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CRISIS HYPERTENSION

Joint National Committee VII

Hypertensive Urgencies and Emergencies


 Patients with marked BP elevations and acute TOD (e.g.,
encephalopathy, myocardial infarction, unstable angina, pulmonary
edema, eclampsia, stroke, head trauma, life-threatening arterial
bleeding, or aortic dissection) require hospitalization and parenteral
drug therapy.

 Patients with markedly elevated BP but without acute TOD usually do


not require hospitalization, but should receive immediate combination
oral antihypertensive therapy.
Target Organ Damage
Stroke
Atherosclerosis*
Vasoconstriction
Vascular hypertrophy Hypertension
Endothelial dysfunction

LV hypertrophy
Fibrosis Heart failure DEATH
Remodeling MI
Apoptosis

GFR
Proteinuria
Renal failure
Aldosterone release
Glomerular sclerosis
*preclinical data
LV = left ventricular; MI = myocardial infarction; GFR = glomerular filtration rate

Adapted from Willenheimer R et al Eur Heart J 1999; 20(14): 9971008, Dahlöf B J Hum Hypertens 1995; 9(suppl 5):
S37S44, Daugherty A et al J Clin Invest 2000; 105(11): 16051612, Fyhrquist F et al J Hum Hypertens 1995; 9(suppl 5):
S19S24, Booz GW, Baker KM Heart Fail Rev 1998; 3: 125130, Beers MH, Berkow R, eds. The Merck Manual of
Diagnosis and Therapy. 17th ed. Whitehouse Station, NJ: Merck Research Laboratories 1999: 16821704, Anderson S
Exp Nephrol 1996; 4(suppl 1): 3440, Fogo AB Am J Kidney Dis 2000; 35(2): 179188
Joint National Committee VII

Target Organ Damage


 Heart
• Left ventricular hypertrophy
• Angina or prior myocardial infarction
• Prior coronary revascularization
• Heart failure
 Brain
• Stroke or transient ischemic attack
 Chronic kidney disease
 Peripheral arterial disease
 Retinopathy
Hypertensive Emergencies :
Definition
• A rapid decompensation of vital organ
function secondary to an inapropriately
elevated BP
• Require lowering of BP within 1 hour to
decrease morbidity
• Not determined by a BP level, but rather
the imminent compromise of vital organ
function
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)
Underlying Etiology?
• Unclear, but some candidates
– ACE DD genotype
– Absence of the b and g subunit of ENaC
– Elevated adrenomedullin levels*
– Elevated natriuretic peptide level*
– Abnormalities in oxidative stress markers and
endothelial dysfunction*
– *Correct after effective BP treatment
Hypertensive Emergency
CNS - encephalopathy,
• Damage
intracranial hemorrhage, Heart - CHF, MI, angina
Grade 3-4 retinopathy

Kidneys - acute kidney


injury, microscopic
hematuria

Vasculature - aortic
Vasculature
dissection,
eclampsia
Hypertensive Emergencies
• CNS - Hypertensive encephalopathy
• CVS
– Acute myocardial ischemia
– Acute cardiogenic pulmonary edema
– Acute aortic dissection
– Post-op vascular surgery
• Renal - Acute renal failure
• Eclampsia
• Catechol excess- Pheochrom, Drugs
Pathophysiology
Sudden increase in
Systemic Vascular Mechanical Stress with endothelial
Resistance injury, increased permeability, Coag/Plt
activation, fibrin deposition

BP
1) Fibrinoid necrosis
2) Ischemia
3) Activation of RAA
4) Proinflammatory cytokines
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
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
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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
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 far can BP be safely
lowered?
• Lower limit usually 25% below MAP
• 50% of chronic hypertensives reached
lower autoregulation limit with 11 to 20%
reduction in MAP
• 50% had lower limit above usual mean
• Most ischemic complications develop with
reductions greater than 20 - 30 % (over 24
to 48 hours)
• Blindness, paralysis, coma, death, MI
Initial Lowering of BP :
Therapeutic Guidelines

• Do not lower BP more than 20% over


the first 1 to 2 hours unless
necessary to protect other organs
• Decreasing to DBP of 110 or patients
“normal” levels may not be safe
• Further reductions should be very
gradual ( days)
• Follow neuro status closely
Management

• Where?
– ICU with close monitoring
– Severe requires intra-arterial BP
monitoring
• Which Parenteral meds?
• Depends on the situation
Preferred Agents
• Beta blockers
– Labetolol
– Esmolol
• Calcium Entry blocker
– Nicardipine
• Dopamine-1 receptor agonist
– Fenoldapam
• Vasodilators - nitroprusside/nitroglucerin
Concept of Hypertensive
Urgencies
• Potentially dangerous BP elevation
without acute, life-threatening end-organ
damage
• Examples (controversial!)
– Retinal changes without
encephalopathy or acute visual
symptoms
– High BP with nonspecific Sx (headache,
dizziness, weakness)
– Very high BP without symptoms
Hypertensive Urgencies
• Severe elevation of BP ( DBP > 115)
• No progressive end-organ disease
• Joint National Committee on Detection,
Evaluation, and Treatment of HBP
– 1984 - lower BP within 24 hours
– 1988 - urgent therapy rarely required
– 1993 - Gradual lowering of BP
• Risks of rapid reduction (cerebral and myocardial
ischemia)