Preoperative Considerations

Pathophysiology of bronchospasm

- concept of smooth muscle contraction as the cause of increased airway resistance in patients with reactive airways is overly simplistic.

- bronchoconstrictor response to trigger is characteristic of asthma

reaction - airway edema - increase secretion - smooth muscle contraction

Studies airway caliber in asthma patients

- marked thickening of submucosa

- inflammation --> increase inflammatory cells in lung of asthma

- asthma clinically as airway obstruction that improves with steroids

- airway narrow by constriction or secretion --> marked increase in resistance

- bronchial hyperresponsiveness increase by airway inflammation

Role of recent infection

- following upper airway viral infection especially influenza --> normal subject increase airway reactivity

- asthma --> most common viral exacerbration

- anesthesia following recent URI result in higher incidence of problems with airway reflex

Medications

- B adrenergic agonist

- mainstay treatment chronic and acute in patient with mild to moderate reactive airways

- inhale B2 agonist- albuterol - pirbuterol- terbutaline - salmeterol- fenoterol

- have LD50 greater than therapeutic dose

- remain significant controversy as to whether there are detrimental effect of chronic use of B adrenergic agonist esp. high potency drug such as fenoterol

- inhaled corticosteroids as first line therapy with B adrenergic agonist reserved for PRN use

- Theophylline

- bronchodilating action

- does not add to therapeutic effects in acute attack

- very low toxic/therapeutic index

- did not provide bronchodilation in dogs anesthesized with ha

lothane when bronchospasm was provoked with histamine

- role --> prophylaxis of acute attack in chronic asthmatic prev

ention nighttime episode of bronchospasm

- chronic lung disease

- theophylline beneficial effects on improvement mucociliary clearance and diaphragmatic contraction

- theophylline increase arrythmias during halothane anesthetic induction, although similar effect are not seen with enflurane or isofluranes

- steroid few hour preoperative useful in patients with moderate to severe asthma and history of required in past

- one day of high dose steroids should not significantly affect wound healing

- steroid course in the week(s) prior to surgery maybe useful in case of ongoing wheezing

- steroids increase rate of wound healing problems or infection are not well founded

- 1991 NIH Expert Panel recommendation that asthmatics with an FEV1 less than 80 % of predicted should receive a preoperative course of oral steroids

- Leukotiene receptor anatagonists or synthesis inhibitors are a recent addition to the anti asthmatic -- mild benefits

Choice Of Anesthesia

RA & GA & mask & LMA

- since instrumentation of airway is major trigger for wheezing during anesthesia

- avoid intubation are useful

- asthmatic patient have wheezing 6.4 % with intubation< 2 % without intubation or RA

- LMA insertion , airway resistance decrease less than following ETT insertion

- high spinal 48 % reduction in expiratory reserve volume --> decrease cough

- it’s a problem in chronic bronchitis or current URI

- most patients with reactive airways, RA is ideal

- high block leading to sympathetic blockade and consequent bronchospasm also appear to be unfounded

- study - asthma no difference between anesthetize with high epidural (T2-T4) and GA with ketamine / isoflurane

- volunteer - document bronchial hyperreactivity found high thoracic epidural did not alter airway resistance and attenuate response to inhale acetylcholine due to systemic absorption of LA rather than any direct effect from epidural

- survey Japan - incidence asthmatic attack with epidural anesth than GA

- However, several case in ASA close claim study with adverse outcome had received RA

- light anesthesia often used with subsequent airway irritation

Induction agents

- thiopental rarely may cause bronchospasm

- airway instrumentation under thiopental anesthesia alone may trigger spasm

- isolate sheep airway --> thio caused tracheal contraction and bronchial relaxation

- ketamine produce smooth muscle relaxation via neural mechanism release of cathecolamine

- lidocaine - prevent reflex bronchoconstriction- little effect toxicity at dose 1.5 mg/kg 1-3 min prior

intubation- direct tracheal lidocaine spray carries hazard of

triggering airway reaction and should be avoid in favor of IV route

- induction of asthmatic with 2.5 mg/kg propofol --> significant lower incidence of wheezing following tracheal intubation when compared with 6 mg/kg thiamylal or methohexital

- propofol result in significant lower respiratory resistance following tracheal intubation than thiopental or etomidate

Inhalation agents

- study in dog with ascaris antigen induce bronchospasm --> halothane and isoflurane were equally effective experimentally in reducing bronchospasm

- halothane better bronchodilate than isoflurane at 1.7 MAC

- halothane induction less cough

- bronchodilating effect of inhale anesthetic following intubation found that sevoflurane was effective bronchodilator as halothane and more effective than isoflurane

Muscle relaxants

- Rapacuronium --> severe bronchospasm

- Mivacurium --> release significance amount of histamine and lead to mast cell degranulation concern in patient history atopy or asthma

--> rabbit --> significance increase airway resistance

Analysis of a Bronchospastic crisis

Why do peak airway pressure rise ?

- airway constrict- coughing and bucking- secretion and mucosal engorgement further

contribute to the problem

- severe case --> air trapping (auto-PEEP) may occur chest become overdistend and less compliance

What is auto PEEP and why is it a problem ?

- increase resistance --> require longer inspiration time to deliver

adequate TV--> shortened expiratory time combine with airway

compression during exhalation may result in incomplete exhalation

- in patient whose volume status is marginal, an increase of just a few cmH2O in intrathoracic pressure can greatly decrease venous return and result in hypotension

Why does the oximeter show a dropping saturation ?

- secretion and spasm have result in airway closure and underventilation of perfuse airway

- hypoxia is generally not a major problem in pure reactive airway disease

- problem --> inadequate perfusion resulting in fasely low reading on oximeter

- keep in mind --> if low saturation is accompanied by hypotension

- trying to treat low saturation with PEEP could just make things worse

Why does pCO2 go up and ETCO2 go down ?

- difference in resistance result in overdistention of some lung units

- V/Q mismatch

- overdistension alveoli may not be perfuse at all especially hypotension --> large increase in dead space

- if increase airway pressure --> decrease minute ventilation

- the compressible volume of typical anesthesia circuit is large enough that wasted ventilation is often 7-10 cc/cmH2O --> as pressure go to 60 --> half liter of each set breath may actually not be delivered to the patient

- anesthesia ventilator --> increase respiratory impedance--> at high pressure, attempt to increase MV are

often unrewarding

- changing to a more powerful ICU type ventilator may be the better approach

Responding to the Crisis

Deepen anesthesia

- even when there is drop in BP --> deepening anesthetic is useful especially since it may lower intrathoracic pressure and improve venous return

- paralysis will decrease respiratory impedance associated with bucking

- halothane and sevoflurane may be a better choice of inhaled anesthetic than isoflurane especially at lower level of MAC

Don’t spare the beta 2 agonists

- very safe agent

- provide further bronchodilation during halothane in animal model

- study, mechanically ventilate patient in ICU found that maximum benefit occur after 15 puffs of albuterol via spacer with no patient benefiting from more puffs

- terbutaline is available as subcutaneous preparation but no evidence superior to inhale route

- salmeterol - long duration of action- use asthmatic prophylactically- don’t use in acute episode because onset

of action 20 min

Ketamine

- incremental dose - quick way of maintaining BP- rapidly deepening anesthesia- avoid problem of delivering an inhale

anesthetic to patient with poor ventilation

Bring in an ICU Ventilator

- our anesthesia ventilator are not design for patient with respiratory failure, too much compressible volume to make adequate ventilation in face of high impedance

- ICU ventilator- pressure as high as 120 cmH2O are feasible- high flow allow for shorter inspiratory time

with adequate time for greater exhalation and lower auto PEEP --> improve circulation

- major disadvantage is need to switch to intravenous from inhalation anesthetic