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Table 1 Causes of difficult weaning

Unresolved underlying disease

Ongoing respiratory failure, fever, sepsis, multiple organ dysfunction, hemodynamic instability, and biochemical derangements contribute to inadequate oxygenation and gas exchange. Obviously, if weaning is initiated before the precipitating illness has resolved significantly, it is more likely to fail. Decreased level of consciousness secondary to the primary illness is common and will also jeopardize the success of weaning if it is started prematurely. Unfortunately, there are no clinical or laboratory indices which reliably define when a patient has recovered sufficiently from the underying condition to begin the weaning process.

Poor respiratory muscle capacity

Impaired central respiratory drive

Poor respiratory muscle capacity appears to be the principal cause of weaning failure. Residual effects of sedative agents will diminish spontaneous ventilation. However, if residual drug effects and premature weaning are excluded, a depressed central respiratory drive is rarely responsible for weaning failure ( Sluis,ky...,199.4).

Respiratory muscle atrophy and fatigue

Difficulty with weaning is usually associated with patients who have received long-term mechanical ventilation, indicating an impairment of global respiratory muscle function with prolonged ventilation. The diaphragm is a major component of respiratory muscles, but its precise contribution in weaning failure is unknown; phrenic nerve function is usually satisfactory.

Concepts of disuse atrophy following prolonged ventilation and muscle fatigue during weaning are widely accepted. Increased work of breathing will lead to respiratory muscle fatigue when respiratory demands exceed capacity. During weaning, this is superimposed on some degree of muscle weakness and atrophy resulting from the period of mechanical ventilation. Unsuccessful weaning has been attributed to respiratory muscle fatigue, as electromyographic and transdiaphragmatic pressure measurements have demonstrated decreased diaphragmatic contractility and slowing of muscle relaxation rate ( Goldstone eta/ 1994).

Nevertheless, the clinical importance of respiratory muscle fatigue remains unclear. Patients who fail a trial of weaning commonly have increased respiratory rates with low tidal volumes. This rapid shallow breathing pattern is seen as an adaptation to spare fatigued respiratory muscles. However, laboratory-induced fatigue (by resistive loading) does not result in rapid shallow breathing. Maximum inspiratory pressure ( Pimax) is a poor determinant of weaning outcome, and thus muscle strength per se may be assumed to be relatively unimportant in sustaining spontaneous breathing. Unfortunately, the pathophysiological mechanisms of respiratory muscle dysfunction, and the roles played by wasting, weakness, and fatigue, are poorly understood ( SlutskyJ994). There are no satisfactory methods of measuring the different components of respiratory function in patients on ventilator support. Techniques to assess respiratory muscle function in the laboratory are not reliably applicable at the bedside. Respiratory muscle function is likely to be impaired in varying degrees, but the clinical significance of this dynamic continuum has not been investigated. Also, data on respiratory muscle function at the time when weaning is initiated are poor.

Myopathies and neuropathies

Of course, weaning difficulties are encountered in neuromuscular diseases (e.g. Guillain-Barre syndrome and motor neuron disease). Persistent paralysis in critically ill patients receiving mechanical ventilation has been reported following administration of corticosteroids or the non-depolarizing muscle relaxants vecuronium and pancuronium. The etiology is not clear, as reported features are inconsistent. Electrophysiological, serum creatine kinase, and muscle biopsy studies have revealed a neuropathic process in some afflicted patients and a myopathic process in others. An increased concentration of a vecuronium metabolite and renal dysfunction in patients who have received long-term vecuronium administration have been proposed as causes. The term 'critical illness polyneuropathy' has been used for patients reported to have unexplained persistent muscle weakness during weaning from mechanical ventilation. Again, the etiology and clinical picture are unclear, but the pathophysiological pattern is neurogenic and not myopathic ( Rapsefa/ 1994). Axonal degeneration involving motor and sensory nerves is seen, and sepsis and multiple organ failure are commonly associated. The diagnosis is made clinically and is unrelated to blood concentrations of cytokines. These myoneuropathies may be manifestations of a common condition caused by toxic or metabolic disturbances following long-term mechanical ventilation. The contribution of neuromuscular diseases to weaning failure is probably underestimated.

Inadequate or inappropriate nutrition

Critically ill patients, including those on mechanical ventilation, are at risk of developing malnutrition. Unfortunately, the nutritional requirements of ventilated patients are difficult to study. Consequently, prospective randomized clinical trials to determine the role of nutritional support for ventilated critically ill patients are not available. Although the energy expenditure of critically ill patients receiving mechanical ventilation has been reported, data on energy requirements during weaning are lacking. Nonetheless, malnutrition affects muscle structure and function in humans. Since respiratory muscle endurance is important for meeting ventilatory demands during weaning, poor nutrition may contribute to weaning failure.

Although the optimal nutritional regimen for ventilated or weaning patients has not been determined, excessive administration of glucose may compromise successful weaning. Increased CO2 production and hypercarbia result from increased glucose combustion and from lipogenesis, as excess glucose is converted to fat.

Excessive respiratory load

Inspiratory load of breathing circuits

Breathing difficulties caused by ventilators and circuits are often overlooked during weaning from mechanical ventilation. Additional work of breathing imposed by weaning circuits commonly contributes to weaning failure. Significant resistance to gas flow, resulting in increased inspiratory work, is imposed by endotracheal tubes, humidifiers, and ventilators. Circuit hoses have relatively small flow resistances as they have a large internal diameter (22 mm). From Poiseuille's law where DP is the pressure gradient across the tube, r is the tube radius, and L is the tube length, small endotracheal tube sizes present very large resistances. In vivo endotracheal tube resistance may be greater, presumably due to kinking and intraluminal secretions.

Bubble or cascade water-bath humidifiers, in which gas is dispersed through heated water, have higher resistances than blow-by or pass-over types, in which gas passes over the water surface. Resistance is higher with low peak inspiratory flows, and, if used, bubble humidifiers contribute to weaning failure.

Ventilators use inspiratory demand valves to respond rapidly to changing spontaneous ventilatory efforts. Unfortunately, these demand valves add considerably to the work of breathing (Beydon... 1988), depending on the way that gas is delivered in response to an initiated spontaneous breath. Ventilators with pressurized gas reservoirs, for example Servo 900C (Siemens Elema AB, Solna, Sweden) and Engstrom Erica (Gambro Engstrom AB, Bromma, Sweden), produce a high gas flow response and can compensate to some extent for demand valve impedance. The high inspiratory loads imposed by the demand valves of some ventilators, particularly older models, are prominent but often unrecognized factors in weaning failure.

Continuous positive airways pressure (CPAP) circuits are available either incorporated in ventilators or as stand-alone units. Valveless circuits obviously impose less inspiratory work. The Bennett 7200a ventilator (Puritan-Bennett Corporation, California, USA) has a 'flow-by' facility for CPAP breathing which uses a separate continuous-flow circuit to bypass the demand valve. CPAP circuits which induce large swings in airway pressure during the respiratory cycle result in greater work of breathing. Weaning will also be severely compromised if breathing circuits do not provide sufficient fresh gas flow during spontaneous inspiration, particularly if the patient increases minute ventilation intermittently.

Intrinsic positive end-expiratory pressure (PEEP)

Patients with obstructive lung disease demonstrate some degree of expiratory flow limitation during weaning, a period when high respiratory rates, short expiratory times, and increased minute volumes are commonly seen. Dynamic hyperinflation results in an alveolar pressure that is greater than atmospheric pressure. This auto-PEEP or intrinsic PEEP imposes an inspiratory load, and the increased work of breathing will compromise successful weaning.

Left ventricular dysfunction

Failure to wean patients with heart or chronic lung disease may be due to the onset of left ventricular failure with cardiogenic pulmonary edema. With the resumption of spontaneous breathing, onset of respiratory distress is accompanied by an abrupt increase in pulmonary artery wedge pressure ( L.e.m.alr§...,e.t..a/ 1988). This left ventricular dysfunction is due to acute myocardial ischemia and is associated with coronary artery disease. Myocardial scintographic studies have shown altered myocardial perfusion, left ventricular dilatation, and decreased left ventricular ejection fraction. Acute impairment of left ventricular function is probably a consequence of increased afterload due to an increase in systemic blood pressure and a change in intrathoracic pressure from positive to negative. The situation is worsened by the work imposed by poorly designed circuits and hypoxemia from any cause. Weaning will be difficult if the cardiopulmonary stress is not recognized.

Severe agitation and delirium

Weaning from mechanical ventilation is a time of physical and emotional stress for the patient. Some patients may be delirious or become extremely agitated, at a time when excessive use of sedative agents is avoided. The patient may experience significant pain. Weaning will not be successful if extreme delirium or agitation is poorly controlled, or if there is oversedation.

Chapter References

Beydon, L., Chasse, M., Harf, A., and Lemaire, F. (1988). Inspiratory work of breathing during spontaneous ventilation using demand valves and continuous flow systems. American Review of Respiratory Disease, 138, 300-4.

Goldstone, J.C., Green, M., and Moxham, J. (1994). Maximum relaxation rate of the diaphragm during weaning from mechanical ventilation. Thorax, 49, 54-60.

Lemaire, F., Teboul, J.-L., Cinotti, L., Giotto, G., Abrouk, F., and Steg, G. (1988). Acute left ventricular dysfunction during unsuccessful weaning from mechanical ventilation. Anesthesiology, 69,

Raps, E.C., Bird, S.J., and Hansen-Flaschen, J. (1994). Prolonged muscle weakness after neuromuscular blockade in the intensive care unit. Critical Care Clinics, 10, 799-813.

Slutsky, A.S. (1994). Consensus conference on mechanical ventilation—January 28-30, 1993 at Northbrook, Illinois, USA. Part 2. Intensive Care Medicine, 20, 150-62.

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