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Patients with COPD may also manifest dynamic hyperinflation and reduced compliance when forced to operate at the less efficient upper margin of the pressure–volume curve. The process of weaning may impose an increased resistive load on the ventilatory muscles, either from the endotracheal tube during an SBT or post-extubation from glottic oedema or increased airway secretions and sputum retention. Cardiac load Many patients will have identified ischaemic heart disease, valvular heart disease, systolic or diastolic dysfunction prior to, or identified during, their critical illness. More subtle and less easily recognised are those patients with myocardial dysfunction, which is only apparent when exposed to the workload of weaning. The transfer of a patient from positive pressure ventilation to spontaneous ventilation is associated with increased venous return and negative intra-thoracic pressure causing increased left ventricular afterload and increased myocardial oxygen consumption. Thus, latent or unrecognised myocardial dysfunction may become manifest at the commencement of the weaning attempts . This is further reflected in the beneficial effects seen with the application of continuous positive airway pressure (CPAP) or NIV in cardiogenic pulmonary oedema. There are several contributors to increased cardiac workload. These include: dynamic hyperinflation (intrinsic PEEP), which increases pulmonary vascular resistance, reduces right ventricular filling and impairs cardiac output; the increased metabolic demand of the weaning process; and unresolved systemic disease (e.g. sepsis). There is an obligatory increase in cardiac output to meet the metabolic demand of a weaning trial. Measurable indices include increased serum lactate and decreased mixed venous oxygen saturation (SV,O2). Weaning failure has been predicted through the use of SV,O2 during SBT or measurement of gastric mucosal pH. 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.
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