Hypertensive Emergency
Deborah DeWaay MD
Medical University of South Carolina
April 16, 2013
Objectives
Knowledge. Residents should be able to:
• Define hypertensive emergency and describe the signs
and symptoms of conditions associated with it
• Describe the epidemiology of hypertensive emergency
• Describe the prognosis of hypertensive emergency
untreated and treated
• Describe the uses of the drugs commonly used to treat
hypertensive emergencies.
Objectives
• Skills
– Understand which physical exam
maneuvers and labs are important to
diagnosing HTN emergency
• Attitude
– Residents should understand and
appreciate that hypertensive emergency is
a serious illness that carries a significant
morbidity and mortality
Key Messages
• 1-2% of patients with systemic
hypertension will develop hypertensive
emergency
• HTN emergency needs to be treated with
IV drips, not IV push
• HTN emergency should be treated in the
ICU
The Old
• Malignant hypertension is not a term that
is used any more
• It was used to mean elevated BP +
encephalopathy or AKI
Hypertensive Emergency
• Elevated blood pressure with symptoms
–
–
–
–
–
–
Shortness of breath (29%)
Chest pain (26%)
Headache (23%)
Altered mental status (20%)
Focal neurologic deficit (11%)
Microangiopathic hemolysis (27%)
• There is no absolute BP cut off
• The rate of increase is as important as the
absolute BP
Hypertensive Urgency
• Elevated blood pressure without
symptoms
• JNC 7 does not specifically define a BP
number for HTN urgency
– Stage 2 hypertension is SBP≥160 mmHg,
DBP≥100 mmHg
– Hypertensive crisis is SBP≥179 mmHg,
DBP≥109 mmHg
Epidemiology
• Systemic hypertension affections 1 billion
people world wide and 65 million Americans
• 1-2% of patients with systemic hypertension will
develop hypertensive emergency
• Men are affected 2x more than women
• More common in the elderly and AfricanAmericans
• Essential HTN accounts for 20-30% of HTN
emergency in whites, but over 80% in AfricanAmericans
Prognosis
• Per one study in 1939, untreated malignant
hypertension has a 79% 1 year mortality with a
median survival of 10.5 months
• Mortality has decreased in recent years
– One study showed that the 5 year survival was 32%
prior to 1977, but between 1977 – 2006 it increased
to 91%
• Per Studying the Treatment of Acute
Hypertension (STAT) registry: in hospital
mortality for HTN emergency was 6.7%, 90 day
mortality of 11%
History
• Medication history
– Anti- HTN meds
– OTC meds
– Illegal drugs: especially cocaine,
amphetamines, phencyclidine
• HTN?
– History of control
– Compliance
Physical Exam
• Blood pressures in both arms and orthostatics
• Pt should be seated with the back supported and
legs uncrossed
• If the cuff is too small, the BP will be falsely
elevated
• Per American Heart Association
–
–
–
–
Arm circumference 22 - 26 cm, small adult cuff, 12x22 cm
Arm circumference 27 - 34 cm, adult cuff, 16x30 cm
Arm circumference 35 - 44 cm, large adult cuff, 16x36 cm
Arm circumference 45 - 52 cm, adult thigh cuff, 16x42 cm
Physical Exam
•
•
•
•
•
•
Neuro exam
Cardiac exam
Pulmonary exam
Ocular exam: only happens in 13% of pts
Extremity exam
[they are critically ill so need a full exam]
Labs to consider
•
•
•
•
•
•
•
BMP
CBC with peripheral smear, LDH
UA
EKG
CXR
CT head
Echocardiogram
Pathophysiology
• The DD genotype of the angiotensinconverting enzyme (ACE) gene has
been found to be associated with
increased risk of HTN emergency
• Overall cause is poorly understood
• One theory is that there is a triggering
factor that causes the release of
humoral vasoconstrictors leading to an
increased in systemic vascular
resistance (SVR)
Pathophysiology
↓organs ability to autoregulate
SVR eventually
blood flow
mechanical wall stress & endothelial injury
Pressure naturesis
RAS
Vasoconstriction
Ischemia
triggers coagulation cascade
fibrin disposition
fibrinoid necrosis of arterioles
• Brain:
The Effects
– CVA: ischemic, hemorrhagic
– Hypertensive Encephalopathy
• Heart:
– Myocardial infarction
– Heart failure: systolic, diastolic
• Aorta:
– Aortic dissection
• Kidney:
– Acute kidney injury
• Blood vessels
– Microangiopathic hemolytic anemia
– Retinal hemorrhages, exudates and papilledema
Pathophysiology
http://www.cardeneiv.com/a3_cardeneiv_ah_py.shtml
Hypertensive Encephalopathy
• Clinical presentation: acute or subacute
lethargy, confusion, headache, visual
disturbance or seizures
• More common in patients with SLE, HUS,
cryoglobulinemia, on cyclosporin or cisplatin
– Diseases with underlying vascular disturbances
Hypertensive Encephalopathy
PRES:
Posterior reversible
encephalopathy syndrome
Typically symmetrical white
matter edema in the
posterior cerebral
hemispheres
www.wikipedia.org
• Normally CBF is unchanged between a MAP of 60-120
• As MAP increases  autoregulation stops  cerebral
vasodilation  edema
• As endothelial damage occurs  capillary leakage 
breakdown of blood brain barrier  edema
http://jap.physiology.org/content/91/5/1986/F1.large.jpg
• Chronically hypertensive patients lose normal
autoregulation in their brain. They require a higher BP
to maintain CBF
• Therefore the BP HTN emergency happens at is
dependent on the patients baseline BP
Goals of Tx: Hypertensive Urgency
– Use oral medications
– BP should be lowered gradually over 1-2
days
– Rapid correction below autoregulatory
range  hypoperfusion  ischemia and
infarction
Goals of Tx: Hypertensive Emergency
•
•
•
•
Altered auto-regulation is present
End-organ damage is already present
Excessive correction can worsen damage
Use IV infusion of a short acting, titratable
medication
• Use intra-arterial BP monitoring if severe
clinical manifestations or labile BP
• Goal: ↓DBP 15-20% or to about 110mmHg
over 1-2hr
– If dissection: this should be done in 5-10 minutes
Other Important Points
• ***Admit to ICU***
– Per STAT registry: only 15% of pts were admitted
1st line
• Once BP is stable, PO should be started as gtt is
titrated off
• Do not use sublingual nifedipine or IV hydralazine
because they lower BP too quickly
Other Important Points
• Don’t use nitroprusside (except with
aortic dissection) because is will
decrease BP to quickly, causes a
decrease in cerebral blood flow and
increases intracranial pressure
• Many patients are volume depleted from
pressure naturesis so use caution with
diuretics  BP will drop too quickly
The Drugs
• Nicardipine:
–
–
–
–
2nd generation dihydropyridine Ca ++ channel blocker
Selective for the peripheral vasculature
Cerebral vasodilatation
Coronary vasodilatation
• Clevidipine
– 3rd generation dihydropyridine Ca++ channel blocker
– Decreases SVR via relaxing smooth muscles of small
arteries, increases CO and SV
– Metabolized by plasma esterases so independent of
liver and kidney function
The Drugs
• Labetalol:
– Alpha 1 and non-selective Beta blocker (1:7 ratio)
– Metabolized by liver
– Maintains cardiac output, decreases SVR 
maintains peripheral blood flow
• Esmolol
– Ultra-short acting cardioselective beta blocker
– Metabolized by RBC esterases, independent of
liver and kidney function
PE
ACS
New S4
Lab
Drug
EKG,
Troponins
CXR, EKG,
BNP
labetalol or esmolol
+ nitroglycerin
nicardipine or
clevidipine + nitro +
loop diuretic
Dia CHF + Crackles,
Pulmonary JVD, LE
Edema
edema
CXR, EKG,
BNP
Aortic
Unequal
Dissection pulses &
BP
Wide
mediastinum
on CXR; CT
chest with
contrast
esmolol or labetalol
or metoprolol or
verapamil + nitro +
loop diuretic
labetalol or
nicardipine +
esmolol or
nitroprusside +
esmolol
Sys CHF + Crackles,
Pulmonary JVD, LE
Edema
edema
PE
Acute Kidney
Injury
Edema, ocular
exam –
retinopathy
HTN
Altered level of
Encephalopathy consciousness
CVA
Hemolytic
anemia
Focal
neurologic
deficits
CBC,
haptoglobin,
LDH, smear,
LFTs
Lab
Drug
elevated Cr, nicardipine,
hematuria on clevidipine,
UA
fenoldopam
CT head;
MRI
nicardipine,
clevidipine,
labetalol
CT head with Same as
angiography encephalop
athy
Anemia,
nicardipine,
schistocytes, clevidipine,
low plts
fenoldopam
Pregnancy related end organ damage: pre-eclampsia, eclampsia, HELLP syndrome
will not be addressed in this lecture.
References
1. Marik P, Rivera R. Hypertensive emergencies: an update. Current Opinion in
Critical Care 2011; 17:569-580
2. Deshmukh A, Kumar G, Kumar N, Nanchal R, Gobal F, Sakhuja A, Mehta J.
Effect of Joint National Committee VII report on hospitalization for
hypertensive emergencies in the United States. American Journal of
Cardiology 2011; 108:1277-1282
3. Franklin S, Neutel J. Initial combination therapy for rapid and effective control
of moderate and severe hypertension. Journal of Human Hypertension 2009;
23: 4-11
4. Aronson S, Dyke C, Stierer K, Levy J, Cheung A, Lumb P, Kereiakes D,
Newman M. The ECLIPSE Trials: comparative studies of Clevidipine to
Nitroglycerin, Sodium Nitroprusside, and Nicardipine for acute hypertension
treatment in cardiac surgery patients. Anesth Analg 2008; 107:1110-21
5. Varon J. Treatment of Acute Severe Hypertension. Drugs 2008; 68(3): 283297
6. Vaughan C, Norman D. Hypertensive Emergencies. Lancet 2000; 356: 41117