Causes reflex tachycardia– Increases cardiac ejection velocity– Increases aortic shear forces– Extends the dissection

Aortic Dissection

• Standard therapy– Beta-adrenergic blocker plus vasodilator– Esmolol + Nicardipine or fenoldopam

• Nitroprusside can be used as well

Acute Post Operative Hypertension

• Frequent in post-operative state (20-75%)

• Hyper-responsiveness to surgical trauma– Increased stress hormones?– Activation of RAA?

• Also hypothermia, hypoxia, carbon dioxide retention, bladder distention

Acute Post Operative Hypertension

• Prevention– Safe to give antihypertensives pre-op– Hold diuretics

• Treatment - BP thresholds vary– Control pain and anxiety– While NPO use nicardipine, esmolol or

labetolol– Resume oral medications when possible

What happened to sodium nitroprusside?

• Mansoor and Friedman. Heart Disease 2002; 4:358– Sodium nitroprusside recommended for all

hypertensive emergencies except eclampsia

• Marik and Varon. Chest 2007; 131:1949– Sodium nitroprusside recommended for

• acute aortic dissection • acute pulmonary edema with systolic

dysfunction

“riding the pride”

• Disadvantages of sodium nitroprusside– Decrease cerebral blood flow and increases

intracranial pressure– Can reduce regional blood flow in coronary artery

disease– Risk of cyanide toxicity

• Use when other agents not effective– Monitor thiocyanate levels– Avoid in renal or hepatic dysfunction

Have we made progress?

• First described by Volhard and Fahr– Die Brightsche Nierenkrankenheit: Klinik

Patholgie und Atlas. Berlin, Germany, Springer 1914:247

• Keith, Wagener, Barker Am J Med Sci, 1939;197:332– Mean survival of patients with htn and

grade 4 retinopathy was 10.5 mo with none living beyond 5 years

We have made progress

• Development of antihypertensive drugs

• Increased diagnosis of hypertension

• Increased ICU settings

• Survival of patients with hypertensive urgency and emergency is 18 years compared to 21 years in those with uncomplicated hypertension

Thank you!

Questions?

Messerli N Engl J Med 1995;3321038.

Messerli N Engl J Med 1995;3321038.