The University of Osaka · Medicine
Professor Takeshi Yoshida's research lab specializes in respiratory physiology and critical care medicine, focusing on the biomechanics of mechanical ventilation and its impact on lung injury. The lab investigates how spontaneous breathing efforts during mechanical ventilation can inadvertently cause or exacerbate ventilator-induced lung injury (VILI), particularly through excessive transpulmonary pressure and tidal recruitment. Using animal models and clinical monitoring techniques like esophageal manometry, the lab aims to optimize ventilatory strategies to balance oxygenation benefits with lung-protective ventilation. Their work emphasizes personalized PEEP titration and the hemodynamic and ventilatory consequences of spontaneous effort in acute respiratory distress syndrome (ARDS).
Figures are computed from collected data and may differ slightly.
Spontaneous breathing effort during mechanical ventilation causes unsuspected overstretch of dependent lung during early inflation (associated with reciprocal deflation of nondependent lung). Even when not increasing tidal volume, strong spontaneous effort may potentially enhance lung damage.
Spontaneous respiratory effort during mechanical ventilation has long been recognized to improve oxygenation, and because oxygenation is a key management target, such effort may seem beneficial. Also, disuse and loss of peripheral muscle and diaphragm function is increasingly recognized, and thus spontaneous breathing may confer additional advantage. Reflecting this, epidemiologic data suggest that the use of partial (vs. full) support modes of ventilation is increasing. Notwithstanding the cent
Even when plateau pressure is limited to <30 cm H2O, combined with increased respiratory rate and tidal volume, high transpulmonary pressure generated by strong spontaneous breathing effort can worsen lung injury. When spontaneous breathing is preserved during mechanical ventilation, transpulmonary pressure and tidal volume should be strictly controlled to prevent further lung injury.
In animals with mild lung injury, spontaneous breathing was beneficial to lung recruitment; however, in animals with severe lung injury, spontaneous breathing could worsen lung injury, and muscle paralysis might be more protective for injured lungs by preventing injuriously high transpulmonary pressure and high driving pressure.
These data support the use of esophageal manometry in acute respiratory distress syndrome. Assuming correct calibration, expiratory Pl derived from Pes reflects Pl in dependent to middle lung, where atelectasis usually predominates; inspiratory Pl estimated from elastance ratio may indicate the highest level of lung stress in nondependent "baby" lung, where it is vulnerable to ventilator-induced lung injury.
Spontaneous effort at low positive end-expiratory pressure improved oxygenation but promoted tidal recruitment associated with pendelluft. Optimized positive end-expiratory pressure (set after lung recruitment) may reverse the harmful effects of spontaneous breathing by reducing inspiratory effort, pendelluft, and tidal recruitment.
Limitation of Vt and Pl(es) by volume-controlled ventilation could not eliminate harm caused by spontaneous breathing unless the level of spontaneous effort was lowered and local dependent lung stress was reduced.
To prevent P-SILI in ARDS, it seems feasible to facilitate 'safe' spontaneous breathing in patients using a higher PEEP strategy in severe ARDS.
Spontaneous ventilation during APRV improves lung aeration by decreasing atelectasis. PSV for gas exchange is effective but not sufficient to improve lung aeration. These results indicate that APRV is more efficient than PSV as a mode of primary ventilatory support to decrease atelectasis in patients with ARDS.
We update and summarize the role of spontaneous breathing during mechanical ventilation in ARDS, which can be beneficial or deleterious, depending on the strength of spontaneous activity and severity of lung injury. Future studies are needed to determine ventilator strategies that minimize injury but maintaining some diaphragm activity.
The role of preserving spontaneous effort during mechanical ventilation and its interaction with mechanical ventilation have been actively investigated for several decades. Inspiratory muscle activities can lower the pleural components surrounding the lung, leading to an increase in transpulmonary pressure when spontaneous breathing effort is preserved during mechanical ventilation. Thus, increased transpulmonary pressure provides various benefits for gas exchange, ventilation pattern, and lung
"Prone Position Reduces Spontaneous Inspiratory Effort in Patients with Acute Respiratory Distress Syndrome: A Bicenter Study." American Journal of Respiratory and Critical Care Medicine, 203(11), pp. 1437–1440
Esophageal manometry is not a complicated technique. There is a large potential to improve clinical outcome in patients with acute respiratory distress syndrome, acting as an early detector of risk of lung injury from mechanical ventilation and vigorous spontaneous effort.
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