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HYPERTENSIVE
EMERGENCIES
Mostafa alshamiri
Discussion
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Categories
Epidemiology
Etiology/pathophysiolog
Managment
Treatment
Prognosis
Take home massage
Case Scenarios
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A 56 yo CM with no significant PMH presents to the ER
with headache,found to have BP 210/110mmHg and
papilledema.
An 82 yo male with h/o HTN,chronic renal insufficiency
presents for a routine physical,found to have BP of
230/130mmHg.
A 76 yo female is brought to the ER by the family due to
altered mental status.BP is 240/110 mmHg with no focal
neuro findings.
Definition
Sustained abnormal elevation of blood
pressure
HYPERTENSION(JNC-7class.)
SBP-mmHg
NORMAL
PREHYPERTENSION
<120
DBP-mmHg
<80
120-139
or 80-89
STAGE 1
140-159
or 90-99
STAGE 2
>=160
>=100
Comparative Prevalence of hypertension and the
expected hypertension
population in each country
Journal of Hypertension 2005, Vol 23 No 6
Benefits of Lowering BP
Average Percent Reduction
Stroke incidence
35–40%
Myocardial infarction
20–25%
Heart failure
50%
Key Point
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For every 20 mm Hg increase in SBP or 10
mm Hg increase in DBP – the risk of death
from stroke, IHD, or vascular disease
DOUBLES!
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For every 20 mm Hg decrease in SBP or
10 mm Hg decrease in DBP – the risk of
death from stroke, IHD, or vascular disease
IS CUT IN HALF!
HYPERTENSIVE
EMERGENCY/URGENCY
Hypertensive Emergencies/crises
Patients with marked BP elevations(> 180/120 mm Hg)
and acute TOD (e.g., encephalopathy, myocardial infarction, unstable
angina, pulmonary edema, eclampsia, head trauma, life-threatening arterial
bleeding, or aortic dissection) require hospitalization and parenteral drug
therapy.
Hypertensive Urgencies
 Patients with markedly elevated BP but without acute TOD usually do not
require hospitalization, but should receive immediate combination oral
antihypertensive therapy.
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Although not specifically addressed in the JNC 7 Report, patients with a systolic
blood pressure greater than 179 mmHg or a diastolic blood pressure that is greater
than 109 mmHg are usually defined as having 'severe or accelerated' hypertension
Historical background of HTN
emergency
The term 'malignant hypertension' has been
used to describe a syndrome characterized
by elevated blood pressure accompanied
by encephalopathy or acute nephropathy .
However, this term has been removed from
national and international blood pressure
control guidelines
Other entity- emergency
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Postoperative hypertension has arbitrarily been defined as a
systolic blood pressure greater than 190 mmHg and/or
diastolic blood pressure greater than 100 mmHg on two
consecutive readings following surgery
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The presence of a systolic pressure greater than 169 mmHg
or a diastolic pressure greater than 109 mmHg in a
pregnant woman is considered a hypertensive emergency
that requires immediate pharmacologic management
ETIOLOGY
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Essential hypertension : Inadequate blood pressure control and noncompliance are common
precipitants
Renovascular
Eclampsia/pre-eclampsia
Acute glomerulonephritis
Pheochromocytoma
Anti-hypertensive withdrawal syndromes
Head injuries and CNS trauma
Renin-secreting tumors
Drug-induced hypertension
Burns
Vasculitis
TTP
Idiopathic hypertension
Post-op hypertension
Coarctation of aorta
Epidemiology of hypertensive
crisis.
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Hypertension is an extremely common clinical
problem, affecting approximately 50 million people
in the USA and approximately 1 billion individuals
worldwide.
Approximately 1% of these patients will develop
acute elevations in blood pressure at some point
in their lifetime
20-30% in patient with emer/urg secondary to
uncontrolled essential HTN while in black it is
80%.
BLOOD FLOW
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BP = PVR X CO (HR X SV)
MAP = DBP + 1/3 PP (SBP-DBP)
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CPP
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Cpp between 70-90 , some consider 50-150
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Increase MAP will increase CPP and vasa versa.
CBF maintained near-constant by auto regulatory mechanism (vasoconestrection/dilation ), despite variation in CPP, however , has upper and
lower limit beyond which CBF can no longer be controlled .
When MAP increases >>> increases CPP >>> and hyperperfusion >> brain
edema & progressive brain dysfunction & ischemia.
Decreased CBF >> brain hypoxia and hypo-perfusion symptoms ( headache ,
nausea , dizziness ,altered sensorium , lethargy & ultimately infarction) .
Normal BP maintain auto regulation of MAP between 50 to 150
Overzealous BP reduction can lead to permanent neurological damage.
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= MAP – ICP (normal, ICP =10)
Auto-regulation curve
PATHOPHYSIOLOGY
NORMAL
AUTOREGULATION
RISE IN BP
ARTERIAL AND
ARTERIOLAR
CONSTRICTION
AUTOREGULATION
FAILURE
RISE IN BP
FAILURE OF
VASOCONSTRICTION
ENDOTHELIAL DAMAGE
(due to shear stress on the
wall)
Normal flow.(flow=P/r)
PATHOPHYSIOLOGY
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BP=PVR*CO(SV*HR)
Rate at which MAP rises more important than absolute rise.
Acute rise in BP
Failure of vasoconstriction
by autoregulation
FIBRINOID
NECROSIS
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Activates coagn and
inflammation
Endothelial
damage
Depsn. of proteins/
fibrinogen in vessel wall
RAAS plays an important role in initiating and perpetuating BP rise by causing
vasoconstriction and fluid retention.
CARDIOVASCULAR SYSTEM
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The cardiovascular system is affected as
increased cardiac workload leads to
cardiac failure; this is accompanied by
pulmonary edema, myocardial ischemia, or
myocardial infarction.
RENAL SYSTEM
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The renal system is impaired when high BP
leads to arteriosclerosis, fibrinoid necrosis,
and an overall impairment of renal
protective autoregulation mechanisms. This
may manifest as worsening renal function,
hematuria, red blood cell (RBC) cast
formation, and/or proteinuria.
CENTRAL NERVOUS SYSTEM
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The CNS is affected as the elevated BP overwhelms the normal
cerebral autoregulation. Under normal circumstances, with an
increase in BP, cerebral arterioles vasoconstrict and cerebral blood
flow (CBF) remains constant.
During a hypertensive emergency, the elevated BP overwhelms
arteriolar control over vasoconstriction and autoregulation of CBF.
This results in transudate leak across capillaries and continued
arteriolar damage. Subsequent fibrinoid necrosis causes normal
autoregulatory mechanisms to fail, leading to clinically apparent
papilledema, the sine qua non of malignant hypertension.
The end result of loss of autoregulation is hypertensive
encephalopathy.
Hypertensive encephalopathy
Hypertensive encephalopathy is an acute organic brain syndrome or
delirium related to cerebral edema
Result from loss of cerebral vascular auto regulatory function in the
setting of severely elevated blood pressure.
Characterized initially by
Headache
Nausea, and vomiting , followed by
Altered mental status and/or seizure if hypertension is not treated.
Hypertensive encephalopathy is a diagnosis of exclusion;
other causes must be ruled out
Management of hypertensive
emergency
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HISTORY
PHYSICAL EX
LABARATORY
DRUGS THERAPY
DRUGS THERAPY
The ideal pharmacologic agent for the
management of hypertensive crises would
be :
 Fast-acting,
 Rapidly reversible
 Titratable
 Without significant side effects
Treatment-1
Initial considerations:
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Place patient who is not in distress in a quiet room and reevaluate after an
initial interview. In one study, 27% of patients with an initial DBP >130 mm
Hg had their DBP fall below critical levels after relaxation without specific
treatment.
Consider the context of the elevated BP (eg, severe pain)
Screen for end-organ damage- Patients with end-organ damage usually
require admission and rapid lowering of BP using iv meds.Suggested meds
depend on the end-organ system damaged.
Patients without evidence of end-organ effects may be discharged with
follow–up.
It is a misconception that a patient should not be discharged from the ER
with elevated BP.Giving oral meds such as nifedipine to rapidly lower BP
may be dangerous as the BP may have been elevated for sometime and
there may be organ hypoperfusion.Acute control has not improved long
term mortality and morbidity rates.
TREATMENT-2
DRUGS THERAPY
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HTN-URGENCY
The initial goal is to reduce blood pressure to 160/110 mm
Hg over several hours to days using conventional oral
therapy.
Mean arterial pressure should be reduced by no more than
25% within the first 24 hours
HTN-EMERGENCY
The ideal rate of blood pressure lowering is unclear, but
reducing the mean arterial pressure by 10% during the first
hour and an additional 15% within the next 2 to 3 hours has
been recommended
TREATMENT - 3
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The majority of patients with severe hypertension (diastolic
pressure > 109 mmHg) will have no acute end-organ damage
(hypertensive urgencies).
In these patients the blood pressure should be lowered
gradually over a period of 24–48 hours, usually with oral
medication.
Rapid reduction in blood pressure in these patients may be
associated with significant morbidity .
In patients with true hypertensive emergencies, rapid but
controlled lowering of blood pressure is indicated to limit and
prevent further organ damage . However, the blood pressure
should not be lowered to normal levels .
TREATMENT - 4
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Most patients with hypertensive emergencies are chronically
hypertensive and will have a rightward shift of the pressure–
flow (cerebral, renal, and coronary) autoregulation curve .
Rapid reduction in blood pressure below the cerebral, renal,
and/or coronary auto-regulatory range will result in a
marked reduction in organ blood flow, leading to ischemia
and infarction.
For this reason all patients with a hypertensive emergency
should be managed in an intensive care unit, where the
patient can be closely monitored.
Intra-arterial blood pressure monitoring may be required in
patients with blood pressure that is labile and difficult to
control.
Treatment-HTN emergency (crisi)-5
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Reductions in diastolic blood pressure by 10–15% or to
about 110 mmHg is generally recommended.
This is best achieved by an continuous infusion of a short
acting, titratable, parenteral antihypertensive agent .
In patients with a dissecting aneurysm this goal should be
achieved within 5–10 min.
In all other patients, this endpoint should be achieved within
1 hour.
RAPID BP REDUCTION
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Acute myocardial ischemia:
- IV NTG, b-blockers,ACE inhibitors.
CHF with pulmonary edema:
- Iv NTG, furosemide, morphine
Acute aortic dissection:
- Iv nitroprusside +b-blockers or iv trimethaphan
b-blockers.
Hypertensive encephalopathy or sub-arachnoid hemorrhage:
- Iv nitroprusside, labetalol or nimodipine.
MAO-tyramine interactions with acute hypertension:
- iv phentolamine.
Treatment ischemic strokes
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Only patients with hypertensive emergencies require immediate reduction
in markedly elevated blood pressure. In all other patients the elevated
blood pressure can be lowered slowly using oral agents.
Lowering BP in patients with ischemic strokes may reduce CBF , which
because of impaired auto-regulation may result in further ischemic injury.
The common practice of 'normalizing' BP following a CVA is potentially
dangerous. When a proximal arterial obstruction results in a mild stroke, a
fall in blood pressure may result in further infarction involving the entire
territory of that artery.
Recommendation of the AHA is that hypertension in the setting of acute
ischemic stroke should only be treated 'rarely and cautiously' .
BP should be carefully observed for the first 1 to 2 hours to determine if it
will spontaneously decrease. Only a persistently MAP over 130 mm Hg or
a SBP over 220 mm Hg should be carefully treated. In this setting, MAP
should be lowered by 15% to 20%.
Treatment hemorrhagic strokes
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In patients with intracerebral hematomas there is almost always a rise in
intracranial pressure with reflex systemic hypertension. There is no
evidence that hypertension provokes further bleeding in patients with
intracranial hemorrhage. However, a precipitous fall in systemic blood
pressure will compromise cerebral perfusion. The controlled lowering of the
BP is currently recommended only when the systolic blood pressure is
greater than 200 mmHg or the diastolic pressure is greater than 110 mmHg
AHA recommends treating hypertension in the setting of an intra-cerebral
bleed only when blood pressure is more than 180/105 mm Hg. Mean
arterial pressure should be maintained below 130 mm Hg.
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Study demonstrated that the rapid decline in BP within the first 24 hours
after presentation was associated with increased mortality in patients with
an intracranial hemorrhage . The rate of decline in BP was independently
associated with increased mortality
Treatment of pregnancy &
hypertensive crisis
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Pregnant patients with hypertensive crises represent a
special group of patients. intravenous drug therapy is
reserved for those patients with SBP persistently greater than
180 mmHg or DBP persistently greater than 110 mmHg (105
mmHg in some institutions) .
Before delivery it is desirable to maintain the DBP greater
than 90 mmHg because this pressure allows for adequate
utero-placental perfusion. If DBP decreases to below 90
mmHg, then decreased utero-placental perfusion may
precipitate acute fetal distress progressing to an in utero
death or to perinatal asphyxia .
PROGNOSIS:
Median survival duration is 144 months for all
patients presenting to ED with hypertensive
emergency.
- 5 yr survival rate is 74%.
So,……….
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A 56 yo CM with no significant PMH presents to the ER
with headache,found to have BP 210/110mmHg and
papilledema. -MALIGNANT HYPERTENSION
An 82 yo male with h/o HTN,chronic renal insufficiency
presents for a routine physical,found to have BP of
230/130mmHg.-ACCELERATED HYPERTENSION
A 76 yo female is brought to the ER by the family due to
altered mental status.BP is 240/110 mmHg with no focal
neuro findings. –HYPERTENSIVE EMERGENCY
Take home points
• Distinguishing between hypertensive emergency (associated
with acute target organ damage) and urgency (no target
organ damage) is crucial to appropriate management.
• Diagnosis of hypertensive emergency requires a thorough
history (evidence of target organ damage, illicit drug use,
and medication compliance) as well as a complete physical
examination, basic laboratory data, and electrocardiogram
to assess for the presence of target organ damage and
determine its severity.
• In general, hypertensive urgency is managed using oral
antihypertensive drugs in outpatient or same day
observational settings, while hypertensive emergency is
managed in an intensive care unit or other monitored
settings with parentral drugs.
Take home points
• The initial goal in hypertensive urgency is a reduction
in mean arterial pressure by no more than 25% within the first
24 hours using conventional oral therapy; in hypertensive
emergency, mean arterial pressure should be reduced
approximately 10% during the first hour and an additional
15% within the next 2 to 3 hours.
• Various medications are available for the treatment of
hypertensive emergency; specific target organ involvement
and underlying patient co-morbidities
Thanks for your Attention!
SPECIFIC TREATMENT
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Hypertensive Encephalopathy:
Goal is to reduce MAP by not>25% or DBP tp100mmHg in the first hour.Nitroprussi(widely used in past)is a
powerful arteriloar dilator,so a rise in ICP may occur.Labetalol,fenoldopam used more now.
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Intracerebral Hemorrhage:
CPP=MAP-ICP.As ICP rises,MAP must rise for perfusion but this raises risk of bleeding from small arteries and
arterioles.A prosp. Obs. study in 1997 did not confirm these concerns but it was obscured by early use of antihypertensives.Cerebral autoregulation curve in chronic hypertensives may be altered,making them less likely to
tolerate aggressive lowering of BP.MAP guidelines:decrease when MAP>130 or SBP>220.Labetalol,esmolol
agents of choice.
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SAH:
Nimodipine decreases vasospasm that occurs due to chemical irritation of arteries by blood.Not recommended
routinely due to high incidence of hypotension.Cognitive status is a guide.Labetalol,esmolol agents of choice.
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Acute Ischemic Stroke:
High BP can cause hemorrhagic transformation of infarct ,cerebral edema.But,if CPP is low,ischemic penumbra
may occur.CPP beyond obstn is low.Distal vessels become dilated with ,loss of autoregulation.A decilne to prestroke values in 4 days has been documented often..A Cochrane review examining 65 RCTs with 11,500 pts.
Concluded that insufficient data exists to evaluate BP lowering post-stroke.AHA guidelines:BP be reduced only if
SBP>220 or DBP>120mmHg.(unless end-organ damage is due to BP).Labetalol,nitroprusside-agents of
choice.For thrombolysis,BP<185/110.
FOLLOW-UP
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The Joint National Committee on High Blood Pressure has
published a series of recommendations for appropriate follow-up,
assuming no end-organ damage.
-For a systolic BP 140-159 mm Hg/diastolic 90-99 mm Hg, confirm
BP within 2 months.
-For systolic BP 160-179 mm Hg/diastolic 100-109 mm Hg, evaluate
within a month.
- For systolic BP 180-209 mm Hg/diastolic 110-119 mm Hg,
evaluate within a week.
-For systolic BP greater than 210 mm Hg/diastolic greater than 120
mm Hg, evaluate immediately.
TRIALS
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HYPERTENSIVE EMERGENCY:1 RCT
HYPERTENSIVE URGENCY:10 RCTS.
CONCLUSIONS:-Evidence about effectiveness of
antihypertensive agents in people with hypertensive
emergencies or hypertensive urgencies is weak.
Studies had small sample sizes and were heterogeneous in
terms of patients, interventions and outcomes reported.
Limited evidence suggests that urapidil is most effective in
emergencies. In urgencies, nicardipine; nitroprusside or
fenolodopam may be used, but not nifedipine.
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Normally autoregulation maintains a constant blood flow
between MAP 50 mmHg and 150 mmHg.
However in traumatised or ischaemic brain, or following
vasodilator agents (volatile agents and sodium
nitroprusside) CBF may become blood pressure
dependent.
Thus as arterial pressure rises so CBF will rise causing
an increase in cerebral volume.
Similarly as pressure falls so CBF will also fall, reducing
ICP, but also inducing an uncontrolled reduction in CBF.