Mechanical ventilation is used to sustain life in patients with acute respiratory failure. A major concern in mechanically ventilated patients is the risk of ventilator-induced lung injury, which is partially prevented by lung-protective ventilation. Spontaneously breathing, nonintubated patients with acute respiratory failure may have a high respiratory drive and breathe with large tidal volumes and potentially injurious transpulmonary pressure swings. In patients with existing lung injury, regional forces generated by the respiratory muscles may lead to injurious effects on a regional level. In addition, the increase in transmural pulmonary vascular pressure swings caused by inspiratory effort may worsen vascular leakage. Recent data suggest that these patients may develop lung injury that is similar to the ventilator-induced lung injury observed in mechanically ventilated patients. As such, we argue that application of a lung-protective ventilation, today best applied with sedation and endotracheal intubation, might be considered a prophylactic therapy, rather than just a supportive therapy, to minimize the progression of lung injury from a form of patient self-inflicted lung injury. This has important implications for the management of these patients.

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Mechanical Ventilation to Minimize Progression of Lung Injury in Acute Respiratory Failure

Objective
The incidence, pathophysiology, and consequences of patient-ventilator asynchrony are poorly known. We assessed the incidence of patient-ventilator asynchrony during assisted mechanical ventilation and we identified associated factors.

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Patient-ventilator asynchrony during assisted mechanical ventilation

As management of respiratory distress syndrome (RDS) advances, clinicians must continually revise their current practice. We report the fourth update of “European Guidelines for the Management of RDS” by a European panel of experienced neonatologists and an expert perinatal obstetrician based on available literature up to the end of 2018. Optimising outcome for babies with RDS includes prediction of risk of preterm delivery, need for appropriate maternal transfer to a perinatal centre and timely use of antenatal steroids. Delivery room management has become more evidence-based, and protocols for lung protection including initiation of CPAP and titration of oxygen should be implemented immediately after birth. Surfactant replacement therapy is a crucial part of management of RDS, and newer protocols for its use recommend early administration and avoidance of mechanical ventilation. Methods of maintaining babies on non-invasive respiratory support have been further developed and may cause less distress and reduce chronic lung disease. As technology for delivering mechanical ventilation improves, the risk of causing lung injury should decrease, although minimising time spent on mechanical ventilation using caffeine and, if necessary, postnatal steroids are also important considerations. Protocols for optimising general care of infants with RDS are also essential with good temperature control, careful fluid and nutritional management, maintenance of perfusion and judicious use of antibiotics all being important determinants of best outcome.

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European Consensus Guidelines on the Management of Respiratory Distress Syndrome - 2019 Update.

The act of breathing depends on coordinated activity of the respiratory muscles to generate subatmospheric pressure. This action is compromised by disease states affecting anatomical sites ranging from the cerebral cortex to the alveolar sac. Weakness of the respiratory muscles can dominate the clinical manifestations in the later stages of several primary neurologic and neuromuscular disorders in a manner unique to each disease state. Structural abnormalities of the thoracic cage, such as scoliosis or flail chest, interfere with the action of the respiratory muscles-again in a manner unique to each disease state. The hyperinflation that accompanies diseases of the airways interferes with the ability of the respiratory muscles to generate subatmospheric pressure and it increases the load on the respiratory muscles. Impaired respiratory muscle function is the most severe consequence of several newly described syndromes affecting critically ill patients. Research on the respiratory muscles embraces techniques of molecular biology, integrative physiology, and controlled clinical trials. A detailed understanding of disease states affecting the respiratory muscles is necessary for every physician who practices pulmonary medicine or critical care medicine.

Disorders of the Respiratory Muscles

Mechanical ventilation is a life-saving intervention for the management of acute respiratory failure. Its objective is to reduce excessive respiratory effort while improving gas exchange. By applying positive pressure to the airway, the mechanical ventilator assumes to a varying extent the work necessary to breathe, thereby unloading the respiratory muscles. In its most basic form, called controlled mechanical ventilation, a pre-set tidal volume is delivered at a fixed rate, irrespective of the patient’s own breathing pattern. If the mechanical and natural respiratory cycles are not matched, however, the patient ‘fights’ the ventilator, causing discomfort, gas exchange deterioration and cardiovascular impairment 1 . To avoid discoordination between the patient and the ventilator, it is often necessary to suppress the patient’s intrinsic respiratory drive with the use of hyperventilation, sedation or even muscle paralysis, which increase the risk of complications due to excessive ventilation 2‐3 , drug-related adverse effects

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Neural control of mechanical ventilation in respiratory failure.

Intersubject comparison of the crural diaphragm electromyogram, as measured by an esophageal electrode, requires a reliable means for normalizing the signal. The present study set out 1) to evaluat...

Voluntary activation of the human diaphragm in health and disease.

Objective:To compare the effect of pressure support ventilation and neurally adjusted ventilatory assist on breathing pattern, patient-ventilator synchrony, diaphragm unloading, and gas exchange. Increasing the level of pressure support ventilation can increase tidal volume, reduce respiratory rate,

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Patient-ventilator interaction during pressure support ventilation and neurally adjusted ventilatory assist.

We compared crural diaphragm electrical activity (EAdi) with transdiaphragmatic pressure (Pdi) during varying levels of pressure support ventilation (PS) in 13 intubated patients. With changing PS, we found no evidence for changes in neuromechanical coupling of the diaphragm. From lowest to highest PS (2 cm H2O ± 4 to 20 cm H2O ± 7), tidal volume increased from 430 ml ± 180 to 527 ml ± 180 (p < 0.001). The inspiratory volume calculated during the period when EAdi increased to its peak did not change from 276 ± 147 to 277 ± 162 ml, p = 0.976. Respiratory rate decreased from 23.9 ( ± 7) to 21.3 ( ± 7) breaths/min (p = 0.015). EAdi and Pdi decreased proportionally by adding PS (r = 0.84 and r = 0.90, for mean and peak values, respectively). Mean and peak EAdi decreased (p < 0.001) by 33 ± 21% (mean ± SD) and 37 ± 23% with the addition of 10 cm H2O of PS, similar to the decrease in the mean and peak Pdi (p < 0.001) observed (34 ± 36 and 35 ± 23%). We also found that ventilator assist continued during the diap...

https://www.atsjournals.org/doi/pdf/10.1164/ajrccm.164.3.2009018

Electrical activity of the diaphragm during pressure support ventilation in acute respiratory failure.

Although it has been postulated that central inhibition of respiratory drive may prevent development of diaphragm fatigue in patients with chronic obstructive pulmonary disease (COPD) during exercise, this premise has not been validated. We evaluated diaphragm electrical activation (EAdi) relative to maximum in 10 patients with moderately severe COPD at rest and during incremental exhaustive bicycle exercise. Flow was measured with a pneumotachograph and volume by integration of flow. EAdi and transdiaphragmatic pressures (Pdi) were measured using an esophageal catheter. End-expiratory lung volume (EELV) was assessed by inspiratory capacity (IC) maneuvers, and maximal voluntary EAdi was obtained during these maneuvers. Minute ventilation (V˙ e) was 12.2 ± 1.9 L/min (mean ± SD) at rest, and increased progressively (p < 0.001) to 31.0 ± 7.8 L/min at end-exercise. EELV increased during exercise (p < 0.001) causing end-inspiratory lung volume to attain 97 ± 3% of TLC at end-exercise. Pdi at rest was 9.4 ± 3.2...

https://www.atsjournals.org/doi/pdf/10.1164/ajrccm.163.7.2007033

Jennifer Beck

Papers

Neural control of mechanical ventilation in respiratory failure.

Voluntary activation of the human diaphragm in health and disease.

Patient-ventilator interaction during pressure support ventilation and neurally adjusted ventilatory assist.

Electrical activity of the diaphragm during pressure support ventilation in acute respiratory failure.

Diaphragm activation during exercise in chronic obstructive pulmonary disease.