HYPERTENSIVE EMERGENCIES Trevor Langhan PGY-2 September 2, 2004.
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HYPERTENSIVE EMERGENCIES
Trevor Langhan PGY-2
September 2, 2004
CASE
67 y male 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 RUL consolidation ?collapse Increased vascular markings bilaterally
CASE
Further Hx: 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:
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 BIPAPMedications: 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 IV Lasix
40 mg x 2 Any better than oral?
CASE (our management)
We chose venous and arteriolar vasodilatation + lasix
labetalol – decrease cardiac contractility COPD Known previous bronchospasm
Hydralazine – increase cardiac work, causes alpha blockade
Pulmonary edema
Pts with CHF usually have increased PVRAcute elevations in their BP may be secondary to hypoxia and subsequent catecholamine releaseAggressive treatment of the pulmonary edema will help decrease the BP Nitrates Morphine Lasix Oxygen
Hypertension
HTN will present to the ED in a variety of ways: 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: Malignant hypertension
Hypertensive encephalopathy Microangiopathic hemolytic anemia Acute renal failure
Aortic dissection Eclampsia/preeclampsia Severe HTN in setting of:
MI Left ventricular failure Bleeding Thrombolytic therapy
Hypertensive Urgency
Situation where blood pressure elevation is an imminent risk for target-organ 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” Maintains perfusion at relatively stable level Prevents increased pressure from being
transmitted downstream to smaller vessels
As BP further increases, autoregulation failsElevated 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 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 hourKeeping DBP > 110 mmHgReduction to pt’s relative normal BP by 4-6 hours is more long term goalWhat agents? 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 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 sideBP 160/100, HR 94, RR 14, sats 99%O/E left facial droop, markedly weak left upper/lower extremityEKG a fib, nil acuteChest exam unremarkable
Case 3
Management?
How do you treat her elevated BP?
Stroke syndromes
Most patients with this presentation are ischemic strokes (85%) not hemorrhagicLikely don’t have acutely elevated BP***caution*** with lowering BP as Watershed area sensitive to hypoperfusionLowering BP may worsen ischemic brain injury
Stroke syndromes
Rarely may see stoke with grossly elevated DBP > 140Pts receiving reperfusion therapy may require BP reduction, as BP > 185/110 is contraindication to tPAWhat 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, palpitationsBP 170/90, HR 150 sinus, RR 18Otherwise healthyTreatment: 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 agoWhen do you treat HTN in pregnancy? DBP > 110 SBP > 160 Treat to goal of 140-155 and 90-105
What agents? 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 MONAYou order IV metoprolol to be hungBefore the Beta blocker, any concerns? 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 Immediate lowering of BP indicated to prevent
myocardial damage Also lower BP if pt to undergo reperfusion tx
NTG agent of choice Beta block ACE-I (shown improvement in mortality) CCB (if BB is contraindicated)
Anything that’s contraindicated? 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: 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: Pheo Excess steroids
Often iatrogenic Cushings
Look for hypokalemia Volume overload from Na retention
Hypertension
Other causes include: Withdrawal of sedative drugs
EtOH, benzo 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 dose onset duration indication Contra-indication
nitroprusside 0.3-10 ug/kg/min
1-2 min
1-2 min Any hypertensive emergency
Pregnancy
Prolong use
Renal failure
nitroglycerin 10-100 ug/kg/min
2-5 min
3-5 min AMI, CHF
hydralazine 5 mg
5-10mg q20min
10-20 min
3-8 h pregnancy AMI, aortic dissection
esmolol 500ug/kg then 50-300 ug/kg/min
1-2 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 CAD, aortic dissection, eclampsia, hypertensive crisis
CHF, heart block, asthma, catecholamine excess
phentolamine 5 mg q 1-2 min
1-2 min
10-30 min Catecholamine excess
AMI
Drug choices
Key concepts
Presence of acute target organ damage determines HTN crisisAll pts with persistent elevation of BP should be investigated of EODER doc should be familiar with indications and contraindications of meds to treat HTN crisisGoal of treat is relative decrease in MAP of 25% in first hour, DBP should not fall <110 mmHgPts without EOD rarely require urgent management of HTN and should be referred for outpt pharmacotherapy adjustments
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