Anesthetic Considerations

A. Preoperative Management
The emphasis in evaluating patients with asthma should be on determining the recent course o
f the disease and whether the patient has ever been hospi- talized for an acute asthma attack, a
s well as on ascertaining that the patient is in optimal condition. Patients with poorly controlle
d asthma or wheezing at the time of anesthesia induction have a higher risk of perioperative c
omplications. Conversely, well- controlled asthma has not been shown to be a risk factor for i
ntraoperative or postoperative complica- tions. A thorough history and physical examination a
re of critical importance. The patient should have no or minimal dyspnea, wheezing, or coug
h. Com- plete resolution of recent exacerbations should be con rmed by chest auscultation. Pa
tients with fre- quent or chronic bronchospasm should be placed on an optimal bronchodilatin
g regimen. A chest radio- graph identi es air trapping; hyperin ation results in a attened diaph
ragm, a small-appearing heart, and hyperlucent lung elds. PFTsparticularly expiratory air o
w measurements such as FEV1, FEV1/FVC, FEF25-75%, and peak expiratory ow ratehelp
in assessing the severity of airway obstruction and reversibility a er bronchodilator treatment.
Comparisons with previous measure- ments are invaluable.2 Asthmatic patients with active b
ronchospasm presenting for emergency surgery should be treated aggressively. Supplemental
oxygen, aerosol- ized 2-agonists, and intravenous glucocorticoids can dramatically improve
lung function in a few hours. Arterial blood gases may be useful in man- aging severe cases.
Hypoxemia and hypercapnia are typical of moderate and severe disease; even slight hypercap
nia is indicative of severe air trapping and may be a sign of impending respiratory failure.Som
e degree of preoperative sedation may be desirable in asthmatic patients presenting for elec- ti
ve surgeryparticularly in patients whose disease has an emotional component. In general, b
enzodiaz- epines are the most satisfactory agents for premedi- cation. Anticholinergic agents
are not customarily given unless very copious secretions are present or if ketamine is to be us
ed for induction of anesthesia. In typical intramuscular doses, anticholinergics are not e ective
in preventing re ex bronchospasm fol- lowing intubation. e use of an H2-blocking agent (suc
h as cimetidine, ranitidine, or famotidine) is the- oretically detrimental, since H2-receptor acti
vation normally produces bronchodilation; in the event of histamine release, unopposed H1 ac
tivation with H2 blockade may accentuate bronchoconstriction.Bronchodilators should be con
tinued up to the time of surgery; in order of e ectiveness, they are -agonists, inhaled glucocor
ticoids, leukotri- ene blockers, mast-cell stabilizers, theophyllines, and anticholinergics. Patie
nts who receive chronic glucocorticoid therapy with more than 5 mg/day of prednisone (or its
equivalent) should receive a graduated supplementation schedule based on the severity of the
illness and complexity of the surgical procedure. Supplemental doses should be tapered to ba
seline within 12 days.
B. Intraoperative Management
The most critical time for asthmatic patients under- going anesthesia is during instrumentation
of the airway. General anesthesia by mask or regional anesthesia will circumvent this proble
m, but nei- ther eliminates the possibility of bronchospasm. In fact, some clinicians believe th
at high spinal or epi- dural anesthesia may aggravate bronchoconstriction by blocking sympat
hetic tone to the lower airways (T1T4) and allowing unopposed parasympathetic activity. Pa
in, emotional stress, or stimulation dur- ing light general anesthesia can precipitate bron- chos
pasm. Drugs o en associated with histamine release (eg, atracurium, morphine, and meperidin
e) should be avoided or given very slowly when used. e goal of any general anesthetic is a sm
ooth induc- tion and emergence, with anesthetic depth adjusted to stimulation. e choice of ind
uction agent is less important, if adequate depth of anesthesia is achieved before intubation or
surgical stimulation. iopental may occasionally induce bronchospasm as a result of exaggera
ted histamine release. Propofol and etomi- date are suitable induction agents; propofol may al
so produce bronchodilation. Ketamine has bron- chodilating properties and is a good choice f
or patients with asthma who are also hemodynamically unstable. Ketamine should probably n
ot be used in patients with high theophylline levels, as the com- bined actions of the two drug
s can precipitate seizure activity. Halothane and sevo urane usually provide the smoothest inh
alation induction with bronchodi- lation in asthmatic children. Iso urane and des u- rane can p
rovide equal bronchodilation, but are not normally used for inhalation induction. Des urane is
the most pungent of the volatile agents and may result in cough, laryngospasm, and bronchos
pasm.Re ex bronchospasm can be blunted before intubation by an additional dose of the induc
tion agent, ventilating the patient with a 23 minimum alveolar concentration (MAC) of a vol
atile agent for 5 min, or administering intravenous or intra- tracheal lidocaine (12 mg/kg). N
ote that intra- tracheal lidocaine itself can initiate bronchospasm if an inadequate dose of indu
ction agent has been used. Administration of an anticholinergic agent may block re ex bronch
ospasm, but causes exces- sive tachycardia. Although succinylcholine may on occasion induc
e marked histamine release, it can generally be safely used in most asthmatic patients. In the a
bsence of capnography, con rmation of cor- rect tracheal placement by chest auscultation can
be di cult in the presence of marked bronchospasm.Volatile anesthetics are most o en used for
maintenance of anesthesia to take advantage of their potent bronchodilating properties. Venti
lation should incorporate warmed humidi ed gases whenever possible. Air ow obstruction dur
ing expiration is apparent on capnography as a delayed rise of the end-tidal CO2 value (Figur
e 242); the severity of obstruction is generally inversely related to the rate of rise in end-tidal
CO2. Severe broncho- spasm is manifested by rising peak inspiratory pres- sures and incomp
lete exhalation. Tidal volumes of 68 mL/kg, with prolongation of the expiratory time, may al
low more uniform distribution of gas ow to both lungs and may help avoid air trapping. e Pa
co2 may increase, which is acceptable if there is no contraindication from a cardiovascular or
neurologic perspective.Intraoperative bronchospasm is usually mani-fested as wheezing, incre
asing peak airway pressures (plateau pressure may remain unchanged), decreasing exhaled tid
al volumes, or a slowly risingwaveform on the capnograph. Other causescan simulate broncho
spasm: obstruction of the tracheal tube from kinking, secretions, or an overin ated balloon; br
onchial intubation; active expiratory e orts (straining); pulmonary edema or embolism; and pn
eumothorax. Bronchospasm should be treated by increasing the concentration of the volatile a
gent and administering an aerosolized bronchodilator. Infusion of low dose epinephrine may
be needed if bronchospasm is refractory to other interventions.Intravenous hydrocortisone can
be given, par- ticularly in patients with a history of glucocorticoid therapy.At the completion
of surgery, the patient should ideally be free of wheezing. Reversal ofnondepolarizing neurom
uscular blocking agents with anticholinesterase agents does not precipitate bronchoconstrictio
n, if preceded by the appropri- ate dose of an anticholinergic agent. Deep extu- bation (before
airway re exes return) reduces bronchospasm on emergence. Lidocaine as a bolus (1.52 mg/
kg) may help obtund airway re exes dur- ing emergence.
Paco2 dapat meningkat, yang dapat diterima jika tidak ada kontraindikasi dari perspektif kard
iovaskular atau neurologis. Bronchospasme intraoperatif biasanya termanifestasi sebagai men
gi, meningkatkan tekanan saluran napas puncak (tekanan plateau mungkin tidak berubah), me
ngurangi volume tidal yang dihembuskan, atau bentuk gelombang yang perlahan naik pada ca
pnograf. Penyebab lainnya dapat mensimulasikan bronkospasme: penyumbatan tabung trakea
dari kinking, sekresi, atau balon yang terlalu banyak; Intubasi bronkial; Ekspirasi aktif (tegan
g); Edema paru atau emboli; Dan pneumotoraks. Bronkospasme harus ditangani dengan meni
ngkatkan konsentrasi zat volatil dan pemberian bronkodilator aerosol. Infus epinefrin dosis re
ndah mungkin diperlukan jika bronkospasme refrakter terhadap intervensi lain. Hidrokortison
intravena dapat diberikan, terutama pada pasien dengan riwayat terapi glukokortikoid. Setela
h selesai operasi, pasien sebaiknya bebas dari mengi. Pembalikan agen penghambat neuromus
kular nondepolarisasi dengan agen antikolinesterase tidak memicu terjadinya bronkokonstriks
i, jika didahului dengan dosis yang tepat dari agen antikolinergik. Deep extubation (sebelum r
eflek jalan nafas kembali) mengurangi bronkospasme saat kemunculan. Lidokain sebagai bol
us (1,5-2 mg / kg) dapat membantu refleks saluran nafas pada saat kemunculan