Continued Vigorous Inspiratory Effort as a Predictor of Noninvasive Ventilation Failure

To the Editor:

This letter is in response to an article by Tonelli and colleagues published in a recent issue of the Journal (1). The authors’ observation that a reduction in the magnitude of spontaneous respiratory effort after initiation of noninvasive ventilation (NIV) predicts the success of the NIV trial appears expected. Nevertheless, I do have a few interesting observations and explanations. V̇e is influenced by respiratory drive, which in turn is guided by hypoxia, hypercarbia, systemic oxygen delivery, or cardiac output (2). A significant reduction in V̇e (7.6 vs. 1.1 L/min) after 2 hours of NIV in the NIV success group with an almost similar expiratory Vt (Vte) and respiratory rate (RR) change seems surprising. The V̇e drive is always the primary determinant of the mechanical changes in the respiratory dynamics (3). An equal magnitude of mechanical pressure support and a similar Vte in both the groups should have been supported by an almost similar reduction in tidal change in esophageal pressure (∆Pes) and tidal change in transpulmonary pressure (∆Pl). As expected, the ∆Pl, Vte, and V̇e (slightly reduced because of a reduction in RR) remain unchanged before and after initiation of NIV in the failure group. A reduction in ∆Pes was compensated by positive pressure to maintain the ∆Pl. A similar Vte in the NIV success group with a significantly lower ∆Pl indicated a higher lung compliance than the failure group. A differential change in ∆Pes to ∆Pl (31.5→39.5 cm H₂O [∆8 cm H₂O] vs. 11→30.5 cm H₂O [∆19.5 cm H₂O]) with a similar level of pressure support and positive end-expiratory pressure (PEEP), 2 hours after the NIV trial in the failure and the success group, needs further clarification. Interestingly, Vte/∆Pl was lower in the NIV success group than the NIV failure group despite having a significantly lower ∆Pl. Even if a similar compliance is assumed for both groups, a persistent higher V̇e indicates reduced cardiac output or systemic oxygen delivery in the NIV failure group. The success of mechanical ventilation and spontaneous breathing is inherently linked with cardiorespiratory interactions (4). A greater inspiratory drive in the NIV failure group resulted in lower intrapleural pressure, which could have further reduced the cardiac output and systemic oxygen delivery by increasing afterload and reducing the blood flow from the intrathoracic to the extrathoracic part of the aorta (5). In addition, an exaggerated venous return due to a higher negative intrapleural pressure coupled with increased afterload could have led to additional pulmonary congestion and deterioration in chest X-rays in the NIV failure group. Furthermore, a persistent higher inspiratory effort in the NIV failure group despite a nonsignificant difference in HACOR (Heart Rate, Acidosis, Consciousness, Oxygenation, Respiratory Rate) score suggests a different pathophysiology of hypoxemia. A continued higher V̇e requirement did not allow ∆Pes to reduce significantly in the NIV failure group. Therefore, a reduction in V̇e could also have been a potential predictor of NIV success with reasonable accuracy. Furthermore, titration of pressure support and PEEP during the NIV trial may be guided by a reduction in V̇e and work of breathing as the majority of the clinical parameters (RR, Po₂/Fi_O2, and Vte/∆Pl) did not reach statistical significance to achieve the role of potential predictors.