Management of acute hypertension 

Hypertensive Urgency
- >180/110 without target organ dysfunction
- ha, sob, epistaxis
- manage with oral agents
- often precipitated by medication non adherence, high salt load ("I ate a bunch of Chinese food"), missing dialysis

Hypertensive Emergency
- cerebral blood flow is constant at a MAP of 60-120 - outside of that, autoregulation fails
- at high perfusion pressures -- shear stress on endothelium, platelet aggregation (leading to MI, HF, stroke, DIC/MAHA etc) - fibrinoid material in vascular wall, increased permeability, thrombosis.

Management
- Immediate: 15-20% reduction (or map 100-120)
- Over next 2-6 hours: Goal 160/100
- exception: ischemic strokes - goal higher BP (permissive to 220/120)
- exception: aortic dissection - goal SBP < 100, goal HR < 60, so beta-blocker gtt i.e. esmolol -- believed that tachycardia is what's causing the shear stress against aorta, so should get HR down first (i.e. dont give hydralazine without having b-blocker on board). Avoid nicardipine as it can cause reflex tachycardia without a b-blocker on board.
- acute MI/CVA - can't give thrombolytics if SBP > 185
- acute HF - don't drop SBP < 120

Blood pressure in ischemic stroke
- 85% of people who have a stroke have HTN - often transient. May be 2/2 the body's response to increase CPP, stress, autonomic dysregulation.
- Bradycardia (possible increased CPP), deep T wave inversions
- First 24-48 hrs after stroke, cerebral autoregulation in penumbra is lost - area is vulnerable. I.e. brain is reliant on CPP to perfuse. If you can maintain perfusion to that area, you can save it.
- American stroke association: treat BP in first 48 hrs only if SBP > 220, DBP > 120, unless you're giving lytics - goal SBP ~ 185
- Fluids and pressors to maintain pressures in first 48 hours

IV antihypertensive agents
- Nipride - arterial and venodilator, onset 1-2 mins, lasts 3-4 mins. limitations: can worsen cerebral edema, cyanide and thioocyanate toxicity (in pts with renal and hepatic failure) - signs of CN toxicity: venous hyperoxemia, lactic acidosis, signs of TCN tox: abdominal pain, AMS, seizures
- Nicardipine - onset 5-15 mins, lasts 4-6 hrs, lim: reflex tachycardia, longer half life - must couple with b-blocker esp in dissection
- Clevidipine - on 2-4 mins, lasts 5-15 mins, 3rd gen dihydropyridine CCB, can't be used in people with egg allergies
- Fenoldopam - DA agonist, onset < 5 mins, lasts 30-60 mins - CI in glaucoma
- Labetaolol - alpha and b-blocker (ratio 1:7) onset 2-5 mins, lasts 24 hrs, limitations: heart block, CHF, bronchospasm, bradycardia - don't use in acute HF as its a negative inotrope, good in pregnancy as minimal placental transfer
- Esmolol - on 1-2 mins, lasts 10-20 mins (T-1/2 : 9 mins) Same limitations as labetalol - plus its a 60cc/hr drip so don't use in ppl who are volume overloaded. Also esmolol drip = ICU stay.
- Phentolamine - a blocker - use to treat htn 2/2 catechol surge like pheo, cocaine
- Nitro - venodilator (some arterial dilation at high doses) - reflex TA, HA, tolerance. Used in ACS.
- Enalaprilat - IV ACE, on 15-30 mins, lasts 6 hrs, limitations: can cause precipitous drop in BP (may explain why outcomes worse in HF) variable response.
- Hydralazine - peripheral vasodilator from direct sm mm relaxation - onset 5-15 mins, lasts up to 12 hours (often way less). Limitations: prolonged and unpredictiable effects, reflex tachycardia. Used often in pregnancy.
- Lasix - reduce volume overload

Avoid:
- ACE-I in acute MI, pregnancy, bilateral RAS
- IV B-blockers in acute HF, reacitive airway dx
- SL nifedipine - big drop in BP