Asthma

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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