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Acute Care I - Spring 2017 > Module 11: Hypertensive Urgency & Emergency > Flashcards

Module 11: Hypertensive Urgency & Emergency Flashcards

1
Q

hypertensive urgency

A

sbp>180 and/or DBP >110

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2
Q

hypertensive emergency

A

SBP > 180 and/or DBP >110 and evidence of end organ damage

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3
Q

etiology of hypertensive urgency

A

abrupt rise in SBP > 180 and/or DBP > 110 usually d/t uncontrolled HTN -no end organ damage yet (body has likely been compensating, a more chronic issue)

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4
Q

causes of hypertensive emergency

A

common causes: 1. unexplained rapid rise in BP on top of uncontrolled chronic HTN 2. abrupt poor compliance with medications causing rebound effect other causes 1. renal parenchymal disease (glomeruli disorders) 2. renovascular disease (renal artery stenosis) 3. endocrine disorders (phenochromocytoma, cushings syndrome, primary aldosteronism) -drugs (cocaine, amphetamines, clonidine withdrawal) -coarctation of aorta -pre/eclampsia

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5
Q

what is the physiology of hypertensive urgency/emergency?

A

-failure of autoregulatory function occurs, precipitated by one or more of a host of potential causes ->leads to increased systemic vascular resistance which causes release of inflammatory markers which ultimately causes endovascular injury & fibrin necrosis of arterioles & release or more vasoconstrictors

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6
Q

physiology pathway

A

shear stress –> endothelial dysfunction –> end organ effect

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7
Q

RAAS?

A

renin-angiotensin aldosterone system plays a role in cascade of HTN decreased renal perfusion and lower tubular sodium concentration which stimulates aldosterone to increase blood pressure by maintaining excess volume through sodium retention and potassium excretion futher potentiating the cycle of uncontrolled blood pressure

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8
Q

myocardial autoregulation

A
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9
Q

cerebral autoregulation?

A
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10
Q

exam & ROS for hypertensive emergency

A
  • focus on s/sx of end organ dysfunction to guide treatment
  • Neuro: hx of stroke, spinal cord injury, brain injury/tumor
    • ROS: ams, confusion, visual changes, headache, focial weakness, syncope, seizures, nausea/vomiting
  • cardiac: h/o MI, CAD, angina, arrhythmias, or family history
    • ROS: CP, SOB, symptoms of CHF, palpitations, DOE
  • renal: h/o CKD
    • ROS: anuria, oliguria, color (look for symptoms of hypoperfusion/something sudden)
  • endocrine: h/o DM, thyroid disease, cushings
    • ros: diaphroesis, tremors, palpitations, apapetitie changes
  • social history: drugs, etoh
    • medications: steroids? compliance?
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11
Q

drugs that may precipitate a htn emergency

A

oral contraceptives

maoi

tca

steroids

nsaid

nasal decongestatns

cold remedies

appetitie suppressants

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12
Q

what should be on a focused physical exam?

A
  • eyes: fundoscopic exam, looking for papilledema (a sign of ICP)
    • flame hemorrhages, cotton wool spots, arteriovenous nicking suggest a long standing history of uncontrolled htn/dm
  • neck: jvd, enlarged thyroid/goiter
  • cardiac: irregular rate/rhythm, displaced apical pulse, gallop, murmur
  • pulmonary: rales, wheezing
  • abdomen: auscultation for renal artery bruit
  • neuro: ams, focal weakness or other focal finding
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13
Q

what diagnostics should you order?

A
  • Neuro:
    • ct head (ischemia/hemorrhage)
    • urine drug screen
  • cardiac
    • ekg (lvh, acute event)
    • cxr (widened mediastimum indicative of dissection, chf, signs of pulmonary edema)
    • cardiac enzymes (acute event)
    • ct chest (for high suspicion of dissection)
  • renal
    • chemistry (kidney function)
    • urinalysis (proteinuria, aki)
      *
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14
Q

how to treat?

A

literature lacks guidance for acute managment of patients presenting w/ htn, expecially severe actue elevates of BP

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15
Q

treatment of htn urgency

A
  • htn urgency usually develops over days/weeks. if showing no signs of end organ damage, could be something they’ve lived with for a while
  • a rapid decrease in BP can actually cause symptomatic hypotension, resulting in hypoperfusion to organs
  • use: rapid onset ORAL anti-hypertensive agents such as clonidien, labetal, captopril as they are easily titrated
  • goal: gradual, short term reduction of bp over 24-48 hours while patient is being monitored for potential htn related organ damange/symptomatic hypotension in observational hospital setting
  • once achieved BP goal: long term agents can be chose to prevent htn (lisinopril, metoprolol, amlodipine)
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16
Q

treatment for htn emergency

A
  • use iv anti-htn medications
  • these patients are in crisis
  • specific drug recommendations for certain end organ dysfunction
  • need continuous BP monitoring via arterial line
  • acute goal: reduce bp by 10-25% within 1st hour then to goal 160/100 by 2-6 hours
  • preserve brain, kideny, and heart function -> treat clinical symptoms, do not focus on numbers
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17
Q

drugs for dissecting aneurysm

A

nitroprusside + beta blocker

nicardipine +/- beta blocker

labetalol

trimethaphan

avoid direct vasodilators alone (nitroprusside diazoxide, hydralazine)

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18
Q

drugs for pulmonary edema

A

nitroprusside

nitrates

nicardipine

fenoldopam

diuretics

avoid: beta blockers, trimethaphan

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19
Q

drugs for angina/MI (w/o CHF)

A

beta blockers

nitrates

nicardipine

calcium blockers

avoid: direct vasodilators alone, phentolamine

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20
Q

drugs for cerebral hemorrhage

A

no treatment

nitroprusside

nicardipine

avoid: trimethaphan, methyldopa, clonidine

21
Q

drugs for hypertensive encephalopathy

A

nitroprusside

nicardipine

labetalol

fenoldopam

drugs to avoid: methyldopa, clonidine, reserpine, beta blockers

22
Q

drugs for catecholamine excess

A

phentolamine

trimethaphan

nicardipine

nitroprusside + beta blocker

benzodiazepine as adjunct

avoid: beta blockers alone, diazoxide

23
Q

drugs for post operative htn

A

nitroprusside

nicardipine

esmolol

avoid: long acting agents

24
Q

drugs for pre eclampsia

A

labetalol, nicardipine

drugs to avoid: ace inhibitors

25
Q

nipride

A
  • direct acting arterior venous dilator
  • almost immediate onset & rapid termination of action
  • breaks down nitric oxide
  • low dose reductions on SVR may be offset by increase CO
  • dose dependent decrease in cerebral blood flow - can cause increased ICP
  • 40% cyanide metabolized to thiocyanate which is cleared by kidney and is contraindicated in pregnancy & liver failure
26
Q

cyanide toxicity

A
  • tachyphylaxis (increased dose but not working anymore) = important sign of impending toxicity
  • neurological manifestations: hyperpena, headache, vertigo, ams, coma, seizures
  • lab: lactic acidosis, increased base deficit
  • treatment of toxicity: sodium thiosulfate and 3% sodium nitrate
27
Q

nitrates?

A
  • primary venodilator, immediate onset, short duration of action
  • b/c patient is in acute htn crisis and volume depleted, decreasing preload can reduce CO
  • very useful in setting of MI, HTN, CHF, pulmonary edema
  • may cause headache, increased hr, vomiting, elevated icp (increased blood flow leads to increased icp)
  • considerations: tachyphylaxis w/in hours, coronary ischemia
28
Q

nipride vs. nitroglycerin

A
29
Q

calcium channel blockers

A
  • dihydropyridines (-dipines ex: nicardipine, amlodipine)
    • systemic & coronary vasodilation by blocking VGCC’s –> less intracellular Ca+ –> less smooth muscle contraction
  • non-dihydropyridine (verapamil, diltiazem)
    • also blocks Ca+ during plateau phase of action potential during cadiac conduction = negative inotropy & chronotropy (doesn’t really help with SVR)
  • for acute BP control
    • nicardipine is best choice
    • clevidipine - is designer CCB
30
Q

nicardipine

A
  • arterial selective vasodilator
    • significant decrease in SVR
    • cerebral and coronary vasodilator
  • vascular smooth muscle selective
    • minimal myocardial depression
    • no av nodal depression, good in cardiac patients
  • no significant increase in ICP
  • after discontinuation concentration declines rapdily
31
Q

clevidipine

A
  • Ca channel blocker
    • highly selective for vascular smooth muscle
  • no effect on myocardial contractility or conduction
  • faster metabolization than nicardipine
  • concern for hyper-triglyceridemia, so if on it for longer than 72 hours need to follow triglycerides
32
Q

labetalol

A
  • combined a<*** onset 2-5 minutes
  • easy transition to PO
  • paradoxical HTN w/ low doses, b blocking only, unopposed alpha
  • not for use w/ CHF, COPD & cocaine intoxicaiton
    • no beta blockers w/ cocaine**
33
Q

esmolol

A
  • exremely rapid onset & duration of action
  • rapidly metabolized by RBC
  • does not depend on hepatic / renal function for elimination
  • effective in patients who hvae both HTN & tachycardia, safe in patients w/ MI
34
Q

ace inhibitors

A
  • prevent conversion of angiotensin 1 to angiotensin 2
  • few side effects if adjust for renal failure; patient is volume depleted
  • hyperkalemia common; renal artery stenosis, nsaids
  • contraindicated in pregnancy
35
Q

hydralazine

A
  • direct arteriolar vasodilator
  • metabolized hepatic & renal elimenation
  • risk: overshoot, reflex tachycardia, coronary ischemia and aortic dissection worse)
  • long term therapy - risk of lupus like syndrome
36
Q

clonidine

A
  • central acting alpha 2 agonist
  • rebound when discontinued
  • can cause somnolence
  • helpful if htn is associated w/ etoh, narcotics, or nicotine withdrawal d/t somnolence it produces.
37
Q

fenoldopam (corlopam)

A
  • peripheral dopamine agonist, arterial/arteriolar vasodilator
  • onset 5 minutes, duration <10 minutes
  • particularlly effective at dilating renal and coronary afteries,
    • increase renal perfusion & cause naturesis
  • side effects
    • contains sulfite group (allergies)
    • reflex tachycardia is common - don’t combine w/ beta blocker so that you can see the reflex tachycardia
    • headache and increse intraocular pressure
  • issues with overall long term mortality with using this drug - that’s why it’s not really used anymore
38
Q

diuretics?

A
  • most pt’s w/ HTN crisis end up w/ volume depleted
    • diruetics are genreally avoided unless: overt heart failure, pulmonary edema, obvious fluid overload
39
Q

acute ischemic stroke treatment

A
  • may be hypertensive as a result of perfusing past area of ischemia/stenosis
  • goal <220/120 to maintain penumbra
  • unless TPA then goal <185/110, if over this number increase risk for hemorrhage
  • IV nicardipine (no end effects in ICP) or labetalol
40
Q

acute intracranial hemorrhage treatment

A
  • may by hypertensive to perfuse given acute rise in ICP
  • MAP-ICP=CPP (crebreal perfusion pressure)
  • goal CPP>60
    • SBP<160 & monitor clinical symptoms
      • want to get to this goal quickly so don’t bleed in head
  • iv nicardipine, labetalol
  • nimodipine (CCB) in SAH (sub arachnoid hemorrhage) patients, helps prevent vasospasm
41
Q

hypertensive encephalopathy

A
  • neurological dysfunction caused by persistently elevated BP
  • BBB getting leaky and leaking into brain tissue
  • headache is common
  • confusion, somnolence, stupor, numbness, twitching
  • reduce blood pressure over 2-6 hours
  • symptoms resolve w/ resolution of HTN
    • as BBB stops leaking things get better since the extra fluid that shouldn’t be tehre stops coming in
42
Q

treatment for posterior reversible encephalopathy syndrome (PRES)

A
  • symptoms associated w/ occipital lobe only
    • headache, confusion, seizure, vision loss
  • treat the BP & symptoms will resolve
  • recommed nicardipine & clevidipine, labetalol
  • on MRI looks like swollen occipital area, not really seen on CT scan, can hvae somre flare signal chagnes
43
Q

myocardial infarction

A
  • during myocardial ischemia - reducing afterload will decrease wall stress and increase myocardial perfusion
  • caution with nitroprusside - tends to divert blood away from most ischemic areas of the heart
  • labetalol, nicardipine & beta blockers (Beta blocker reduce myocardial O2 consumption)
44
Q

acute pumonary edema

A
  • may need assistance with ventilation until better under control
  • result of excessive LV afterload - usually responds when SVR lowered
  • reduce afterload w/
    • nitropruside
    • nicardipine/clevidipine
  • if MI at same time, NTG is good
  • if volume overloaded, consider diuretics/dialysis
45
Q

aortic dissection

A
  • suspect w/ severe HTN + chest / back pain (could be subtle)
    • arm/leg BP difference, absent LE pulses, asymmetry in BP between arms
    • watch for h/o cocaine use
  • CXR shows widened mediastinum, confirm w/ stat ct chest, mri, aortography
  • treatment:
    • decrease BP asap - forget the rules
    • goal is to decrease shear force
    • beta blocker in conjunction with a vasodilator (nitroprusside / nicardipine) or a mixed beta blocker (labetalol)
    • vascular/cardiac surgery consult
46
Q

renal failure

A
  • may be the cause or result of HTN (glomerulonephritis, vasculitis, RAS)
  • HTN caused kidney injury
    • reversible perfusion related increases BUN & Cr are frequently followed by BP reduction
  • despite BP generally lowering after increase in BUN & Cr, lower the BP
  • labatelol, nicardipine, clevidpine
47
Q

catecholamine excess

A
  • abrupt increase in alpha adrenergic tone (withdrawal of clonidine, phenochromocytoma, cocaine, lsd, maoi crisis)
  • avoid beta blockers
  • IV nicardipine, clevidipine + benzo (especially w/ withdrawal situation)
48
Q

eclampsia

A

iv labetalol or nicardipine & call someone else

Acute Care I - Spring 2017 (10 decks)

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