Transcript Severely Increased Blood Pressure In The ED

Severely Increased Blood
Pressure In The ED: Treating The
Mercury?
Rick Blubaugh, D.O.
Cornerstone Physician’s Management Group
Skaggs Community Health Center
Branson, MO
Case History
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50 y/o male
History of hypertension
Hasn’t taken meds in 1 year
C/O headache & malaise for 2 days
Exam: remarkable only for BP 210/120 &
grade I retinopathy
Questions For EP
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Is patient stable?
Is further WU indicated? & if so, what?
Does pt require immediate intervention? &
if so, what?
Does pt require admission or monitoring,
or if D/C’d, how soon should he be seen in
follow up?
Background
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Prolonged & severely increased BP causes
cerebral, cardiovascular, and renal disease
(Target Organs).
Morbidity & mortality can be improved
with treatment
Limited data concerning acutely elevated
blood pressure
Physiology
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Affects heart, brain, kidneys, & large
arteries
Chronic HTN causes right shift in pressure
flow autoregulation curve
When BP decreases, cerebral vasodilation
occurs
When BP increases, constriction occurs
Cerebral perfusion pressure remains
constant despite fluctations in MAP
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Normal individuals: cerebral blood flow remains
constant for MAP of 60-150mmHg
When MAP decreases to less than lower limits of
autoregulation, the brain becomes hypoperfused
& cerebral hypoxia occurs.
MAP = Diastolic + 1/3 (Systolic – Diastolic)
Cerebral perfusion pressure = MAP – Intracranial
pressure
Chronic hypertension: lower limit of
autoreguation is increased
Autoregulation might fail at MAPs well tolerated
in normotensive individuals
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Lower limit of autoregulation is
approximately 25% of MAP
Therefore, MAP should not be lowered by
more than 20-25%
Autoregulation Curve
Fig. 4.
Gao, E. et al. Am J Physiol Heart Circ Physiol 274: H1023-H1031 1998
Copyright ©1998 American Physiological Society
Clinical Evaluation
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BP 180/110: immediate or evaluation
within 1 week (Joint National CommitteeVI Guidelines)
Recheck BP: many spontaneously reduce
Seated, arm at level of heart, both arms
Automated cuff inaccurate in A-Fib or irreg
Manage pain or underlying causes
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Fundoscopic exam: retinal hemorrage or
papilledema
Cardiovascuar exam: Identify heart failure
Neuro exam: LOC, visual fields, motor &
sensory deficits
Serum creatinine
ECG
Med History including OTC
Urine drug screen: cocaine, amphetamine
Stratification of Hypertensive
Events
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Emergent
Urgent
Uncontrolled hypertension
Hypertensive Emergency
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Rapid, progressive decompensation or
damage of target organs
Hypertensive encephalopathy, or brain
hemorrage
Acute aortic dissection, acute LV failure,
AMI, unstable angina, symptomatic aortic
aneurysm.
Acute glomerulonephritis,kidney transplant
Hypertensive Emergency
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Pheochromocytoma
Sympathomimetic use
Severe burns
Severe epistaxis
Eclampsia/preeclampsia
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Requires immediate (1-2 hours) BP
reduction
Parenteral agent
Nitroprusside – most events
Labetalol – intracranial disorders (does not
dilate cerebral vessels)
B- blockers – aortic dissection (blocks
reflex tachycardia)
Oral agents – should not be used (limited
data, high failure rates, not titratable,
uncontrolled hypotension)
Emergent Blood Pressure
Reduction
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Should not exceed 20%-25% of
pretreatment BP
1st 30-60 Min: Reduce MAP to 110-115
Further reduction over next 24 hours
Hemorrhagic & Ischemic CVA
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When systolic BP is reduced, cerebral
autoregulation might fail leading to
extension of CVA
Some believe that elevated MAP is
protective in CVA
AHA: reduce BP in CVA only when MAP is
> 130mm Hg or SBP > 220 mm Hg
Esmolol & labetalol are good choices
Nipride – cerebral vasodilation
Cardiovascular Emergencies
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CHF – nitroprusside & ACE inhibitor
ACS – nitroglycerine – reduce BP to
normal levels
Aortic Dissection – nitroprusside + Bblocker.
Hypertensive Urgency
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Controversial
History of prior target organ disease (CHF,
CAD, angina, renal insuff, TIA, or CVA)
Treatment strategy should be initiated in
ED, although BP does not necessarily need
to be reduced in ED
Reliance on specific numbers is
inadequate
Hypertensive Urgency
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VA Cooperative Study: no adverse
outcomes within first 3 months in patients
who had DBP 115-130mm Hg
No evidence to support practice of treating
hypertension by reducing BP acutely in ED
Numerous reports of adverse outcomes
with acute, rapid reduction of BP in ED.
Uncontrolled Hypertension
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Asymptomatic elevated BP without
evidence of target organ disease
Represents majority of patients with
elevated BP in ED
Goal: lifelong BP control
Treat pain or infection
Refer for recheck after primary problem
resolved ( 1 week)
Uncontrolled Hypertension
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If patient has quit taking antihypertensive
meds – then restart them
1/3 of patients in ED with DBP > 95
mmHg were normotensive at follow-up
Initial Oral Drug Choices
Case Revisited
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Tx: analgesia for headache
Lab: Serum creatinine, UA, ECG
CT: if findings on H&P suggest CNS
involvement
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If history or CT scan shows prior CVA,
then patient qualifies as hypertensive
urgency – justifying initiation of
maintenance treatment
Best regimen is one that previously
worked
Otherwise – diuretic & B-blocker
Follow up in 1 week or observation
Case
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If clinical exam & work up is negative &
BP remains elevated after resolution of
headache, then patient is stratified as
uncontrolled hypertension
Follow –up with PCP
Summary
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Hypertensive Emergency – rapidy,
progressive end-organ damage.
Needs parenteral meds & ICU
Caution in cerebrovascular events
Summary
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Hypertensive Urgency – BP elevated >
180/110 & history of end- organ disease.
Initiate oral meds & short term follow up
or observation
Uncontrolled Hypertension –
asymptomatic
Referral to PCP & education