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Failure of ventilation in the neuromuscular diseases presents as one of two symptom complexes: one occurs in patients with acute generalized weakness, such as Guillain-Barre syndrome and my asthenia gravis, and the other in patients with subacute or chronic diseases, such as motor neuron disease, certain myopathies (acid maltase, nemaline), and muscular dystrophy The review by Polkey and colleagues provides a more extensive list Patients in whom respiratory failure evolves rapidly, in a matter of hours, become anxious, tachycardic, and diaphoretic; they exhibit the characteristic signs of diaphragmatic paralysis They experience paradoxical respiration, in which the abdominal wall retracts during inspiration, owing to the failure of the diaphragm to contract, while the intercostal and accessory muscles create a negative intrathoracic pressure Or, there is respiratory alternans, a pattern of diaphragmatic descent only on alternate breaths (this is more characteristic of airway obstruction) These signs appear in the acutely ill patient when the vital capacity has been reduced to approximately 10 percent of normal, or approximately 500 mL in the average adult Patients with chronic but stable weakness of the respiratory muscles, demonstrate signs of CO2 retention, such as daytime somnolence, headache upon awakening, nightmares, and, in extreme cases, papilledema The accessory muscles of respiration are recruited in an attempt to maximize tidal volume, and there is a tendency for the patient to gulp or assume a rounded sh mouth appearance in an effort to inhale additional air In general, patients with chronic respiratory dif culty tolerate lower tidal volumes without dyspnea than do patients with acute disease, and symptoms in the former may occur only at night, when respiratory drive is diminished and compensatory mechanisms for obtaining additional air are in abeyance Treatment of the two conditions differs The chronic type of respiratory failure may require only nighttime support of ventilation, which can be provided by negative pressure devices such as a cuirass or preferably, by intermittent positive pressure applied by a tight- tting mask over the nose (BIPAP or CPAP) These measures may also be used temporarily in acute situations, but in many cases there will be need of a positive-pressure ventilator that provides a constant volume with each breath This can be effected only through an endotracheal tube In patients with chronic weakness, the use of a cough-assist machine to provide an arti cial cough three or four times a day is remarkably effective in preventing pulmonary infection Typical ventilator settings in cases of acute mechanical respiratory failure, if there is no pneumonia, are for tidal volumes of 8 to 10 mL/kg, depending on the compliance of the lungs and the patient s comfort, at a ventilator rate between 4 and 12 breaths per minute, adjusted to the degree of respiratory failure The tidal vol-.

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ume is kept relatively constant in order to prevent atelectasis, and only the rate is changed as the diaphragm becomes weaker or stronger Decisions regarding the need for these mechanical devices are frequently dif cult, particularly since patients with chronic neuromuscular illnesses often become dependent on a ventilator Further details regarding the management of ventilation in acute neuromuscular weakness are given in the section on Guillain-Barre syndrome on page 1126 The presence of oropharyngeal weakness as a result of the underlying neuromuscular disease may leave the patient s airway unprotected and require endotracheal intubation before mechanical ventilation becomes necessary It is also dif cult to decide when to remove the endotracheal tube in cases of oropharyngeal weakness Because the safety of the swallowing mechanism cannot be assessed with the tube in place, one must be prepared to reintubate the patient or to have a surgeon prepared to perform a tracheostomy after extubation, in the event that aspiration occurs Not infrequently we encounter a patient in whom the earliest feature of neuromuscular disease is subacute respiratory failure; this is manifest as dyspnea and exercise intolerance but without other overt signs of neuromuscular disease Most such cases turn out to have motor neuron disease, but rare instances of myasthenia gravis, acid maltase de ciency, polymyositis, nemaline myopathy, Lambert-Eaton syndrome, or chronic in ammatory demyelinating polyneuropathy may present in this way The neurologist may be consulted in these cases after other physicians have found no evidence of intrinsic pulmonary disease The spirometric ow-volume loop examination in mechanical-neuromuscular forms of respiratory failure shows low air ow rates with diminished lung volumes that together simulate a restrictive lung disease Among such patients we have also found instances of an apparently isolated unilateral or bilateral phrenic nerve paresis, which had followed surgery or an infectious illness The problem is probably akin to brachial neuritis (Parsonage-Turner syndrome, page 1165), in which the phrenic nerve can be implicated Neuromuscular Respiratory Failure in Critically Ill Patients Neurologists increasingly are being called upon to address the question of an underlying neuromuscular cause for respiratory failure in a critically ill patient Aside from the acute neuromuscular diseases listed above, Bolton and colleagues have delineated a critical illness polyneuropathy, which accounts for the majority of instances in which there is an inability to wean the patient from a ventilator once the more conventional causes of pulmonary insuf ciency such as malnutrition and hypokalemia have been addressed Such a critical illness polyneuropathy has been identi ed by electromyography (EMG) in as many as 40 percent of patients in medical intensive care units Most of the patients have had an episode of sepsis or have had multiple-organ failure (see Chap 46) Less often, a critical illness myopathy occuring in relation to administration of high-dose corticosteroids (Chap 51) has been the cause of generalized weakness and respiratory failure This unique polymyopathy occurs mainly in patients who are receiving neuromuscular postsynaptic blocking drugs such as pancuronium with the high-dose steroids (page 1237) Severe hypophosphatemia is another cause of acute generalized weakness.

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