Acute severe asthma
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Acute severe asthma

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    Acute severe asthma Acute severe asthma Presentation Transcript

    • Acute Severe Asthma
      By: Kane Guthrie
    • Objectives
      Pathophysiology of ASA
      Assessing the patient with ASA
      Emergency department management
      NIV vs Mechanical Ventilation in ASA
    • Case Study
    • Case Study
    • Vital Signs
    • Epidemiology of Asthma
      Over 2.2 million Aussie’s have asthma
      Over 400 hundred die each year
      Highest risk of death >70years
      Severe acute asthma is a life threatening condition.
    • Pathophysiology
    • Acute Severe Asthma
      2 distinct phenotypes of ASA identified:
    • Differential Dx:
    • Assessment
    • Assessing Severity
    • Investigations
      Diagnostic test generally provide limited information, compared to clinical assessment
    • CXR
      Limited Use
      Hyperinflation 5-10%
      Infiltrates 5%
      PTX <1%
      Pnemomediastinum <1%
    • Blood Gas
      Respiratory alkalosis typical
      Inaccurate predictor of outcome
      Seldom alters treatment plan
      Clinical assessment gives better information
      Painful
    • Pulse Oximetry
      Simple, less invasive and painful, compared to blo0d gas.
      Provides continuous o2 measurement
      Aim >Spo2 94%
    • PEFM
      Objective measurement of lung function
      Useful to assess response to treatment
      Limited role in ASA
    • Complications of ASA
    • ED Management
      The sick and dying asthmatic!!!
    • Nursing Care
      Apply o2/neb (humidified)
      Monitor BP,HR,RR, Spo2, EtCo2, Temp, GCS
      IVC x2
      Monitor electrolytes/arrhythmias closely
      ECG
      FBC
      IDC
    • o2
      Asthmatic die from hypoxia
      Keep Sp02 > 94%
      A slight ∧ in Pco2 may occur, (not clinically significant)
    • Bronchodilators
      Salbutamol
      First line therapy
      Nebulizer (back to back nebs)
      Dose?
      Not improving consider IV (back door)
      Monitor K
      Salbutamol toxicity= ∧Lactic acidosis
    • Anticholinergics
      Ipratropium bromide
      Blocks muscarinic receptors in smooth muscle, resulting in bronchodilation
      Dose: 500mcg
      Can give up to 3 dose’s initially then ever 4/24
    • Mg
      Controversial
      Best evidence is in the sick/dying asthmatic
      Cause smooth relaxation, inhibits histamine & acetylcholine release from nerve endings
      Indicated when bronchodilators are failing
      Dose: 2-4mg over 30-60mins
    • Steroids
      Prednisolone vs Hydrocortisone
      Given within 1st hour greatly reduces hospital admission
      Target airway oedema and secretions via anti-inflammatory role
      Dose: Pred 50mg PO, Hydrocort 100-200mg IV
    • Adrenaline
      Given via Neb or IV
      Alpha effects target ∨ airway oedema
      Beta effect target ∨bronchodilation
      Used as a rescue therapy in the hypotensive, poor responding asthmatic
      Dose: Neb 1-6mg in 3ml Nacl
      Dose: IV 6mg in 100mls 5% dextrose (1-15mls/Hr), “also push dose’s 0.10-0.50mcg”.
    • AB’s
      Not routinely indicated
      Give
      Underlying pneumonia/bacterial cause
      Preventing VAP
    • Airway Management
    • NIV
      Becoming more popular, (research, case reports)
      Unloads resp muscles, augments alveolar ventilation until asthma resolves.
      CPAP vs BiPAP
      Start with low IPAP & EPAP
      Good indicator which patients need intubating
    • What the literature says on NIV.
      Clinical Evidence:
    • Mechanical VentilationIndications
    • Intubating
      Ketamine for bronchodilator effects
      Use rapid sequence intubation
      Fluid bolus before (pre-load)
      Allow permissive hypercapnea
    • Challenges of Mechanical Ventilation
      Effective pre-oxygenation difficult
      No margin for error or delay
      Need to be intubated by most senior person available
      Develop high Intrathoracic pressure after RSI
      Intubation causes higher mortality via= lung hyperinflation, VILI, cardiovascular collapse.
    • The BIG issue
      Asthmatics require prolonged expiratory times
      Severe asthma pt initiates inspir before expir ceases
      Results in increase lung volume, auto-peep and hyperinflation
      Minimizing hyperinflation and avoiding excessive airway pressures are the goals
      Use low RR and prolonged exhalation times
      Allow Co2 to rise, but keep pH .7.15
      Monitor (P plat) >30 cm H20 against expir time
    • Initial Ventilator Settings
      Assist control mode
      Tidal volume 7-8mL/kg (use ideal body weight)
      RR 10-12bpm
      Fi02: 100%
      PEEP: 0cm H20
      Patients require deep sedation to tolerate the Vent.
    • Crashing Ventilated Asthmatic
      D.O.P.E.S.
    • Take Home Points
      Assessment skills are paramount
      Maximizing therapy to prevent MV is the GOAL!!!
      Mg works in the sick asthmatic
      NIV works
      Experience makes a big difference
      These patients will challenge you
    • Questions
    • Thank-you