Hypertensive Emergencies

Hypertensive Emergencies

Ingrid Berling29/09/2010

Aims

Epidemiology/pathophysiology

Definitions/common types Clinical evaluation Goals of treatment Pharmacotherapy Specific treatment

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

Pathophysiology

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.”

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

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

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

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

Clinical EvaluationHypertensive emergencies, look like EMERGENCIES.

Therefore your approach is going to be simultaneous resuscitation and information

gathering.

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

Examination

BP in both arms Fundoscopy

examination Cardiovascular

examination Neurological

examination

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

Investigations FBC; schistocytes Electrolytes;

Urea/creat Urinalysis; proteins B-hCG CXR ECG Head CT ? Urine drug screen

Goals of Treatment

Within 1-2 hrs. Lower MAP 20-25%

Controlled environmentUse IV titratible meds

MAP = 1/3 SBP + 2/3 DBP

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

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)

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

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

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

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

Specific situations….

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)

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

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.

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.

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.

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

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

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

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

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

Summary – Other emergencies

Eclampsia and HELLP

Catecholamine excess

Goal DBP ~90; magnesium, hydralazine, labetalol, delivery!

labetolol for ~25% reduction over several hours

Scenarios3 quick questions

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

A. Aortic dissection

In all the other scenarios, such a precipitous drop in BP is likely to worsen outcome

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

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.

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

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

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.