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Myocardial ischaemia may become manifest during SBT. This may result in reduced left ventricular compliance, pulmonary oedema and increased WOB. Neuromuscular competence Liberation from mechanical ventilation requires the resumption of neuromuscular activity to overcome the impedance of the respiratory system, to meet metabolic demands and to maintain carbon dioxide homeostasis. This requires an adequate signal generation in the central nervous system, intact transmission to spinal respiratory motor neurons, respiratory muscles and neuromuscular junctions. Disruption of any portion of this transmission may contribute to weaning failure. Depressed central drive With complete absence of central drive, patients do not exhibit any ventilatory activity upon discontinuation from the ventilator, and this persists despite hypercapnia and hypoxaemia. Examples of this may include, but are not limited to, encephalitis, brainstem haemorrhage/ischaemia and neurosurgical complications. It is more challenging to identify a reduction in ventilatory drive. The carbon dioxide responsiveness test may be used to assess this but there are few studies evaluating its utility in critically ill patients. The responsiveness of central drive to carbon dioxide assessed from the 100-ms occlusion pressure has been shown to predict weaning success in a small case series. Central drive may be impeded by metabolic alkalosis, mechanical ventilation itself or the use of sedative/hypnotic medications. Of these three possible contributors, there are only data that link sedative/hypnotic medication use to prolonged weaning. The importance of the contribution of daily awakening and heightened awareness over sedation to prolonged weaning and ICU stay has been established in the literature. Myopathy may be confirmed on muscle biopsy and type II fibre drop-out with a loss of myosin filaments is a consistent finding. Three studies have shown that diaphragmatic electrophysiological abnormalities are common in patients with locomotor electroneuromyographic abnormalities and were more prevalent when the limb weakness was more severe. The bedside evaluation of respiratory neuromuscular weakness is difficult. Maximum inspiratory pressure and vital capacity are dependent on patient comprehension and cooperation and are hindered by the endotracheal tube. As a result, many have questioned their ability to detect respiratory neuromuscular dysfunction that contributes to prolonged weaning. Twitch transdiaphragmatic pressure in response to bilateral stimulation of the phrenic nerves can give an effort-independent measure of diaphragmatic contractility. Clinical applicability is limited as this requires placement of both an oesophageal and gastric balloon. The airway pressure at the end of the tracheal tube in response to phrenic nerve stimulation has been proposed to be a noninvasive alternative measure and may have a role in monitoring inspiratory muscle contractility as its correlation to twitch transdiaphragmatic pressure is weak. The contribution of CINMA to prolonged mechanical ventilation has been studied in 10 cohorts of ICU patients. Four studies have shown an association between CINMA and an increased duration of weaning or weaning failure. Two of these used multivariable analysis to control for confounding factors and showed that CINMA was an independent risk factor for duration of mechanical ventilation and weaning failure, including the need for tracheostomy. Neuromuscular dysfunction related to CINMA usually improves over weeks but some disability may persist over months and interfere with activities of daily living .
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