Laryngoscopy and Intubation
Hypoxemia and hypercarbia are potential complications of laryngoscopies
and intubations that are not successful in a reasonable amount of time. Careful
evaluation of the airway can screen out most patients who cannot be adequately ventilated
by mask or intubated. The pulse oximeter is essential for detecting desaturation
during this time. If neither mask ventilation nor intubation can be accomplished,
the insertion of a supraglottic airway device such as the LMA or Combitube should
be performed with TTJV or a surgical airway reserved for when less invasive maneuvers
are unsuccessful.
There is an increased risk of aspiration in the patient with a
full stomach and a difficult airway, but aspiration can also occur in the properly
fasting patient who does not present special difficulties. Rapid-sequence induction
and conscious intubation have been described as means of protecting the patient from
aspiration. Aspiration remains a concern but less so in the patient with a properly
placed, cuffed endotracheal tube.
Cardiovascular responses to laryngoscopy include hypertension,
tachycardia, and dysrhythmias. In children, bradycardia may occur, but hypoxemia
must always be considered as the primary cause. In healthy patients, these responses
are generally well tolerated; however, in patients with limited coronary or myocardial
reserve, myocardial ischemia or failure may follow. The patient with a vascular
lesion at risk such as an intracranial vascular anomaly or trauma of the thoracic
aorta may also suffer serious sequelae. The clinician must be careful to not overtreat
these responses and create more difficulties than the responses themselves.
Because the minimum alveolar concentration (MAC) for endotracheal
intubation is about 30% higher than the MAC for surgical incision, a relatively deep
level of anesthesia must be established. Because deep anesthesia may not be tolerated
by many patients, drugs that tend to block the response to airway instrumentation
or antihypertensives may be used. Narcotics are one option as an adjunct. Fentanyl
has been best studied and requires doses of at least 3 to 4 µg/kg to be effective.
Alfentanil has a more rapid onset of action and is effective for this purpose, and
remifentanil is likely to be similarly effective. Intravenous lidocaine may be used
to supplement the narcotic effect on hemodynamics, although some studies have called
the effectiveness of lidocaine in this setting into doubt.[46]
Topical anesthesia with lidocaine has been a less effective method for blunting
hemodynamic responses because laryngoscopy precedes intratracheal administration
of lidocaine. Transtracheal anesthesia avoids laryngoscopy but is stimulating in
its own right. Glossopharyngeal and superior laryngeal nerve blocks may also be
effective methods to blunt adverse hemodynamic responses. A variety of antihypertensive
agents have also been used to diminish the blood pressure and heart rate responses
to intubation. These include β-adrenergic blockers, phentolamine, nitroprusside,
clonidine, captopril, nitroglycerin, and hydralazine, but their relative efficacy
is not established. However, one study reported that a 150-mg esmolol bolus was
superior to intravenous high-dose lidocaine or low-dose fentanyl in preventing
the tachycardia associated with intubation.[47]
All three treatments provided equivalent blunting of blood pressure increases.
In treated (with drugs other than β-blockers) hypertensive adult patients, a
single, 100-mg intravenous bolus of esmolol given before laryngoscopy appears to
control heart rate and blood pressure without excessive hypotension.[48]
Dysrhythmias during or immediately after laryngoscopy and intubation generally resolve
with adequate ventilation and establishment of adequate anesthetic depth.
The respiratory response of laryngospasm has been described.
In predisposed individuals, laryngoscopy alone may also cause bronchospasm. In healthy
volunteers, intubation results in an increase in airway resistance that is greater
than the resistance of breathing through the tube held externally. This doubling
of the expected resistance even in topically anesthetized airways represents reflex
bronchoconstriction to the mechanical irritation of the tube.[49]
Bronchospasm may be especially severe in the lightly anesthetized patient with reactive
airways. Propofol may be the intravenous induction agent of choice in patients prone
to bronchospasm.[50]
Clinically, it appears that
bronchospasm is blunted by the prior administration of anticholinergics, steroid,
inhaled β2
-agonists, lidocaine (topical, nerve block, or intravenous),
and narcotics. After intubation, deepening anesthesia with intravenous or inhaled
agents and the administration of inhaled or intravenous β-agonists helps treat
the bronchospasm. Muscle relaxants may improve ventilation, and in extreme situations,
a small amount of positive end-expiratory pressure may improve oxygenation when it
is unsatisfactory on 100% oxygen. With the tube in situ, it is important to ensure
that the audible wheezing is not caused by some form of mechanical obstruction of
the tube: kinking, clot, mucus, active biting or passive mouth closure, foreign
body, cuff overinflation, bevel against tracheal wall, or endobronchial intubation.
Less likely problems such as tension pneumothorax, a nasogastric tube in the trachea,
and heart failure must also be eliminated before definitively treating wheezing as
bronchospasm. Visual inspection and passage of a suction catheter (or preferably,
a fiberoptic bronchoscope) along with cuff deflation and 90-degree rotation of the
tube can rule out several of these possibilities.
The patient with elevated intracranial pressure (ICP) who has
minimal reserve in intracranial compliance is at risk for brainstem herniation and
sudden death during laryngoscopy and intubation. Instrumentation of the airway may
result in a sudden increase in cerebral blood flow because of increases in cerebral
metabolic activity and systemic cardiovascular effects. The normal autoregulation
mechanism may not be effective because of disease or because its upper pressure limit
(normally, mean arterial pressure of 150 mm Hg) may be exceeded. Coughing or bucking
decreases venous return from the head and may increase ICP. Induction drugs that
result in cerebral vasoconstriction are most useful. In practice, drugs have included
thiopental and lidocaine, although etomidate and propofol can also be considered.
Narcotics are somewhat useful, although they do not have a great direct effect on
central brain function. Ketamine is best avoided. Adjunctive measures may include
voluntary or mask hyperventilation, mannitol, steroids, and establishment of ICP
monitoring before laryngoscopy and intubation.
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