Neuromuscular Blockade

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Neuromuscular blocking agents facilitate airway management of selected patients in the emergency department. There are two major classes of drugs, depolarizing and nondepolarizing. Depolarizing neuromuscular blocking agents have high affinity for cholinergic receptors of the motor end plate, and are resistant to acetylcholinesterase. Initially they produce transient muscle fasciculations, followed by paralysis. This type of blockade is not antagonized, and may be enhanced, by anticholinesterase agents. Nondepolarizing neuromuscular blocking agents compete with acetylcholine for the cholinergic receptors, and can usually be antagonized by anticholinesterase agents. Succinylcholine, a depolarizing agent, inhibits neuromuscular transmission as long as an adequate concentration remains at one receptor site. However, succinylcholine is rapidly hydrolyzed by plasma cholinesterase. Potential adverse effects are listed in Table 15:4.. In contrast, pancuronium, vecuronium, atracurium, cisatracurium, rocuronium, and mivacurium are nondepolarizing agents (Table 15-5).

TABLE 15-4 Succinylcholine

Paralytic Agent Ventilator Management

TABLE 15-5 Nondepolarizing Neuromuscular Relaxants

In the ED, neuromuscular blockade can facilitate tracheal intubation, improve mechanical ventilation, and help control intracranial hypertension. Paralysis improves oxygenation and decreases peak airway pressures in a variety of disorders, including refractory pulmonary edema and the respiratory distress syndrome. Patients with refractory status asthmaticus, status epilepticus, or tetanic spasms resulting from clostridial infections or a variety of toxins, including strychnine, may improve with blockade.

In addition, extremely violent, agitated patients who jeopardize aeromedical personnel or their own airway security, spinal cord integrity, or fracture stability may require the ultimate pharmacologic restraint.

For the conditions mentioned above, nondepolarizing agents are preferable to succinylcholine. Although the onset of action is delayed, nondepolarizing agents have fewer adverse cardiovascular and histaminic effects coupled with a longer duration of paralysis. The delayed onset (1 to 5 min) and prolonged duration of action (25 to 120 min) require that the patient be ventilated with a bag-mask unit or other alternative, should intubation fail.

After documentation of the neurologic examination, including pupil size, presedation with an induction agent is advised unless there are other mitigating circumstances such as significant head injury or overdose. Neuromuscular blockers (NMBs) are neither anxiolytics nor analgesics. Omission of sedation is a common error in patients who remain aware of their paralysis. The resultant increased sympathetic tone can also exacerbate dysrhythmias.

The normal sequence in RSI is to induce sedation prior to administration of the depolarizing NMB agent. If a nondepolarizing agent is selected, some physicians reverse the sequence of administration, giving the nondepolarizing agent first because of its longer onset of action. Giving a rapid-acting hypnotic agent seconds later results in both medications having a synchronized peak effect.


When the indication for neuromuscular blockade is tracheal intubation, succinylcholine is the most commonly used agent. It has a more rapid onset (30 to 60 s) and shorter duration of action (average 5 to 6 min) than do the nondepolarizing agents. After a brief fasciculation, complete relaxation occurs at 60 s, with maximal paralysis at 2 to 3 min.

The dosage of succinylcholine is 1.0 to 1.5 mg/kg IV for adults. Succinylcholine can result in excellent intubation conditions in the ED. There are some significant potential complications.

Before injection of succinylcholine, atropine 0.01 mg/kg IV may attenuate the muscarinic vagal effects, especially in vagotonic adults and adolescents. An additional pretreatment to consider is a subparalytic dose of 0.01 mg/kg vecuronium or another nondepolarizing agent of similar duration to prevent the initial muscle fasciculations, which may cause long bone fractures to become displaced. Such fasiculations are most pronounced in muscular adolescents.

Succinylcholine increases intraocular pressure. In addition, the increased intragastric pressure will predispose to aspiration, hence the importance of cricoid pressure. Another concern with succinylcholine is its potential to increase the ICP. This increase in ICP is greater in patients with central nervous system (CNS) neoplasms and may not be clinically significant in those with acute CNS hemorrhage or trauma.

There are other, less preventable side effects of succinylcholine. The serum potassium will transiently rise an average of 0.5 meq/L with succinylcholine. A clinically significant hyperkalemic response following succinylcholine administration in prescreened ED patients is uncommon. 14 Nevertheless, hyperkalemia may be pronounced hours after muscle trauma or burns. It should not be a factor in the immediate aftermath of such injury. Still, it is advisable to avoid depolarizing agents in patients with burns, muscle trauma, crush injuries, myopathies, rhabdomyolysis, narrow-angle glaucoma, renal failure, or neurologic disorders. Any patient with "denervated musculature" (e.g., Guillain-Barre syndrome or spinal cord injury) is particularly at risk. Genetically susceptible individuals may develop acute malignant hyperthermia.

Dantrolene sodium should always be available. Patients with an atypical pseudocholinesterase will require prolonged ventilatory support, as will those with burns, cirrhosis, or carcinomas who have low plasma pseudocholinesterase levels.

Also, patients recently abusing cocaine may have a prolonged duration of neuromuscular blockade, since cocaine is metabolized by plasma cholinesterase, reducing the amount of enzyme available for succinylcholine metabolism.

Nondepolarizing Agents

Pancuronium is a nondepolarizing agent which is less likely than most others to cause histamine release. However, it more commonly results in tachycardia, so should be avoided in patients with underlying cardiac disease. While still commonly used, agents with a shorter duration of action and fewer cardiac effects have supplanted its use in some institutions.

Vecuronium bromide is an intermediate- to long-acting nondepolarizing agent. This drug is approximately one-third more potent than pancuronium. The duration of action is one-third to one-half as long. The usual dose of vecuronium is 0.08 to 0.15 mg/kg IV. Maximal paralysis occurs within 2 to 4 min, with full blockade lasting for 25 to 40 min. Vecuronium does not cause the degree of tachycardia commonly seen after pancuronium, since it has one-twentieth of the vagolytic effect. This simplifies interpretation of a tachycardia developing in the trauma patient.

A major advantage is the lack of hemodynamic alterations. Hypersensitivity reactions are rare, doses are only minimally cumulative, and excretion is biliary. Despite the lack of histamine release, hypotension may occur through two other mechanisms. Blockage of sympathetic ganglia occurs, and venous return is decreased from both absent muscle tone and the positive-pressure ventilation.

Doxacurium chloride is a long-acting nondepolarizing NMB used to facilitate prolonged mechanical ventilation after tracheal intubation. It provides skeletal muscle relaxation with no dose-related cardiovascular effects.

Atracurium is an agent well suited for patients with hepatic or renal failure. Elimination is via ester hydrolysis and Hoffman degradation, a nonenzymatic process. This nondepolarizing agent's elimination half-life is approximately 20 min, versus 65 to 75 min for vecuronium. Recovery time is consistent and unaffected by anticonvulsants. Consider this agent for intubated patients requiring brief diagnostic or therapeutic procedures.

Atracurium also offers advantages when continuous infusion is essential to maintain a precise, required level of neuromuscular blockade. A disadvantage is that histamine release can cause bronchospasm and hypotension. The risk with prolonged infusion is accumulation of laudanosine, a neuroexcitatory metabolic by-product.

Other nondepolarizing options include cisatracurium, rocuronium, and mivacurium. Cisatracurium is an intermediate-duration NMB agent. None of the metabolites have NMB activity, and excretion is independent of hepatorenal function. Rocuronium also has an intermediate duration of action, but the onset of action is much faster. Excretion is predominantly hepatic. Mivacurium is the nondepolarizing agent with the shortest duration of action. Histamine release can be minimized by slow infusion.

The reversal of nondepolarizing muscle relaxants is rarely necessary in the ED. Reversal should not be attempted prior to some sign of motion or spontaneous recovery. Reversal requires atropine 0.01 mg/kg IV to prevent muscarinic side effects, followed by edrophonium 0.5 to 1.0 mg/kg IV. The onset of action is 30 to 60 s, with a duration of 10 to 30 min. This reversal may be shorter than the duration of the muscle relaxant. Edrophonium is an acetylcholinesterase inhibitor with a faster onset and fewer muscarinic side effects than the longer-acting neostigmine.


DIFFICULT AIRWAY The management of the difficult airway in the ED is, in many regards, more challenging than in the controlled setting of the operating room. The patient generally has not been fasting and is not premedicated. There is rarely time for a leisurely evaluation of the "airway history" and "airway physical examination." The difficult airway constitutes the clinical scenario in which mask ventilation or tracheal intubation is challenging. Approximately 2 to 3 percent of tracheal intubations prove impossible with standard techniques. Difficult mask ventilation is defined as the inability to maintain the Sa o2 above 90 percent. Intubation is defined as difficult if more than three attempts are necessary or if conventional laryngoscopy requires more than 10 min. Many emergency physicians prefer to assure the availability of the appropriate airway equipment by customizing the contents of a portable airway kit (TabJeJ 5-6).

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TABLE 15-6 "Difficult Airway" Kit

In some stable ED patients, it may be feasible to screen for those physical findings that might suggest a difficult laryngoscopy. The three most predictive tests include assessments of atlantooccipital extension, thyromental distance, and the Mallampati criteria 15 (Fig 15-4).

Malampati Criteria

FIG. 15-4. The classification of tongue size relative to the size of the oral cavity as described by Mallampati and colleagues. 15 Class I: faucial pillars, soft palate, and uvula can be visualized. Class II: faucial pillars and soft palate can be visualized, but the uvula is masked by the base of the tongue. Class III: only the base of the uvula can be visualized. Class IV: none of the three structures can be visualized.

Proper visualization of the larynx requires flexion of the lower cervical vertebrae coupled with extension at the atlantooccipital joint (the "sniffing position"). In addition, the mandibular opening in a normal adult should be at least 4 cm or two to three finger breadths. A thyromental distance less than 6 cm or a mandibular length less than 9 cm correlates with difficulties. Finally, the size of the tongue relative to the oral cavity affects visualization of the glottis. The Mallampati criteria ( Fig 15-4) help predict the degree of difficulty in visualizing the vocal cords.15 The ability to visualize the faucial pillars, base of the uvula, and the soft palate predicts the degree of difficulty in laryngeal exposure.

These clinical findings should affect the judgment of the emergency physician who is considering the feasibility of the various approaches to airway management. The decision is basically centered on two initial considerations: will a nonsurgical approach succeed, and is preservation versus ablation of spontaneous ventilation wise

FIG. 15-5. Difficult airway algorithm.

* Options include bag-valve-mask intubation, endotracheal intubation, nasotracheal intubation, rapid-sequence intubation, digital intubation, fiberoptic transillumination, laryngeal mask airway, Combitube, retrograde tracheal intubation, translaryngeal ventilation, and cricothyrotomy. (Adapted from American Society of Anesthesiologists,5 with permission.)

CEREBRAL RESUSCITATION Patients with suspected acute intracranial hypertension require aggressive airway management. Direct laryngoscopy can elevate the ICP. Prior to oral or nasal intubation, pretreatment with intravenous lidocaine may help blunt this deleterious cardiovascular response. Fentanyl will also blunt the hemodynamic changes.

Since in certain situations succinylcholine may also increase ICP, the intubator should consider prior use of a defasciculating dose of a nondepolarizing NMB agent. If one is selected, the use of a priming dose will shorten the onset of action. However, a significantly prolonged duration of action may be the result, extending the risks if a difficult airway is encountered. Another consideration is the use of a short-acting sedative induction agent. Several of these drugs, including thiopental, fentanyl, and etomidate, directly decrease the ICP.

Effective oxygenation and ventilation during cerebral resuscitation often requires prolonged neuromuscular blockade. Autoregulation of cerebral blood flow (CBF) over a range of perfusion pressures may be impaired. As a result, CBF becomes pressure-dependent ( CBF = CPP/CVR, where CPP is cerebral perfusion pressure and CVR is cerebral vascular resistance). Autoregulation is usually intact when the CPP ranges between 50 and 130 mmHg. The CPP equals the mean arterial pressure minus the ICP.

In traumatic brain injury, the goal is therefore to maintain the mean arterial pressures over 90 mmHg throughout the patient's course; this will usually maintain the CPP over 70 mmHg. Other treatment modalities, such as mannitol administration and hyperventilation, do have the potential for exacerbation of intracranial ischemia. Therefore, prophylactic hyperventilation therapy (P co2 less than 35 mmHg) should be avoided during the first 24 h after injury.16

On the other hand, brief hyperventilation therapy should rapidly be initiated in the ED in patients with definite acute signs of intracranial hypertension. If the intracranial hypertension does not respond to adjunctive osmotic diuretics, sedation, neuromuscular blockade, and neurosurgical drainage of cerebrospinal fluid, protracted hyperventilation may be necessary.

After blockade, select the Fio2 sufficient to maintain an arterial Po2 of 100 mmHg, fully saturating hemoglobin. Positive end-expiratory pressure (PEEP) of up to 5 cmH2O may help prevent atelectasis. Higher levels will impair cerebral venous drainage because of the elevated intrathoracic pressure. Avoid other modalities that also increase the ICP, including excessively tight ET tube straps, tight cervical collars, or Trendelenburg positioning.

CARDIOPULMONARY DISEASE Tracheal intubation and mechanical ventilation can also have other significant physiologic consequences. In a prospective investigation of 297 tracheal intubations in an intensive care unit setting, there were 7 deaths. 17 These occurred predominantly among those requiring emergent tracheal intubation. Mortality risk, however, was greatest among those receiving prior vasopressor therapy. Any conditions that result in the cardiovascular system's reliance on preload to maintain perfusion will predispose to hypotension and cardiac decompensation. Particular caution is needed when intubating previously hypotensive patients who require vasopressor support. In addition, patients with hypercarbia and chronic obstructive pulmonary disease (COPD) require special consideration. As mentioned, mechanical ventilation increases the positive intrathoracic pressure. This decreases the preload by decreasing venous return. Hypotension may be anticipated. Additional physiologic considerations include the decreased left ventricular compliance and the fact that most of the medications useful in RSI decrease the sympathetic tone.

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