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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
- terbutaline
- fenoterol
- pirbuterol
- salmeterol
- 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 halothane when bronchospasm was provoked with
histamine
- role --> prophylaxis of acute attack in chronic
asthmatic prevention 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