Protecting the Lungs and the Diaphragm during Mechanical Ventilation

Protecting the Lungs and the Diaphragm during Mechanical Ventilation

  • Issue 76

The Young Teaching Recognition Award, 2018

Protecting the Lungs and the Diaphragm during Mechanical Ventilation

Tom Schepens, MD, MMed
Antwerp University Hospital, Edegem, Belgium
tom.schepens@uza.be

Introduction

The potential harm of mechanical ventilation (MV) on the lungs is well known. The injury this caused was termed ventilator-induced lung injury (VILI),1a term that covers the combination of volutrauma, atelectrauma, and biotrauma. The volutrauma is a result of excessive lung stress and strain,2and the atelectrauma is a result of repetitive opening and closing of alveoli. The resulting inflammation has systemic consequences and is the biotrauma associated with MV.3The insights into VILI have led to the specific ventilation strategies that are lung-protective. These include ventilation with low tidal volumes, prone positioning, and neuromuscular blockade in early ARDS.4-6Adopting these strategies in clinical practice has resulted in decreased morbidity and mortality in ventilated patients.

A different type of injury (myotrauma) resulting from MV was more recently described: ventilator-induced diaphragm dysfunction (VIDD).7This term is used to cover the effects of MV on respiratory muscles, predominantly the diaphragm. The diaphragm has a crucial role in liberating (weaning) the patient from the ventilator once the lung parenchyma has recovered from acute lung injury. As with VILI, respiratory muscle (diaphragm) weakness results in morbidity and mortality as well.8The first studies on this subject, about a decade ago, showed muscle atrophy on diaphragm biopsies of long-term ventilated patients.9Further research has looked at biological pathways and at the physiological basis of how the ventilator interferes with respiratory muscle function. These novel insights have recently laid the foundation for what a muscle-protective ventilation strategy may look like in the future. Integrating both muscle- and lung-protective ventilation targets is a challenge we face but may lead to improved patient outcome.

Ventilator-Induced Diaphragm Dysfunction

Muscle weakness is common in the intensive care unit (ICU). Both limb muscles and respiratory muscles are affected, and both independently impact the length of ventilation and patient survival.8,10There are multiple reasons why muscle dysfunction is so frequently seen: the patient’s disease and the therapy we administer often affect the muscles. Recently, diaphragm muscle injury by the ventilator has been brought forward as a major contributor to the diaphragm dysfunction observed in the ICU.

The diaphragm

During normal tidal breathing, the diaphragm provides about 70% of respiratory activity in adults.11In young children, the diaphragm is even more important, as their accessory respiratory muscle strength has not been developed completely. It is a thin (a few millimetres thick) muscle with a dome-like shape. When inspiring, the diaphragm contracts, pulling the lungs downward.

Risk factors

Multiple factors have an impact on diaphragm strength, most of them present in almost any patient admitted in the ICU. Even before admission to the ICU, critically ill patients frequently exhibit diaphragm weakness.12During their illness, one of the most important contributors to muscle weakness is sepsis,13which may impact the diaphragm even more than other muscles.14Other factors include the use of certain drugs, including neuromuscular blocking agents, corticosteroids, and aminoglycosides.15-17The presence of metabolic derangements like acidosis and hypokalaemia, and comorbidities like endocrinopathies and malnutrition, seem to affect muscle function as well.15,16These factors are also risk factors for ICU-acquired weakness (ICU-AW),18together with immobility and microvascular injury, and thus VIDD probably shares some characteristics with ICU-AW.19,20

In ventilated patients, the possible additional impact of mechanical ventilation on the diaphragm is present. The pathophysiological process is complex and not fully understood, but reactive oxygen species, mitochondrial dysfunction, and an activation of caspase/calpain proteolytic pathways seem to be at the base.13,21,22The lack of muscle activity during MV is an important part in this process, essentially creating disuse atrophy of the diaphragm.23This implicates that some degree of maintained inspiratory activity will be important in mitigating VIDD.23

Monitoring diaphragm activity

Different techniques are available to monitor diaphragm activity during mechanical ventilation. We can measure the pressures generated by the diaphragm with oesophageal manometry,24or look at the electrical activity with diaphragm electromyography (EMG). Ultrasound offers us the possibility to visualize diaphragm activity. Diaphragm excursion can be measured with subcostal M-mode views, but only as long as there is no downward displacement of the diaphragm by positive pressure ventilation. The other ultrasound technique looks at the diaphragm in the 8th or 9th intercostal space between the mid- and anterior-axillary lines. This is called the zone of apposition, where the diaphragm is parallel to the chest wall. Here, both diaphragm thickness and change in thickness from expiration to inspiration (the thickening fraction) can be measured.25The thickening fraction is a parameter for inspiratory activity.26,27These recordings have demonstrated excellent reproducibility in ventilated patients.28

Diaphragm protective ventilation

The lack of muscle activity results in diaphragm atrophy and thus dysfunction. Furthermore, a certain degree of inspiratory muscle activity during mechanical ventilation seems to be able to mitigate atrophy and dysfunction.23,29However, the flipside of this coin seems to be that excessive amounts of diaphragm activity are undesirable as well, causing muscle fatigue and worse respiratory outcome,23and potentially patient self-inflicted lung injury (P-SILI). A novel approach, a diaphragm protective ventilation, will thus need to incorporate a way of titrating diaphragm activity to an appropriate level: keeping the muscle active but supporting it adequately.

Conclusion

Intensivists used to focus on the lungs when setting ventilator targets. Recent evidence adds the diaphragm as an element in the respiratory system not to ignore. The challenge will be how to define optimal levels of inspiratory activity, and to merge the goals for lung-protective ventilation with these of diaphragm-protective ventilation. Diaphragm ultrasound will be able to serve as a diagnostic tool for dysfunction, and possibly as a way of titrating respiratory support as well.

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