HYPERTENSIVE EMERGENCIES

1
HYPERTENSIVEEMERGENCIES

• Louis Muller
• 11 March 2009

2
Content

• Introduction
• Definitions
• Prevalence/morbidity/mortality
• Etiology pathophysiology
• Diagnosis
• Causes
• Differential diagnoses
• Workup
• Management
• Treatment
• Pharmacology IV Anti-hypertensives
• References

3
Introduction

• Hypertension(HPT) very common Western soc.
• 50 mil. US affected (world - approx. 1 billion
  people)
• Despite awareness treatment still 30 adults
  unaware
• 40 known with HTN - not on treatment
• 60 on treatment BP not controlled to lt140/90 mm
  Hg
• New data shown incr. lifetime risk of HPT
• - incr. risk of CVS
  complications with normal
• BP levels

4
Classification

• Joint National Committee (JNC 7) introduced a
  new classification system for HTN 2004
• Normal SBPlt120 and DBPlt80
• Prehypertension SBP 120-139 or DBP 80-89
• Stage I hypertension SBP 140-159 or DBP 90-99
• Stage II hypertension SBP gt160 or DBP gt100
• Stage II HPT further divided into
• Hypertensive urgency
• Hypertensive emergency

5
Other Terminology

• Severely elevated BP (JNC VII)
• Defined as BP gt 180/120
• accelerated HPT
• term used to describe individuals with chronic
  hypertension with associated group 3
  Keith-Wagener-Baker retinopathy
• malignant HPT
• describe those individuals with group 4 KWB
  retinopathy changes papilledema

6
Definitions

• HPT emergency(crisis) Is characterized by a
  severe elevation in BP, complicated by evidence
  of impending or progressive target/end organ
  dysfunction
• VS
• HPT urgency is a severe elevation in BP without
  progressive target organ dysfunction
• NB these definitions do not specify absolute BP
  levels

7
Conditions constituting evidence of EOD

• Hypertensive encephalopathy
• Intracerebral heamorrhage
• Stroke
• Head trauma
• Ischemic heart disease (most common)
• AMI
• Acute LVF with P/oedema
• Unstable angina
• Aortic dissection
• Eclampsia
• Life threatening arterial bleed

8
Prevalence/ morbidity/ mortality

• Prevalence
• With progress in anti-hypertensive Rx
  decrease in the lifetime incidence of HPT
  emergencies from 7 to 1
• Hypertensive crisis more common among elderly and
  black patients
• Studies HPT related problems amount for 25 of
  all pt visits to medical section of ED. 33 of
  these - HTN emergencies.
• Morbidity/mortality
• - Dependent on the extent of EOD on
  presentation and the degree to which BP is
  controlled subsequently.
• 1year survival rate has increased from 20 to
  more than 90 with appropriate treatment.
• 10-year survival rate approaches 70 with approp
  treatment
• 1-year and 5-year mortality rate - following
  untreated HPT emergency are 70 to 90 and 100
  respectively

9
Etiology

• Most common
• - rapid unexplained rise in BP in pt with
  chronic essential HPT
• most have history of poor treatment/compliance or
  an abrupt discont of their meds
• Other causes
• Renal parenchymal disease (80 of sec.causes)
• Systemic disorders with renal involvement (SLE)
• Renovascular disease (Atheroscleroses/fibromuscula
  r dysplasia)
• Endocrine ( phaeochromocytoma/cushing syndrome)
• Drugs (cocaine/amphetam/clonidine withdrawal/diet
  pills)
• CNS (trauma or spinal cord disorders
  Guillain-Barre
• Coarctation of the aorta
• Preeclampsia/Eclampsia
• Postop. HPT

10
Pathophysiology

• Not well understood
• Failure of normal autoregulation abrupt rise in
  SVR
• Increase in SVR due to release of humoral
  vasoconstrictors from the stressed vessel wall.
• Endothelium plays a central role in BP
  homeostasis via substances as Nitric oxide and
  prostacyclin
• Increased pressure starts a cycle of
• -
  endothelial damage
• - local
  activation of clotting cascade
• - fibrinoid
  necrosis of small vessels
• - release
  of more vasoconstrictors
• Process leads to progressive increase in
  resistance and further endothelial dysfunction

11
Pathophysiology

• Single organ inv. in approximately 83
• Two organ inv found in 14
• Multiorgan involvement found in 3 of pts
• Most common clinical presentations
• - cerebral
  infarction(24)
• - pulmonary
  oedema (22)
• - HPT
  encephalopathy(16)
• - Cong. HF
  (12)
• Less common presentations IC hemorrhage, aortic
  dissection and eclampsia

12
Case example - HPT Encephalopathy

• 52yr male presents to ED
• worsening headache and confusion, numbness and
  weakness involving right side of body, blurry
  vision over past 12 hrs
• PMx HPT, bilateral artery stenosis, cocaine
  abuse, hyperlipidemia.
• Exam
• BP 213/134
• confused, papilledema on fundoscopy
• Mild motor weakness (4/5) right arm
• Lab studies rased creatinine
• ECG LVH
• CT Brain diffuse bilateral white matter changes
  HPT encephalopathy

13
Case example HPT Encephalopathy

• Mx
• admitted ICU
• started on IV Nitroprusside
• BP decreased to 190/100 mmHg over first 3hrs
• Outcome
• Neurology symptoms resolved within 5hrs
• he was switched to his usual oral regimen on
• 3rd day in hospital
• discharged day 5 controlled BP

14
Hypertensive encephalopathy

• Clinical manifestation of cerebral edema and
  microhemorrhages seen with dysfunction of
  cerebral autoregulation
• Defined as an acute organic brain syndrome or
  delirium in the setting of severe hypertension

15
HTN Encephalopathy

• Symptoms
• Severe headache
• Nausea and vomiting
• Visual disturbances
• Confusion
• focal or generalized weakness

• Signs
• Disorientation
• Focal neurologic defects
• Focal or generalized seizures
• nystagmus

16
HPT Encephalopathy

• Not adequately treated cerebral heamorrhage,
  coma and death.
• BUT with proper treatment completely reversible
• Clinical diagnoses (exclusion)

17
Hypertensive Retinopathy

• Fundoscopy used to be considered a definitive
  tool in diagnosing HTN encephalopathy
• NOW still usefull in recognizing acute EOD as
  in HTN encephalopathy, but the absence of retinal
  exudates, hemorrhages, or papilledema does not
  exclude the diagnoses.
• Fundoscopy findings

18
HPT Retinopathy - Fundoscopy

• Keith-Wagener classification
• Stage I arteriolar sclerosis with thickening,
  irregularity and tortuosity
• Stage II AV dipping or compression
• Stage III Flame shaped haemorrhages and cotton
  wool spots
• Stage IV Papilledema
• presence of stage III and IV lesions implies
  failure of the CNS vascular autoregulation and
  makes the Dx of Malignant HPT definitive

19
HPT Retinopathy
20
AV crossing changes
21
HPT retinopathy
22
HPT retinopathy
23
PanOptic ophtalmoscope
24
Diagnosis

• History
• 1) focus on presence of Sx of end-organ
  dysfunction(eod)
• 2) any identifiable etiology
• Hypertension Hx
• last known normal BP
• prior diagnoses Rx
• dietary and social factors
• Medication
• Steroid use
• Estrogens
• Sympathomimetics
• MAO inhibitors
• Social history
• smoking, alcohol
• illicit drugs (cocaine, stimulants)
• Family history
• early HPT in family members
• cardiovascular and cerebrovascular disease

25
Diagnoses

• History (cont)
• Symptom spesific Hx suggesting EOD
• CVS Hx
• previous MI/angina/arrhythmias
• chest pain/SOB/Sx of CF/claudication/flank or
• back pain
• Neurologic Hx
• prior strokes, neuro dysfunction
• visual changes, blurriness, loss of visual
  fields, severe headaches, nausea and vomiting,
  change in mental status
• Renal Hx
• Underlying renal disease (RF)
• Acute onset changes in renal frequency
  (anuria/oliguria)
• Endocrine Hx
• diabetes, thyroid dysfunction, Cushings syndrome

26
Diagnoses

• Examination
• Confirm elevated BP
• Proper position, appropriate cuff size
• Supine and standing and both arms
• Asses EOD present
• Fundoscopy
• Chronic HPT will have findings
• Acute changes
• new retinal bleeds
• Superficial/flame shaped
• Deep/punctuate
• exudates
• hard/cotton wool spots
• papilledema
• Neck
• Enlarged thryoid, carotid bruit, jugular venous
  distention
• CVS
• Enlarged heart, S3, asymmetric pulses,
  arrhythmias
• Pulmonary

27
Workup

• Lab studies
• Electrolytes, urea and creatinine
• FBC and smear
• Urinalysis dipstix microscopy
• Optional - tox screen
• - BHCG
• - Endocrine testing
• Imaging studies
• CXR (chest pain or SOB)
• Head CT/MRI brain (abn neurology)
• Chest CT/TEE/Aortic angio (Aortic dissection)
• Other Tests
• - ECG

28
Management

• ED considerations
• Many HPT pts only small number will require
  emergent treatment
• Primary goal of EP?
• The pts syptoms of EOD and require immediate iv
  parenteral therapy.
• VS
• The pt with acutely elev BP(SBPgt200 or DBPgt120)
  without EOD symptoms, who require initiation of
  medical therapy and close follow up as outpatient
  /inpatient

29
Management

• The EP must be capable of
• Appropriately evaluating pts with an elevated BP
• Correctly classify the HPT
• Determine the aggressiveness and timing of
  therapeutic interventions
• Making disposition decisions
• Remember - treat the patient and not the number

30
Treatment

• Prehospital care
• Address the manifestations of a HPT emergency
  eg.chest pain or HF
• Reduction of BP not indicated in prehospital
  setting
• Rapid lowering of BP can critically decrease
  end-organ perfusion

31
Treatment

• ED Care - general principles
• Consider context of elevated BP (pain, anxiety)
• Screen for EOD (Hx/workup)
• - Pts without evidence of EOD
  d/c f/up
• Misconception - never d/c
  patient from ED with elevated BP ?
• -
  oral nifedipine NOT indicated and may be
  dangerous!
• - Pts with EOD require ICU admission
  and rapid but gradual lowering of BP - using IV
  meds.
• 3. BP should not be lowered to normal
  levels
• Rapid reduction in BP below the autoregulatory
  range results in reduction in organ blood flow
  risk of ischemia and infarction
• General rule the MAP should be lowered by no
  more than 20 - 1st hour
• remains stable - BP lowered
  to 160/110 in next 2-6hrs
• NB Exceptions
• BP goals best achieved by a continuous infusion
  of a short-acting, titratable,
  
  parenteral anti-HPT
  agent, along with constant intensive patient
  monitoring

32
(No Transcript)
33
Treatment

• Medication options
• Oral antihypertensives
• Chronic hypertensive
• Hypertensive urgency
• IV antihypertensives
• Hypertensive emergency

34
Pharmacology IV anti-HPT

• Vasodilators
• Sodium nitroprusside
• Nitroglycerin
• Nicardipine
• Fenoldapam
• Hydralazine
• Enalapril
• Adrenergic inhibitors
• Labetalol
• Esmolol
• Phentolamine

35
IDEAL IV ANTI-HYPERTENSIVE

• Lower the BP without compromising blood flow to
  critical organs
• Vasodilators generally considered 1st , because
  they preserve organ blood flow in the face of
  reduced perfusion and also tend to increase CO.

36
Profile of an ideal IV antihypertensive

• Preserves GFR and renal blood flow
• Few or no drug reactions
• Little or no potential for exacerbation of
  co-morbid conditions
• Rapid onset and offset of action
• Minimal hypotension overshoot
• Minimal need for continuous BP monitoring and
  frequent dose titration
• No acute tolerance
• Ease of use and convenience
• Safe and no toxic metabolites
• Multiple formulations for short and long term use
• Minimal symphathetic activation

37
Sodium Nitroprusside (Hypoten L)

• MoA
• Direct smooth muscle dilator (art ven)
• Nitric oxide compound
• Potent preload and afterload reducer
• Causes cerebral vasodilation
• Ultra short acting
• Immediate onset - DoA 10min
• Dose
• 0.1-0.5mcg/kg/min IV infusion
• titrate to desired effect
• ratesgt10mcg/kg/min cyanide
  toxicity
• Adverse affects/Precautions
• Cyanide and thiocyanate toxicity (pts with
  liver/renal dysfunction)
• Max dose, max 10min
• Can cause precipitous drop in BP (hypotensive
  effects unpredictable)
• Ideally Art.line with continuous BP
  monitoring
• Causes significant reflex tachycardia ( incr
  Oxygen demand)

38
Nitroglycerin(Nitrocine / Isoket / Tridal)

• MoA
• Potent vasodilator (nitric oxide compound)
• Primary affects the venous system, decrease
  preload (CO BP)
• Decreases coronary vasospasm
• Dose cont infusion
• start 5mcg/min, incr by 5mcg/min
  
• every 3-5min to 20mcg/min
• If NO Response
• increase by 10mcg/min every
  3-5min,up
• 200mcg/min
• Onset 2-5min/DoA 5-10min
• Adverse effects/precautions
• Constant monitoring is essential
• Tolerance from uninterrupted use (12hr
  withdrawal)
• Headache, tachycardia, flushing
• Contra ind

39
Nicardipine(Nimodipine Nimotop)

• Ca channel blocker selective arterial
  vasodilator
• Onset 1-5min
• DoA 15-30min
• Dose start 5mg/hr IV infusion, titrate every
• 15min to max 15mg/hr.
• Advantages
• Cause cerebral and coronary vasodilatation
• Precautions can worsen/cause HF and
• liver failure
• can exacerbate renal
  insuff.
• Ideal for CNS emergencies
• Not available SA

40
Fenoldapam(Carlopam)

• New (not available SA)
• MoA
• Peripheral dopamine agonist (high vs low doses)
• causes selective neuro vasodilatation
• mesenteric vasodilatation
• increases renal blood flow and sodium excretion
• Onset lt5min, but more gentle, lasts for 30min
  (titratable, predictable and stable)
• Standard BP monitoring is sufficient, no toxic
  metabolites
• Dosing
• Start at 0.1-0.3mcg/kg/min IV infusion
• May be increased in increments of
  0.05-0.1mcg/kg/min every 15min, until target BP
  reached
• Max infusion rate 1.6mcg/kg/min
• Precautions
• Pts with glaucoma or intraocular hypertension
• Dose related tachycardia can occur angina
• Close BP monitoring
• Close K monitoring
• Caution with raised ICP
• Drug of choice

41
Hydralazine(Apresoline)

• MoA
• Decreases systemic resistance by direct
  vasodilation of arterioles
• Dose
• 5-20mg IV bolus or 10-40mg IM repeat every
  4-6hrs
• old school
• used too much
• boluses takes 20min to work
• not titratable
• Adverse effects/Precautions
• tachycardia, flushing, headache
• sodium and water retention
• increased ICP
• adjust dose in severe renal dysfunction
• response may be delayed and unpredictable
• Still drug of choice in pregnancy(Eclampsia), but
  B-blocker/Labetalol and Fenoldapam are also safe
  options
• Only available PO, Dihydralazine discontinued

42
Enalaprilat

• The active component of Enalapril (hydrolyzed in
  liver and kidney)
• MoA
• ACE inhibitor
• Dose
• 0.625-2.5mg every 6hr IV
• Not titratable
• Onset within 30 min long half life
• Adverse effects/Precautions
• Contra-indicated volume depletion, renal
  vascular disease
• Prolonged ½ life
• Expensive, not available SA

43
Labetalol(Trandate)

• MoA
• selective alpha blocker will reduce vascular
  smooth m. resistance
• non-selective Beta blocker decrease cardiac
  inotropy and miocard O2 consumption, will prevent
  reflex tachycardia
• Dose
• Bolus effect in 5-10min,max effect at 20min.
  (DoA 2-6hrs)
• 1st dose 20mg then every 10-20min
• 2nd dose 40mg, 3rd dose 80mg.
• Cont. infusion 0.5 2mg/min titrate to
  response,max 300mg total dose
• Difficult to titrate due to very wide dose range
• Advantages
• smooth onset
• Transition to oral Rx easy (dose equivalent)
• Improve cerebral bloodflow stroke pt
• No need for ICU/Arterial line
• Adverse effects/precautions
• Relative CI Heart failure, heart block, Asthma
  (bronchoconstriction)

44
Esmolol(Brevibloc)

• MoA
• highly selective beta blocker
• Dose (titratable)
• bolus 250-500mcg/kg IV over 1-3min
• infusion 50-100mcg/kg/min
• may repeat bolus after 5min or increase
• infusion rate to 300mcg/kg/min
• Onset 1-2min / short acting
• Adverse effect/Precautions
• Hypotension common
• nausea
• Asthma
• 1st degree AV block
• heart failure
• Contraindications
• Sinus bradycardia
• Heart block
• Cardiogenic shock
• Bronchial asthma

45
Phentolamine(Regitine)

• MoA
• alpha adrenergic receptor blocker
• Dose
• load 5-20mg IV every 5min or
• infusion 0.2-0.5mg/min
• Onset 1-2min
• Adverse effect/precautions
• tachycardia
• flushing/headache
• MI
• cerebrovascular spasm
• Contra-indications
• renal impairment
• Concurrent use with PDE-5 inhibitors
• coronary or cerebral arteriosclerosis
• Drug of choice
• Cocaine associated HPT crisis
• Pheochromocytoma HPT crisis
• Not available in SA anymore

46
Neurological emergencies

• Hypertensive encephalopathy
• reduce MAP by 25 or diastole to 100mmHg
• over 8 hrs
• If neurology worsens, suspend Rx
• Drug of choice
• Sodium nitroprusside
• Labetalol

47
Neurological emergencies

• Acute Ischemic stroke
• often loss of cerebral autoregulation
• ischemic region more prone to hypoperfusion
• thus BP reduction not recommended
• unless SBPgt220 or DBPgt120
• UNLESS planning fibrinolysis SBPlt185
• and DBPlt 110
• Drug of choice
• Labetalol
• Nicardipine
• Sodium Nitroprusside

48
Neurological emergencies

• Acutes ICH/SAH
• Treatment based on clinical/radiographic evidence
  of raised ICP
• Raised ICP MAPlt130 (1st 24hrs)
• No raised ICP MAPlt110
• Drug of choice
• Sodium Nitroprusside
• Labetalol
• Nicardipine

49
Cardiovascular emergencies

• ACS
• treat if SBPgt160 and/or DBPgt100
• Reduce MAP by 20 -30 of baseline
• nitrates should be given till symptoms
• subside or until DBPlt100
• Drug of choice
• Nitroglycerine
• Labetalol
• Nicardipine

50
CVS emergencies

• Acute HF (pulmonary edema)
• treat with vasodilator (additional to diuretics)
• Sodium Nitroprusside in conjunction with
• morphine, oxygen and loop diuretic
• Enalaprilat also an option

51
CVS emergencies

• Aortic dissection
• anti-hypertensive Rx is aimed at reducing the
  
• shear stress on aortic wall (BP and Pulse)
• immediate lowering of BP lifesaving
• maintain SBPlt110, unless signs of end
• organ hypoperfusion
• preferred Rx is combination of Morphine,
• B-blocker and vasodilator
• Nitroprusside Labetalol

52
Other disorders

• Cocaine toxicity/pheochromocytoma
• Hpt and tachycardia rarely require spesific Rx
• Alpha adrenergic blockers preferred
• B blockers can be added, but only after
• alpha blockade.
• Drug of choice
• Phentolamine
• Labetalol
• Diazepam

53
Other disorders

• Pre-eclampsia/Eclampsia
• Goal SBPlt160 and DBPlt110 in pre-and-
  intrapartum periods.
• Platelets lt 100 000, BP should be maintained lt
  150/100
• IV Magnesium to prevent seizures
• Drug of choice
• Methyldopa
• Hydralazine

54
Other disorders

• Perioperative hypertension
• target BP to within 20 of baseline, except if
  potential for life threatening arterial bleeding
• typically related to catecholamine surge
  post-op.
• Drug of choice
• B-blocker
• Labetalol

55
Local

• Tygerberg
• F1(medical outpatients)
• Nitroglycerine
• Cardiology ICU
• Nitroglycerine
• Renal unit
• Labetalol
• Obstetrics
• Labetalol
• Hydralazine

56
Local

• Grootte Schuur (C15)
• Nitroglycerine (Tridal)
• Victoria
• Nitroglycerine (Tridal/Nitrocine)
• Labetalol
• Can get Sodium nitroprusside

57
Summary

• HPT crisis - serious condition - associated with
  EOD, if left untreated
• High mortality - untreated
• Main causes non-compliance and poorly
  controlled chronic hypertension.
• Urgency vs emergency
• Treatment should be tailored to the individuals
  condition
• HPT urgency initial goal max 25 drop in MAP in
  first 3 hours
• Precipitous drop just as bad good continuous
  monitoring essential

58
References

• Joint National Committee on prevention,
  detection, evaluation and treatment of high blood
  pressure.Seventh Report. Hypertension 422003
  1206-1252
• Kitiyakara C, Guzman NJ. Malignant hypertension
  and hypertensive emergencies.J Am Soc Nephrol
  19989135
• Vaidya CK, Ouellette JR. Hypertensive Urgency and
  Emergency. Hospital Physician March 2007 43-50
• Vidt D. Hypertensive Crises emergencies and
  urgencies. The Cleveland clinic disease
  management project. 12 Jan 2006. Available at
  www.clevelandclinicmeded.com/diseasemanagement/nep
  hrology/crises/crises.htm
• McCowan C. Hypertensive Emergencies. Available at
  www.emedicine.medscape.com/emergencymedicine/cardi
  ovascular. Updated Jan 26, 2009
• Hollander JE. Cocaine intoxication and
  hypertension. Ann Emerg Med. Mar 200851S18-20
• Characteristics and management op patients
  presenting to the emergency department with
  hypertensive urgency. J.Clin Hypertens.
  8200612-18
• Peck TE, Hill SA, Williams M.Pharmacology for
  anaesthesia and intensive care. 3rd
  Edition.Chapters 15 16,p246-269.
• AggarwalMD, Khan IA. Hypertensive Crisis
  Hypertensive emergencies and Urgencies.Cardiology
  Clinics 242006135-146
• Flanigan JS.Vitberg D.Hypertensive Emergency and
  Severe Hypertension What to Treat, Who to Treat,
  and How to Treat. Med Clin N Am 902006439-451