Asthma Listen to Audio General Pathophysiology Treatment Preoperative management Intraoperative management GENERAL -affects 5 - 7% of general population -hallmark: bronchiolar inflammation, hyperreactivity response of airways due to varying stimuli (ex. pollen, dust) -clinical manifestation: episodic attacks of dyspnea, cough and wheezing -airway obstruction is generally reversible -asthma is generally classified as acute or chronic asthma Airway obstruction caused primarily by: -constriction of bronchial smooth muscles -increased secretions within the bronchial airways -edema of airways Possible precipitating factors: -pollen -animal dander -dust -pollutants -ingestion of asprin, NSAIDs, sulfiting agents, dyes -exercise -emotional excitement -viral infections PATHOPHYSIOLOGY -release of local inflammatory mediators within the airway -degranulating mast cells may provoke bronchospasm -possible overactivity of parasympathetic nervous system ex. normal bronchial tone is maintained by the parasympathetic nervous system normal diurnal variation in tone with peak airway resistance usually at 6 am intense vagal parasympathetic stimulation may lead to bronchoconstriction mediated by increased levels of cGMP -increase in the work of breathing may fatigue respiratory muscles -increase number of inadequately ventilated alveoli leads to a lower V/Q mismatch hence promoting hypoxemia -increasing PaC02 generally indicates impending respiratory failure due to increased work of breathing requirement not met by the pt -severe airway obstruction also indicated by pulsus paradoxus and ECG signs of right ventricular strain Mediators possibly involved in bronchoconstriction: -histamine -bradykinin -leukotrienes C, D and E -prostaglandins PGE2, PGF2alpha, PGD2 -platelet-activating factor -chemotactic factors from neutrophils and eosinophils During an acute asthmatic attack: -total lung capacity (TLC) is increased -residual volume (RV) is increased -functional residual capacity (FRC) is increased -RV may be increased by more than 400% -FRC may be increased by more than 100% TREATMENT Beta adrenergic agonist (sympathomimetic) Methylxanthines Glucocorticoids Anticholinergics Leukotriene blockers Mast cell stabilizing agents Cromoyln sodium Nedocromil Sympathomimetic agents: ex.albuterol, bitolterol, epinephrine, isoproterenol, metaproterenol, salmeterol, terbutaline -generally most useful and most commonly used agents -stimulation of beta2 receptors produces bronchodilation by relaxation of bronchilar smooth muscle relaxation -beta2 receptor stimulation activates adenylate cyclase creating cAMP -beta2 selective agonist (albuterol, terbutaline) decreases/avoids stimulation of beta1 cardiac receptors and subsequent effects Methylxanthines ex. theophylline, aminophylline -promotes bronchodilation by inhibition of phosphodiesterase and therefore preventing breakdown of cAMP -more complex pulmonary involvement compared to beta agonist -pulmonary effects include: histamine release blockade, catecholamine release, and stimulation of the diaphragm theophylline oral preparations: used for patients with nocturnal symptoms,however, has a narrow therapeutic range aminophylline the only available intravenous preparation of theophylline Glucocorticoid ex. beclomethasone, triamcinolone, flunisolide, and budesonide -provide anti-inflammatory and membrane-stabilizing effects for both acute treatment and maintenance therapy -synthetic steroids (ex.budesonide) often used for maintenance therapy administered by a metered-dose inhaler (MDI) -intravenous hydrocortisone or methyprednisolone are used acutely for severe asthmatic attacks Anticholinergics ex. ipratroprium -produce bronchodilation and may inhibit reflex bronchoconstriction by the antimuscarinic effects -given either by metered-dose inhaler or aerosol -moderately effective bronchodilator PREOPERATIVE MANAGEMENT -investigate into recent course of disease -investigate into any hospitalizations due to an acute asthmatic attack -ever been intubated due to severe pulmonary dysfunction -review patients peak flow diary if available -consider whether the patient is clinically optimized for the procedure (presense/absense of wheezing, coughing, dyspnea) -investigate into current drug regimine -evaluate any previous or current pulmonary function tests (FEV1/FVC, peak expiratory flow rate) -review chest xray:assess for air-trapping, hyperinflation with flattening of diaphragm, small appearing heart, hyperlucent lung fields -arterial blood gases -moderate to severe asthmatic disease are often associated with hypoxemia and hypocarbia -hypercapnia is indicative of air-trapping and may be a sign of impending pulmonary failure -FEV1 < 40% of predicted value also may be a sign of impending pulmonary failure Asthmatic patient with active bronchospasm for emergent surgery: if possible period of intensive treatment consisting of: -supplemental oxygen -aerosolized beta2 agonist -intravenous glucocorticoid Asthmatic patient optimized for elective surgery: -preoperative sedation may be beneficial especially for the emotional predisposing related factor to some asthmatic patients -benzodiazepines are generally a good selection for preoperative sedation -histamine blockers (ex.cimetidine, ranitidine) may be a poor choice which may accentuate bronchoconstriction -bronchodilators should be continued until the time of surgery INTRAOPERATIVE MANAGEMENT Goal for general anesthesia:smooth induction and emergence along with the depth of anesthetic maintenance adjusted to stimulation -most critical time for asthamtic patients undergoing general anesthesia is during the instrumentation (ex.intubation) of the airway Bronchospasm: -may be stimulated by: pain, emotional distress, stimulation upon light general anesthesia -may possibly be caused during a high spinal or epidural anesthesia by inhibiting the sympathetic tone (T1-T4) of lower airways -inhibition of the sympathetic tone may accentuate the parasympathetic mediated bronchoconstriction -drugs which promote histamine release may induce bronchospasm (ex. curare, atracuronium, mivacuronium, morphine, meperidine) Anesthetic induction agents -generally the depth of anesthesia before intubation and surgical incision is more important than the actual anesthetic agent chosen -thiopenthal although the most commonly used induction agent used in adults may be associated with histamine release -exaggerated histamine release associated with thiopenthal use may induce bronchospasm -propofol and etomidate oftenly are preferred due to avoidance of histamine release and bronchospasm -ketamine only bronchodilating intravenous anesthetic induction agent; often a good choice for hemodynamically unstable patients -ketamine should not be used in patients with high theophylline levels due to possibilities of seizure activity w. both drugs combined -halothane provides both a smooth induction along with bronchodilating properties beneficial in asthmatic children -sevoflurane and desflurane also provide bronchodilation although may create mild irritant effects amongst the airways Blunting reflex bronchospasm prior to intubation -additonal dose of thiopenthal: 1-2 mg/kg -ventilating patient with 2-3 MAC of volatile anesthetic for 5 minutes -bolus of intravenous lidocaine 1.5 mg/kg -bolus of anticholinergic ( i.v. atropine 2mg, i.v. glycopyrrolate 1mg) Maintenace anesthesia for asthmatic patients -volatile anesthetics generally are used for maintenance anesthesia especially due to thier beneficial bronchodilating effects -although halothane is a potent bronchodilator, it may sensitize the myocardium to epinephrine-induced dysrhythmias -halothane is generally avoided and not used in adult patients -severity of expiratory airflow obstruction can be sensed on the capnograph -severity of expiratory airflow obstruction is inversely related to the rate of rise of the capnograph measureing the exhaled C02 ex.slow rate of rise of the capnograph indicates a highly severe obstruction to the expiratory airflow likely due to bronchoconstriction -uniform distribution of gas flow to both lungs may occur with a prolonged expiratory time and tidal volumes less than 10ml/kg -air-trapping may be avoided with a more prolonged expiratory time Intraoperative bronchospam usually manifested as: -wheezing -increased peak airway pressure -plateau pressure is often normal -decreased exhaled tidal volumes -capnograph revealing a slow rising C02 waveform Treatment of intraoperative bronchospasm -deeping the level of volatile anesthetic -beta adrenergic delivered as aerosol or MDI in the inspiratory limb of breathing circuit -intravenous hydrocortisone (1.5 - 2 mg/kg) Rule out other causes of increased peak airway pressure: -kinked ETT -impacted secretions -over-inflation of the ETT cuff -endobronchial intubation -active straining respiratory efforts secondary to light anesthesia -pulmonary edema -pneumothorax -pulmonary embolism Emergence of anesthesia in asthmatic patients: -patient should be free of wheezing -reversal of NDMR with use of anticholingerics to prevent bronchospasm -deep extubation may prevent bronchospasm upon emergence -bolus intravenous lidocaine 1.5 - 2 mg/kg may help to blunt the airway reflexes upon emergence