Transcript hypertensive emergencies - Calgary Emergency Medicine

HYPERTENSIVE
EMERGENCIES
Trevor Langhan PGY-2
September 2, 2004
CASE
67 y male
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Known small cell lung CA, prev CVA, DM,
COPD, chronic steroids.
Admitted to CCU one month ago with ACS
Today was at TBCC getting CT scan for
malignancy staging
Brought directly by wife after acute c/o
SOB and mild chest pain
CASE
BP 190/100, HR 140, RR 33, sats 81% r/a
Working hard to breathe, mottled skin,
diaphoretic
Doesn’t want to lay down for EKG, IV pokes
Swollen legs R > L
Portable CXR
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RUL consolidation ?collapse
Increased vascular markings bilaterally
CASE
Further Hx:
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Received 2 units PRBC 3 days prior
Chemotherapy yesterday with large volume load
Volume of fluid IV with contrast for CT
Known LV dysfunction from prev echo
Documented LEVEL II care in chart (NO intub)
Clinical exam:
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accessory muscle use
elevated JVP
inspiratory/expiratory wheezes bilat
minimal air entry
CASE (our management)
Unable to get IV access
Couple/three NTG SL sprays
ABG - 7.09/61/98/30
Move to code room
Femoral langhan – i mean line
CASE (our management)
Started on BIPAP
Medications:
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IV NTG
 5 ug/min to maximum 100 ug/min (we went to
200 ug/min and he improved)
 Mechanism: venous and mild arteriolar dilator
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IV Lasix
 40 mg x 2
 Any better than oral?
CASE (our management)
We chose venous and arteriolar
vasodilatation + lasix
labetalol –
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decrease cardiac contractility
COPD
Known previous bronchospasm
Hydralazine –
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increase cardiac work, causes alpha blockade
Pulmonary edema
Pts with CHF usually have increased PVR
Acute elevations in their BP may be
secondary to hypoxia and subsequent
catecholamine release
Aggressive treatment of the pulmonary
edema will help decrease the BP
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Nitrates
Morphine
Lasix
Oxygen
Hypertension
HTN will present to the ED in a variety
of ways:
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1. Hypertensive crisis/emergency
2. Hypertensive urgency
3. Mild hypertension without EOD
4. Transient hypertension
Hypertensive Emergency
Severely elevated blood pressure with
signs of acute damage to target organs
Brain, eyes, heart, kidneys
Hypertensive Emergency
Conditions defined by Rosen’s as HE:
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Malignant hypertension
 Hypertensive encephalopathy
 Microangiopathic hemolytic anemia
 Acute renal failure
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Aortic dissection
Eclampsia/preeclampsia
Severe HTN in setting of:
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MI
Left ventricular failure
Bleeding
Thrombolytic therapy
Hypertensive Urgency
Situation where blood pressure
elevation is an imminent risk for targetorgan damage
No acute end organ damage but risk is
high if BP elevation continues
Relative increase in BP more important
than specific numbers
Brief pathophysiology
Mild to moderate increase in BP leads to
initial vasoconstriction
“autoregulation”
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Maintains perfusion at relatively stable level
Prevents increased pressure from being
transmitted downstream to smaller vessels
As BP further increases, autoregulation fails
Elevated BP disrupts vasc endothelium,
causing narrowing
Brief pathophysiology
Chronic increase in BP causes arteriolar
hypertrophy
Will decrease the amount of pressure
passed on to more distal vessels
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Chronically hypertense people need
diastolic BP’s >130 for symptoms
Normotensive people can have
hypertensive crisis at DBP > 100
Case 2
45 y male c/o 12 hour history of
SOBOE, mild chest heaviness
Vomiting, drowsy
Bi-frontal headache
Blurred vision both eyes
BP 240/150, HR 102, RR 16, sats 95%
Case 2
PMHx: ? HTN, was on a “water pill”
many years ago. No DM, no CAD,
generally healthy
Labs normal, except Creat: 150
DDx? Mgnt?
Case 2
Goal of therapy is to reduce MAP by 25% in
the first hour
Keeping DBP > 110 mmHg
Reduction to pt’s relative normal BP by 4-6
hours is more long term goal
What agents?
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Nitroprusside - 0.25-0.5 ug/kg/min, up to 10
ug/kg/min, titratable, easy off, potential toxicity
labetalol – infusion 0.5-2 mg/min, or bolus 20 mg
then 20-80 mg q 10 minutes (up to 300mg), alpha
and beta blocker
Hypertensive Encephalopathy
Cerebral edema by breakthrough hyper-perfusion
from severe and sudden increase BP
BP has exceeded the capacity of autoregulation
Elevated BP in vessels that can’t accommodate the
pressure – leakage and edema
Autoregulation must be considered during treatment
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I.e. Hypertrophied vessels can’t vasodilate, so caution with
lowering blood pressure to avoid a relative hypoperfusion
and resultant ischemia
Hypertensive Encephalopathy
HE is a true medical emergency
Is an acute presentation, but reversible
Progression of untreated cerebral edema
leads to coma and death
Admission and invasive BP monitoring is the
recommended mainstay of therapy
Case 3
67 y female known CAD, DM, smoker,
atrial fib.
Presents with c/o weakness left side
BP 160/100, HR 94, RR 14, sats 99%
O/E left facial droop, markedly weak left
upper/lower extremity
EKG a fib, nil acute
Chest exam unremarkable
Case 3
Management?
How do you treat her elevated BP?
Stroke syndromes
Most patients with this presentation are
ischemic strokes (85%) not hemorrhagic
Likely don’t have acutely elevated BP
***caution*** with lowering BP as
Watershed area sensitive to
hypoperfusion
Lowering BP may worsen ischemic
brain injury
Stroke syndromes
Rarely may see stoke with grossly elevated
DBP > 140
Pts receiving reperfusion therapy may require
BP reduction, as BP > 185/110 is
contraindication to tPA
What do you think about nitroprusside here?
Titrate labetalol diligently in 5 mg increments
to achieve slow decrease in MAP by a max of
20%
Case 4
32 y female awaiting “sweatgland” surgery
from plastics for hyperhydrosis, c/o H/A,
palpitations
BP 170/90, HR 150 sinus, RR 18
Otherwise healthy
Treatment:
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Nitroprusside if emergency
Phentolamine – 1-5 mg IV boluses (alpha-block)
 Followed by beta-blockade
Case 4
Pheochromocytoma
Rare tumor – 0.2% of pts with essential HTN
Episodic H/A, tachycardia, sweating, HTN
Tumor secreting norepinephrine and
epinephrine
Diagnosis radiographic, measurement of
urinary and plasma levels of catecholamines
and metabolites
Case 5
25 y G2P1, LMP 6 months ago
When do you treat HTN in pregnancy?
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DBP > 110
SBP > 160
Treat to goal of 140-155 and 90-105
What agents?
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Hydralazine (older agent of choice)
Labetalol (preferred modality now)
Case 6
33 year male stock broker. Snorted a
“couple of rails” of cocaine ½ hour ago.
Presents with crushing retrosternal
chest pain, diaphoresis and H/A
BP 190/100, HR 130, RR 28, sats 96%
EKG ST segment elevation V1-V3
Nurse asks “what do you want to give?”
Case 6
Give MONA
You order IV metoprolol to be hung
Before the Beta blocker, any concerns?
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Beta antagonism will decrease heart rate, but will
also block B2 receptors
Will have unopposed alpha agonism by cocaine
toxicity – dangerous HTN crisis
Need alpha blockade first
Like pheo can use phentolamine, some sources
say hydralazine
Case 7
55 year male smoker, HTN, DM,
unstable angina getting worse.
Shoveling snow and developed left
RSCP that radiated to his jaw.
HR 120, BP 190/90, RR 19, sats 99%
EKG obvious ant/lateral infarct
How do you treat his pressure?
Case 7
Agents of choice in HTN during ACS
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Immediate lowering of BP indicated to prevent
myocardial damage
Also lower BP if pt to undergo reperfusion tx
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NTG agent of choice
Beta block
ACE-I (shown improvement in mortality)
CCB (if BB is contraindicated)
Anything that’s contraindicated?
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Hydralazine – reflex tachycardia
Nitroprusside – reflex tachycardia
Hypertension
What is normal BP?
 SBP < 140
 DBP < 90
What is hypertension?
 SBP >160
 DBP >100
Anything in between GRAY.
Hypertension
Possible cardiovascular causes of
increased BP:
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Loss of vessel elasticity with age
Coarctation of aorta
 Delayed femoral pulses
 Hypertensive upper extremities
 Bruit in upper back
Hypertension
Endocrine causes for elevated BP:
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Pheo
Excess steroids
 Often iatrogenic
 Cushings
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Look for hypokalemia
Volume overload from Na retention
Hypertension
Other causes include:
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Withdrawal of sedative drugs
 EtOH, benzo
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Tyramine toxicity in MAO-I patients
Aortic dissection
Sympathomimmetic drug intoxication
Withdrawal of clonidine or beta blocking agents
Reno-vascular disease
Renin-angiotensin system abnormality
Drug choices
drug
dose
onset
duration
indication
nitroprusside
0.3-10
ug/kg/min
1-2
min
1-2 min
Any
hypertensive
emergency
nitroglycerin
10-100
ug/kg/min
2-5
min
3-5 min
AMI, CHF
5 mg
5-10mg
q20min
10-20
min
3-8 h
pregnancy
hydralazine
Contra-indication
Pregnancy
Prolong use
Renal failure
AMI, aortic
dissection
esmolol
500ug/kg then 1-2
50-300
min
ug/kg/min
10-20 min CAD, aortic
dissection
CHF, heart
block, asthma,
catecholamine
excess
labetalol
20mg then
20-80 q10
min to max
300 OR 1-2
mg/min
2-10
min
2-4 h
CHF, heart
block, asthma,
catecholamine
excess
phentolamine
5 mg q 1-2
min
1-2
min
10-30 min Catecholamine
excess
CAD, aortic
dissection,
eclampsia,
hypertensive
crisis
AMI
Key concepts
Presence of acute target organ damage determines
HTN crisis
All pts with persistent elevation of BP should be
investigated of EOD
ER doc should be familiar with indications and
contraindications of meds to treat HTN crisis
Goal of treat is relative decrease in MAP of 25% in
first hour, DBP should not fall <110 mmHg
Pts without EOD rarely require urgent management
of HTN and should be referred for outpt
pharmacotherapy adjustments