Pharmacologic Adjuncts to Intubation

Endotracheal (ET) intubation in the emergency setting presents a challenge distinct from that associated with intubation of fasted, premedicated patients in the operating room (OR). Patients in the emergency department (ED) are frequently uncooperative and unstable and may have medical problems or anatomic abnormalities that are completely unknown to the treating clinician. It is challenging that within a matter of minutes and with scant data the clinician must assess and control the airway while diagnosing and managing the patient's other life-threatening problems.

In 1979, Taryle and colleagues reported that complications occurred in more than half the patients intubated in a university hospital ED. They called for improved house officer training in ET intubation, including “more liberal use of the procedures and agents used in the OR, including sedatives and muscle relaxers.” Since this report, the use of neuromuscular blockade and rapid-sequence intubation (RSI) have become the standard for emergency medicine practice.

In addition to RSI, emergency physicians now use airway devices such as videoscopes and flexible fiberoptic bronchoscopes to manage difficult and complex airways. In high-risk patients it is increasingly common for awake intubation techniques to be utilized. This allows for the safe management of an emergent airway without the risk of completely eliminating the patient's airway reflexes. A related approach that has been described as delayed-sequence intubation has emerged in recent years. This technique may be considered as procedural sedation to allow preoxygenation prior to intubation. Both awake intubation and delayed-sequence intubation techniques have their own unique pharmacologic considerations. Clinicians must concentrate not only on the manual skills of airway management, but also on selection of the appropriate drugs to achieve specific objectives. These objectives include: (1) immediate airway control, including induction of unconsciousness and muscle paralysis; (2) analgesia and sedation in awake patients; (3) minimization of the adverse physiologic effects of intubation, including systemic and intracranial hypertension; and (4) prevention of harm during the postintubation period, including inadequate sedation, hemodynamic instability, or oversedation.

This chapter reviews the mechanisms and strategic use of the drugs that are currently available to facilitate intubation in the ED.

Overview of RSI

The sequential process for quickly intubating a patient in an emergency situation is referred to as rapid-sequence intubation . The steps in performing RSI are often described by the six “P's”: preparation, preoxygenation, pretreatment, paralysis and induction, placement of the tube, and postintubation management ( Fig. 5.1 ). This sequential technique of rapidly inducing unconsciousness (induction) combined with muscular paralysis to create optimal conditions for intubation has gained broad acceptance among ED clinicians. Many patients do not afford the clinician the time or opportunity to comply with the ideal scenario of tracheal intubation described in this chapter. RSI, as described in this chapter, is the ideal method of emergency airway management for intubations that are not anticipated to be difficult. Consider awake techniques of intubation in high-risk patients with airways that are anticipated to be difficult.

Figure 5.1, The 6 “P's” of rapid-sequence intubation. IV, Intravenous; RSI, rapid-sequence intubation.

Preparation occurs before and during preoxygenation. Assess the airway to determine the likelihood of a difficult intubation. Simultaneously, establish an intravenous (IV) line and connect the patient to cardiac, pulse oximetry, and end-tidal CO ₂ monitors when available. Assemble all necessary drugs and equipment for oral intubation and the desired backup equipment for airway management.

Begin RSI preoxygenation as soon as possible by administering 100% oxygen. The intent is to displace nitrogen from the lungs and replace it with an oxygen reserve that will last several minutes. Under optimal conditions, breathing 100% oxygen for 3 minutes has been demonstrated to maintain acceptable oxygen saturation for up to 8 minutes in previously healthy apneic individuals. Another method is to give four vital capacity (maximal) breaths of 100% oxygen from a face mask, which can also maintain acceptable saturation for 6 minutes. Comparable results may not be extrapolated to the ED setting because of differences in the underlying health and cooperation of the patient population.

A recent advance in preoxygenation of patients prior to intubation is the Nasal Oxygenation During Efforts Securing A Tube (NO DESAT) technique. In the NO DESAT technique a nasal cannula is placed underneath the non-rebreather face mask. In awake patients, the nasal cannula can be comfortably set to 5 L/min of oxygen. After induction agents are given, this can be safely increased to 15 L/min of oxygen. The nasal cannula may be left on throughout the attempt to intubate, as it will not interfere with the ability to place an orotracheal tube. This has the potential to prolong the time to desaturation, but clinical studies of this technique's application in the ED are currently lacking.

Pretreatment consists of the administration of medications to mitigate the potential untoward responses to intubation. Pretreatment during RSI usually occurs 2 to 5 minutes before induction of unconsciousness or muscular paralysis. Although preoxygenation should be maintained for as long as practical before beginning intubation, the ideal situation and circumstances are not always present, and clinical judgment is the deciding factor for this portion of RSI. The clinical utility of routine pretreatment to improve patient-oriented outcomes in ED RSI has been challenged.

Paralysis and induction involve the induction of a state of unconsciousness with a sedative agent, followed immediately by muscle paralysis. A protocol for ED-based RSI is summarized in Box 5.1 .

Box 5.1

Rapid-Sequence Intubation Protocol

1.
Preoxygenate (denitrogenate) the lungs by providing 100% oxygen by mask. Apply nasal cannula at high flow at this time if using nasal cannula for apneic oxygenation.
2.
Assemble the equipment required:
- Bag-valve-mask device connected to an oxygen delivery system.
- Suction with a Yankauer tip.
- ET tube with an intact cuff, stylet, syringe, and tape.
- Laryngoscope and blades, in working order.
- Backup airway equipment.
3.
Check to be sure that a functioning, secure intravenous line is in place.
4.
Continuously monitor cardiac rhythm and oxygen saturation.
5.
Premedicate as appropriate:
- Fentanyl: 2 to 3 µg/kg given at a rate of 1 to 2 µg/kg per min intravenously.
- Atropine: 0.01 mg/kg by intravenous push for children or adolescents.
- Lidocaine: 1.5 to 2 mg/kg intravenously over a period of 30 to 60 seconds.
6.
Induce anesthesia with one of the following agents administered intravenously: ketamine, etomidate, fentanyl, midazolam, or propofol.
7.
Give succinylcholine, 1.5 mg/kg by intravenous push (use 2 mg/kg for infants and small children) or rocuronium 1.2 mg/kg.
8.
Apnea, jaw relaxation, and/or decreased resistance to bag-mask ventilation (use only when oxygenation before rapid-sequence intubation cannot be optimized by spontaneous ventilation) indicates that the patient is sufficiently relaxed to proceed with intubation.
9.
Perform ET intubation. If unable to intubate during the first 20-second attempt, stop and ventilate the patient with the bag-mask device for 30 to 60 seconds. Monitor pulse oximetry readings as a guide.
10.
Treat bradycardia occurring during intubation with atropine, 0.5 mg by intravenous push (smaller dose for children; see item 5).
11.
Once intubation is completed, inflate the cuff and confirm ET tube placement by auscultating for bilateral breath sounds and checking the pulse oximetry and capnography readings. Ultrasound for lung sliding on both sides may be a useful adjunct.
12.
Secure the ET tube.

ET, Endotracheal.

ET intubation and RSI have also expanded beyond the ED into the prehospital setting. Prehospital RSI protocols use a sedative plus a paralytic for patients not in cardiac arrest, with success rates as high as 92% to 98%. Without a full complement of medications, prehospital intubation becomes significantly more difficult, and success rates drop to approximately 60%. Rates of misplaced ET tubes and complications by paramedics may be much higher than previously reported. Studies indicate that outcomes may be worse for patients with traumatic brain injury intubated in the prehospital setting than in the ED. For these reasons many prehospital systems have moved away from the use of RSI.

The technique for proper ET tube placement is discussed in Chapter 4 . Postintubation monitoring should assess for proper tube placement, adequate tissue oxygenation, and response to previously administered drugs. After laryngoscopy, ensure ongoing analgesic and anxiolytic therapy.

Pretreatment: Preventing the Complications of Intubation

Numerous reports have highlighted the physiologic responses to tracheal intubation and attempted to define their immediate or long-term adverse effects and to offer interventions to ameliorate potential organ injury. It is certain that intubation and adjunctive medications have the potential to alter reflexes, intracranial pressure (ICP), blood pressure, and pulse rate, and may induce disturbances in cardiac rhythms, but the actual clinical consequences of these commonly observed changes are largely unknown. Clinical experience suggests that most transient alterations in physiology occurring with ED intubation produce no specific or readily documented long-term sequelae, or are often consequences that cannot easily be monitored or prevented. Prudent clinicians are aware of the potential adverse effects of intubation and are cognizant of potential methods to minimize them. Careful monitoring of the postintubation condition will guide specific interventions.

Overzealous attempts to suppress the physiologic responses that normally accompany airway manipulation may be counterproductive. It would be desirable to provide airway control under the best of circumstances and with the least amount of injury to the patient, but the ideal approach to the physiologic responses to intubation is simply unknown. Most information has been extrapolated from experimental animal models or from the anesthesia experience and similar issues may not apply to the milieu of the ED experience. It is critical to prevent hypotension and hypoxia during intubation, particularly in those with neurologic injury. Patients that theoretically would benefit the most from pretreatment medications are those that may be least able to tolerate any delay in obtaining a definitive airway. The following discussion serves as a general clinical guide to alterations in the physiologic response to intubation.

The Pressor Response

In addition to the ubiquitous sinus tachycardia, a number of dysrhythmias have been reported after intubation. They are primarily ventricular in origin and include ectopic beats, bigeminy, and short runs of ventricular tachycardia. No studies have established a direct relationship between the response and subsequent clinical deterioration in a large patient population. It is also unclear whether attenuation of the pressor response prevents dysrhythmias or electrocardiographic evidence of ischemia. Ideally, it would be desirable to avoid sudden increases in blood pressure in unstable patients with acute cardiac or vascular disease. Unfortunately, it is unclear if outcomes are improved by attempting to mitigate the pressor response.

Multiple medications have been evaluated to attempt to reduce the pressor response. Lidocaine has been the most extensively evaluated, but it has not been shown to improve outcomes. A dose of 1.5 to 2 mg/kg may slightly reduce the heart rate or blood pressure increase caused by intubation. One small trial demonstrated that nebulized tetracaine reduced increases in heart rate during intubation, but this is not commonly done in emergency practice. Fentanyl dosed at 2 to 5 µg/kg is likely to be more effective at blunting the pressor response than lidocaine. Fentanyl will be discussed in more detail later, in relation to its possible benefit in preventing increases in ICP.

Lidocaine and fentanyl are the drugs with the largest evidence base supporting their use to decrease the pressor response. Other drugs, including thiopental, sodium nitroprusside, labetalol, nitroglycerin, verapamil, nifedipine, clonidine, fentanyl, sufentanil, etomidate, and magnesium, have shown variable responses. In light of the uncertainty of the benefit of any premedication in improving patient outcomes, these other medications cannot be recommended for routine use. In patients at very high risk for harm by transient increases in heart rate or hypertension (such as those experiencing hypertensive emergency or having an active myocardial infarction), it would be reasonable to consider fentanyl or lidocaine. Given the lack of patient-oriented outcomes in the available literature, it is also very reasonable to not premedicate these patients and proceed with intubation without delay.

Hypotension

A more pressing concern for the majority of patients intubated in the ED is the importance of avoiding hypotension. Postintubation hemodynamic instability occurs in over 10% of emergency intubations. Unlike the uncertainty regarding patient harm as a result of transient hypertension, transient hypotension is associated with poor patient outcomes. This is of even higher concern in patients with known or suspected traumatic brain injury.

Avoid hypotension by initiating adequate resuscitation prior to attempts at intubation. If the patient's clinical condition permits, pursue appropriate volume resuscitation with blood in actively bleeding patients and fluids in hypovolemic patients prior to intubation. Even relatively hemodynamically stable drugs, such as etomidate, may contribute to hypotension in critically ill patients by reducing the endogenous catecholamine response. The physiologic changes that contribute to hypotension following intubation include both the reduced venous return from positive pressure ventilation and the effects of medications given during intubation. It is a challenge to balance the need for airway control and the need to adequately resuscitate prior to intubation.

Once hypotension has occurred during or after intubation, the fastest way to correct this is with the use of vasopressors. If time permits clinically, it is advisable to start vasopressors prior to attempting to intubate if a patient is already hypotensive. Due to the necessary delays in setting up a vasopressor through a pump, there has been recent increased attention to the use of push-dose vasopressors to treat peri-intubation hypotension ( Box 5.2 and Fig. 5.2 ). Further details about how to mix a dilute solution of vasopressor for this purpose will be provided later. It is certainly reasonable to administer temporary vasopressors for this purpose through a peripheral IV line to avoid further delays in intubation to place a central line. Although currently we lack patient-oriented data on whether push-dose pressors improve outcomes in hypotensive patients, the clear harm of even transient hypotension makes the use of these agents a reasonable approach until additional data is generated.

Box 5.2

How to Make Push-Dose Epinephrine

1.
Gather materials: 10 mL saline flush, blunt-tip needle, and 10-mL syringe of 1 : 10,000 epinephrine from code cart ( Fig. 5.2 A ).
2.
Waste 1 mL of saline flush into sink ( Fig. 5.2 B ).
3.
Draw up 1 mL of epinephrine into flush syringe using the blunt tip. This creates a 1 : 100,000 mixture of epinephrine ( Fig. 5.2 C ).
4.
Shake vigorously after drawing a little air into syringe to evenly mix ( Fig. 5.2 D ).
5.
Clearly label syringe as 1 : 100,000 epinephrine. This syringe must be clearly labeled to avoid unintentional bolus of 0.1 mg of epinephrine if someone mistook it for a regular saline flush ( Fig. 5.2E ).
6.
Administer 1 mL to 2 mL of this 1:100,000 epinephrine every 2 to 5 minutes IV as needed for hypotension. This medication is dilute enough to be reasonably safe even if it extravasates, as this is the same concentration of epinephrine found in standard lidocaine with epinephrine syringes.

Intracranial Hypertension

Stimulation of the respiratory tract by maneuvers such as laryngoscopy, tracheal intubation, and ET suctioning is commonly associated with a brief rise in ICP. The exact mechanism responsible for this rise is unknown. One potential mechanism is the coughing and gagging that frequently follow manipulation of the upper airway and subsequent transmission of intrathoracic pressure to the cerebral circulation. An alternative explanation is the release of catecholamines that accompanies laryngoscopy, which causes a rise in mean arterial pressure and cerebral perfusion pressure. A small rise in ICP has been reported after the administration of succinylcholine. The value of pretreatment with defasciculating doses of neuromuscular blockers (NMBs) to prevent rises in ICP is unknown.

Although the exact significance of a transient rise in ICP is not known, it is possible that it may be detrimental in patients with head trauma or intracranial hypertension. This theoretical harm comes from a possible reduction in cerebral blood flow if a rise in intracranial hypertension is not compensated for by a rise in systemic blood pressure. A number of drugs, including lidocaine, succinylcholine, and the majority of anesthesia induction agents, have been studied to determine whether their use prevents this response. Many of the existing clinical data are not particularly relevant to the ED setting because they are derived from patients in various stages of general anesthesia, during which a wide variety of drug combinations and doses are utilized.

Good evidence suggests that deep general anesthesia prevents the rise in ICP associated with intubation. Depending on the drug used, anesthesia may compromise cardiovascular performance and critically reduce cerebral blood flow. The ideal anesthetic agents to facilitate intubation of patients with acute intracranial pathology may be those that have minimal effects on cardiovascular performance, such as etomidate or fentanyl. Etomidate has been demonstrated to prevent changes in both cerebral perfusion pressure and ICP after tracheal intubation of patients with space-occupying intracranial lesions.

Fentanyl is perhaps the agent with the best evidence supporting its use in prevention of increased ICP during intubation. The dose is 2 to 5 µg/kg, and is higher than dosages typically used for other indications of fentanyl. To be effective, this dose must be given well before intubation, preferably at least 3 minutes prior to intubation.

Ketamine is traditionally contraindicated in patients with head injuries, but this has come into question. Whereas there may be minimal increases in ICP with ketamine, this effect is offset by a rise in systemic blood pressure. This appears to preserve cerebral blood flow and may in fact be cerebroprotective. There are no current studies that have demonstrated poor patient outcomes due to the use of ketamine in critically ill patients.

Atropine for Prevention of Bradycardia

Bradycardia is not infrequent during intubation, especially in young children and neonates. Traditionally, premedication with atropine has been advocated to reduce the incidence of bradycardia. A dose of 0.01 mg/kg given intravenously is the standard dose for premedication. While there may be a slight decrease in the incidence of bradycardia with this medication, patient-oriented outcomes have not been proven to benefit. It is not unreasonable to use atropine only in response to bradycardia, as opposed to using it as a premedication.

Bronchospasm

Patients with reactive airway disease may have further bronchospasm during the process of intubation. Lidocaine has traditionally been used to decrease the incidence of bronchospasm in asthma patients who require intubation. A dose of 1.5 to 3 mg/kg given intravenously has been advocated. This medication has not been proven to reduce the incidence of bronchospasm, but nebulized albuterol has been shown to be of benefit.

At the present time, the clinical consequences of intubation-induced physiologic changes are not thoroughly understood. The role of drugs in preventing these changes is equally unclear. Despite this lack of data, it may be intuitively reasonable to attempt to protect patients at theoretical risk. The approach outlined in Box 5.3 is recommended.

Box 5.3

Sample Protocol for Intubation of a Head-Injured Adult Patient ^a

a The benefit of this traditional protocol is unproved but can be supported if contraindications do not exist.

1.
Preoxygenate with 100% O ₂ for 2 to 3 minutes.
2.
Administer lidocaine, 1.5 to 2 mg/kg intravenously.
3.
Sedate with fentanyl, 3 to 5 µg/kg.
4.
Induce anesthesia with etomidate, 0.3 mg/kg.
5.
Paralyze with succinylcholine, 1.5 mg/kg or rocuronium 1.2 mg/kg.
6.
Perform intubation.
7.
Maintain postintubation analgesia and sedation.
8.
Maintain paralysis if indicated (vecuronium, 0.1 mg/kg).

Induction Agents

After premedication, a sedative agent is used to induce loss of consciousness. A number of diverse drugs are available in the ED to induce unconsciousness before intubation, including barbiturates, benzodiazepines, etomidate, ketamine, opiates, and propofol. The choice of a particular induction agent depends on the experience and training of the clinician, the patient's clinical status, drug characteristics, and institutional protocols ( Box 5.4 ). Considerable evidence indicates that the selected sedative agent influences the quality of intubation conditions and the rapidity of their attainment. These effects persist even when paralytic agents are used. Commonly used drugs and their doses are summarized in Table 5.1 .

Box 5.4

Adapted from Caro D, Walls RM, Grayzel J: Sedation or induction agents for rapid sequence intubation in adults. https://www.scribd.com/document/72424186/Sedation-or-Induction-Agents-for-Rapid-Sequence-ion-in-Adults .

Recommendations for Sedation of Patients Undergoing Rapid-Sequence Intubation in Specific Circumstances

The most appropriate medications for sedation before rapid-sequence intubation are based on evaluation of the clinical scenario, and no specific recommendations are appropriate for all circumstances. Different situations, too complex to list here, lend themselves to the use of certain agents (see text). There are no specific standards that must be followed, and the medical literature can be confusing, contradictory, or inadequate. The following conditions and sedation agent recommendations may guide the clinician. Note that appropriate paralytic drugs should also be used.

Head Injury or Potentially Elevated Intracranial Pressure

Pretreatment with the various medications described in the text are appropriate but of unproven value. Adequate cerebral perfusion pressure should be maintained to prevent secondary brain injury. Etomidate is suggested for induction of these patients, but ketamine is also likely to be safe in this population. For hypotensive patients, etomidate or ketamine may be used.

Status Epilepticus

Midazolam or thiopental may be used for induction. Reduced doses should be used in the unusual circumstance of seizure with hypotension. Midazolam may be used for induction in those with adequate blood pressures. Ketamine and propofol may also be used for induction as they may have some antiepileptic properties.

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