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Boston, MA
Dr. Loring is Associate Professor, Beth Israel Deaconess Medical Center and Harvard Medical School. Dr. Malhotra is Assistant Professor, Brigham and Women’s Hospital, Beth Israel Deaconess Hospital, and Harvard Medical School.
Correspondence to: Stephen H. Loring, MD, Beth Israel Deaconess Medical Center and Harvard Medical School, Department of Anesthesia, 330 Brookline Ave, DA 717, Boston, MA 02215; e-mail: sloring{at}bidmc.harvard.edu
A growing body of literature suggests that mechanical ventilation can promote lung damage when excessive transpulmonary pressures are applied.1 Although stretch-mediated lung injury has received much attention,2 lung hyperinflation leading to gross barotrauma is also a concern, particularly if lung volume exceeds total lung capacity (TLC). Human lungs are normally prevented from overdistension by the felicitous match between maximal inspiratory muscle pressures (Pmus-max) and the pressures required to inflate the respiratory system to its maximal volume (ie, TLC). This protective equilibrium may not apply to patients making forceful inspiratory efforts on mechanical ventilation, especially during pressure-control or pressure-support ventilation when applied pressures could conceivably combine with Pmus-max to overdistend the lungs.
In this issue of CHEST (see page 711), Sinderby et al3 provide observations that make the possibility of involuntary hyperinflation seem less likely. Maximal lung volume (ie, TLC) is quite reproducible in trained individuals; repeated inhalations yield TLC values clustering within 5%. What limits TLC in healthy subjects? Early reports456 that abdominal muscles become active when subjects inhale to TLC, thereby raising the abdominal pressure, led to suggestions that TLC is limited by the reflex action of the expiratory abdominal muscles. In addition, glottal closure during sustained inhalation to TLC led to the conclusion that airway reflexes also limit maximal lung volume.6 Later, Mead et al7 showed that inhalation to TLC could be performed with or without abdominal muscle contraction, observing substantial abdominal muscle contraction only in untrained subjects. In fact, modest abdominal muscle contraction during active inhalation at TLC has only minimal expiratory effect. The study by Mead et al7 led to the current understanding that TLC is limited by a mechanical equilibrium between Pmus-max and the elastic recoil of the lung and chest wall (Fig 1 ). Subsequent demonstration that the diaphragm is maximally active during inhalation at TLC8910 implied that reflexes are not normally important in limiting maximal lung volume.
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What has the article by Sinderby et al3 contributed to this understanding? Using neurally adjusted ventilatory assist (NAVA), they explored the interactions between mechanical ventilation and respiratory muscle action in healthy subjects making maximal inhalations. NAVA applies pressure in proportion to electromyogram activity in the diaphragm in an attempt to maximize comfort, which is somewhat similar to proportional assist ventilation (PAV). As they increased ventilatory assist from zero to a level that provided all of the pressure required for lung inflation, they observed a decrease in diaphragmatic activation such that the sum of inspiratory Pmus-max and ventilator pressures continued to exactly match the pressure required for lung inflation. When the subjects voluntarily made maximal inspiratory efforts, the maximal diaphragm activity was similarly reduced to a level at which the inspiratory capacity remained near the unassisted values, and, despite airway pressures that were equal to those normally supplied by Pmus-max, lung volume at TLC remained nearly unchanged. These observations suggest that in healthy subjects diaphragmatic activation is limited, perhaps by reflex, to maintain maximal lung volume constant in the face of externally applied inspiratory pressures. While this reflex is not the same as that proposed by early investigators, it does suggest that maximal lung volumes will not be exceeded during NAVA in patients who are also using their inspiratory muscles. Two important caveats need to be mentioned. These studies were conducted in healthy subjects making voluntary inspiratory efforts, not in dyspneic patients with injured lungs making involuntary inhalations. Heterogeneously diseased lungs may experience high shear forces at relatively low transpulmonary pressures, particularly at the junctions of normal and abnormal lung tissue. Furthermore, these experiments suggest that inspiratory muscle actions are limited at high lung volumes, but forceful inspiratory efforts at low lung volumes could also produce regional overexpansion in a heterogeneously diseased lung.
As in PAV, NAVA relies on the concept that ICU patients should determine their own respiratory rate and tidal volume. NAVA has a potential advantage over PAV in that inflation is triggered at the start of the inspiratory effort (even with auto-positive end-expiratory pressure), rather than requiring the patient to initiate airflow. On the other hand, NAVA requires the continuous assessment of electromyogram activity in the diaphragm, a signal that may be difficult to record reliably for prolonged periods. For the physiologist, this article provides support for a possible inhibitory reflex that can reduce diaphragm activation to prevent lung overexpansion. For the clinician, questions remain about when NAVA should be used and whether this technique improves patient/ventilator synchrony, safety, and comfort.
Footnotes
Dr. Loring has reported to the ACCP that no significant conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article. Dr. Malhotra has received research support from Respironics, Inc.
References
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