Transcript Hypertensive-Emergencies

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Ingrid Berling
29/09/2010
 Epidemiology/pathophysiology
 Definitions/common
 Clinical
evaluation
 Goals of treatment
 Pharmacotherapy
 Specific treatment
types
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Prevalence of hypertension in Australia is 11%
An estimated 30% of hypertensive patients are
undiagnosed
29% of diagnosed patients are inadequately controlled
Hypertensive crisis are uncommon, about 1-2% of the
hypertensive population
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It is hypothesized that the final common pathway is a
sudden increase in systemic vascular resistance (SVR) 
an increase in BP due to the action of circulating
vasoconstrictors
The ↑ BP damages the endothelium, leading to the release
of local vasoconstrictors, such as endothelin, which cause
further vasoconstriction
Damage to the endothelium impairs auto-regulatory
function.
Further release of humoral vasoconstrictors perpetuates
the “vicious circle.”
JNC-VII, 2003;
 Normal:
<120 over <80
 Pre-hypertension: 120-139 over 80-89
 Stage I: 140-159 over 90-99
 Stage II: >160 over ≥ 100-109
 Stage III: >180 over >110
JOINT NATIONAL COMMITTEE ON PREVENTION, DETECTION, EVALUATION AND
TREATMENT OF HIGH BLOOD PRESSURE 1997/ 2003
A Hypertensive Emergency exists when acute elevation of
blood pressure is associated with acute and ongoing organ
damage to the kidneys, brain, heart, eyes or vascular system
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Does not specifically include BP levels, but
 Systolic >240mmHg
 Diastolic > 120 - 140mmHg
REQUIRES IMMEDIATE BLOOD PRESSURE REDUCTION
A Hypertensive Urgency exists when there is acute or chronic
blood pressure elevation not associated with any observable
acute organ damage
This can be hard to distinguish on clinical evaluation alone.
BP control over hours to days
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CVS
o Acute MI
o Acute LVF
o Aortic dissection
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SAH
RENAL
o Glomerulonephritis
o Collagen vascular disease
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PREGNANCY
o
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PERIOPERATIVE
o Coronary Bypass
o Carotid endarterectomy
o AAA stenting
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EXCESS CATECHOLAMINES
o Phaeochromocytoma
o withdrawal of anti-hypertensives
o Toxicological
• Interaction: MOAIs
• Ingestions: Cocaine, cold
medications
• Glucocorticoid therapy
CNS
o Hypertensive encephalopathy
o Stroke: Ischaemic, cerebral bleed,
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Pre-eclampsia and Eclampsia
ENDOCRINE
o Phaeochromocytoma crisis
o thyrotoxicosis
Hypertensive emergencies, look like EMERGENCIES.
Therefore your approach is going to be simultaneous
resuscitation and information gathering.
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Cardiovascular
o Chest pain/syncope
o Back pain
o Dyspnoea
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Neurological
o Seizures/altered MS
o Focal weakness
o Headache/visual disturbance
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Renal
o Decreased UO
o Bloody or frothy urine
o Non-specific abdominal pain
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General
o Malaise
MI, unstable Angina, dissection
Dissection
Pulmonary Oedema, CHF
Encephalopathy
CVA/TIA
Central nervous system compromise
 BP
in both arms
 Fundoscopy
examination
 Cardiovascular
examination
 Neurological
examination
HTN Retinopathy (Keith-Wagner)
 Grade I
o Mild arteriolar narrowing and
sclerosis
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Grade II
o Definite focal narrowing and AV
nicking
o Moderate to marked sclerosis of
the arterioles
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Grade III
o Retinal haemorrhages, exudates
and cotton wool spots
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Grade IV
o Severe grade III and papilledema
 FBC;
schistocytes
 Electrolytes;
Urea/creat
 Urinalysis; proteins
 B-hCG
 CXR
 ECG
 Head CT
 ? Urine drug screen
Within 1-2 hrs.
Lower MAP 20-25%
Controlled environment
Use IV titratible meds
MAP = 1/3 SBP + 2/3 DBP
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Lancet, Hypertensive Emergencies,
2000; 356(9227):411-417
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Maintains blood flow to
vital organs, despite
variations in systemic BP
Classically maintained
between MAP 60120mmHg
However, in chronically
hypertensive patients the
curve is shifted to the right
The average lower limit of
auto-regulation is about
20-25% below the resting
MAP.
↓ CO: inhibit contractility or decrease filling pressure
 ↓ filling pressure: Act on venous tone or blood volume
 ↓ PVR: relax smooth muscle of resistance vessels or
interfere with systems that produce constriction (SNS)
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Vasodilators
Adrenergic Inhibitors
NITRATES
 Sodium nitroprusside (SNP)
 Nitroglcerin
α+β BLOCKER
 Labetolol
CALCIUM CHANNEL BLOCKERS
 Nicardipine
β BLOCKER
 Esmolol
ACE INHIBITOR
 Enlaprilat
ARTERIAL VASODILATOR
 Hydralazine
DOPAMINERGIC RECEPTOR AGONIST
 Fenoldopam
DRUG
DOSAGE (IV)
ONSET/DUR
ADV.EFF
Nitroprusside
0.25-10 mcg/kg/min Instant/1-2 min
Cyanide poisoning,
Coronary steel
Nitro-glycerine
5-100mcg/min
1-5 min/ 3-5min
Flushing, headache,
methaemoglobin
Nicardipine
(dihydropyridine)
5-15mg/hr.
5-10min/1-4hr
Reflex tachycardia,
flushing
Hydralazine
10-20mg
5-15min/ 3-8hrs. Flushing, reflex
tachycardia
Enalapril
1.25-5mg IV q6hr
20-30min / 6hrs
Hypotension, renal
failure, hyperkalaemia
DRUG
DOSAGE
ONSET/DUR
Labetalol
(α + β blocker)
20-80mg IV bolus
5-10min/3-6hrs
every 10 mins, 2mg
min IV infusion
Heart block,
Ortho-hypotension
Avoid: heart failure,
asthma
Esmolol
(β1 selective
blocker)
200-500 mcg/kg/min
for 4 mins, then 150300 mcg/kg/min
Hypotension
Avoid: heart failure,
asthma
1-2 mins/ 10-20
min
ADV.EFF
DRUG
DOSAGE
ONSET/DUR
ADV.EFF
Clonidine
0.1-0.2 mg hr.
Up to max 0.8mg
in 24hrs.
30-60min/612hrs.
Sedation
Bradycardia
dry mouth
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α2 agonist-centrally acting
Results in a reduction in sympathetic outflow from the CNS
The decrease in plasma norepinephrine is correlated
directly with the hypotensive effect
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Reduction of BP is at the risk of causing hypo-perfusion of the
peri-ischaemic area, resulting in an extension of the stroke.
However, high BP can cause haemorrhagic transformation of
infarct
A Cochrane review examining 65 RCTs with 11,500 pts.
Concluded that insufficient data exists to evaluate BP lowering
post-stroke
AHA guidelines: BP be reduced only if SBP>220 or
DBP>120mmHg. (unless end-organ damage is due to BP)
Labetalol and nitroprusside are agents of choice.
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Thrombolysis  BP<185/110. (increased risk intracranial bleeding)
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No strong evidence for blood pressure management in
intracerebral haemorrhage. In trials, nil adverse events
from BP reduction of less than 20%
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Guidelines: decrease when MAP>130 or SBP>220.
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Labetalol and esmolol agents of choice.
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DO NOT use nitrates as they theoretically increase ICP
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Nimodipine decreases vasospasm that occurs due to
chemical irritation of arteries by blood.
Not recommended routinely due to high incidence of
hypotension.
Guidelines suggest SBP< 160 MAP <110
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Labetalol and esmolol agents of choice.
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The aim is to reduce myocardial work and promote coronary
blood flow, thus reducing ischaemia.
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IV GTN agent of choice
(β-Blockers)
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Avoid hydralazine, as it increases myocardial oxygen
demand.
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Usually associated with pulmonary oedema and
diastolic/systolic dysfunction.
Titrate until BP controlled and signs of heart failure
alleviated.
IV nitroprusside and GTN agents of choice.
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Symptoms:
o Mental status change – somnolence, confusion, lethargy, stupor,
coma, seizure
o Headache –
o Nausea and vomiting
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Hypertensive encephalopathy is a diagnosis of exclusion –
thus, exclude the other possibilities!
Only definitive criteria is a favourable response to BP
reduction.
However clinical improvement may lag behind BP
improvement by hours to days
Agent of choice – SNIP or labetalol
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Worsening of the dissection dependent on:
o Level of elevated BP
o Slope of the pulse wave. This increases the “shear force” on the
dissection, leading to propagation of the dissection
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Goal is to reduce both the BP and the slope of the pulse wave!
BP goal is SBP of 100-120
If patient presents with normal BP, still need to decrease the shear
forces!!
Labetalol
IV SNIP + B-blocker!!
o Do not use alone, as vasodilation causes reflex activation of SNS leading to
enhanced ventricular contraction and increased aortic shear stress
Do not use hydralazine, increased shear stress
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Labetalol traditional agent of choice, but experimental
studies not positive for use.
Nicardipine (or phentolamine in older texts) choice agent
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β-blocker - May be added to control tachycardia
Not for use as sole agent – as may result in β-receptor
antagonism and unopposed α adrenergic activity - ↑BP
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Benzodiazepines - May be helpful in cocaine/amphetamine
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Hypertensive
encephalopathy
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Embolic CVA
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Hemorrhagic CVA
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SAH
Nitroprusside, goal
~25 reduction
 Only if >220/120
or>185/110 for t-PA
 Labetalol for ~10-20%
reduction
 Nimodipine 60 mg
Q4hrs x 21 days
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Aortic dissection
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Acute LV failure
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Acute coronary
syndrome
Nitroprusside +
Esmolol or Labetalol –
SBP ~100
 NTG, Lasix, MS04 for
symptoms and ~1015% reduction
 NTG, MgS04, betablocker for symptom
improvement
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Eclampsia and HELLP
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Goal DBP ~90;
magnesium,
hydralazine, labetalol,
delivery!
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Catecholamine excess
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labetolol for ~25%
reduction over several
hours
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3 quick questions
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A. Aortic dissection
B. Thrombo-embolic CVA
C. Hemorrhagic CVA
D. Subarachnoid hemorrhage
E. Hypertensive encephalopathy
In all the other scenarios, such a precipitous drop in BP is
likely to worsen outcome
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A. Aortic dissection – esmolol + SNIP
B. Aortic dissection – labetalol
C. Eclampsia – magnesium +/- hydralazine
D. Pheochromocytoma – esmolol
E. Acute LV failure - NTG
Although use of Labetalol is controversial and possibly
indicated, a pure beta-blocker like esmolol is grossly
inappropriate in emergencies caused by catecholamine
excess.
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A. Persistent BP >185/110 is a contraindication to
thrombolytics
B. Hemorrhagic CVAs tend to have higher BP than embolic
C. Lowering the BP in the acute setting may worsen
outcome
D. If BP needs lowering in hemorrhagic CVA, SNIP is the
agent of choice
Nipride and other vasodilators are relatively contraindicated in
hemorrhagic CVA as they may worsen ICP.
Labetalol is the agent of choice IF BP needs to be lowered
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1. Hoshide, S., et al., Hemodynamic cerebral infarction triggered by
excessive blood pressure reduction in hypertensive emergencies.
Journal of the American Geriatrics Society, 1998. 46(9): p. 1179-80.
2. Kitiyakara, C. and N.J. Guzman, Malignant hypertension and
hypertensive emergencies. Journal of the American Society of
Nephrology, 1998. 9(1): p. 133-42.
3. Epstein, M., Diagnosis and management of hypertensive
emergencies. Clinical Cornerstone, 1999. 2(1): p. 41-54.
4. Kriegisteiner, S., et al., Hypertensive emergencies. Lancet, 2000.
356(9239): p. 1443.
5. Mansoor, G.A. and W.H. Frishman, Comprehensive management
of hypertensive emergencies and urgencies. Heart Disease, 2002. 4(6):
p. 358-71.
6. Vaughan, C.J. and N. Delanty, Hypertensive emergencies. Lancet,
2000. 356(9227): p. 411-7.