Transcript Hypertensive Emergencies - Calgary Emergency Medicine

Hypertensive
Emergencies
Alyssa Morris, R3
March 5, 2009
Thanks to Dr Gant!
Definitions
 Hypertensive 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 SVR
CO= HR x SV
Think of the components as:
• CO= heart
• BP= arteries
• SVR= arterioles
CPP=MAP-ICP
CASE 1
Hypertensive Encephalopathy
 Uncommon syndrome
 Acute and reversible
 Results 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 Presentation
 Severe h/a
 Drowsiness
 ALOC
 Vomitting
 Seizures
 Focal 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 Options
 VASODILATORS
 CALCIUM CHANNEL
• Nitroprusside
BLOCKERS
• Nitroglycerin
• Enalaprilat/enalipril
• Fenoldopam
 ALPHA BLOCKERS
• Hydralazine
• Phentolamine
 BETA BLOCKERS
• Labetalol
• Esmolol
• 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
Nitroglycerine
1) 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
Labetalol
 Selective α-1 blocker and nonselective β-blocker
 α:β blockade ratio between 1:3 and 1:7
 Not a significant drop in CO like other βB
 Does not affect cerebral blood flow or renal fxn
 BP starts to fall in 5-10m, max effect at 30m
 How 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 agent
 Used for the Mx of catecholamine-induced HTV
crisis
 MAOI, Pheo, Cocaine
 Immediate effect
 Effect lasts up to 15 mins
 1-5mg IV boluses
CASE 2
PRES
 Posterior reversible encephalopathy syndrome
 Pathophysiology
Cerebral vasospasm leading to cytotoxic edema
2. Vasodilattion leading to vasogenic edema
1.
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
stroke
 For 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 decision
 More 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 study
Hemorrhage 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) Cerebellum
2) Pons
3) Basal ganglia
4) 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 esmolol
 Can use nipride after have sufficiently BB b/c will blunt
the reflex tachycardia and increased SV
Case 6
Drug Summary
 Nitroprusside
• 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