Hypertensive Emergencies:

Diagnosis and Treatment

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

Question 1

What is the primary reason for

hypertensive emergencies
today?
1. Renovascular Disease
2. Pheochromocytoma
3. Non-adherence to anti-hypertensive
medication
4. Hyperaldosteronism
5. Erythropoeitin

What is the primary reason for

hypertensive emergencies in
today?
1. Renovascular
Disease
2. Pheochromocytom
a
3. Non-adherence to
anti-hypertensive
medication
4. Hyperaldosteronis
m
5. Erythropoeitin

10

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
CNS - encephalopathy,

Damage

intracranial hemorrhage,
Grade 3-4 retinopathy

Kidneys - acute kidney

injury, microscopic
hematuria

Vasculature Vasculatur
e aortic dissection,
eclampsia

Heart - CHF, MI, angina

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)

Pathophysiology
Sudden 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.
2.
3.
4.
5.

Neurologic defect
Gross Hematuria
Chest pain
Headache
Epistaxis

What is the most common complaint in

hypertensive emergency?

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.
2.
3.
4.
5.

Systolic > 225 mm Hg

Diastolic > 110 mm Hg
Systolic > 250 mm Hg
Diastolic > 120 mm Hg
All of the above

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

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.
2.
3.
4.
5.

Sublingual Nifedipine
Labetolol
ACE Inhibitors
Nicardipine
1 and 3

Which of the following drugs should

not be used to treat hypertensive
emergency?
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.
2.
3.
4.
5.

Phentolamine
Benzodiazepine
Labetolol
Nicardipine
Fenoldopam

Which of the following drugs should

be avoided in sympathetic crises
with hypertensive emergency?
1.
2.
3.
4.
5.

Phentolamine
Benzodiazepine
Labetolol
Nicardipine
Fenoldopam

Sympathetic Crisis
Beta-adrenergic antagonists will
result in unopposed alphaadrenergic 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 (2075%)

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