Intubation can be performed under sedation assistance (absence of neuromuscular blockade) or rapid sequence (coadministration of neuromuscular blockade and sedatives) (Table 35-3). Rapid-sequence intubation is suggested when the stomach may be full to minimize the risk of distending the stomach with air, triggering vomiting and gastric aspiration.
Table 35-3.Commonly Used Medications for Induction ||Download (.pdf) Table 35-3. Commonly Used Medications for Induction
|Drug ||Dose ||Onset of action ||Duration of effect ||Indications ||Precautions |
|Fentanyl ||1-2 μ/kg IV push over 1-2 min ||Within 2-3 min ||30-60 min ||Preinduction, blunts ICP rise ||Respiratory depression, hypotension, rare muscle wall rigidity |
|Lidocaine ||1-1.5 mg/kg IV 2-3 min before intubation ||45-90 s ||10-20 min ||Preinduction, blunts ICP rise ||Avoid if allergic or high-grade heart block if no pacemaker |
|Etomidate ||0.3 mg/kg IV push ||30-60 s ||3-5 min ||Induction, sedation; good in hypotension. Decreases CBF, ICP; preserves CPP ||Decreases seizure threshold, decreases cortisol synthesis; avoid in sepsis |
|Propofol ||2 mg/kg very slow IV push ||9-50 s ||3-10 min ||Induction, sedation, reduces ICP and airway resistance, anticonvulsive effects ||Hypotension, myocardial depression |
|Ketamine ||2 mg/kg IV push ||1-2 min ||5-15 min ||Induction, analgesia, sedation, amnesia, bronchodilatory effects; good in hypotension ||Catecholamine surge, possible increase in ICP, “reemergence” phenomenon if not pretreated with benzo-diazepines |
|Thiopental ||3 mg/kg IV push ||30-60 s ||5-30 min ||Normotensive, normovolemic status epilepticus or increased ICP patients ||Hypotension, bronchospasm |
|Succinylcholine ||1.5-2 mg/kg IV push ||30-60 s ||5-15 min ||Preferred paralytic unless contraindicated ||Caution in hyperkalemia, myopathy, neuropathy/denervation; avoid if history of malignant hyperthermia |
|Rocuronium ||0.6 mg/kg IV push ||45-60 s ||45-70 min ||Paralysis when succinylcholine contraindicated ||Caution in DMV and DI |
|Vecuronium ||0.1 mg/kg IV push ||Within 3 min ||35 min ||Least preferred paralytic for RSI ||Caution in DMV and DI |
Fentanyl has a rapid onset and short duration of action and reduces the hypertensive response to laryngoscopy.19 Because it suppresses the sympathetic response to hypotension, caution must be used in shock states or hypovolemia. Fentanyl derivatives such as remifentanil, sufentanil, and alfentanil are increasingly utilized worldwide and may be more efficacious in blunting the tachycardic response.17
Lidocaine at a dose of 1.5 mg/kg intravenously blunts ICP rise during laryngoscopy by reducing tachycardia, airway hyperactivity, cerebral blood flow, cerebral vascular resistance, and cerebral metabolism.20 It can, however, also decrease mean arterial pressure (MAP) and CPP.21, 22 The use of lidocaine to reduce ICP during intubation is controversial,19, 23 but has been shown to be effective in patients with cerebral neoplasms,24 closed head injuries,25 and known elevated ICPs.26 Its side-effect profile includes hypotension, a decreased seizure threshold, and a low incidence of ventricular tachy-arrhythmias.27
Pretreatment with low-dose nondepolarizing neuromuscular blocking agents prior to the administration of succinylcholine is often recommended in order to prevent fasciculation and ICP rise.28, 29, 30 This practice may be effective, but it is not supported by published data.17, 31
Etomidate is one of the most commonly used medications for facilitating endotracheal intubation,32 with powerful sedative and muscle relaxant properties. It is a γ-aminobutyric acid (GABA) agonist without analgesic properties. Etomidate is popular because of its hemodynamically neutral effects and a tendency to reduce ICP and cerebral oxygen demand while purportedly preserving CPP.32, 33, 34 Side effects include increases in airway resistance, myoclonus, nausea, and vomiting; reduction of the seizure threshold; and adrenal insufficiency. The clinical sequelae of this well-described adrenal insufficiency are unknown; there is growing concern about the use of etomidate in septic patients, in whom an increased mortality rate has been observed.35, 36
Propofol is a GABA agonist that delivers sedation and anesthesia but not analgesia. It reduces airway resistance, has anticonvulsive and antiemetic effects, and suppresses sympathetic activity. This includes a reduction in cardiac inotropy, systemic vascular resistance, intracranial pressure (by decreasing cerebral blood flow), cerebral blood volume, and cerebral metabolism.37 Propofol provides deeper anesthesia than etomidate and creates intubating conditions similar to succinylcholine when used with a nondepolarizing neuromuscular blocker or opiate.17 However, propofol causes a reduction in systolic blood pressure by 15% to 33%.38 Extreme caution should be exercised when using propofol as an induction agent in patients who require a higher cerebral perfusion pressure and those patients with known cardiomyopathy or low ejection fraction.
Thiopental causes sedation and amnesia through its GABA-agonist properties. It decreases cerebral blood flow, cerebral metabolism, cardiovascular contractility, systemic vascular resistance, and venous return to the heart. Major side effects include hypotension, allergic reactions (2%), laryngo-spasm, bronchospasm, hypersalivation, and immune suppression.
Ketamine is a “dissociative” anesthetic that provides sedation, amnesia, and analgesia. It is an appealing agent in critical illness because it does not cause vasodilation or hypotension. Ketamine binds to catecholamine receptors, causing an increase in heart rate, cardiac output, contractility, mean arterial pressure, and cerebral blood flow.39 Prior studies have demonstrated that ketamine increases ICP,40, 41,42, 43, 44, 45 and some authors have recommended against its use in patients with intracranial hypertension. This recommendation is probably obsolete, however, as improvements in CPP have been clearly demonstrated despite elevated ICP when ketamine was used in conjunction with a GABA agonist.46, 47, 48, 49 Clinicians should be aware of the potential for dangerous agitation with ketamine when it is given with inadequate sedation, and that it has been poorly studied in the neurocritically ill.
Neuromuscular blocking agents cause profound skeletal muscle relaxation, creating ideal intubating conditions, and have hemodynamically neutral effects. They are always employed in conjunction with sedation. Succinylcholine is a depolarizing agent that activates the acetylcholine receptor, resulting in defasciculation and transient skeletal muscle paralysis. It has the shortest onset and duration of action (typically < 5 minutes) of all the neuromuscular blockers. Side effects include hyperkalemia, myalgias, and rarely malignant hyperthermia in genetically susceptible patients. Some studies suggest that succinylcholine increases intracranial pressure,50 but this has been disputed.31, 51 The effect of succinylcholine on ICP is transient and of questionable significance17, 52 and should not preclude its use when needed.
Neurocritically ill patients may be at higher risk for succinylcholine-induced hyperkalemia.53, 54,55 Conditions leading to an upregulation of acetylcholine receptors cause greater potassium efflux from myocytes with nerve depolarization. This includes patients with disuse atrophy, such as stroke or TBI patients with a sudden onset of weakness or paralysis, occurring after as little as 24 to 72 hours of immobility, and patients with upper or lower motor neuron defects.56 This risk may be averted by “precurization”—administration of a small dose of nondepolarizing neuromuscular blockers a few minutes before the succinylcholine—or by simply using a nondepolarizing agent instead.