Hypertensive

Emergencies Jason R. Frank MD MA(Ed) FRCPC

Dept of Emergency Medicine

Case 1

Case 1

• 82 yo female• CC: acute onset severe

headache, n/v• Noted by family to be confused• Denies trauma• PMHx: HTN, elevated

cholesterol

Your Assessment

• VS: HR-110, BP-230/150 RR 32, O2 96% RA

• GCS 14 (speech confused)• No focal neurological signs• No signs of trauma• CVS/Resp: bilateral crackles

What now?

• What concerns you about this pt?• Differential diagnosis?• Investigations?• Immediate management?

Concerning Features

• VS: HR-110, BP-230/150 RR 32, O2 96% RA

• GCS 14 (speech confused)• No focal neurological signs• No signs of trauma• CVS/Resp: bilateral crackles

Differential Diagnosis

62 yo with headache, confusion, HTN• CVA• ICH: spontaneous, traumatic• CNS Infection: meningitis, encephalitis, abscess• CNS neoplasm: primary or mets• Migraine HA• Metabolic or toxic encephalopathy• Hypertensive encephalopathy

MCC Objectives

MCC OBJECTIVES – HTN EM

KEY objectives:• Differentiate “malignant”

HTN from secondary conditions

• Conduct initial HTN lowering treatment

OBJECTIVES:• Differentiate non-localizing

neurologic symptoms• Determine presence of

other hypertensive emergencies

• Interpret clinical & lab findings

• Conduct an effective management plan, including specific Rx

HYPERTENSION

Standard Definition• Based on 3 measurements, each 1 wk apart

> 140 systolic> 90 diastolic

Most important # acutely: DiastolicMAP = 1/3 Systolic, 2/3 Diastolic

Primary or Secondary

• Majority (90-95%) essential HTN

• Of Secondary: ½ have a potentially curable cause

Secondary HTN

Increased CO:• RF with fluid

overload• Acute renal disease• Hyperaldosteronism• Cushing’s syndrome• Coarctation of the

Aorta

Increased vascular resistance:

• Renal Artery Stenosis• Pheochromocytoma• Drugs• Cerebrovascular (CVA,

ICH, SAH)

Renal Artery Stenosis

• most common treatable cause (1-5%)• compromised renal perfusion => activation of

RAA • 2 pt groups:

– Elderly with atherosclerotic disease– Young females with fibromuscular dysplasia

• Clinical: abdo bruit (40-80%), retinopathy, HTN resistant to Rx, hypoK

Aldosteronism

• Uncommon but treatable• Na retention, volume expansion,

increased CO• Hypernatremia & Hypokalemia

typical• Primary: Adrenal adenoma,

hyperplasia• Secondary: Cushing’s, CAH,

exogenous mineralcorticoids

Pheochromocytoma

• Tumour, usually in adrenal medulla• Produces xs catecholamines (epi, NE)• Paroxysmal HTN…difficult to

recognize• Episodic HTN, HA, palpitations,

diaphoresis, anxiety…not a panic attack!

• Easy to diagnose: elevated urinary catecholamines, metanephrines, vandillylmandelic acid

Coarctation of the Aorta

• Rare but early surgical intervention can improve prognosis

• Clinical triad:1) upper extremity HTN2) systolic murmur over back3) delayed femoral pulses

Drugs

• Cocaine, amphetamines• ETOH withdrawal• Withdrawal from clonidine, beta

blocker• MAOI + tyramine containing foods or

certain Rx (meperidine, TCA, ephedrine)– Tyramine causes release of NE– Usually rapidly destroyed by MAO

Thinking About HTN:

1. Chronic HTN2. Transient HTN3. “White coat HTN”4. Hypertensive “Urgencies”5. Hypertensive “Emergencies”

Hypertensive “Urgencies”

• Elevated BP WITHOUT evidence of acute end-organ damage

• BP arbitrary levels• In past, treated with SL nifedipine• Demonstrated adverse outcomes (stroke, MI) • “rarely requires therapy”• Consider initiating chronic Rx

Malignant Hypertension

Severe HTN

& Evidence of acute end-organ damage

• Diastolic BP usually > 130 mm Hg or MAP > 160

• Relative rise much more important than #• Affects 1% of hypertensive patients

End-Organ Damage

• CNS: Hypertensive encephalopathy• CVS: Cardiac Ischemia Pulmonary Edema Aortic Dissection• Renal: ARF• Heme: microangiopathic hemolytic anemia• Eclampsia/Pre-eclampsia

Case 1

• 62 yo female• CC: acute onset severe headache, n/v• Noted by family to be confused• Denies trauma• PMHx: HTN, elevated cholesterol

Your Assessment

• VS: HR 110, BP 230/150, RR 32,O2 96% RA

• GCS 14• No focal neurological signs• No signs of trauma• CVS/Resp: bilateral crackles

Case 1

• What is your initial management for this pt?• What is causing her symptoms?

Cerebral Perfusion

• Autoregulation: cerebral blood flow maintained through normal range of BP by afferent arterioles

• N: autoregulation for MAP > 60• Chronic HTN: level of

autoregulation in elevated

Hypertensive Encephalopathy

Abrupt, sustained raised in BP (DBP > 140)=> exceeds capacity of autoregulation

uncontrolled cerebral blood flow

vasospasm, ischemia, punctate hemorrhages,

increased vascular permeability => ischemia, cerebral edema

Hypertensive Encephalopathy: Clinical

• Acute in onset & reversible• Severe HA, N/V, drowsiness, confusion• +/- seizures, coma, focal neurological deficits,

blindness• Papilledema usually present• EMERGENCY….untreated pts may die within

hrs!

How to Differentiate?

• Focal deficits do not usually follow a singular anatomic pattern

• Onset: usually hours to days• Can be associated with hemorrhage• CT usually N• EEG non-specific• CSF: clear, increased opening pressure

Management

ABC’sControl BP!• Goal reduce MAP by 25% or diastolic to minimum

of 110 mm Hg over 1 hr– IV Nitroglycerine– IV Nitroprusside– Labetolol: selective alpha & non-selective beta

blocker

Physical Exam in HTN• Eye:

– Acute: papilledema, retinal hemorrhages, vasospasm

– Chronic: AV nicking, cotton wool spots, silver wiring

• CVS: – Pulm edema: S3, rales JVD, peripheral edema– LVH: displaced apex– Coarctation murmur

• Renal– Bruit– Fluid overload

Other End-Organ Effects

Cardiovascular End-Organ Damage

• Pulmonary Edema• Aortic Dissection• ACS

Pulmonary Edema

• Long standing HTN myocardial hypertrophy• Eventually leads to LVF & dilatation• Stress of pulmonary edema to xs

catecholamines leading to HTN• Standard treatment causes fall in levels & BP

returns to normal

Pulmonary Edema

• In some, sudden, severe HTN precipitates acute LVF, causing pulmonary edema

• BP must be lowered to reverse the process

Management of Pulmonary Edema

• Standard Therapy: nitrates, O2, Furosemide, ACEI

Focused antihypertensive Rx:• Nitroglycerin IV• Nitroprusside IV• ACEI as an adjunct

Cardiac Ischemia

• If severe HTN associated with angina, lower BP to prevent myocardial damage

• Nitroglycerin SL, IV• Beta-blockers (careful in

setting of poor LVF)• ACEI• Nitroprusside NOT used as

may cause reflex tachycardia

Aortic Dissection

• Classic: acute onset ‘tearing” chest pain radiating to back

• Widened mediastinum on CXR• CT angio modality of choice• Immediate control of BP to limit

extent of dissection• Type A: involve ascending Ao, Tx: OR• Type B: treated medically

Management Aortic Dissection

• Goal to reduce BP to sys 100-120 mm Hg• Reduce ejection force of heart• Rx

– Vasodilator (e.g. nitroprusside, fendolopam)PLUS Beta blocker

– Or monotherapy with Labetolol (alpha/beta blocker)

Acute Renal Failure

• Urine dip: protein, RBC• Labs: BUN, Cr, electrolytes• Management• Nitroprusside IV, Labetolol IV• ACE-I, although takes a few hours• CCB IV (nicardipine)

Specific Therapies in Acute Hypertensive Emergencies

• Labetolol– 20mg IV, may incrementally increase dose (40mg, 80mg) q20

min, max 300mg/24 hr

• Nitroprusside: 0.3 mcg/kg/min, titrate up to 10 mcg/kg/min

• Nitroglycerin: start at 10-20 mcg/min, titrate up

• Special cases: Eclampsia, pre-eclampsia

• MgSO4 (for seizures) 4-6gm/1 hr

• Hydralazine 10 mg IV

Acute Hypertension: Overview

• Most pts do NOT require emergent treatment for their HTN (do no harm)

• With severe HTN, evaluate immediately for end-organ effects

• Appropriate BP measurement• Rapid recognition & appropriate reduction in BP for

hypertensive emergencies• Careful of over-treatment of HTN & risk of cerebral

ischemia

Hypertensive Emergencies

Questions?

Jason R. Frank MD MA(Ed) FRCPC

Dept of Emergency Medicine