Module 11: Hypertensive Urgency & Emergency

Question 1

hypertensive urgency

Answer 1

sbp>180 and/or DBP >110

Question 2

hypertensive emergency

Answer 2

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

Question 3

etiology of hypertensive urgency

Answer 3

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)

Question 4

causes of hypertensive emergency

Answer 4

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

Question 5

what is the physiology of hypertensive urgency/emergency?

Answer 5

-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

Question 6

physiology pathway

Answer 6

shear stress –> endothelial dysfunction –> end organ effect

Question 7

RAAS?

Answer 7

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

Question 8

myocardial autoregulation

Answer 8

Question 9

cerebral autoregulation?

Answer 9

Question 10

exam & ROS for hypertensive emergency

Answer 10

• 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?

Question 11

drugs that may precipitate a htn emergency

Answer 11

oral contraceptives

maoi

tca

steroids

nsaid

nasal decongestatns

cold remedies

appetitie suppressants

Question 12

what should be on a focused physical exam?

Answer 12

• 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

Question 13

what diagnostics should you order?

Answer 13

• 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)
    *

Question 14

how to treat?

Answer 14

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

Question 15

treatment of htn urgency

Answer 15

• 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)

Question 16

treatment for htn emergency

Answer 16

• 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

Question 17

drugs for dissecting aneurysm

Answer 17

nitroprusside + beta blocker

nicardipine +/- beta blocker

labetalol

trimethaphan

avoid direct vasodilators alone (nitroprusside diazoxide, hydralazine)

Question 18

drugs for pulmonary edema

Answer 18

nitroprusside

nitrates

nicardipine

fenoldopam

diuretics

avoid: beta blockers, trimethaphan

Question 19

drugs for angina/MI (w/o CHF)

Answer 19

beta blockers

nitrates

nicardipine

calcium blockers

avoid: direct vasodilators alone, phentolamine

Question 20

drugs for cerebral hemorrhage

Answer 20

no treatment

nitroprusside

nicardipine

avoid: trimethaphan, methyldopa, clonidine

Question 21

drugs for hypertensive encephalopathy

Answer 21

nitroprusside

nicardipine

labetalol

fenoldopam

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

Question 22

drugs for catecholamine excess

Answer 22

phentolamine

trimethaphan

nicardipine

nitroprusside + beta blocker

benzodiazepine as adjunct

avoid: beta blockers alone, diazoxide

Question 23

drugs for post operative htn

Answer 23

nitroprusside

nicardipine

esmolol

avoid: long acting agents

Question 24

drugs for pre eclampsia

Answer 24

labetalol, nicardipine

drugs to avoid: ace inhibitors

Question 25

nipride

Answer 25

* 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

Question 26

cyanide toxicity

Answer 26

* 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

Question 27

nitrates?

Answer 27

* 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

Question 28

nipride vs. nitroglycerin

Answer 28

Question 29

calcium channel blockers

Answer 29

* 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

Question 30

nicardipine

Answer 30

* 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

Question 31

clevidipine

Answer 31

* 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

Question 32

labetalol

Answer 32

* 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**

Question 33

esmolol

Answer 33

* 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

Question 34

ace inhibitors

Answer 34

* 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

Question 35

hydralazine

Answer 35

* 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

Question 36

clonidine

Answer 36

* 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.

Question 37

fenoldopam (corlopam)

Answer 37

* 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

Question 38

diuretics?

Answer 38

* most pt's w/ HTN crisis end up w/ volume depleted * diruetics are genreally avoided unless: overt heart failure, pulmonary edema, obvious fluid overload

Question 39

acute ischemic stroke treatment

Answer 39

* 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

Question 40

acute intracranial hemorrhage treatment

Answer 40

* 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

Question 41

hypertensive encephalopathy

Answer 41

* 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

Question 42

treatment for posterior reversible encephalopathy syndrome (PRES)

Answer 42

* 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

Question 43

myocardial infarction

Answer 43

* 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)

Question 44

acute pumonary edema

Answer 44

* 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

Question 45

aortic dissection

Answer 45

* 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

Question 46

renal failure

Answer 46

* 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

Question 47

catecholamine excess

Answer 47

* 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)

Question 48

eclampsia

Answer 48

iv labetalol or nicardipine & call someone else