⅙ Other extraglottic device, according to institutional preference F. Surgical: • Needle-guided percutaneous cricothyro- tomy set, for example, Melker or PCK, with cuffed cannula • Surgical cricothyrotomy equipment: scalpel handle, #11 blade, tracheal hook, Trousseau dilator, #6.0 ETT, Shiley cuffed tracheostomy (#4) tubes G. Other Equipment: • End-tidal CO 2 (ETCO 2 ) detector • Twill tape • Esophageal detector device (EDD), for example, 60 cc catheter-tip (Toomey) syringe • 10 cc syringes for cuff inflation • Suction catheters: rigid tonsillar (e.g., Yankauer) and flexible endotracheal tube suction catheters • Magill forceps • Bite blocks • Adult airway exchange catheter • Materials for application of topical airway anesthesia: tongue depressors; Mucosal Atomization Device (e.g., MADgic®) or DeVilbiss atomizer; Jackson forceps; cotton pledgelets; Lidocaine 10% spray, 2% gel, 5% ointment, 4% liquid Sample Pediatric Equipment Note: Departments with significant pediatric volumes may wish to consider organizing equip- ment in a color-coded fashion according to Broselow tape sizes. • Broselow tape • Oxygen masks: newborn, pediatric • Manual resuscitator with infant and child- sized masks • Oral airways: 3.5, 5, 6, 7 cm • Laryngoscope blades: straight (e.g., Miller) 0, 1, 2; & curved (Macintosh) 1,2, and 3 • ETT: uncuffed—2, 2.5; cuffed and uncuffed— 3, 3.5, 4, 4.5; cuffed—5, 5.5, 6, 6.5, 7 • Stylet: 6 Fr, 8 Fr • Bougie: pediatric • LMA: 1, 1.5, 2, 2.5, 3; or other pediatric extra- glottic devices • +/- Lightwand: infant and child sizes • +/- Pediatric fiberoptic stylet: Shikani or Brambrinck • Small Magill forceps • ETCO 2 detector, pediatric size • #18, #16, and #14 G IV catheters for cricothy- rotomy Finally, the presence of an “airway drug kit” with all the necessary pharmacologic agents, in one location, is highly recommended. RESPONSE TO AN ENCOUNTERED DIFFICULT AIRWAY 209 This page intentionally left blank This page intentionally left blank Chapter 13 Airway Pharmacology 211 and respiratory consequences, in the at-risk patient. • Succinylcholine remains in widespread use for several reasons: (a) it has a very rapid onset; (b) it usually has a very short duration of action; and (c) clinicians are familiar with its use. • Rocuronium use avoids the need to con- sider many of the contraindications to, and precautions associated with succinyl- choline use. • A decrease in blood pressure is common following induction and intubation. • The initial response to hypotension from almost any cause should be circulatory volume expansion. However, clinicians should also be comfortable with the indica- tions for, and use of short-acting vasopressors. ᭤ INTRODUCTION Airway management, including endotracheal intubation, requires a competent understanding of airway pharmacology. A small number of medications are used to facilitate airway man- agement, for various indications as shown in Table 13–1. Successful airway intervention without patient compromise requires a good working knowledge of these agents, together with an appreciation of expected physiological responses to manipulation of the airway. ᭤ KEY POINTS • For the patient requiring emergency airway management, preservation of oxy- genation and blood pressure often takes priority over attenuation of undesirable reflexes. • There is strong evidence that in the head- injured patient, hypoxia or hypotension occurring during patient resuscitation can significantly increase mortality. • Ketamine produces excellent amnesia and is the only induction agent to also provide analgesia. • Although ketamine can indirectly raise blood pressure by sympathetic nervous system stimulation, intrinsically, it is a myocardial depressant. • Etomidate is remarkable for its stable hemodynamic effects and has become the induction agent of choice in many North American emergency departments. • Etomidate does cause adrenal suppression. Unless risk/benefit assessment suggests otherwise, an alternative agent should be used for induction in the septic patient. • In airway management, the primary role of midazolam is as a light sedative for the patient undergoing an awake intubation. • The advantageous effects of pretreat- ment agents must be balanced against their potential adverse hemodynamic Copyright © 2008 by The McGraw-Hill Companies, Inc. Click here for terms of use. ᭤ THE PHYSIOLOGIC RESPONSE TO LARYNGOSCOPY AND INTUBATION Laryngoscopy and intubation are powerful stimuli that can provoke intense physiologic responses from multiple body systems. 1,2 These responses, including hypertension, tachycardia, increased intracranial pressure (ICP), and bron- choconstriction, are generally transient, and of little consequence in most individuals. How- ever, for some patients, if these responses are not attenuated, significant morbidity may ensue. It should be appreciated that most of the data supporting the attenuation of these adverse physiologic responses has been gathered from generally healthier, elective surgical patients. For the patient requiring emergency airway management, preservation of oxygenation and blood pressure often takes priority over atten- uation of undesirable reflexes. Stimulation of the oropharynx and upper airway activates both arms of the autonomic nervous system. In adults, the sympathetic response usually predominates, with an increase in circulating levels of catecholamines. In young children (and some adults) airway instrumenta- tion may cause a predominately vagal response, including bradycardia. It is important to note that intubation tech- niques other than direct laryngoscopy will still elicit these responses. 3 Systems primarily 212 CHAPTER 13 ᭤ TABLE 13–1 MEDICATIONS COMMONLY USED FOR AIRWAY MANAGEMENT Procedure Medication Type Indication Sample Medications Awake intubation Topically applied or Airway anesthesia for Lidocaine spray, regionally injected awake intubation jelly, ointment, local anesthetic injectable agents Awake intubation Adjuvant sedative Anxiolysis, analgesia, Benzodiazepines, agents and sedation during Opioids, Buty awake intubation rophenones, Propofol, Ketamine Awake intubation Opioid and Use in case of overdose Naloxone, benzodiazepine of opioid or Flumazenil anatogonists benzodiazepine Rapid-sequence “Pretreatment” agents Attenuation of undesirable Atropine, Lidocaine, intubation physiologic reflexes Opioids, Neuromus- during laryngoscopy cular blockers and intubation Rapid-sequence Induction agents and Induction of unconsciousness Etomidate, Propofol, intubation neuromuscular (control of ICP), and Thiopental, blockers subsequent skeletal muscle Ketamine. relaxation to facilitate Succinylcholine, laryngoscopy Rocuronium Rapid-sequence Miscellaneous rescue Treatment of Dantrolene intubation agents succinylcholine-induced malignant hyperthermia Awake or Rescue vasopressor Treatment of postintubation Ephedrine, rapid-sequence and other agents hypotension Phenylephrine intubation affected by direct laryngoscopy and/or intuba- tion include the cardiovascular, respiratory, and central nervous systems. When indi- cated, local anesthesia and systemic medica- tions can be used to minimize these undesirable effects. The following sections will review the responses in question. Cardiovascular Response to Laryngoscopy and Intubation Laryngoscopy and intubation causes an increase in both sympathetic and sympathoadrenal activity. This usually results in transient hyper- tension and tachycardia, correlating with a rise in catecholamine levels. Under “light general anesthesia,” systolic blood pressure has been shown to rise an average of 53 mm Hg in response to laryngoscopy and intubation, while the heart rate increases by 23 beats per minute. 1 In smokers and individuals with preexisting hypertension, the rise in blood pressure can be more pronounced. 4 In healthy patients, these hemodynamic effects are usually of little conse- quence. However, patients in whom attenuation of this pressor response may be important include: • The patient with coronary artery disease. Significant rises in heart rate and blood pres- sure (BP) could result in myocardial ischemia due to increased myocardial oxygen demand. • The patient with an unruptured cerebral or aortic aneurysm, or aortic dissection. A dramatic increase in mean arterial pressure (MAP) could lead to aneurysm rupture or worsening dissection, respectively. • Patients with significant preexisting hypertension, including women with pregnancy-induced hypertension. Further increases in BP could overcome the limits of cerebral autoregulation and potentially lead to increased ICP or cerebral hemorrhage The pressor response to laryngoscopy and intubation can be attenuated by one of a number of drug regimens, including deep anesthesia and/or vasoactive agents. However, in the volume-depleted emergency patient, any pressor response to laryngoscopy and intubation may by counteracted by the vasodilating and negative inotropic effects of induction agents. Such a drop in blood pressure during a resuscitation can be associated with increased morbidity and mortality. 5 The best approach must take into consideration the individual patient, the experience of the physician, and the available medications. Respiratory System Response to Laryngoscopy and Intubation Coughing, laryngospasm, and bronchospasm are all potential responses to airway manipula- tion. Laryngospasm may be more common in the pediatric population. Gagging may lead to vomiting and potential aspiration. All of these responses are more likely in the inadequately anesthetized patient and those with underlying respiratory pathology. Coughing, gagging, and laryngospasm can be abolished with the use of neuromuscular blocking agents. Bronchospasm does not respond to muscle relaxants since these agents do not block smooth muscle receptors in the airways. Bronchoconstriction can be attenuated by deep anesthesia and the use of drugs that promote bronchial smooth muscle relaxation. Obviously, hypoxia and hypercarbia are potential complications of laryngoscopy and intubation, especially if prolonged attempts at intubation are made without intervening bag- mask ventilation (BMV). Central Nervous System Response to Laryngoscopy and Intubation Laryngoscopy and intubation results in a tran- sient rise in ICP. 1 This increase in ICP may be a direct response to central nervous system (CNS) stimulation, causing an increase in cere- bral blood flow (CBF). ICP may also rise if sys- temic blood pressure is profoundly raised AIRWAY PHARMACOLOGY 213 and/or venous outflow is obstructed (e.g., by straining or coughing). Although this is of little consequence in most individuals, in patients in whom ICP is already elevated or in whom cerebral autoregulation is impaired, these effects could complicate an already dan- gerous situation. As discussed in more detail in Chap. 14, the focus in management of the patient with trau- matic brain injury has shifted from simply preventing an ICP rise with endotracheal intubation, to maintenance of cerebral perfu- sion pressure (CPP). CPP is determined by the difference between mean arterial pressure (MAP) and the ICP, that is, CPP = MAP – ICP. There is now evidence that in the head-injured patient, hypoxia or hypotension occurring during patient resuscitation can signifi- cantly increase mortality. 6 Therefore, the importance of avoiding a lowered MAP during intubation may assume greater clinical signifi- cance than a transient increase in ICP. Although deep anesthesia can block the direct effect of laryngoscopy and intubation on ICP, this approach can also result in a signifi- cant decrease in MAP and CPP. In the head- injured patient, a pre-intubation fluid bolus and special care in choosing the dosage of induc- tion medication is needed to help avoid signifi- cant drops in CPP. ᭤ INDUCTION SEDATIVE/ HYPNOTICS Induction sedative/hypnotics are used pri- marily to induce unconsciousness in the patient as part of an RSI. In lower doses, some can also be used as sedative agents. In modern practice it is accepted that, except in unusual circumstances, the use of muscle relax- ants requires the concomitant use of an induc- tion agent to ensure lack of awareness. To this extent, induction sedative/hypnotics are gener- ally considered a mandatory component of RSI, at all ages. There is some evidence suggesting that use of induction sedative/hypnotics as part of an RSI actually improves intubating conditions and decreases time needed to perform RSI. 7,8 How- ever, this data is difficult to interpret and may in part simply reflect the rapid onset and potency of the sedative/hypnotic compensating for attempted intubation before full onset of neu- romuscular blockade. In determining the appropriate dosage of induction agent, several factors must be consid- ered. These include: A. Patient weight: Drug dosing is based pri- marily on patient weight. The appropriate loading dose of an agent is largely depen- dent on the volume of distribution. The volume of distribution reflects the medica- tion’s lipid solubility. How the drug is dis- tributed in turn impacts the decision to dose based on ideal body weight (IBW) or total body weight (TBW). 9 With obesity, both lean and fat mass increase, but fat increases pro- portionally more. Clinical data on how to dose induction sedative/hypnotics in obese patients is limited. For propofol and thiopental, the recommendation is for dosing based on TBW. 9 However, for many drugs, the situation is indefinite. For this reason, many clinicians dose agents based on a weight that lies somewhere between IBW and TBW. B. Age: With the exception of neonates, anes- thetic requirements decrease with advancing age. An 80-year old will typically require only half the induction dose of a 20-year old. C. Hemodynamics: Hypotension is common following intubation. One study quotes a 25% incidence of life-threatening hypoten- sion in the initial phase of mechanical ven- tilation. 10 It is important to note that all induction sedative/hypnotics can cause a drop in blood pressure. As this is more dra- matic in patients with preexisting hypov- olemia, volume status must be taken into account when determining the dose of induction agent. 214 CHAPTER 13 AIRWAY PHARMACOLOGY 215 D. Level of Consciousness: The purpose of using an induction sedative/hypnotic is to induce a state of unconsciousness and amnesia. If this is already present, either from drugs (e.g., the overdose patient) or pathology (e.g., the head-injured, hypoten- sive, or arrested patient), the need for addi- tional induction agent is diminished (but often still necessary). This can sometimes be a difficult decision, as airway manipula- tion is intensely stimulating and especially in an overdose situation may “awaken” an apparently unconscious patient. Provided the hemodynamics will tolerate it, the authors would generally recommend admin- istration of an induction sedative/hypnotic (even to the unconscious patient) whenever muscle relaxants are used. Propofol Propofol is an intravenous sedative/hypnotic agent that works primarily via gamma amino butyric acid (GABA) receptors to produce hyp- nosis. 11,12 Propofol has become popular because of its rapid onset and short clinical dura- tion. Recovery from the effects of propofol is notable for the lack of residual sedation. Propofol causes a dose-dependent decrease in level of consciousness. Small doses (0.25–0.5 mg/kg) result in sedation while larger doses (1–3 mg/kg) are used to induce uncon- sciousness. Propofol does not possess intrinsic analgesic properties and although it may produce amnesia, this effect is not as reli- able as that seen with the benzodiazepines. Fol- lowing a bolus of 2 mg/kg to a healthy adult, unconsciousness is generally produced within 30 seconds, with recovery taking 5–15 minutes. As a potent respiratory depressant, apnea is common following an induction dose. Propofol decreases airway reflexes to intubation in a dose-dependent manner. Propofol is a myocardial depressant and also results in peripheral vasodilation. This results in a decrease in blood pressure following a bolus dose. For this reason, a fluid bolus is commonly given before its administration. In patients with hypovolemia or impaired heart function, this drop in blood pressure can be quite marked. The hemodynamic effects are more pronounced in the elderly, in whom the dose should also be lowered. Although propofol lowers ICP, a decrease in CPP can still result from its administration, because of its adverse effect on blood pres- sure. This decrease in CPP may be particularly detrimental in the head-injured patient who is also hypovolemic and has impaired autoregula- tion. Propofol may offer a degree of cerebral protection, 13 but the clinical significance of this is unknown. Prolonged high-dose propofol infusions have been associated with poor outcomes in the ICU setting. This phenomenon, called “propofol infusion syndrome” has been described mainly in children but recently also in adults. 12 As such, caution should be exercised when propofol infusions are to be administered in high doses for more than 48 hours. The manufacturer does not recommend propofol for long-term seda- tion in pediatric ICU patients. 14 For emergency intubations and to facilitate procedures, how- ever, even in children, propofol has been safely used outside the OR. 15 Propofol may cause pain on injection. This can be minimized by injecting into a large vein. The addition of 1–2 cc of 1% lidocaine to the syringe of propofol just prior to injection may also decrease discomfort. Propofol is supplied as a 10 mg/mL emul- sion containing 10% soybean oil and 1.2% puri- fied egg phosphatide. In theory, individuals with egg or soybean allergies could be sensi- tive, but in practice, allergic reactions to propofol are exceedingly rare. This preparation has been shown to be a growth medium for certain microorganisms, so that sterile technique should be utilized when handling propofol: it should be drawn up immediately before use and unused portions discarded. 14 P ROPOFOL AS A S EDATIVE A GENT Propofol can be used as an agent to blunt aware- ness for an ‘awake’ intubation, but does not address anxiety or discomfort associated with the procedure in the way that benzodiazepines or narcotics, respectively, are able to do. If used for sedation, propofol should be administered in small doses (e.g., 0.25 mg/kg), maintaining verbal contact with the patient. In the critically ill patient, even when used in small doses, it can cause loss of consciousness and hypoten- sion. Use of propofol to achieve a state of deep sedation for intubation will impair protective airway reflexes, while not providing the facili- tated conditions provided by RSI with a muscle relaxant. S UMMARY Drug: Propofol. Drug type: Anesthetic induction sedative/ hypnotic. Indication: Induction of unconsciousness; sedation. Contraindications: Uncorrected shock states are relative contraindications, at least requiring a significant decrease in dose. Pediatric long- term infusions are contraindicated. Dose: Induction dose is 1–3 mg/kg (average 75 kg = 150 mg). Dosage should be decreased in the elderly and volume-depleted patient. Onset/Duration: Onset is ~30 seconds. Clinical duration is 5–15 minutes. Potential Complications: Hypotension and apnea; pain on injection. Thiopental Thiopental is a barbiturate sedative/hypnotic, and until the introduction of propofol, it was the primary agent used for induction of general anesthesia. Despite the popularity of propofol, thiopental is still widely used in many operating rooms (ORs) and emergency departments (EDs). The barbiturates exert their main effect by binding to and potentiating GABA receptors in the central nervous system (CNS). They produce a dose-dependent CNS depression, ranging from sedation to pharmacologic coma. Thiopental has a rapid onset with clinical effects seen within about 30 seconds. Following a single dose, recovery generally takes 5–10 minutes. Recov- ery may be substantially longer following repeated doses or infusions. Thiopental is a potent respiratory depres- sant, and apnea is the norm following an induc- tion dose. This agent has also been associated with clinically relevant histamine release, which may induce bronchospasm. In fact, the manu- facturer lists status asthmaticus as an absolute contraindication. 16 Despite this, thiopental has been used successfully in the management of severe asthma. 17 Thiopental, like propofol, causes a decrease in ICP and cerebral oxygen consumption, the- oretically making it an attractive choice for use in the brain-injured patient. As with propofol, however, care must be taken to not lower ICP at the expense of a profound reduction in blood pressure, as thiopental is also a potent myocardial depressant. In the presence of hypovolemia, a significant drop in blood pres- sure can result. The dose of thiopental for RSI is 3–5 mg/kg, although this dose should be lowered in elderly or hypovolemic patients. It is supplied as a powder, which must be dissolved in sterile water to produce a 2.5% solution (25 mg/mL). The resulting solution is highly alkaline and care must be taken to avoid interstitial or intraarterial injec- tion. Care must also be taken to avoid direct inter- action with acidic solutions (e.g., most of the neuromuscular blockers) as this may result in precipitation and loss of intravenous (IV) access. T HIOPENTAL AS A S EDATIVE A GENT Thiopental is not generally used as a sedative agent to facilitate awake intubations. S UMMARY Drug: Thiopental. Drug type: Anesthetic induction agent; sedative/ hypnotic. 216 CHAPTER 13 Indication: Induction of unconsciousness. Contraindications: Uncorrected shock states are relative contraindications that require a marked decrease in dose. Dose: Dose is 3–5 mg/kg (average 75 kg = 250 mg), depending on hemodynamics. Onset/Duration: Onset is about 30 seconds. Clinical duration is 5–10 minutes. Potential complications: Hypotension and apnea. Ketamine Ketamine is unique among the sedative/hyp- notic agents in both its mechanism of action and its clinical effects. Ketamine produces a state of “dissociative amnesia,” referring to a dissociation occuring between the thalamocortical and limbic systems on electroencephalogram (EEG). Clinically, the result is a catatonic state in which the eyes often remain open, with obvi- ous nystagmus. The patient may sporadically move, but nonpurposefully, and not generally in reaction to painful stimuli. Ketamine pro- duces excellent amnesia and is the only induction agent to also provide analgesia. Ketamine may exert some of its analgesic prop- erties via opioid receptors, although these effects are not consistently antagonized by naloxone. 18 Ketamine has a centrally stimulating effect on the sympathetic nervous system (SNS) by decreasing catecholamine reuptake. These effects are responsible for many of the observed clinical effects. For example, via SNS stimulation, ketamine relaxes bronchial smooth muscle, in turn causing a decrease in airway resistance and improved pulmonary compli- ance. At higher doses, ketamine may also act directly to relax bronchial smooth muscle, although clinical benefit has not been clearly demonstrated. 18,19 These effects make ketamine a particularly attractive agent for induction of the patient with acute bronchospasm. Ketamine tends to preserve ventilatory drive, although a large, rapidly administered bolus dose may still result in apnea. Ketamine may result in an increase in secretions, an effect which can be managed (although rarely indi- cated) by pretreatment with a drying agent such as glycopyrrolate or atropine. In addition, keta- mine when used alone (i.e., not part of an RSI) has been associated with laryngospasm. 18,20 This may be more common in infants, to the extent that ketamine sedation may be con- traindicated under 3 months of age. 20 SNS stimulation is also responsible for an increase in heart rate (by about 20%) and blood pressure (a rise of around 25 mm Hg) with ket- amine use. Care should thus be exercised in patients with coronary artery disease, as ketamine has the potential to aggravate myocar- dial ischemia. Due to its ability to raise blood pressure, it has been suggested that ketamine would be particularly suited for use in patients with unstable hemodynamics. It must be remembered, however, that the hemodynamic effects are secondary to SNS stimulation and that intrinsically, ketamine is in fact a myocar- dial depressant. Thus, ketamine could theoreti- cally lower blood pressure in patients who are already maximally sympathetically stimulated. Therefore, as with all induction seda- tive/hypnotics, caution should be used in patients with severe shock, and the induc- tion dosage reduced. Much controversy has centered around the use of ketamine in patients with intracranial pathology. Historically, ketamine has been con- sidered to be contraindicated in patients with decreased intracranial compliance due to reports that it could increase ICP and increase cerebral oxygen demand. However, the data upon which these recommendations were made did not involve patients with traumatic brain injury. 21 Indeed, more recent data using human and animal subjects suggest that low-dose bolus ketamine may have a beneficial effect on CPP in this setting. 21,22 When used in conjunction with a GABA agonist (such as propofol or mida- zolam), ketamine has actually been shown to lower ICP. 23 A cerebral protective effect has AIRWAY PHARMACOLOGY 217 been shown with ketamine use in animals, pos- sibly mediated through NMDA receptor blockade, and a similar effect is being investigated in humans and appears to show promise. 22 How- ever, at this time, ketamine cannot be recom- mended for routine use in patients at risk of increased ICP, unless they also are also hypoten- sive (in relative or absolute terms), in which case ketamine’s hemodynamic effects may help preserve CPP. Ketamine has been associated with unpleasant emergence reactions characterized by “bad dreams,” disorientation and perceptual distur- bances. 18 This is relatively uncommon in chil- dren and seems in part to be related to the “state of mind” at the time of the drug’s administra- tion. 18,20,24 At least in children, this phenomenon is not reduced by concomitant administration of benzodiazepines. 18,20,24,25 Emergence reactions are not generally a consideration in the patient requiring RSI in emergencies. Ketamine is supplied as either a 10 or 50 mg/mL solution. The induction dose of keta- mine is 1-2 mg/kg as an IV bolus. Onset time is generally within 1 minute and clinical duration is 15–20 minutes. A lower dose should be used for the patient in profound shock. Conversely, the higher end of the dose range should be used if bronchodilation is the goal. An “off-label” combination of ketamine with propofol (each in 10 mg/mL concentrations) drawn up in a single syringe (“ketafol”) has been used in recent years, primarily for procedural sedation in emergency departments. 26,27 The mixture has also been used as an induction agent for RSI, with at least a theoretic advantage of maintenance of stable hemodynamics. K ETAMINE AS A S EDATIVE A GENT Ketamine is usually administered as a single predetermined dose to achieve a state of disas- sociation. However, smaller doses of ketamine can be used as a sedative for awake intubation or “awake look” laryngoscopy in the uncooper- ative patient. Used in this way, in divided doses of 0.25–0.5 mg/kg, it has the advantage of main- tained respiratory drive and good analgesia. How- ever, it can also increase secretions, which as mentioned can increase the risk of laryngospasm, particularly in the pediatric patient. A theoreti- cal risk of under-dosing relates to ketamine’s use as a “street drug,” where it may induce, or worsen an intoxicated, uncooperative state. S UMMARY Drug: Ketamine. Drug type: Anesthetic induction agent, seda- tive/hypnotic, analgesic. Indication: Induction of unconsciousness, especially for patients with severe bron- chospasm or unstable hemodynamics. Seda- tive to facilitate non-RSI intubations. Contraindications: Known coronary artery disease or an elevated ICP are relative con- traindications (see text). Dose: Dose is 1–2 mg/kg IV (average 75 kg = 100 mg). Onset/Duration: Onset is within 60 seconds. Clinical duration is 15–20 minutes. Potential Complications: Increase in heart rate (HR) and BP, with potential myocar- dial ischemia. Increase in ICP. Emergence reactions. Etomidate Etomidate is a sedative-hypnotic which has been available for use in the United States since 1983. Its mechanism of action probably involves GABA receptors, although it has a dif- ferent drug-receptor interaction than that seen with the barbiturates and propofol. As with other induction agents, it has a predictably rapid onset and short duration of action (5–15 minutes following a standard induction dose). Etomidate has become the induction seda- tive/hypnotic of choice in many EDs through- out North America. 28 Etomidate is remarkable for its hemo- dynamic stability. 29,30 This makes it particularly 218 CHAPTER 13 [...]... succinylcholine similarly increases the ICP of brain-injured patients.69 In brain tumor patients undergoing elective surgery, two studies have shown an attenuation of a succinylcholine-induced rise in ICP with nondepolarizing agent pretreatment.70, 71 However, to date there is no similar data supporting the use of defasciculating agents prior to succinylcholine use in brain-injured patients In practice, succinylcholine... succinylcholine should be used Succinylcholine may cause cardiac dysrhythmias Bradydysrhythmias are most common and are more likely following a repeat dose of succinylcholine In this regard, it is recommended that atropine be administered prior to giving a second dose of succinylcholine, even in a tachycardic patient Succinylcholine has been shown to increase intraocular pressure (IOP) However, in patients... Contraindications: Predicted inability to either bag-mask ventilate or intubate Dose: Dose is 1 mg/kg IV (average 75 kg = 80 mg) Onset/Duration: Onset is within 1–1.5 minutes Clinical duration is 45 80 minutes, depending on dose administered Potential Complications: Hypoxia, hypercarbia Pain on injection Vecuronium Vecuronium is an intermediate-acting nondepolarizing muscle relaxant An intubating dose of 0.1 mg/kg... muscle relaxation post-intubation Contraindications: Predicted inability to either bag-mask ventilate or intubate Dose: Intubating dose is 0.1 mg/kg IV (average 75 kg = 8 mg initially; 1–2 mg for maintenance of post-intubation paralysis) As a pretreatment agent before succinylcholine, 01 mg/kg (average = 0.5–1.0 mg) Onset/Duration: Onset is within 5 minutes Clinical duration is 60–90 minutes Potential Complications:... prevents succinylcholine-induced increases in intracranial pressure Anesthesiology 1 987 ;67(1):50–53 71 Minton MD, Grosslight K, Stirt JA, et al Increases in intracranial pressure from succinylcholine: prevention by prior nondepolarizing blockade Anesthesiology 1 986 ;65(2):165–169 72 Silber SH Rapid sequence intubation in adults with elevated intracranial pressure: a survey of emergency medicine residency programs... alpha-2 receptor agonist, currently approved for sedation in an intensive care setting Delivered by infusion in an initial dose of 1 µg/kg over 10 minutes, followed by ongoing infusion at 0.2–0.7 µg/kg/h, it is remarkable for not significantly suppressing ventilatory drive Case reports and series47, 48 are appearing on its use to facilitate awake intubations in the OR setting In time, its use for this indication... in patients with open eye injuries, no adverse effects from succinylcholine administration have been reported, despite extensive use.67 Coughing and straining during intubation will raise intraocular pressure significantly more than succinylcholine use alone Rocuronium may be a better choice for patients with open-eye injuries, in that during RSI, compared to succinylcholine, it has been shown to significantly... consciousness Clinician experience is also invaluable in making drug choices and choosing dosages The drug indications and dosages outlined in this text should therefore be used only as a guide Intravenously injected agents act quickly The clinician using these drugs must have a solid knowledge of their indications, contraindications, dosing, and expected clinical effect It is incumbent on the clinician to... anesthetic induction agents: propofol versus ketamine Anesthesiology 1999; 90(3) :82 2 82 8 Green SM, Krauss B Clinical practice guideline for emergency department ketamine dissociative sedation in children Ann Emerg Med 2004;44(5): 460–471 Sehdev RS, Symmons DA, Kindl K Ketamine for rapid sequence induction in patients with head injury in the emergency department Emerg Med Australas 2006; 18( 1):37–44... by pseudocholinesterase in the blood stream The duration of muscle relaxation following a single dose of 1–2 mg/kg is typically 5–10 minutes, although initial return of spontaneous respiration will often occur in less than 5 minutes Adequate intubating conditions are consistently achieved in less than 1 minute following an IV bolus 1–2 mg/kg of succinylcholine When dosing succinylcholine, it is better . data supporting the use of defasciculating agents prior to succinylcholine use in brain-injured patients. In practice, suc- cinylcholine is commonly used to facilitate intu- bation in this population. 72 Succinylcholine. gastrointestinal (GI), and gen- itourinary (GU) tracts. Clinically, atropine results in an increase in heart rate, decrease in secre- tions, and potential bronchodilation. In toxic doses, atropine. phar- macologic aid in airway management. It has a relatively slow onset time, taking up to 15 minutes for peak effect following an IV injection. In addi- tion, morphine can result in histamine