Hypertensive Emergencies

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Hypertensive Emergencies

• Jason R. Frank MD MA(Ed) FRCPC
• (N. Wolpert MD FRCPC)
• Dept of Emergency Medicine

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Case 1

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

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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

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What now?

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

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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

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Differential Diagnosis

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

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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

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HYPERTENSION

• Standard Definition
• Based on 3 measurements, each 1 wk apart
• gt 140 systolic
• gt 90 diastolic
• Most important Diastolic
• MAP 1/3 Systolic, 2/3 Diastolic

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Primary or Secondary

• Majority (90-95) essential HTN
• Of Secondary ½ have a potentially curable cause

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Secondary HTN

• Increased CO
• RF with fluid overload
• Acute renal disease
• Hyperaldosteronism
• Cushings syndrome
• Coarctation of the Aorta

• Increased vascular resistance
• Renal Artery Stenosis
• Pheochromocytoma
• Drugs
• Cerebrovascular (CVA, ICH, SAH)

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Renal Artery Stenosis

• most common treatable cause (1-5)
• compromised renal perfusion gt 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

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Aldosteronism

• Uncommon but treatable
• Na retention, volume expansion, increased CO
• Hypernatremia Hypokalemia typical
• Primary Adrenal adenoma, hyperplasia
• Secondary Cushings, CAH, exogenous
  mineralcorticoids

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Pheochromocytoma

• Tumour, usually in adrenal medulla
• Produces xs catecholamines (epi, NE)
• Paroxysmal HTNdifficult to recognize
• Episodic HTN, HA, palpitations, diaphoresis,
  anxietynot a panic attack!
• Easy to diagnose elevated urinary
  catecholamines, metanephrines, vandillylmandelic
  acid

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Coarctation of the Aorta

• Rare but early surgical intervention can improve
  prognosis
• Clinical triad
• upper extremity HTN
• systolic murmur over back
• delayed femoral pulses

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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

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Thinking About HTN

1. Chronic HTN
2. Transient HTN
3. White coat HTN
4. Hypertensive Urgencies
5. Hypertensive Emergencies

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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

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Malignant Hypertension

• Severe HTN
• Evidence of acute end-organ damage
• Diastolic BP usually gt 130 mm Hg or MAP gt 160
• Relative rise much more important than
• Affects 1 of hypertensive patients

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End-Organ Damage

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

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Case 1

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

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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

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Case 1

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

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Cerebral Perfusion

• Autoregulation cerebral blood flow maintained
  through normal range of BP by afferent arterioles
• N autoregulation for MAP gt 60
• Chronic HTN level of autoregulation in elevated

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Hypertensive Encephalopathy

• Abrupt, sustained raised in BP (DBP gt 140)
• gt exceeds capacity of autoregulation
• uncontrolled cerebral blood flow
• vasospasm, ischemia, punctate hemorrhages,
• increased vascular permeability
• gt ischemia, cerebral edema

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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!

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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

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Management

• ABCs
• Control 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

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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

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Other End-Organ Effects
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Cardiovascular End-Organ Damage

• Pulmonary Edema
• Aortic Dissection
• ACS

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Pulmonary Edema

• Long standing HTN gt myocardial hypertrophy
• Eventually leads to LVF dilatation
• Stress of pulmonary edema gt to xs catecholamines
  leading to HTN
• Standard treatment causes fall in levels BP
  returns to normal

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Pulmonary Edema

• In some, sudden, severe HTN precipitates acute
  LVH, causing pulmonary edema
• BP must be lowered to reverse the process

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Management of Pulmonary Edema

• Standard Therapy nitrates, O2, Furosemide, ACEI
• Focused antihypertensive Rx
• Nitroglycerin IV
• Nitroprusside IV
• ACEI as an adjunct

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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

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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

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Management Aortic Dissection

• Goal to reduce BP to sys 100-120 mm Hg
• Reduce ejection force of heart
• Rx
• Vasodilator (eg nitroprusside, fendolopam)
• PLUS Beta blocker
• Or monotherapy with Labetolol (alpha/beta
  blocker)

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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)

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Specific Therapies in Malignant Hypertension

• 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

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Malignant 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 measuring
• Rapid recognition appropriate reduction in BP
  for hypertensive emergencies
• Careful of over treatment of HTN risk of
  cerebral ischemia

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QUESTIONS?