Michael F. Murphy
Stephen Beed
Ron M. Walls
The Clinical Challenge
Airway management of the critically ill patient, whether in the intensive care unit (ICU), the emergency department, or elsewhere is characterized by the following:
1. The physical environment often presents patient access and positioning challenges.
2. The airways of critically ill patients are frequently characterized as “difficult.”
3. The patients have limited “physiological reserve”; they poorly tolerate airway manipulation and the medications employed to facilitate airway management.
4. Knowing when and how to extubate is challenging.
5. An array of routine and rescue airway management equipment is often unavailable.
Physicians who practice in the emergency department or ICU environment, or who respond to airway emergencies in inpatient units, must be prepared to deal with the challenges listed above. This chapter emphasizes the ICU environment, but the principles apply equally, regardless of the patient's physical location within the health care system.
Approach to the Airway
The Physical Environment
The American College of Critical Care Medicine describes three echelons of ICUs, all of which demand expertise in airway management:
1. A level one center provides multidisciplinary, comprehensive care and is typically located in a large urban hospital environment affiliated with an academic medical center.
2. A level two center provides comprehensive care, although not all disciplines may be accessible.
3. A level three center provides limited intensive care support and stabilization of the critically ill patient.
In addition to the psychological stress associated with the “crisis-like atmosphere” that colors most airway management events in the ICU, the physical environment of the ICU presents additional challenges to the airway manager. For example, physical barriers, such as mechanical ventilators, monitors, infusion pumps, dialysis machines, and intravenous lines can make it difficult even to get to the head of the bed. Specialized apparatus for patient care (e.g., air beds, cervical spine collars, orthopedic frames) in an already overcrowded environment also contribute to the difficulty in accessing the airway or positioning the patient for airway management, particularly in an emergency. Space limitations may make it difficult for other members of the resuscitation team to access the patient. Finally, finding room for the equipment needed for airway management, such as the difficult airway cart and the bronchoscopy cart, can be a challenge.
Difficult Airways in the ICU
There are several dimensions to this issue:
· The skills and abilities of the practitioner as they relate to airway management
· The stress of the environment
· The physical barriers to care
· The effects of compromised physiological reserve on the choices of medications used in managing the airway
· An increased incidence of difficult mask ventilation, laryngoscopy and intubation, and cricothyrotomy; in addition, successful rescue with an extraglottic device is less likely Although many intensive care practitioners have significant expertise in airway management, not all “intensivists” are airway experts. Varying routes of entry to critical care medicine (e.g., internal medicine, surgery, anesthesia, pediatrics, emergency medicine) result in intensivists with varying skill levels and comfort with airway management, especially for this challenging patient population.
Considered as a population, critically ill patients requiring airway management are prone to difficulty in each of the four dimensions of the difficult airway discussed in Chapter 7:
1. Bag-mask ventilation is more difficult due to several factors: upper airway edema associated with prior intubation or the underlying condition is more common, these patients tend to be older and more obese, and they suffer increased airways resistance and reduced pulmonary compliance.
2. Laryngoscopy and intubation difficulty may be encountered due to a limited capacity to preoxygenate; increased incidence of anatomical abnormalities such as airway edema as noted previously; and neck immobilization in the case of trauma victims.
3. Cricothyrotomy is made more difficult by the width of the ICU bed and, often, access to the neck or the ability to position the neck appropriately.
4. Rescue with extraglottic devices is more challenging due to a variety of factors, particularly increased airway resistance and reduced pulmonary compliance in these patient populations.
Physiological Reserve
As described in Chapters 4 and 8, the larynx is the most heavily innervated sensory structure in the body. Laryngoscopy and endotracheal intubation stimulate these sensory organs and produce adverse physiological effects. The intensity of these physiological responses is related to the intensity of stimulation, which in turn depends on the duration of laryngoscopy, the aggressiveness of laryngoscopy, the degree of attendant hypoxemia/hypercarbia, stimulation of the carina by the endotracheal tube (ETT), and the device used. These stimuli, if unchecked, have the potential to produce significant responses and, potentially, adverse end-organ consequences. Depending on which organ systems are involved in a particular critically ill patient, the following organ system responses to endotracheal intubation may be the most important to consider:
· Increased intracranial pressure (ICP) and cerebral blood flow, particularly if autoregulation is disturbed
· Increased airways resistance
· The autonomic nervous system
· Adrenergic responses: Endotracheal intubation causes increased adrenergic activity with activation of the sympathetic nervous system and elevated circulating catecholamines. This in turn results in
· An increased systolic blood pressure and mean arterial pressure (up to two times normal)
· Increased diastolic blood pressure (up to 50% increase)
· Increased heart rate (up to 50% increase)
· Increased cardiac work and myocardial oxygen consumption
· Ventricular dysrhythmias (increased automaticity/irritability due to increased circulating catecholamines and increased blood pressure)
· Decreased gastric emptying (increased gastric volume and risk of aspiration)
· Decreased gut motility (ileus)
· Cholinergic responses:
· Bronchoconstriction and bronchorrhea
· Bradycardia: rarely but occasionally in children and infants, especially if hypoxemic
BOX 31-1 High-Risk Conditions
· Upper airway and respiratory system
· Reactive airways disease
· Cardiovascular system
· Major vessel aneurysm rupture (congenital, traumatic, or atherosclerotic)
· Aortic or major vessel dissection and rupture
· Ischemic heart disease
· Left ventricular (LV) systolic or diastolic dysfunction (“failure”) from any etiology (e.g., ischemic, hypertensive, congestive)
· Valvular heart disease: stenotic lesions limit the heart's ability to provide an adequate cardiac output to meet the needs of the body; regurgitant lesions may see increased retrograde flow in the face of increased systemic vascular resistance (SVR)
· L to R shunts (e.g., ventricular septal defect) will increase as SVR and LV systolic pressure increase
· Cor pulmonale: the stress of intubation increases pulmonary vascular resistance and, in the face of cor pulmonale, may produce acute right heart failure
· Ventricular and atrial arrhythmias may be induced
· Brain
· Patients with intracranial hypertension or increased intracranial pressure
Box 31-1 lists the most important underlying conditions that place the patient at higher risk of adverse effects.
Both nonpharmacological and pharmacological approaches can be used to mitigate or prevent adverse physiological responses to intubation in these patients. The nonpharmacological methods include limiting the intensity (rigor) and duration of laryngoscopy, maintaining oxygen saturation and keeping the ETT off the carina. Some alternatives to direct laryngoscopy, such as use of the Trachlight, have been shown to reduce adrenergic responses.
Pharmacological interventions are a double-edged sword in the critically ill patient. Although they may mitigate many of the adverse effects outlined previously, the agents themselves may cause adverse effects, especially hypotension, respiratory depression (during the pretreatment interval), and hypercapnia. Consider the following:
· The additive or potentiating effects of one technique or drug on another (e.g., the obtunded overdose patient may need less induction agent)
· The patient's physiological reserve: Patients with reduced cardiac reserve [decreased left ventricular (LV) function and valvular heart disease] are more sensitive to myocardial depressants such as induction agents; as are patients who are hypovolemic, such as those with uncontrolled hypertension, blood loss, or dehydration.
· The potential of an adverse outcome related to the physiological response to intubation: The physiological response to intubation may be especially detrimental in patients with severe asthma, ischemic heart disease, elevated ICP, intracranial hemorrhage, and aneurysm rupture or major vessel dissection.
· Underlying sympathetic tone: If the sympathetic nervous system is already maximally stimulated (e.g., hemorrhagic shock) and the patient is barely compensated, one must be cautious with any drug that can reduce sympathetic tone. This potentially includes all sedative hypnotic agents (benzodiazepines, barbiturates), neuroleptics (haloperidol and droperidol), opioids, lidocaine, and any drugs that release histamine. Etomidate, ketamine, succinylcholine, vecuronium, and rocuronium are the most hemodynamically stable drugs in their respective classes. For sedation, small titrated doses of ketamine or haloperidol are probably safer than benzodiazepines or barbiturates. Although still a good choice for induction, etomidate is avoided as an infusion because of its ability to suppress the adrenal axis.
When using medications to mitigate the adverse physiological responses to intubation in patients with marginal pulmonary or cardiovascular reserve (e.g., those who are critically ill), administer conservative doses and err on the side of too little rather than too much. If postintubation hypertension and tachycardia occur, they can be managed by administering small doses of the induction agent or by titrating a benzodiazepine and opioid (e.g., fentanyl).
Specific Clinical Considerations
Acute Pulmonary Edema
The patient with acute pulmonary edema due to LV failure who requires intubation presents several challenges to the physician performing the intubation: preoxygenation will provide little in the way of oxygen reserve because these patients have little or no functional residual capacity (FRC). Oxyhemoglobin desaturation will occur rapidly; the patient may be unable to lie flat and is often struggling and uncooperative, presenting airway access difficulties; foamy secretions may obscure visualization of the airway; high airway resistance and low pulmonary compliance are likely to render bag-mask ventilation difficult or ineffective; cardiac reserve varies such that the patient who is hypertensive is more likely to tolerate opioids and induction agents than one who is normotensive, who in turn is more likely to tolerate opioids and induction agents than a hypotensive patient. Finally, laryngoscopy and intubation are likely to exacerbate any element of bronchospasm.
All these points emphasize the fact that there is little margin for error in these patients and that intubation should be carefully planned. This argues strongly for the superior pharmacological and physiological control, and success rates provided by rapid sequence intubation (RSI). Even when a difficult airway is identified, other factors, especially the immediacy of the need for intubation and the inability of the patient to tolerate a sedated “awake look,” may make RSI the best choice, although often with a double setup.
Patients in acute pulmonary edema are difficult to preoxygenate, although it should be attempted with 100% oxygen, even though it may not be as effective as in patients with normal lungs. Assist ventilation to maintain oxygen saturation if at all possible. Bilevel positive airway pressure has been used in many patients with heart failure and may be useful for optimizing preoxygenation, even if it is ultimately unsuccessful in averting intubation (see Chapter 38). Even after the best attempts at preoxygenation, the patient may require positive-pressure ventilation throughout the intubation sequence to maintain adequate oxygen saturation. The cardiovascular system will tolerate the procedure, medications, and ventilation better in the supine position, but the patient usually prefers to be erect. It may be best to administer drugs with the patient erect and then to place the patient in a supine position for intubation as consciousness is lost.
Patients who are hypertensive and hyperdynamic have the capacity to respond in exaggerated fashion to intubation and may require medications to attenuate this response. Use caution in patients who are normotensive and extreme caution in those who are hypotensive. Have both intravenous nitroglycerine and pressors, such as dobutamine or dopamine, available. Alpha agent pressors such as phenylephrine and methoxamine are inappropriate because they increase blood pressure at the expense of myocardial work. An exception is the patient with significant aortic or mitral stenosis and a fixed cardiac output, in which case alpha-adrenergic agonists may be preferable. The patient should be pretreated with lidocaine or fentanyl as for any other patient, but fentanyl is avoided when sympathetic tone is required to maintain cardiac output. Etomidate is probably the induction agent of choice, as is succinylcholine as a neuromuscular blocking agent.
If the intubation is anticipated to not be difficult, use the largest ETT possible to minimize resistance to ventilation and facilitate pulmonary toilette (8 mm inner diameter [ID] in an adult female; 9 mm ID in an adult male). If a difficult laryngoscopy is anticipated, a smaller tube may enhance success and minimize stimulation. Place a stylet in the tube.
Once the patient is intubated, initiate mechanical ventilation with caution because irreversible hypotension immediately following intubation and positive-pressure ventilation in this setting (and in patients with chronic obstructive pulmonary disease) is not uncommon. Immediately after intubation, bag ventilate the patient to assess compliance and resistance. Appreciate the time needed to complete expiration. Note the effect of positive-pressure ventilation on blood pressure. Obtain a chest x-ray and look especially carefully for a right mainstem intubation because one-lung ventilation is even less well tolerated when the patient has pulmonary edema. Set the inspired fraction of oxygen (Fio2) at 100%. A tidal volume of 8 mL/kg at a rate of 12 to 14 breaths/minute, as usual, is a good place to start. An elevated mean intrathoracic pressure due to positive-pressure ventilation may impede venous return and improve LV function in the setting of acute LV failure, although peak airway pressures exceeding 35 to 40 cm of water pressure (CWP) are associated with an increased risk of pneumothorax. In the event that the lungs are stiff and high airway pressures are compromising venous return and cardiac output, faster rates at lower tidal volumes may be required. If there is significant bronchospasm, the rate may have to be decreased to extend the expiratory time and the tidal volume increased, if possible, to maintain minute volume. Positive end-expiratory pressure (PEEP) beginning at 5 CWP or other forms of pressure support may be introduced to enhance FRC and oxygenation if the cardiac output will tolerate it. Increase the PEEP as needed and as tolerated. Treat the pulmonary edema aggressively according to its cause.
Dramatic falls in blood pressure caused by drugs (especially nitrates and histamine releasers) and ventilation may provide clues to underlying significant valvular heart disease. The patient who has worrisome hypertension caused by the intubation will respond to small repeated doses of thiopental (25–50 mg) or propofol (10–20 mg), which may be used to both sedate and lower the blood pressure. However, postintubation hypertension that persists is the result of inadequate sedation and excessive sympathetic tone. Lorazepam, supplemented with fentanyl or morphine, constitutes a good approach (see Chapter 3). Nitrates may also be useful. Circulation times are slowed in these patients, and medication onset time may be considerably delayed.
Cardiogenic Shock
The patient in cardiogenic shock is gravely ill with a high mortality rate. This fact serves to emphasize the attention to detail that is required in managing the intubation. Provided the patient is not in pulmonary edema, the FRC is probably intact, and preoxygenation is useful. By definition, there is no cardiac reserve, and medications that reduce cardiovascular performance are contraindicated. Induction agents, in particular, must be carefully selected. An amnestic agent, such as midazolam 1 to 4 mg, may be well tolerated. Etomidate and ketamine in much-reduced doses (e.g., etomidate 0.1 mg/kg or ketamine 0.5 mg/kg) are also reasonable, although, as for midazolam, either may depress cardiac function. Long-term sedation with lorazepam in small titrated doses of 0.25 to 1 mg may be tolerated. Circulation times are prolonged, so drug effects are substantially delayed.
As with the patient in pulmonary edema, RSI is usually the safest, most controlled, and best approach. Be prepared to handle surges in blood pressure and myocardial oxygen demand after intubation, rather than pre-emptively. No pretreatment medications are indicated, and in fact, they are contraindicated. Depending on the patient's circulatory status, either no induction agent or a greatly reduced dose, such as 0.05 mg/kg of midazolam or 0.5 mg/kg of ketamine or 0.1 mg/kg of etomidate should be used. This is immediately followed by succinylcholine 1.5 mg/kg. When initiating mechanical ventilation, be cautious of impeding venous return and cardiac filling. Paralytic agents such as succinylcholine do not have substantial cardiovascular activity. Pancuronium has cardiac muscarinic blocking properties, so may exacerbate tachycardia, although this may be difficult to detect in the setting of cardiogenic shock, where sympathetic activity is already maximal. Histamine-releasing agents, such as sodium thiopental or the benzyl isoquinoline neuromuscular blocking agents, should be avoided.
Septic Shock
Septic shock may be hyperdynamic or hypodynamic; myocardial contractility and systemic vascular resistance are compromised. The challenge is to maintain cardiac output and oxygen delivery to the tissues. Any agent that may compromise myocardial contractility or systemic vascular resistance must be considered with great caution, and alternatives should be sought, if at all possible.
The approach to airway management in the patient with septic shock is no different from that in the patient in cardiogenic shock (see previously recommended sequence). Ventilation should be initiated at 8 mL/kg at 12 to 14 breaths/minute. However, as most patients in septic shock are also acidemic, consideration should be given to carefully increasing minute ventilation by 20% to 30%, if the cardiac output will tolerate it, until arterial blood gases can be obtained. However, be cautious with ventilation. Any reduction in venous return will not be tolerated. Pressure support may reduce shunt fraction and improve oxygenation, provided cardiac output is maintained. The use of etomidate in patients with sepsis is discussed in Chapter 18.
Anaphylaxis
The patient suffering from a systemic anaphylactic reaction demonstrates hypotension due to release of vasoactive mediators, intense bronchoconstriction, and upper airway edema. The patient may be profoundly acidemic (respiratory and metabolic). Orotracheal intubation may be difficult or impossible because of upper airway edema, so a small-diameter ETT and surgical airway equipment should be readily at hand. Transtracheal needle ventilation and other supralaryngeal rescue airway devices such as the Combitube or laryngeal mask airway will be ineffective because of the combination of upper airway obstruction and bronchospasm. Hypotension limits the spectrum of pharmacological options for sedation. Intense bronchospasm will challenge the ability to ventilate the patient effectively.
Intense bronchospasm and hypotension will limit the effectiveness of preoxygenation and gas exchange in the preintubation period. Therefore, expeditious intubation is desirable. Be prepared to perform a surgical airway. If you are confident in your ability to intubate the patient, maximize the success rate by using RSI, with cricothyroidotomy prepared as a backup. If severe upper airway edema or stridor is present, an awake technique or primary cricothyrotomy is recommended. Treat the anaphylaxis aggressively with intravenous epinephrine during preparation for intubation. Steroids and antihistamines may be helpful, but epinephrine is the primary agent. Ketamine provides the best blood pressure support and is a bronchodilator.
Pretreat with lidocaine 1.0 mg/kg, if time permits; induce with ketamine, 1 to 1.5 mg/kg; and paralyze with succinylcholine. When initiating mechanical ventilation, the substantial increase in airways resistance will mandate slow rates and moderate tidal volumes with permissive hypercapnia to achieve acceptable oxygenation, minimal barotrauma, and optimum cardiac output, as for asthma (see Chapter 29). Excessive mean intrathoracic pressure is likely to compromise venous return and cardiac output. Manage hypotension and bronchospasm with intravenous epinephrine. Pancuronium, rocuronium or vecuronium are preferred for paralysis after intubation. Benzyl isoquinoline derivatives (e.g., curare, cisatracurium) are to be avoided because of their ability to release histamine.
When and How to Extubate
Extubation in a patient who has been intubated for some time carries significant risk, and a strategy to manage this risk is mandatory. The extubation of patients who were easily intubated and in whom no intervening event has occurred to jeopardize their airways might be regarded as a routine extubation. Those who were easily intubated but who are at greater risk of requiring reintubation (due to hypoxemia, hypercapnia, inadequate clearance of secretions, inability to protect their airway or airway obstruction) are intermediate-risk extubations. Those in whom airway management is likely to be challenging or complex if reintubation were to be required represent high-risk extubations. The last group includes (a) patients with a difficult tracheal intubation (failure to visualize the glottis, requiring multiple attempts or alternative techniques); (b) those with interval complications (airway edema, extrinsic compression, glottic injuries); and (c) those with clinical conditions associated with difficult ventilation or intubation. This latter group would include, for example, patients with paradoxical vocal cord motion, morbid obesity, obstructive sleep apnea, airway surgery, maxillofacial surgery (particularly when it involves intermaxillary fixation), deep neck infections, cervical surgery, or prolonged intubation.
Patients in critical care units often have limited physiological reserve, altered secretions, or an impaired capacity to protect their airways, elevating the risk of reintubation. In these instances, the practitioner may have limited clinical information, equipment, supportive personnel, and preparation time. Furthermore, the patient may be hemodynamically unstable with associated airway obstruction, hypoxemia, and acidosis. There may be a reluctance to administer paralytics when there is uncertainty about the airway. Topical anesthesia may be ineffective due to time constraints or the presence of secretions and edema leading to a struggle between the caregiver and a confused and possibly hypoxic patient. Generally, any urgent reintubation is likely to be more challenging than the original procedure.
Perhaps the most troublesome accompaniment of prolonged intubation in an ICU patient leading to postextubation upper airway obstruction and reintubation is the presence of upper airway edema. In adults, the swelling is generalized involving all glottic and supraglottic structures. In children, subglottic swelling predominates. The degree of edema is increased by positioning (e.g., prone or Trendelenburg), angioedema, thermal injuries, or with conditions associated with generalized swelling such as anaphylaxis and volume overload. In addition, injuries sustained during intubation or ensuing after intubation may exacerbate swelling in the upper airway.
Because of the hazards associated with extubation of the injured or edematous airway, several techniques to assess the degree of injury or swelling have evolved, some better than others. Direct visualization of the glottis with a laryngoscope prior to extubation is of limited value unless the image can be magnified, in which case the assessment of the anatomy is reasonable. Direct examination of the airway using a bronchoscope through an LMA during spontaneous ventilation after extubation provides a good assessment of both form and function.
Tissue swelling may encroach on an ETT at any point along its length. For this reason, a “cuff leak test” has been recommended to determine if air is moving around the ETT. For this test, the oropharynx is suctioned, and the cuff is slowly deflated. The patient is asked to inhale and exhale slowly as the ETT is occluded. An audible leak indicates the flow of air around the ETT. This has been found to be a useful predictor of successful extubation in pediatric trauma and burn victims as well as children with croup. However, its reliability in adults in predicting postextubation stridor and the need for reintubation is poor. Administering the test during controlled mechanical ventilation permits one to quantify the leak volume, and this method has been shown to be a better predictor of postextubation stridor, the need for reintubation, or both.
Airway edema may be reduced by head elevation and the use of racemic epinephrine. Steroids, fluid restriction, and diuretics have been employed with varying results.
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Figure 31-1 • Extubation algorithm for moderate- and high-risk patients. See text for details. |
Patients who meet moderate and high-risk extubation criteria must be treated cautiously. Figure 31-1 is an algorithm designed to guide one through the extubation of such patients. The algorithm is predicated on the following:
· That a pre-extubation evaluation of the airway is performed
· That the patient has adequate weaning parameters
· That an ETT exchange catheter is incorporated into the plan
· That the ability to rapidly perform a cricothyrotomy is assured
Several commercially available ETT exchange catheters are available on the market, including the Cook Airway Exchange Catheter (Cook Critical Care), the Endotracheal Ventilation Catheter (CardioMed Industries), and the Sheridan Tracheal Tube Exchanger (Hudson Respiratory Care). Substitutes (e.g., gum elastic bougie, nasogastric tube) are not acceptable because they are not sufficiently stiff to guide the replacement tube into position. The dedicated exchange catheters are hollow and are supplied with adapters to permit some degree of gas exchange (insufflation or ventilation). The catheter is inserted through the existing ETT with the distance markings on the tube exchange catheter aligned with those on the ETT to ensure it is positioned correctly in the mid trachea. The tube exchange catheter remains in the airway after the ETT is withdrawn. The patient tolerates the exchange catheter better if lidocaine is instilled down the ETT prior to the insertion of the exchange catheter.
Once the decision to extubate has been made, Figure 31-1 guides subsequent decisions. An exchange catheter is inserted, and the ETT removed. The exchange catheter is taped to the cheek and the forehead to prevent movement of the device. If all is well after a period of time, the exchange catheter is removed. The period of time the exchange catheter ought to be maintained in situ after the ETT is removed remains uncertain and is a matter for clinical judgment. If the patient becomes hypoxic while the exchange catheter is in place, supplemental oxygen by face mask is administered. If this fails to rectify the problem and reintubation is required, an ETT is inserted over the exchange catheter. It is crucial that the ETT size approximate that of the exchange catheter to the extent possible to prevent the leading edge of the ETT from impinging on airway structures and preventing passage. It is also imperative that a laryngoscope be used to move oral tissue out of the way and minimize the angle of approach to the glottis (in much the same fashion as intubation over an Eschmann introducer, see Chapter 6). If this maneuver fails, oxygenation through the exchange catheter should be attempted while one prepares another approach to the airway. If oxygenation via the exchange catheter is unsuccessful, it must be removed and bag-mask ventilation attempted while a cricothyrotomy or intubation is performed.
ICU Airway Equipment
Just as in the operating room (OR) and the emergency department, the ICU ought to have adequate airway management equipment to meet its needs, and there ought to be policies overseeing its management (responsibility, checking, restocking, etc). Routine airway management equipment, as well as devices to manage a difficult or a failed airway, must be immediately available. Moreover, all staff must be familiar with how to use and support the use of these devices.
Evidence
1. Is there evidence to suggest that managing the adverse physiological effects of intubation improves outcome? There is substantial evidence that orotracheal intubation produces adverse responses and that those responses lead to adverse patient outcomes (1,2,3,4,5,6,7). It is also clear from the literature that obtunding those adverse responses results in an improved outcome (5,6,7). The critically ill patient has the most to lose and the most to gain from obtunding the responses. The mainstays of controlling the responses are the technique chosen (8,9,10) and medications. Less stimulating techniques, such as the lighted stylet and nontracheal devices (e.g., LMA), produce less response than traditional laryngoscopic intubation. Opioids, such as fentanyl, alfentanil, sufentanil, and recently, remifentanil, are the mainstays of the pharmacological strategy. However, induction agents, nitrates, beta-blockers (e.g., esmolol), and others have also been used successfully (4,5,7,11,12,13,14,15,16,17,18).
2. How common is it to have to manage an airway in an ICU patient? It is not uncommon for airway management to be performed outside the controlled OR environment.
A recent review of cardiac arrest associated with emergency airway management outside the OR in 3,035 patients confirms that the many of these occur in the ICUs (19). Furthermore, we know that the incidence of cardiac arrest in the ICU setting is as high as 2%, much higher than the 0.068% rate in the OR (20). Interestingly, the authors of these two cited studies note that hypoxemia is a prearrest factor and comment that improvements have been seen since the introduction of more experienced staff and the use of ancillary airway devices in ICU. In addition, nonintubated patients with cardiorespiratory decompensation are admitted to the ICU for monitoring. Some of these patients will deteriorate, as with the patient described previously, and require tracheal intubation and mechanical ventilation.
3. How are most ICUs equipped when it comes to airway management? A recent survey of ICUs revealed that most maintain an airway cart, but only about 50% maintain a “difficult” airway cart, and less than 5% conform to the suggested list of equipment offered by American Society of Anesthesiologists guidelines (21). Devices used to confirm tracheal intubation and detect esophageal intubation are present in 93% of ICUs, but they are only routinely used in 68% of cases. Only 4% of ICUs had both a bulb syringe and end-tidal carbon dioxide detectors, as suggested by the American Heart Association (22). A fiberoptic bronchoscope (FOB) is the most popular device selected for use in a difficult airway situation, even though it is immediately available less than one-third of the time. Fifty-one percent of respondents believed that the FOB was the primary backup when conventional intubation fails. In a “can't intubate, can't ventilate” situation, 20% believed that the FOB was the method of choice, an LMA (which was in only 50% of the airway kits) was only chosen 36% of the time, and a cricothyrotomy was the first choice for 32% of respondents. The authors commented on the underutilization of the LMA and the need for “continued efforts to educate medical personnel on airway management in the ICU setting” (22).
References
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