Hypertensive Crisis/Urgency/Emergency Flashcards
Definition of hypertensive crisis
SBP >180mmHg, DBP >120mmHg, or both
Definition of hypertensive urgency
acute condition of very high BP without evidence of new or worsening target organ damage
Definition of hypertensive emergency
acute condition of very high BP and evidence of new or worsening target organ damage
End-organ dysfunction: CV system
acute pulmonary/flash pulmonary edema, acute LV dysfunction, acute MI
End-organ dysfunction: neurological
hypertensive encephalopathy, acute intracranial bleeding, cerebral infarction, seizures
End-organ dysfunction: vascular system
acute aortic dissection, eclampsia/preeclampsia
End-organ dysfunction: renal
AKI
End-organ dysfunction: liver
elevated function tests, acute liver failure
End-organ dysfunction: other
Retinopathy, retinal hemorrhage
Risk factors for hypertensive crisis
Female, obesity, hypertensive/coronary heart disease, presence of a somatoform disorder, higher number of antihypertensive agents at baseline
Common causes of hypertensive crisis
Non-adherence
Abrupt withdrawal of certain antihypertensives → rebound HTN: Clonidine, beta-blockers
Substance abuse: Cocaine, amphetamines, ecstasy
DDIs: Serotonin syndrome
Drug-food interactions: Tyramine containing foods with MAOIs
Drug-disease state interactions: NSAIDs, sympathomimetics in patients with HTN
Withdrawal: alcohol, opioids, BZDs
Clinical presentation of hypertensive crisis
May appear asymptomatic (urgency) or with evidence of target organ damage (hypertensive emergency)
Symptoms of hypertensive crisis
HA, N/V, epistaxis, SOB, chest pain, dizziness, paresthesia, vision changes
Signs of hypertensive crisis
focal neurological deficits, crackles on lung auscultation, increased SCr/BUN, LFTs, new/worsening hematuria/proteinuria, EKG changes, changes on fundoscopic examination of the eye, changes on CT of the head (bleed), MRI evidence of CVA
Timing of BP lowering in hypertensive urgency
Lower BP slowly over 24-48 hours using PO medication, no need for ICU admission
Timing of BP lowering in hypertensive emergency: 1st hour
decrease DBP by 10-15% or MAP by 25% with a goal DBP ≥100mmHg
Timing of BP lowering in hypertensive emergency: hours 2-6
SBP 160mmHg and/or DBP 100-110mmHg
Timing of BP lowering in hypertensive emergency: hours 6-24
Maintaining above goals from the first 6 hours
Timing of BP lowering in hypertensive emergency: hours 24-48
gradually decrease BP to normal outpatient goal
Special considerations: aortic dissection
SBP ≤120mmHg within first hour, ideally the first 20 minutes (and HR <60 BPM)
Aortic dissection treatment
Esmolol, then a vasodilator (nicardipine, clevidipine, nitroprusside)
Special considerations: ischemic stroke
tPA: BP <185/110 before tPA and <180/105 during tPA infusion
No tPA: SBP <220mmHg
Treatment for ischemic stroke
Nicardipine, clevidipine, labetalol
Avoid sodium nitroprusside
Special considerations: hemorrhagic stroke
SBP >220mmHg: lower with infusion and monitor
SBP 150-220 mmHg: <140mmHg in 60 minutes
Treatment for hemorrhagic stroke
Same as ischemic stroke
Special considerations: severe preeclampsia or eclampsia
SBP <140mmHg in 60 minutes
Preeclampsia/eclampsia treatment
Hydralazine, labetalol, nicardipine
AVOID RAAS INHIBITORS AND SODIUM NITROPRUSSIDE
Vasodilators used in hypertensive crisis/emergency
Sodium nitroprusside, NTG, hydralazine
Sodium nitroprusside MoA
Breaks down into NO → relaxation/dilation of smooth muscle
Direct venous and arterial vasodilator
Onset of sodium nitroprusside
<2 mins
Duration of sodium nitroprusside
1-10 minutes
Sodium nitroprusside dosing
0.25-10mcg/kg/min
Sodium nitroprusside ADEs
Potent hypotension, N/V, muscle twitching
Cyanide toxicity; accumulation occurs most commonly at higher doses (>2mcg/kg/min) and longer treatment duration
Sodium nitroprusside pearls
Caution in high intracranial pressure, azotemia, CKD
NTG MoA
NTG converted into NO → activates guanylate cyclase → increase of cGMP in smooth muscle → dephosphorylation of myosin light chains → vasodilation
NTG onset
Immediate
NTG duration
3-5 mintues
NTG dosing
5-200mcg/min IV infusion
NTG ADEs
Hypotension, HA, methemoglobinemia, tolerance with prolonged use
NTG pearl
Most often used in situations with coronary ischemia
Hydralazine MoA
Direct-acting smooth muscle relaxant and acts as a vasodilator primarily in the smooth muscle of the arterial bed
Hydralazine onset
10-80 minutes
Hydralazine duration
Up to 12 hours
Hydralazine dosing
IV bolus: 10-20mg IV q4-6h
Hydralazine ADEs
Hypotension, tachycardia, flushing, HA
Hydralazine pearls
Concern with unpredictable PK profile → difficult to assess what the effect will be and how long it will last
Safe in pregnancy
Beta-blockers used in hypertensive emergency
Labetalol, metoprolol, esmolol
Beta-blocker MoA
Competitively block the binding of NE and epinephrine to beta-adrenergic receptors
Beta-blocker ADEs
Hypotension, bradycardia/heart block
Labetalol-specific ADE
orthostatic hypotension
Labetalol onset
5-10 minutes
Labetalol duration
180-360 mins
Labetalol dosing
Bolus: 10-20mg IV q10min
Infusion: 0.5-2mg/min
Labetalol pearls
Used in most HTN emergencies
Safe in pregnancy
Caution in acute HF
Metoprolol onset
5-20 minutes
Metoprolol duration
120-360 mins
Metoprolol dosing
Bolus: 5-15mg IV q5-15min
Metoprolol pearl
Caution in acute HF
Esmolol onset
1-2mins
Esmolol duration
10-20mins
Esmolol dosing
Bolus: 250-500mcg/kg/min
Infusion: 50-100 mcg/kg/min
Esmolol pearls
Drug of choice in aortic dissection
Caution in acute HF
CCBs used in hypertensive emergency
Clevidipine, nicardipine
CCBs MoA
Bind to and block voltage-gated L-type calcium channels found on smooth muscle cells of arterial vessels → vasodilation
Clevidipine onset
2-4 mins
Clevidipine duration
5-15 mins
Clevidpine dosing
1-2mg/hr infusion
Clevidipine ADEs
Hypotension, HA, tachycardia, hypertriglyceridemia (lipid formulation)
Clevidipine pearls
Most hypertensive emergencies
Caution in coronary ischemia
CI’ed in soy/egg allergy
Nicardipine onset
5-10mins
Nicardipine duration
15-30 minutes
Nicardipine dosing
2.5-5mg/hr
Nicardipine ADEs
Hypotension, tachycardia, HA, flushing, local phlebitis
Nicardipine pearls
Most hypertensive emergencies
Not generally utilized in acute HF
Caution with coronary ischemia