Hypertensive Emergencies

Alyssa Morris, R3March 5, 2009

Thanks to Dr Gant!

DefinitionsHypertensive Emergency• Acute, life threatening, usually a BP>

180/120• Target organ damage

Hypertensive Urgency• Asymptomatic, severe HTN, usually

>180/120• NO target organ damage

Hypertensive Emergencies

Neurological • Hypertensive

Encephalopathy

• CVA• SAH• ICH

Cardiovascular• MI/ischemia• Acute LV dysfxn• Ao dissection

Pulmonary• Acute edema

Other• Acute renal

failure/insufficiency

• Retinopathy• Eclampsia• MAHA

Components of BP

BP= CO x SVRCO= HR x SV

Think of the components as: • CO= heart• BP= arteries• SVR= arterioles

CPP=MAP-ICP

CASE 1

Hypertensive Encephalopathy

Uncommon syndromeAcute and reversibleResults from an abrupt, sustained

rise of BP that exceeds the limits of cerebral autoregulation of the small resistance arteries in the brain

Arises from “breakthrough” hyperperfusion and leakage of fluid thru BBB

Clinical PresentationSevere h/aDrowsinessALOCVomittingSeizuresFocal neuro deficits Blindness

Tx

Various recommendations 25% over 3-4hrs 10% in first hour, 15% in next 2-3 hours

*will not be able to perfuse brain if you drop it too fast or too much

CPP=MAP-ICP

Drug OptionsVASODILATORS• Nitroprusside• Nitroglycerin• Fenoldopam• Hydralazine

BETA BLOCKERS• Labetalol• Esmolol

CALCIUM CHANNEL BLOCKERS• Enalaprilat/

enaliprilALPHA BLOCKERS• Phentolamine • Clonidine

Nitroprusside Potent smooth muscle relaxing agent Reduces both preload and afterload Rate of onset rapid, duration very short Also a cerebral vasodilator

Can increase ICP secondary to increased cerebral blood flow

Unstable in UV light, therefore wrapped in tinfoil

Infusion at 0.25-0.5ug/kg/min -then increase by 0.5mcg/kg/min Max of 10 mcg/kg/min

Nitroglycerine1) Activates guanylate cyclase

2) Accumulation of cGMP

3) Sequestration of Ca into SR

4) Relaxation of Vascular smooth muscle Dose dependent

Low dose: venodilator (preload) High dose: veno and arteriodilator (afterload) Therefore, usually reduce BP by reducing

preload and CO Start with 10-20ug/min infusion Titrate up 5-10ug/minQ3-5min

Hydralazine Direct arteriolar vasodilator Used to be used as first line in pregnancy htv

emergencies Starting dose is 5mg IV Repeat doses of 5-10mg IV every 20 mins to

maintain desired BP Complications:• Marked hypotension • Reflex tachycardia (can give angina)• Flushing and nausea• H/a

LabetalolSelective α-1 blocker and nonselective β-

blockerα:β blockade ratio between 1:3 and 1:7Not a significant drop in CO like other βBDoes not affect cerebral blood flow or

renal fxnBP starts to fall in 5-10m, max effect at

30mHow much do you guys give?

Esmolol Selective β-1 blocker Very short acting Elimination ½ life of 9 minutes No intrinsic sympathomimetic activity

Phentolamine α-blocking agentUsed for the Mx of catecholamine-

induced HTV crisisMAOI, Pheo, Cocaine

Immediate effectEffect lasts up to 15 mins1-5mg IV boluses

CASE 2

PRES

Posterior reversible encephalopathy syndrome

Pathophysiology1. Cerebral vasospasm leading to cytotoxic

edema2. Vasodilattion leading to vasogenic edema

CASE 3

HTN Mx in Ischemic Stroke

Stroke. 2007;38:1655-1711.

HTN Mx in Ischemic Stroke

HTN common in 1st hours after stroke• SBP>160 found in 60% pts with

acute ischemic strokeFor every 10mmHg raise >180, risk of

neurologic deterioration increases by 40% and risk of poor outcome by 23%

HTN Mx in Ischemic Stroke

Theoretical reasons for lowering BP in stroke• Decrease formation of brain edema• Lessening risk of hemorrhagic

transformation of infarction• Preventing further vascular damage• Forestalling early recurrent stroke

BUT remember aggressive tx of BP may lead to neurologic worsening by decreasing perfusion pressure to ischemic areas of brain

CPP=MAP-ICP

CASE 4

HTN Mx in Ischemic Stroke

A lot of studies showing harm with reduction of BP

Most pts have a decrease in BP a few hours post-stroke w/o intervention

Oliveira-Filho et al. Neurology. 2003;61:1047-1051• Found >90% pts had a decrease in

SBP by 28% in 24hrs post-stroke with no intervention

Consensus Statement“ emergency administration of

antihypertensive agents should be withheld unless DBP>120 and SBP>220”

“reasonable goal to decrease blood pressure by 15-25% within 24 hours”

This is a case-by-case decisionMore research needs to be done

Case 4

Stroke, 2007;38:2001-2023

HTN Mx in Hemorrhagic Stroke

Primary rational for reducing BP is to avoid hemorrhagic expansion from potential sites of bleeding

BP is correlated with increased ICP and volume of hemorrhage

Difficult to determine whether increased BP is a cause of hemorrhage growth or an effect of increased volumes of ICH and increased ICP

HTN Mx in Hemorrhagic Stroke

Summary of studies Isolated SBP<210 is not clearly related to

hemorrhagic expansion or neurologic worsening Decrease in MAP by 15% does not result in

decreased CBF Baseline BP was not associated with growth of

ICH in largest prospective studyHemorrhage enlargement occurs more

frequently in pts with increased SBP but it is not clear if this is an effect of increased growth of ICH with associated increase in ICP or a contributing cause to the growth of ICH

Evidence supports maintaining CPP >60mmHg

HTN Bleeds

Where do you get HTN bleeds in the brain?1)Cerebellum2)Pons3)Basal ganglia4)Thalamus

Case 4

HTN Mx in Ao Dissection

Remember to check BP in legs if you are thinking dissection b/c the flap can give you falsely low BP in arms

Want to avoid shear stress and wide pulse pressures Reduce the LV ejection force

Goal is to get SBP 90-110 but just do what you can

Use labetalol or esmololCan use nipride after have sufficiently BB b/c will

blunt the reflex tachycardia and increased SV

Case 6

Drug SummaryNitroprusside• 0.25-0.5ug/kg/min• Inc by 0.5ug/kg/min quickly

Nitro• 10-20ug/min• Inc by 5-10ug/min Q3-10min

Labetalol• 10-20mg IV Q5-10min• Infusion at 1-2mg/min