Anesthesia in the patient with
with lung disease arrive at respiratory patterns optimal for their condition.
This can include the recruitment of auxiliary muscles, changes in inspiratory
and expiratory flow rates, respiratory rate, and arterial carbon dioxide
tension. Because anesthesia can disturb these delicate adjustments, many
anesthesiol-ogists prefer to resort to regional anesthesia, where practical. Two
major issues must be considered, however:
The potential respiratory effects of the intended regional
anesthetic. For exam-ple, a thoracic-level epidural anesthetic block begins to
compromise inter-costal muscle activity, reduces FRC, limits the patient’s ability
to cough, and theoretically can stimulate bronchospasm by blocking dilatory
sympathetic innervation to the bronchi. Some approaches to the brachial plexus
have a high incidence of unilateral phrenic nerve paralysis and an occasional
pneu-mothorax. While the average patient can tolerate the loss of intercostal
mus-cles, a “pulmonary cripple,” who at rest uses accessory muscles to breathe,
might be left with inadequate respiratory muscle strength.
The respiratory depressant effects of sedative medications might be
accen-tuated in these patients. While it is preferable to attempt an anesthetic
that avoids airway instrumentation, this preference turns into a liability if
the need for emergent tracheal intubation arises should the patient slip into
patient with well-controlled asthma should sail through general anesthe-sia
without much difficulty. All asthma medications, and particularly steroids,
should be continued pre-operatively. Nebulized albuterol (or another 2
ago-nist) administered in the pre-operative holding area provides
bronchodilation just before anesthesia. Because instrumentation of the airway
can stimulate bronchospasm, patients with refractory asthma might benefit from
anesthetic techniques that avoid airway manipulation, such as regional or local
anesthesia with gentle intravenous sedation. Should general anesthesia be
required, several options for induction and airway management are available.
Small doses of either thiopental or propofol can ease the patient to sleep, at
which point one of the halogenated inhalation anesthetics can be slowly
introduced. These agents are bronchodilators. Ketamine is a bronchodilator as
well and may be used, provided its potential side effects can be accepted. A
laryngeal mask airway (LMA) is a lesser stimulus to bronchospasm than an
endotracheal tube. When tracheal intubation becomes necessary, the goal at
induction will be to completely block the airway reflexes that stimulate
bronchospasm. Intravenous lidocaine (0.5–1.0 mg/kg) can prove helpful.
Intravenous opioids (but not morphine which tends to release histamine) can be
used. But remember that some patients develop respiratory difficulties (a
“stiff chest”) in response to large doses of opioids, the treatment of which
requires muscle relaxation.
warm and humidified gases can reduce bronchospasm. Mechanical ventilation
requires consideration of the pulmonary pathology. Asth-matics have a prolonged
expiratory phase. If we do not give them enough time for exhalation, they will
trap air (“dynamic hyperinflation”), resulting in increased intrathoracic
pressures. This “auto-PEEP” reduces venous return and cardiac out-put. A
prolonged expiratory time allows for full exhalation. Simply lengthening the
exhalation time steals time from inhalation, which in turn might require high
inspiratory pressures (the same tidal volume must be given over a shorter
the tidal volume and/or respiratory rate would help, but will necessarily
reduce minute ventilation and entail the potential for hypercarbia. “Permissive
hypercapnea” can become necessary when minute ventilation cannot be main-tained
without risk of barotrauma (pneumothorax).
stimulation of the trachea can trigger bronchospasm, removal of the endotracheal
tube may be best accomplished during deep anesthesia. This is only appropriate
in patients at low risk for aspiration and obstruction of the upper airway.
Prophylactic supplemental oxygen in the post-operative period can prevent
hypoxia-induced airway reactivity.
sleep apnea (OSA) occurs when the soft tissues of the pharynx collapse during
sleep, obstructing the airway and resulting in hypoxemia. Sleep apnea plagues
obese patients who snore heavily with intermittent bouts of obstruction to the
point of apnea (reported by partner) and repeated awakening. During the day,
they are often somnolent. The apneic periods cause hypoxemia and hypercar-bia,
resulting in (i) cardiac irritability with bradycardia and premature
ventricular contractions (PVCs), (ii) vasoconstriction, both peripherally
(leading to increased systemic vascular resistance and hypertension) and in the
pulmonary circulation (with pulmonary hypertension and potentially right heart
failure), and (iii) ery-thropoeisis (resulting in polycythemia). Because of the
potential of thrombosis and unfavorable rheology, a polycythemic patient should
be phlebotomized if the hematocrit is too high (>55%).
you obtain a history of OSA during the anesthesia pre-operative evalu-ation,
you may have to order further studies including ECG and possibly
echocar-diogram to look for evidence of pulmonary hypertension and right heart
compro-mise. In a subset of patients (“Pickwickians”), ABG analysis might
demonstrate daytime CO2 retention with potentially impaired
hypercarbic respiratory drive. Therapeutic interventions include nasal CPAP
during sleep, weight loss, and surgi-cal correction. OSA patients are
particularly sensitive to opioids and sedatives and can develop airway
obstruction with even low doses of respiratory depressants. Finally, patients
with excess pharyngeal tissue and obesity present difficulties with airway
management. Not only can intubation be tough, we may be unable to
mask–ventilate or even use an LMA. Thus ventilation may be very difficult to
provide once we render the patient unconscious and paralyzed.