Bronchospasm successful management Presented by R 1 supervised

Bronchospasm: successful management Presented by R 1林至芃 supervised by VS詹偉弘

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.

Preoperative considerations • Pathophysiology of bronchospasm Smooth muscle contraction. Exaggerated bronchoconstrictor response to trigger airway edema , increased secretions, smooth muscle contraction. Airway inflammation increases bronchial hyperresponsiveness.

Preoperative considerations • Role of recent infection Upper airway viral infection, especially influenza, increased airway reactivity. Exacerbation of asthma.

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

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 q 8 h iv. Taper within 24 hrs.

Medications

Beta-adrenergic agonists • Both acute and chronic treatment. • Safety underestimated by anesthesiologists. • Inhaled beta 2 -agonists

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

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

Steroids • Onset of benefit within few hours. • Useful as pre-op medication in patients with moderate to severe asthma. • One day high dose steroid doesn’t affect wound healing and wound infection. • Inhalation steroids, MDI preparation.

Choice of Anesthesia

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?

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 doesn’t. • propofol induction 2. 5 mg/kg.

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

Analysis of a bronchospastic crisis

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

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.

What is auto-PEEP? • Airway resistance increase =>longer inspiratory time =>shorter exp time+airway compression =>incomplete exhalation. • In-line manometer is not helpful! • Resistor btw alveoli and circuit. • Patients with marginal volume status, decrease venous return and hypotension.

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

Keep in mind!!

If low saturation is accompanied by hypotension, trying to treat the low saturation with PEEP could just make things worse!!

Why does p. CO 2 go up and ETCO 2 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.

Why does p. CO 2 go up and ETCO 2 go down? • Overall minute ventilation declines as airway pressure rise. • Large compressible volume in circuit (7 -10 ml/cm. H 2 O). • Inability of our ventilator to maintain flow. • Changing to more powerful ICU type ventilator.

Responding to the crisis

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.

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

Don’t 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-

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

Bring in an ICU ventilator • Not design for patient of respiratory failure. • Too much compressible volume. • Major disadvantage of ICU ventilator => shift to iv anesthetics.

Currently available beta-2 agonists in NTUH • • Ventolin (Albuterol) , nebules. Ventodisk Bricanyl (Terbutaline) MDI, nebules. Alupent (Metaproterenol), tab Berotec (fenoterol) MDI , nebule, liquid.

The End