Ventilator Weaning — Practical Guide (Akella 2022)

Since the inception of critical care medicine and artificial ventilation, literature and research on weaning has transformed daily patient care in intensive care units (ICU). As our knowledge of mechanical ventilation (MV) improved, so did the need to study patient-ventilator interactions and weaning predictors. Randomized trials have evaluated the use of protocol-based weaning (vs. usual care) to study the duration of MV in ICUs, different techniques to conduct spontaneous breathing trials (SBT), and strategies to eventually extubate a patient whose initial SBT failed. Despite considerable milestones in the management of multiple diseases contributing to reversible respiratory failure, in the application of early rehabilitative interventions to preserve muscle integrity, and in ventilator technology that mitigates against ventilator injury and dyssynchrony, major barriers to successful liberation from MV persist. This review provides a broad encompassing view of weaning classification, causes of weaning failure, and evidence behind weaning predictors and weaning modes.

Weaning is an intricate intervention that demands the attention and expertise of critical care specialists. Seventy years ago, Dr Ibsen introduced the revolutionary technique of positivepressure ventilation during the polio epidemic in Copenhagen that saved countless lives.1,2 In 1955, Dr Carl-Gunnar Engström introduced the first volume oriented-ventilator.3 In

1961, Drs. Henrik Bendixin and Henning Pontoppidan

founded the first respiratory intensive care unit (ICU) at Massachusetts General Hospital and conducted ventilator weaning research. 4 By 1977, Henning, Shubin and Weil were using esophageal-balloon catheters to make detailed measurements of the work of breathing. 5 In the 1970s, synchronized intermittent mandatory ventilation (SIMV) was widely used as the weaning mode of choice in most ICUs. Prior to the application of SIMV, weaning techniques comprised of disconnecting patients from the ventilator for 3–4 minutes at a stretch every thirty minutes and ascertaining their tolerance to abrupt discontinuation. In the 1980s, patient-ventilator interactions studies showed the limitations of SIMV as a weaning mode.

By the mid 1990’s, there was a shift in intensivists comparing various modes of weaning from MV. 1 Initially, patients require full ventilatory support to manage acute respiratory failure. Thereafter, recovering PaO2/FiO2 ratios, lower FiO2 requirements and lower ventilator settings might indicate the initiation of weaning readiness assessments. Various clinical and objective readiness assessment criteria must be met. 8 A patient undergoes measurements of weaning predictors while on a spontaneous breathing trial (SBT) for a prescribed amount of time. Weaning success is defined by extubation and absence of ventilatory support 48 hours after extubation.

9 Conversely, weaning failure is defined as the inability to pass a SBT or the need for reintubation within 48 hours following extubation. 10 Weaning can be classified as simple, difficult, or prolonged. 8,9,11 Simple weaning is associated with a higher incidence (30-60%) of success and a lower mortality (5-10%). The main objective for this group is to identify readiness to wean as soon as possible, and ensure a systematic approach to ventilator discontinuation. 8 In difficult weaning, a patient

Weaning is defined as a gradual decrease in ventilatory support from patients whose underlying cause for respiratory failure is improving and should be thought of as a continuum.6,7 requires up to three SBTs or as long as seven days to wean. For the difficult-to-wean patient, a major objective is identifying and addressing reversible causes for SBT failure. Finally, prolonged weaning occurs when a patient fails more than three SBTs or requires more than 7 days to be liberated from MV. In combination, difficult and prolonged weaning groups are associated with lower incidence (15-40%) of success and higher mortality (10-30%).7,9 In the prolonged weaning patient, preventive measures such as encouraging early spontaneous breathing, well controlled use of sedation, and early mobilization may help.8

In order to address reversible causes of weaning failure, a simple structured approach allows for a systematic review of the pathophysiology of weaning failure (Table 1). Discontinuation failure may depend on several factors and is

• ften consequent to more than a single cause. Irrespective of the underlying disorder leading to the need for MV, the most common mechanism is generally an imbalance between the force generating capacity of the respiratory muscles and the load they must face once MV is discontinued.11–13

Table 1. Pathophysiology of Weaning Failure.

Causes of Weaning

Failure Airway & lung dysfunction Weaning-induced cardiac dysfunction Cognitive dysfunction Endocrine & metabolic dysfunction Diaphragm dysfunction Nutrition Interventions Inhaled bronchodilators Inspiratory occlusion

Diagnostic Bronchoscopy during SBT

Diuretics Thoracentesis

EKG during SBT

Echocardiography before & after SBT

Bedside Cardiac POCUS

Afterload reduction strategies Delirium screening tools Reorientation techniques

Early Mobilization

Reducing noise/light during sleep Behavioral therapy Anxiolytics Electrolytes and Blood gas Plasma cortisol and thyroid hormone levels

Diaphragm EMG

Transdiaphragmatic pressure using gastric and esophageal balloon catheters Diaphragm muscle biopsy Indirect calorimetry EKG = electrocardiogram; PEEP = positive-end-expiratory pressure; SBT = spontaneous breathing trials; POCUS = point-of-care ultrasound; EMG = electromyography.

Airway and Lung Dysfunction

Airway and lung dysfunction can be broadly viewed through the prism of illnesses that increase airway resistance and those that reduce compliance.10 Causes of upper airway resistance are presence of an endotracheal tube, tracheal injury such as tracheal stenosis, tracheomalacia, granulation tissue formation, and small airway diseases such as asthma and chronic

• bstructive pulmonary disease (COPD).9,11,13 However, in general, it is a misconception that, after extubation, upper airway resistance decreases. In fact, the work of breathing in patients mechanically ventilated for ± 5.5 days increased after extubation, a probable consequence of upper airways edema.14 In a study of COPD patients failing an SBT, airway resistance significantly increased (9 ± 2 cm H2O up to 15 ±

2 cm H2O; p <0.05), whereas successfully weaning patients, airway resistance stayed the same.15,16 Additionally, increased airway resistance is associated with the development of intrinsic positive end-expiratory pressure (PEEPi). PEEPi may develop because of increased flow resistance, expiratory flow limitation, high breathing frequency, and loss of elastic recoil of the lungs.10 Pulmonary hyperinflation resulting from PEEPi places the diaphragm at a suboptimal position on the lengthtension curve, impairing the ability to generate negative pressure. PEEPi is associated with patient-ventilator asynchrony and, in particular, with ineffective triggering (Figure 1). Causes of reduced compliance include: pulmonary edema, pleural fluid, ascites, elevated abdominal pressures, obesity, pneumonia, interstitial lung diseases (ILD), and alveolar edema.10 Compliance of the respiratory system (Crs) is dependent on PEEP and plateau pressure (Pplat) and is calculated as per: Vt/(Pplat – PEEPtotal). Normal static lung compliance is 200 mL per cm H2O for non-intubated patients and 60 mL Figure 1. Ineffective triggering on a ventilator: airway pressure and flow waveforms. per cm H2O or lower for patients who need mechanical ventilation. Flexible bronchoscopy is the gold standard for diagnostic assessment of potential causes of upper airway resistance such as tracheal injury, tracheostomy malposition, tracheomalacia and thick respiratory secretions.9–11 Interventions such as non-invasive ventilation and endotracheal stents can be used to relieve resistance.17,18 Furthermore, in patients with small airway diseases, applied PEEP should match the level of PEEPi, as estimated by the expiratory occlusion technique.10 Bronchoconstriction can be reduced by routine use of bronchodilators.19 Diuretics can reduce lung and chest wall edema,20,21 while thoracentesis and paracentesis can resolve pleural fluid and ascitic fluid respectively,11,13,22 and help improve atelectasis thereby improving compliance and facilitating weaning.8–10 Laryngeal edema is associated with prolonged intubation and induces post-extubation stridor, which increases the risk

• f reintubation. A cuff leak test can be used as a surrogate indicator of laryngeal edema and to guide critical decisions to extubate patients or to continue mechanical ventilation. A recent meta-analysis and systematic review points to the excellent specificity and moderate sensitivity of the cuff leak test to predict post-extubation airway obstruction. The most salient risk factors for post-extubation stridor include traumatic intubation, intubation for longer than six days, a large endotracheal tube, female gender, and reintubation after unplanned extubation.23

The cuff leak test is a useful tool in the decision-making about extubation, but the low sensitivity suggests that a negative test cannot completely exclude post-extubation airway

• bstruction and that patients still need to be closely monitored post-extubation.23 Furthermore, systemic steroid therapy reduces both the reintubation rate and post-extubation stridor (PES) rate.23 The ATS/ACCP clinical practice guideline suggests performing cuff leak test in mechanically ventilated adults who meet extubation criteria and deemed high risk for

PES and suggest that for adults who have failed a cuff leak test but are otherwise ready for extubation, systemic steroids should be administered at least 4 h before extubation.11,18,23–25 In the context of uniquely primary respiratory disorders, such as chronic obstructive pulmonary disease, cystic fibrosis,

• besity hypoventilation syndrome, neuromuscular disorders and pediatric disorders prone to chronic hypercapnic respiratory failure, IMV and non-invasive ventilation have become a wellestablished treatment option.17 Special considerations need to be accounted for while managing these patients during weaning attempts and well-defined algorithms have been proposed by the German Respiratory Society for treating chronic respiratory failure.17 proposed mechanisms for cardiac dysfunction and weaninginduced left ventricular (LV) dysfunction (Figure 2).

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