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* From the Medical-Surgical Intensive Care Unit (Dr. Reynolds), University Health Network and Mount Sinai Hospital, Toronto, ON, Canada; and the Division of Pulmonary and Critical Care Medicine, Allergy, and Clinical Immunology (Dr. Heffner), Medical University of South Carolina, Charleston, SC.
Correspondence to: John Heffner, MD, FCCP, Medical University of South Carolina, 169 Ashley Ave, PO Box 250332, Charleston, SC 29425; e-mail: heffnerj{at}musc.edu
| Abstract |
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Key Words: airway management ICU induction agents intensivist intubation neuromuscular blocking agents rapid-sequence intubation respiratory failure
| Introduction |
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Unfortunately, multiple factors complicate rapid stabilization of the airway for critically ill patients in the ICU. Patients who require emergency intubation frequently become combative during intubation attempts. Conditions that complicate assisted ventilation and airway intubation, such as supraglottic edema, may go undetected before airway placement attempts. Also, critical care physicians cannot always count on having the most highly skilled members of the nursing and respiratory therapy staff on duty to assist with difficult intubations.
All of these factors warrant the standardization of the approaches used for emergency intubation in the ICU to ensure proper airway placement. Emergency medicine physicians have adopted algorithmic approaches for airway assessment and for rapid-sequence intubation (RSI) as the primary approach for emergency airway management.34 RSI is the nearly simultaneous administration of a potent induction agent with a paralyzing dose of a neuromuscular blocking agent (NMBA). When applied by skilled operators for appropriately selected patients, RSI increases the success rate of intubation to 98% while reducing complications.456789101112131415 Moreover, adjunctive medications incorporated into the RSI algorithm reduce the physiologic pressor response to endotracheal intubation, which can induce cardiovascular complications. The present review outlines these standardized approaches for airway assessment and RSI with the intent of widening the use of these techniques in the ICU setting.
| Airway Assessment |
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Examination of the airway to predict difficulties with face mask ventilation and intubation is an essential component of the preoperative assessment of patients who are scheduled for elective surgery. Multiple approaches exist to identify patients with a difficult airway. Unfortunately, the utility of these airway assessment methods has not been adequately evaluated in critically ill patients who undergo urgent intubation. Moreover, a recent retrospective analysis by Levitan and coworkers18 has indicated that performing a thorough airway assessment of a critically ill patient in the emergency department is often not feasible in 70% of patients. Nevertheless, intensivists who are skilled in intubation should have an understanding of these techniques to allow their application when it is practical to do so.
| Assessment for Difficult Ventilation |
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| Assessment for Difficult Intubation |
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The Mallampati classification system,24 as modified by Samsoon and Young,25 is a widely utilized approach for evaluating patients in the preoperative setting. This system predicts the degree of anticipated difficulty with laryngoscopy on the basis of the ability to visualize posterior pharyngeal structures (Fig 1 ). The Mallampati class is devised by having patients sit up, open their mouth, and pose in the "sniffing position" (ie, neck flexed with atlantoaxial extension) with the tongue voluntarily protruded maximally while the physician observes posterior pharyngeal structures. A tongue blade is not used. A Mallampati class of I or II predicts a relatively easy laryngoscopy. A Mallampati class > II indicates an increased probability of a difficult intubation and the need for specialized intubation techniques.
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Other factors that predict a difficult intubation include a mouth opening < 3 cm (ie, two fingertips), a cervical range of motion of < 35° of atlantooccipital extension, a thyromental distance of < 7 cm (ie, three finger breadths), large incisor length, a short, thick neck, poor mandibular translation, and a narrow palate (ie, three finger breadths).2728293031 Models developed by multivariate analysis have incorporated multiple clinical factors to derive highly accurate predictive models (sensitivity, 86.8%; specificity, 96.0%) for identifying difficult intubations among patients who are undergoing elective intubations in the operating room.32 Because the incidences of both difficult laryngoscopy (1.5 to 8.0%) and failed intubation (0.1 to 0.3%) are low in the operating room with expert anesthesiologists working with patients from the healthy population, these models have a high negative predictive value (99.7%) but a low positive predictive value (30.7%).323334 Their routine use in the operating room, therefore, has questionable cost-effectiveness. Although the incidence of difficult intubations is higher in the ICU, these multivariate predictive models have not been tested in that setting. In the emergency department, nearly 70% of patients undergoing RSI have either altered mental status or cervical spine collars in place that prevent the assessment of these predictive factors.18 Consequently, no data support the value of these predictive models for routine use of RSI in the ICU to identify patients who will experience a difficult or failed intubation.
Despite the absence of validation studies to demonstrate the utility of airway assessment techniques to identify patients who will experience difficult intubations in the ICU, a quick examination of the patient for functional and anatomic factors has been shown to be predictive in the operating room setting and can assist preintubation planning.
| Advanced Airway Pharmacology |
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Preinduction Drugs
Stimulation of the airway with a laryngoscope and endotracheal tube presents an extremely noxious stimulus,39 which is associated with an intense sympathetic discharge resulting in hypertension and tachycardia (called the pressor response). The physiologic consequences of this pressor response are well-tolerated by healthy persons undergoing elective intubation. A hypertensive response, however, may induce myocardial and cerebrovascular injury in critically ill patients with limited reserves for adequate tissue oxygenation.2 Moreover, critically ill patients who require emergent intubation experience hypoxia, hypercarbia, and acidosis, which induce an extreme sympathetic outflow that is associated with tachycardia, labile BP, and an increased myocardial contractility.40 Attenuation of these physiologic stresses after the placement of an airway may unmask relative hypovolemia and/or vasodilation, which result in postintubation hypotension.40 Endotracheal intubation also can provoke bronchospasm and coughing that may aggravate underlying conditions, such as asthma, intraocular hypertension, and intracranial hypertension. Patients who are at risk for adverse events from airway manipulation benefit from the use of preinduction drugs, which include opioids, lidocaine, ß-adrenergic antagonists, and non-depolarizing neuromuscular blockers (Table 2
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Caution is advised when using opioids in patients who are in severe shock states. Opioids can block the sympathetic compensatory response to hypotension, resulting in cardiovascular collapse.
Lidocaine, a class 1B antiarrhythmic drug, has been used to diminish the hypertensive response, to reduce airway reactivity, to prevent intracranial hypertension, and to decrease the incidence of dysrrhythmias during intubation.495051 Demonstrated effectiveness for these end points, however, has varied among reports,505253 and no evidence has clearly established that lidocaine improves outcomes in terms of a lower incidence of myocardial infarction or stroke. North American physicians use lidocaine more commonly as a preinduction agent for patients who are at risk of elevated intracranial pressure compared with physicians in Europe.52 To be most effective, lidocaine should be administered 3 min prior to intubation at a dose of 1.5 mg/kg.
Esmolol is a rapid-onset, short-acting, cardioselective ß-adrenergic receptor-site blocker that effectively mitigates the tachycardic response to intubation with an inconsistent effect on the hypertensive response.4142545556 However, most studies,415456 but not all,53 have indicated that esmolol is more effective than lidocaine or fentanyl in reducing the pressor response. The combined use of esmolol (2 mg/kg) and fentanyl (2 µg/kg) has a synergistic effect for reducing both the tachycardia and hypertension associated with tracheal intubation and laryngeal manipulation.3541 Caution is needed with the use of esmolol in trauma victims and other patients who are at risk for hypovolemia and may require a tachycardic response to maintain BP.
Some protocols for RSI recommend the use of a subparalytic preinduction dose of a non-depolarizing neuromuscular blocking drug for patients with suspected raised intracranial or intraocular pressure (eg, those with acute traumatic brain injury) who will receive succinylcholine during induction for intubation.4257 Succinylcholine can cause fasciculations that may promote transient intracranial hypertension, hyperkalemia, and postintubation myalgia. A low "defasciculating dose" dose (ie, one tenth of the intubation dose) of a non-depolarizing NMBA, such as rocuronium, has been recommended585960 to prevent fasciculations and a succinylcholine-induced rise in intracranial pressure. One systematic literature review,57 however, found no evidence that pretreatment with a defasciculating dose of competitive neuromuscular blockers in patients with acute brain injury is beneficial. The available studies were limited by weak designs and small sample sizes, so a positive effect has not yet been excluded. Level II evidence exists that pretreatment before succinylcholine administration lowers intracranial pressure in patients undergoing neurosurgery for brain tumors.57 It is not the practice of the authors, however, to use a subparalyzing dose of rocuronium or any other non-depolarizing muscle relaxant as an adjunctive premedication because of the limited evidence for efficacy.
| Induction Agents |
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O2). It does not, however, attenuate the pressor response that is related to intubation or provide analgesia. Adverse effects of etomidate include nausea, vomiting, myoclonic movements, lowering of the seizure threshold in patients with known seizure disorders, and adrenal suppression.4349616263 Etomidate, even after a single bolus dose, inhibits cortisol production in the adrenal gland at various enzymatic levels and reduces adrenal responsiveness to exogenous adrenal corticotrophin hormone for up to12 h.4964 Deleterious effects of etomidate-induced adrenal suppression have not been established after a single induction dose.
Because of its rapid onset, short half-life, and good risk-benefit profile, etomidate has become the primary induction agent for emergency airway management. It is especially useful for patients with hypotension and multiple trauma because it does not alter systemic BP.
Propofol is a rapid-acting, lipid-soluble induction drug that induces hypnosis in a single arm-brain circulation time. The characteristics of propofol include a short half-life and duration of activity, anticonvulsive properties, and antiemetic effects. Propofol reduces intracranial pressure by decreasing intracranial blood volume and decreasing cerebral metabolism.6566 These mechanisms may underlie the improved outcomes with the use of propofol that have been demonstrated in patients with traumatic brain injury who are at risk of raised intracranial pressure.426367
At doses that induce deep sedation, propofol causes apnea and produces profound relaxation of laryngeal musculature. This profound muscular relaxation effect allows propofol, when used in combination with a non-depolarizing NMBA (rocuronium) or opioids (remifentanil or alfentanil) to produce intubation conditions that are similar to those obtained with succinylcholine.68697071 However, we continue to favor its use with succinylcholine to ensure adequate intubating conditions. Propofol facilitates RSI, to a greater degree than etomidate, because it provides a deeper plane of anesthesia, thereby attenuating any effects of incomplete muscle paralysis.38
The most important adverse effect of propofol is drug-induced hypotension, which occurs by reducing systemic vascular resistance and, possibly, by depressing inotropy.63 Hypotension usually responds to a rapid bolus of crystalloid fluids and can be prevented by expanding intravascular volume before giving propofol or by pretreating patients with ephedrine.72 Some patients with allergies to soy or eggs may experience hypersensitivity reactions to propofol. Propofol has no analgesic properties.
For hemodynamically stable patients who have either a contraindication to succinylcholine or receive non-depolarizing neuromuscular blockers for paralysis, propofol may be the induction agent of choice. Many clinicians use propofol as an induction drug for patients with isolated head injury or status epilepticus.
Ketamine, a phencyclidine derivative, is a rapidly acting dissociative anesthetic agent that has potent amnestic, analgesic, and sympathomimetic qualities. Ketamine acts by causing a functional disorganization of the neural pathways running between the cortex, thalamus, and limbic system.49 It does so by selectively inhibiting the cortex and thalamus while stimulating the limbic system. Ketamine is also a unique induction agent because it does not abate airway-protective reflexes or spontaneous ventilation.49
The central sympathomimetic effects of ketamine can produce cardiac ischemia by increasing cardiac output and BP, thereby increasing myocardial
O2. Patients can experience "emergence phenomena" as they resurface from the dissociative state induced by ketamine. This frightening event, characterized by hallucinations and extreme emotional distress, can be attenuated or prevented with benzodiazepine drugs. Because ketamine is a potent cerebral vasodilator, intracranial hypertension is a contraindication for its use. Other side effects include salivation and bronchorrhea, both of which can be prevented with the administration of an anticholinergic agent such as glycopyrrolate or scopolamine.
The bronchodilator properties of ketamine make it suitable for patients with bronchospasm due to status asthmaticus or COPD. No outcome studies exist, however, to demonstrate improved outcomes in these clinical settings. The sympathomimetic effects of ketamine warrant avoiding its use in patients with acute coronary syndromes, intracranial hypertension, or raised intraocular pressure.
Sodium thiopental is a thiobarbiturate with a rapid 30-s onset of action and a short half-life. Its use for RSI is limited because it is a controlled substance and propofol has similar characteristics. Barbiturates in general decrease cerebral
O2, cerebral blood flow, and intracranial pressure. They are associated, however, with hypotension secondary to the inhibition of CNS sympathetic outflow, which results in decreased myocardial contractility, systemic vascular resistance, and central venous return.6373 Hypovolemia accentuates barbituate-induced hypotension. Sodium thiopental, therefore, should not be used as an induction agent in patients who have hypovolemic or distributive shock. The central sympatholytic effect induced by barbiturates has a positive effect in its blunting of the pressor response to intubation.587475
Barbituates cause allergic reactions in 2% of patients, and also induce laryngospasm, hypersalivation, and bronchospasm.63 Just as barbiturates are generally not used in the ICU for sedation purposes, they are not used to the same extent for emergency airway management. Sodium thiopental is rarely used in the ICU for emergency intubation, although it has applications for normotensive, normovolemic patients who have status epilepticus or require intubation prior to entering barbiturate coma for the control of intracranial hypertension.
Scopolamine is a muscarinic anticholinergic agent with a short half-life that has sedative and amnestic effects, but no analgesic properties. It can cause tachycardia but otherwise produces no hemodynamic consequences.74 Scopolamine induces less tachycardia, however, compared with other available muscarinic agents (eg, atropine and glycopyrrolate).49 This hemodynamic profile makes scopolamine a preferred induction agent for patients with uncompensated shock when RSI is used. Adverse effects include psychotic reactions in addition to tachycardia and occur related to the dose administered.49 Scopolamine causes profound papillary dilation, complicating neurologic evaluations.
| NMBAs |
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Succinylcholine is the most commonly administered muscle relaxant for RSI, owing to its rapidity of onset (30 to 60 s) and short duration (5 to 15 min).76 Effective ventilation may return after 9 to 10 min. The effects of succinylcholine on potassium balance and cardiac rhythm represent its major complications. It can also induce malignant hyperthermia.77
Most reports767879 of deaths, secondary to succinylcholine-induced hyperkalemia, involve children with previously undiagnosed myopathies who underwent surgery. Although deaths related to succinylcholine-induced hyperkalemia are rare, cardiac arrest has been reported.80818283 Three studies848586 of adult patients have reported that the mean values of serum potassium levels for the study populations before and after an intubating dose of succinylcholine changed by as little as 0.04 mmol/L to as much as 0.6 mmol/L.
The hyperkalemic effect may be exaggerated in patients with subacute or chronic denervation conditions (eg, congenital or acquired myopathies, cerebrovascular accidents, prolonged pharmacologic neuromuscular blockade, wound botulism, critical illness polyneuropathy, corticosteroid myopathies, and muscle disuse atrophy), burns, intraabdominal infections, sepsis, and muscle crush injuries.81838788899091 The exaggerated hyperkalemic response is mediated through the up-regulation of skeletal muscle nicotinic acetylcholine receptors.88 Acute rhabdomyolysis can produce hyperkalemia, which is aggravated by the effects of succinylcholine, through mechanisms of drug-induced increases in muscle cell membrane permeability.838892
A personal or family history of malignant hyperthermia represents an absolute contraindication to succinylcholine therapy, which may trigger a hyperthermic response. Patients who experience masseter spasm on induction with either thiopental or fentanyl are at an increased risk of developing malignant hyperthermia when treated with succinylcholine.9394 Other contraindications that require special precautions include denervation of muscles due to underlying neuromuscular diseases or injury to the CNS, myopathies with elevated serum creatine kinase values, sepsis after the seventh day, narrow-angle glaucoma, cutaneous burns, penetrating eye injuries, hyperkalemia, and disorders of plasma pseudocholinesterase. Succinylcholine may be used safely within 24 h of experiencing acute burns,959697 and within 3 days of experiencing acute denervation syndromes and crush injuries.979899100 The drug should be used with caution in patients with preexisting chronic renal insufficiency, although a literature review101 has indicated that succinylcholine may be used safely in this setting in the absence of other risk factors for drug-induced hyperkalemia. Such patients must be closely monitored for severe hyperkalemia.
Succinylcholine-associated dysrrhythmias are mediated by postganglionic muscarinic receptors and preganglionic sympathetic receptors. Bradydysrrhythmias are most commonly observed, with rare reports of asystole and ventricular tachyarrhythmias. Most instances occur in pediatric patients or in adults after the use of multiple doses of succinylcholine.76102103 Dysrrhythmias may be prevented in adults by premedication with a vagolytic dose of atropine (0.4 mg IV) prior to repeating a dose of succinylcholine.7576
Succinylcholine may cause an increase in intragastric pressure, presumably because of drug-induced muscular fasciculation. Aspiration usually does not occur by way of this effect because of a coincident increase in tone of the esophageal sphincter.104105 Succinylcholine increases both intraocular and intracranial pressure, but these effects are transient and clinically unimportant.106107 Patients should receive succinylcholine only if adequate face-mask ventilation can be achieved if intubation fails.
Because of the extensive risks associated with the use of succinylcholine in critically ill patients, some intensivists have argued that its role in the ICU is obsolete.108 We believe that its superiority to other available neuromuscular blocking drugs (infra vida) warrant its use in patients without risk factors for adverse events. Its use requires extensive education of critical care physicians to ensure their understanding of the contraindications for use of the drug. One survey study109 observed that there was a poor understanding among critical care physicians of the risks of succinylcholine for patients with critical illness polyneuropathy.
Succinylcholine is given in a dose of 1.5 mg/kg for intubation because a lower dose may induce relaxation of the central laryngeal muscles before peripheral musculature. This circumstance may promote aspiration and complicate intubation by relaxing laryngeal muscles and promoting glottic incompetence, while leaving masseter muscle function intact.49 A recent study,110 however, suggests that comparable intubation conditions for surgical patients undergoing elective intubation can be achieved after 0.3, 0.5, or 1.0 mg/kg succinylcholine when induced with propofol or fentanyl. These lower doses allow a more rapid return of spontaneous respiration and airway reflexes.110 In the absence of such data for critically ill patients who require urgent intubation, we continue to recommend the use of succinylcholine, 1.5 mg/kg, for RSI.
Non-Depolarizing NMBAs
Non-depolarizing NMBAs provide an alternative to succinylcholine for RSI. Rocuronium, an aminosteroid drug, has a short onset of action (1 to 2 min) and an intermediate duration of action (45 to 70 min).
A systematic review68 compared relative outcomes with the use of succinylcholine for intubation to those with the use of rocuronium. This study concluded that the use of succinylcholine produced superior intubation conditions compared to that of rocuronium (0.6 mg/kg) when rigorous standards were used to define the term excellent conditions (relative risk of poor conditions with rocuronium use, 0.87; 95% confidence interval, 0.81 to 0.94; n = 1,606). The two agents had similar efficacy when less rigorous definitions were used to define adequate intubation conditions. No differences were found, however, if propofol was used for induction, or if the dose of rocuronium was 1.0 mg/kg. The use of this higher dose of rocuronium prolongs the duration of paralysis. The success rate of intubation was similar for both rocuronium and succinylcholine under all of the study conditions.68
The effects of non-depolarizing blocking drugs can be reversed using acetylcholinesterase inhibitors, such as neostigmine or edrophonium, and vagolytic doses of glycopyrolate or atropine. The only absolute contraindication to the use of rocuronium is allergy to aminosteroid neuromuscular drugs. Extreme caution should be exercised in selecting appropriate patients for its use. Patients for whom intubation appears likely to be difficult may experience hypoxia if face mask ventilation is unsuccessful during the prolonged period of drug-induced paralysis (45 to 70 min) before intubation can be achieved.
| Airway Management in the ICU |
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Although not validated, algorithms reported by Walls and coworkers114 provide a standardized approach to emergency airway management. Such algorithmic approaches for emergent intubation that appropriately select patients for RSI have demonstrated improved outcomes in both emergency department and field intubation settings.567891011121315 Emergency medicine practitioners who utilize airway management protocols that incorporate RSI experience airway failures with a need to progress to emergency cricothyrotomy in only 0.5% of intubations.56 The National Emergency Airway Registry II,6 a data bank of 7,712 intubations, has demonstrated that RSI is the most common technique of intubation with a success rate > 98.5%. These results contrast with the 18% incidence of failed intubation in the absence of RSI reported by Li and coworkers.7 This prospective study compared complications arising from intubation utilizing paralytic agents within an RSI protocol to intubations those arising from intubations without the use of NMBAs. Esophageal intubations and airway trauma occurred with greater frequency in the group that did not receive RSI (18% vs 3%, respectively, and 28% vs 0%, respectively).7
The intubation algorithms modified from Walls and coworkers114 (Figs 2345 ) classify intubation attempts into the following categories: (1) universal; (2) crash; (3) difficult; and (4) failed. The universal algorithm (Fig 2) is the beginning point for intubation for all patients. The initial assessment requires the intensivist to determine whether the patient is unresponsive or near death, or whether a difficult airway appears likely. The former requires activation of the crash airway algorithm (Fig 3), and the latter activation of the difficult airway algorithm (Fig 4). The absence of any of these conditions allows the physician to initiate RSI.
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| RSI |
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Several factors underlie the improved outcomes with RSI. Preoxygenation reduces the need for face-mask ventilation in preparation for intubation, and thereby decreases the risks for gastric insufflation and the aspiration of stomach contents. The use of a potent induction agent with a neuromuscular blocking drug allows the airway to be rapidly controlled, further reducing the risk of aspiration. The use of adjunctive medications in appropriate clinical settings can reduce the pressor response and other physiologic consequences of laryngoscopy and tracheal intubation. Table 5 presents an example of the authors typical RSI protocol.
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The general sequence of RSI consists of the "six Ps," as follows: preparation, preoxygenation, premedication, paralysis, passage of the endotracheal tube, and postintubation care. Preparation begins when the clinician identifies the need for intubation. A period of 5 to 10 min before intubation allows for the evaluation of the patient for signs of a difficult airway, as described above, and for the preparation of the equipment. Among the various mnemonics that are used to assist preparation, the phrase "Y BAG PEOPLE?" (Table 6 ) allows physicians to recall the essential elements of the preparatory phase and emphasizes the need to avoid positive-pressure face mask ventilation whenever possible.
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Premedication entails the use of drugs to provide sedation and analgesia, and to attenuate the physiologic response to laryngoscopy and intubation. Two to three minutes before the patients undergoes laryngoscopy, a combination of drugs individualized to a patients needs and clinical circumstances is administered (Table 2).
The induction and neuromuscular blocking drugs are administered immediately after the patient achieves adequate preoxygenation and receives the preinduction medication. An assistant performs the Sellick maneuver (ie, cricoid pressure) to prevent passive aspiration and reduce gastric insufflation if the patient is receiving positive-pressure ventilation by face mask. If the patient vomits, cricoid pressure should be released and the patient should be log-rolled to allow dependent suctioning of the pharynx.
Although many emergency physicians use etomidate as their primary induction drug, other drugs have specific advantages in certain clinical settings (Table 3). The selection of a neuromuscular blocking drug also depends on clinical circumstances, as previously described. Succinylcholine provides safe and effective neuromuscular blockade for most patients. Rocuronium may be a more appropriate choice for patients if there are contraindications or concerns about the use of succinylcholine.
Forty-five seconds to 1 min after induction and paralysis, the adequacy of paralysis is assessed by checking mandibular mobility. Resistance to motion indicates incomplete paralysis, which requires that the patient start to receive oxygen again, with reassessment of relaxation taking place in 15 to 30 s.
Once the patient is relaxed, laryngoscopy is performed and the vocal cords visualized. Visualization of the vocal cords and the glottic opening may be improved by placing pressure on the thyroid cartilage in a backward, upward, and rightward direction (the mnemonic "BURP" or backwards, upwards, right, and pressure).8 If laryngoscopy is not immediately successful and the patients oxygen saturation level falls to < 90%, assisted ventilation is initiated with a bag-valve-mask device and cricoid pressure to oxygenate and ventilate the patient before attempting laryngoscopy again. After successful tracheal intubation and cuff inflation, the confirmation of intubation is required.
The goal in the immediate postintubation period is to confirm correct tracheal intubation, and the adequacy of oxygenation and ventilation. Epigastric auscultation followed by auscultation of both hemithoraces in the axillas assists in assessing for an esophageal or mainstem intubation. The rise and fall of the chest and the maintenance or improvement of oxygenation should be noted. The measurement of end-tidal CO2 by either a colorimetric or waveform device has become a necessary step in confirming tracheal intubation. Once satisfied that the endotracheal tube is in the trachea, cricoid pressure may be released. The cuff is then rechecked, and the endotracheal tube is secured to the patient. A postintubation chest radiograph and arterial blood gas assessment should be obtained. Many of the induction agents and succinylcholine have a short duration of action. Thus, sedation should be considered at this point.
| Conclusion |
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| Footnotes |
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O2 = oxygen uptake Received for publication April 14, 2004. Accepted for publication August 31, 2004.
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