By Richard Kallet, MS, RRT, FAARC, FCCM
Director of Quality Assurance, Respiratory Care Services, San Francisco General Hospital
Mr. Kallet reports no financial relationships relevant to this field of study.
SYNOPSIS: Rapid loss in diaphragmatic thickness during the first week of mechanical ventilation is common and associated with higher levels of ventilator driving pressure.
SOURCE: Goligher EC, et al. Evolution of diaphragm thickness during mechanical ventilation: Impact of inspiratory effort. Am J Respir Crit Care Med 2015 Jul 13 [Epub ahead of print].
Goligher et al conducted a multicenter trial using daily transthoracic ultrasonography to measure diaphragmatic contractile activity and thickness in 107 critically ill patients with the goal of assessing whether these measurements were affected by the level of inspiratory effort during mechanical ventilation (MV). The trial explored the evolution of diaphragm thickness over time, the impact of diaphragmatic contractile activity on diaphragm thickness, and the role of MV, including ventilator mode and driving pressure (a signifier for ventilator work output) on diaphragmatic contractile activity. Changes in muscle thickness > 10% from baseline in either direction were deemed clinically meaningful.
Diaphragmatic activity varied widely between patients and within individual patients over time. In the first week of MV, 44% of patients had no change in diaphragm thickness, 44% had evidence of clinically significant decreases in diaphragm thickness, and 12% had a significant increase in thickness. Most changes occurred within days of initiating MV. Loss of diaphragmatic thickness did not differ between patients who were ventilated with assist-control or partial support modes. Lower diaphragmatic contractile activity was associated with decreasing diaphragm thickness over time and higher activity with increasing thickness, although this was most pronounced during the first week of MV. Higher daily Sequential Organ Failure Assessment (SOFA) scores also were associated with increased diaphragm thickness, having an additive effect to diaphragmatic contractile activity. Significant inverse relationships were discovered between diaphragm thickness and diaphragmatic contractile activity with ventilator driving pressures; lower driving pressures and partially assisted modes of MV were associated with higher diaphragmatic contractile activity. Most importantly, both reduced and increased diaphragmatic thickness was associated with dysfunction. This suggests that increased thickness likely signifies muscle inflammation and structural injury from excessive inspiratory workloads rather than hypertrophy. No other baseline characteristics were associated with diaphragmatic thickness.
COMMENTARY
This study advances our understanding of the rapidity and variability of respiratory muscle dysfunction in critically ill patients requiring MV. Much of the previous literature has emphasized the problem of “disuse atrophy” during MV, thus indirectly promoting the strategy of “spontaneous breathing” during the entire course of acute respiratory failure. However, this theory neglects the important role of excessive muscular work causing secondary diaphragmatic injury and dysfunction1 and does not advance our practice of MV during critical illness. Refreshingly, the authors provided a balanced view of this nettlesome problem. That a substantial number of patients showed no ill effects of MV on diaphragmatic function was as important as the fact that approximately three out of every five study subjects had evidence of either rapid loss of muscle mass or injury.
The limitation of this study was its observational nature. The ability to quantify the amount of work sharing between patient and ventilator, the duration of activity, and the underlying source of acute respiratory failure (e.g., acute exacerbation of chronic obstructive lung disease vs acute lung injury) are crucial details needed to improve patient management. Future studies should perform ultrasonic measurements of diaphragmatic activity and thickness when both the degree of inspiratory support provided and inspiratory muscle pressure generated can be reasonably controlled. Moreover, measurements of diaphragmatic electromyography and inflammatory mediators would be helpful in further elucidating the mechanisms promoting diaphragmatic dysfunction from both excessive and insufficient stimulation.
An overlooked aspect of this problem is that modern MV began with the birth of the ICU in the mid-1960s, approximately 10 years before intense research into respiratory muscle function began. Thus, the nature of respiratory muscle dysfunction resulting from critical illness and prolonged MV was not well understood. This lack of knowledge leads to a bias toward overemphasizing disuse atrophy and promoting partial MV support early in the course of critical illness. This has probably been detrimental to hypotensive patients, particularly those with severe infection or trauma, and has likely promoted respiratory muscle injury contributing to prolonged dysfunction and ventilator dependence.
On the other hand, those of us who have focused on measuring patient work of breathing (WOB) during MV may have inadvertently promoted the opposite problem. It’s highly unlikely that the evolutionary success of mammals could have occurred without the ability to at least double normal WOB levels for extended periods of time without significant consequences. What became apparent as my own research experience matured (particularly with the advent of lung-protective ventilation) was that MV did not necessarily normalize WOB, so much as sufficiently enhance minute ventilation to levels required by critical illness despite their increased workload. Putting this issue into perspective, approximately 75% of critically ill patients are not ventilator-dependent once they reach the recovery phase.2 Nonetheless, there is ample room to enhance our understanding of the interplay between MV and respiratory muscle function. This will undoubtedly improve our care, regardless of whether “optimization” is a realistic achievement for all patients requiring MV.
REFERENCES
-
Vassilakopoulos T, et al. Is loaded breathing an inflammatory stimulus? Curr Opin Crit Care 2005;11:1-9.
-
Alia I, Esteban A. Weaning form mechanical ventilation. Crit Care 2000;4:72-80.
