Bronchospasm:%20successful%20management

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Bronchospasmsuccessful management

• Presented by R1???
• supervised by VS???

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Bronchospasm

• Many cases of severe bronchospasm do not have
  pre-existing history of bronchospastic disease.
• Very few asthma patients have adverse outcome in
  the perioperative period.
• Routine pre-op PFT would be expensive and
  time-consuming.

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Preoperative considerations

• Pathophysiology of bronchospasmSmooth muscle
  contraction.Exaggerated bronchoconstrictor
  response to trigger - airway edema , increased
  secretions, smooth muscle contraction. Airway
  inflammation increases bronchial
  hyperresponsiveness.

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Preoperative considerations

• Role of recent infectionUpper airway viral
  infection, especially influenza, increased airway
  reactivity.Exacerbation of asthma.

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Preoperative considerations

• For asthma recent course of disease, Tx
• For COPD stop smoking, infection control
  chest physiotherapy, steroid.

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NIH recommendation

• Evaluate the patients asthma over the past half
  year.
• Improve lung function to predicted values before
  surgery, possibly with short course of oral
  steroids.
• Give patients who have received steroids for
  longer than 2 weeks 100 mg hydrocortisone q8h iv.
  Taper within 24hrs.

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Medications
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Beta-adrenergic agonists

• Both acute and chronic treatment.
• Safety underestimated by anesthesiologists.
• Inhaled beta2-agonists

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Aminophylline

• Bronchodilating action.
• Does not add to the therapeutic effects of
  beta-adrenergic agonist.
• Does not provide bronchodilation in dogs
  anesthetised with halothane.
• Prophylaxis of acute attacks in chronic
  asthmatics.

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Aminophylline

• Prevent of nighttime bronchospasm episode.
• Mucociliary clearance and diaphragmatic
  contraction.
• Very low toxic/therapeutic index.

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Steroids

• Onset of benefit within few hours.
• Useful as pre-op medication in patients with
  moderate to severe asthma.
• One day high dose steroid doesnt affect wound
  healing and wound infection.
• Inhalation steroids, MDI preparation.

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Choice of Anesthesia
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RA vs general vs LMA

• Instrumentation of airway is the main trigger for
  wheezing during anesthesia.
• LMA cause less airway resistance increase than
  ETT.
• RA is ideal for reactive airway disease.
• Sympathetic block , bronchospasm?

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Induction agents

• Thiopental rarely cause bronchospasm, but light
  anesthesia.
• Ketamine produce bronchial smooth muscle
  relaxation.
• Lidocaine 1-3 min before intubation prevents
  reflex bronchoconstriction, direct airway spray
  doesnt.
• propofol induction 2.5 mg/kg .

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Inhalation agents

• Halothane vs isoflurane.
• Mask induction less pungency , less cough
  response.
• Intubaton sevoflurane is as effective as
  halothane , more effective than isoflurane.

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Analysis of a bronchospastic crisis
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The manifestation

• Wheezing
• Increase peak inflation pressure
• Decrease exhaled tidal volume
• Slow rising wave form on capnograph
• Desaturation

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Why do peak airway pressure rise?

• Airway constrict, increase resistance.
• Coughing and bucking.
• Secretion and mucosal engorgement.
• Air-trapping in severe case over-distension and
  less compliant.

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What is auto-PEEP?

• Airway resistance increase gtlonger inspiratory
  time gtshorter exp timeairway
  compressiongtincomplete exhalation.
• In-line manometer is not helpful!
• Resistor btw alveoli and circuit.
• Patients with marginal volume status, decrease
  venous return and hypotension.

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Why desaturate?

• Secretion and spasm result in airway closure and
  underventilation of perfused area.
• Inadequate perfusion or just falsely low reading
  due to hypotension.

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Keep in mind!!
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If low saturation is accompanied by hypotension,
trying to treat the low saturation with PEEP
could just make things worse!!
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Why does pCO2 go up and ETCO2 go down?

• Overdistension of some lung units,
  underventilation of others.
• Overdistended alveoli may not be perfused well,
  especially in hypotension, large dead space.
• Increase in V/Q mismatch.

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Why does pCO2 go up and ETCO2 go down?

• Overall minute ventilation declines as airway
  pressure rise.
• Large compressible volume in circuit(7-10ml/cmH2O
  ).
• Inability of our ventilator to maintain flow.
• Changing to more powerful ICU type ventilator.

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Responding to the crisis
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Think before you do!

• Obstruction of the ET tube from kinking,
  secretion, or an overinflated balloon.
• Endobronchial intubation.
• Active expiratory efforts.
• Pulmonary edema or embolism.
• Pneumothorax.

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Deepen anesthesia

• Even hypotension, lower intrathoracic pressure
  and improve venous return.
• Paralysis decrease respiratory impedance
  associated with bucking.
• Choice of agent-Sevoflurane and Halothane

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Dont spare the beta-2 agonists

• Further bronchodilation.
• Inhalation route is just as effective as parental
  therapy but less side effects.
• Spacer devices deliver drug effectively, even via
  ET tube.
• Drug with long duration-

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Ketamine

• Incremental dose.
• A quick way to maintain BP.
• Rapidly deepening anesthesia.
• Avoiding problems of inhaled anesthetics
  delivering to a poor ventilated patient.

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Bring in an ICU ventilator

• Not design for patient of respiratory failure.
• Too much compressible volume.
• Major disadvantage of ICU ventilator gt shift to
  iv anesthetics.

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Currently available beta-2 agonists in NTUH

• Ventolin (Albuterol) , nebules . Ventodisk
• Bricanyl (Terbutaline) MDI, nebules.
• Alupent (Metaproterenol), tab
• Berotec (fenoterol) MDI , nebule, liquid.

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The End