Hypertensive Emergencies
Transcript of Hypertensive Emergencies
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Hypertensive Emergencies
Ingrid Berling29/09/2010
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Aims
Epidemiology/pathophysiology
Definitions/common types Clinical evaluation Goals of treatment Pharmacotherapy Specific treatment
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Epidemiology
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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Pathophysiology
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Pathophysiology 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.”
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Hypertension
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
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DefinitionsA 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
Does not specifically include BP levels, but Systolic >240mmHg
Diastolic > 120 - 140mmHg
REQUIRES IMMEDIATE BLOOD PRESSURE REDUCTION
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DefinitionsA 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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Most Common Presentations
CVSo Acute MIo Acute LVFo Aortic dissection
CNSo Hypertensive encephalopathyo Stroke: Ischaemic, cerebral
bleed, SAH RENAL
o Glomerulonephritiso Collagen vascular disease
PREGNANCYo Pre-eclampsia and Eclampsia
ENDOCRINEo Phaeochromocytoma crisiso thyrotoxicosis
PERIOPERATIVE o Coronary Bypasso Carotid endarterectomyo AAA stenting
EXCESS CATECHOLAMINESo Phaeochromocytomao withdrawal of anti-
hypertensiveso Toxicological
• Interaction: MOAIs• Ingestions: Cocaine,
cold medications• Glucocorticoid therapy
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Clinical EvaluationHypertensive emergencies, look like EMERGENCIES.
Therefore your approach is going to be simultaneous resuscitation and information
gathering.
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History Cardiovascular
o Chest pain/syncopeo Back paino Dyspnoea
Neurologicalo Seizures/altered MSo Focal weaknesso Headache/visual disturbance
Renalo Decreased UOo Bloody or frothy urineo Non-specific abdominal pain
Generalo Malaise
MI, unstable Angina, dissectionDissectionPulmonary Oedema, CHF
EncephalopathyCVA/TIACentral nervous system compromise
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Examination
BP in both arms Fundoscopy
examination Cardiovascular
examination Neurological
examination
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RetinopathyHTN Retinopathy (Keith-Wagner) Grade I
o Mild arteriolar narrowing and sclerosis
Grade IIo Definite focal narrowing and
AV nickingo Moderate to marked sclerosis
of the arterioles Grade III
o Retinal haemorrhages, exudates and cotton wool spots
Grade IVo Severe grade III and
papilledema
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Investigations FBC; schistocytes Electrolytes;
Urea/creat Urinalysis; proteins B-hCG CXR ECG Head CT ? Urine drug screen
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Goals of Treatment
Within 1-2 hrs. Lower MAP 20-25%
Controlled environmentUse IV titratible meds
MAP = 1/3 SBP + 2/3 DBP
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WHY? Auto-regulation
Maintains blood flow to vital organs, despite variations in systemic BP
Classically maintained between MAP 60-120mmHg
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.
Lancet, Hypertensive Emergencies, 2000; 356(9227):411-417
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Treatment
↓ 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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PharmacotherapyVasodilators
NITRATES Sodium nitroprusside (SNP) Nitroglcerin
CALCIUM CHANNEL BLOCKERS Nicardipine
ACE INHIBITOR Enlaprilat
ARTERIAL VASODILATOR Hydralazine
DOPAMINERGIC RECEPTOR AGONIST Fenoldopam
Adrenergic Inhibitors
α+β BLOCKER Labetolol
β BLOCKER Esmolol
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VasodilatorsDRUG 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
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Adrenergic Inhibitors
DRUG DOSAGE ONSET/DUR
ADV.EFF
Labetalol(α + β blocker)
20-80mg IV bolus every 10 mins, 2mg min IV infusion
5-10min/3-6hrs Heart block,Ortho-hypotensionAvoid: heart failure, asthma
Esmolol(β1 selective blocker)
200-500 mcg/kg/min for 4 mins, then 150-300 mcg/kg/min
1-2 mins/ 10-20 min
HypotensionAvoid: heart failure, asthma
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Clonidine
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
DRUG DOSAGE ONSET/DUR ADV.EFF
Clonidine 0.1-0.2 mg hr.Up to max 0.8mg in 24hrs.
30-60min/6-12hrs.
SedationBradycardiadry mouth
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Specific situations….
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Ischaemic Stroke 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.
Thrombolysis BP<185/110. (increased risk intracranial bleeding)
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Haemorrhagic Stroke No strong evidence for blood pressure management
in intracerebral haemorrhage. In trials, nil adverse events from BP reduction of less than 20%
Guidelines: decrease when MAP>130 or SBP>220.
Labetalol and esmolol agents of choice.
DO NOT use nitrates as they theoretically increase ICP
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SAH 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
Labetalol and esmolol agents of choice.
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Myocardial Ischaemia The aim is to reduce myocardial work and
promote coronary blood flow, thus reducing ischaemia.
IV GTN agent of choice (β-Blockers)
Avoid hydralazine, as it increases myocardial oxygen demand.
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Acute LV Failure 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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Hypertensive Encephalopathy
Symptoms: o Mental status change – somnolence, confusion, lethargy,
stupor, coma, seizureo Headache –o Nausea and vomiting
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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Aortic Dissection Worsening of the dissection dependent on:
o Level of elevated BPo Slope of the pulse wave. This increases the “shear force” on the
dissection, leading to propagation of the dissection
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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Catecholamine excess Labetalol traditional agent of choice, but
experimental studies not positive for use. Nicardipine (or phentolamine in older texts) choice
agent
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
Benzodiazepines - May be helpful in cocaine/amphetamine
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Summary – Neurologic emergencies
Hypertensive encephalopathy
Embolic CVA
Hemorrhagic CVA
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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Summary – Cardiovascular
emergency Aortic dissection
Acute LV failure
Acute coronary syndrome
Nitroprusside + Esmolol or Labetalol – SBP ~100
NTG, Lasix, MS04 for symptoms and ~10-15% reduction
NTG, MgS04, beta-blocker for symptom improvement
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Summary – Other emergencies
Eclampsia and HELLP
Catecholamine excess
Goal DBP ~90; magnesium, hydralazine, labetalol, delivery!
labetolol for ~25% reduction over several hours
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Scenarios3 quick questions
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1. In which of the following would a SBP of 100-120 be
appropriate?
A. Aortic dissection B. Thrombo-embolic CVA C. Hemorrhagic CVA D. Subarachnoid hemorrhage E. Hypertensive encephalopathy
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A. Aortic dissection
In all the other scenarios, such a precipitous drop in BP is likely to worsen outcome
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2. Which emergency – medication is LEAST appropriate?
A. Aortic dissection – esmolol + SNIP B. Aortic dissection – labetalol C. Eclampsia – magnesium +/- hydralazine D. Pheochromocytoma – esmolol E. Acute LV failure - NTG
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D. Pheochromocytoma - esmolol
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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3. All the following regarding CVAs are true EXCEPT:
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
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D. If BP needs lowering in hemorrhagic CVA, Nipride 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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References 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.