The Authors Reply: Ventilator Liberation after Pediatric Cardiac Surgery: Balancing the Competing Interests of the Lungs and the Heart

Dear Editor,

In reply:

We thank Wu and Zhu for their thoughtful comments on our recent study examining the association between postextubation arterial blood gas (ABG) derangements and re-intubation in children with congenital heart disease.¹ The authors propose that the acidemia observed in our cohort may reflect an “adaptive perturbation” driven by acute afterload mismatch during the transition from positive-pressure to negative-pressure breathing, and they advocate for evolving extubation readiness testing (ERT) into a multimodal “cardiopulmonary stress test” that incorporates B-type natriuretic peptide (BNP) trajectories, central venous oxygen saturation (ScvO₂) trends, and point-of-care echocardiography.¹ We welcome the opportunity to clarify several points and to expand the discussion.

First, we wish to emphasize that our study was never intended to frame postextubation acidemia as a purely respiratory phenomenon. On the contrary, we explicitly acknowledged in our discussion that acidemia in this population frequently reflects cardiac, hemodynamic, and microcirculatory derangements, including decreased cardiac output, increased work of breathing, and the impact of transitioning from positive- to negative-pressure ventilation on systemic ventricular afterload.¹ Indeed, two of us recently elaborated on precisely this physiology in an editorial on risk analytics and ventilator liberation following neonatal cardiac surgery, highlighting that premature extubation shifts the burden of breathing back to the patient, increases oxygen consumption, raises systemic ventricular afterload, and can ignite a vicious cycle of escalating work of breathing and hemodynamic compromise.² The postextubation ABG is a window into this integrated cardiopulmonary state, not a respiratory-centric snapshot.

Second, the cardiopulmonary interaction framework invoked by Wu and Zhu, while physiologically grounded, rests on an implicit assumption that does not hold across the spectrum of congenital heart disease. The proposition that positive-pressure ventilation uniformly unloads the systemic ventricle, such that its withdrawal predictably precipitates afterload mismatch, describes normal biventricular physiology. It does not describe the universe of patients treated in a high-complexity pediatric cardiac ICU (PCICU) such as ours. For example, children with single ventricle physiology who have undergone superior or total cavopulmonary anastomosis (Glenn and Fontan operations) depend on passive, low-resistance pulmonary blood flow, which is actively impeded by positive intrathoracic pressure. In these patients, continued mechanical ventilation may adversely affect pulmonary blood flow, cardiac output, and tissue oxygen delivery, so expeditious liberation is a therapeutic goal rather than a hemodynamic threat.³ Similarly, children with repaired tetralogy of Fallot and restrictive right-ventricular physiology derive substantial benefit from the negative intrathoracic pressure of spontaneous breathing, which augments systemic venous return and right-ventricular filling. Patients with acute right-ventricular dysfunction may also benefit from spontaneous breathing to reduce afterload imposed by positive-pressure ventilation. For all these subpopulations, the “adaptive perturbation” framing inverts the physiology: The perturbation is mechanical ventilation itself, and extubation is the corrective maneuver.

Third, this heterogeneity is precisely why ventilator liberation in the PCICU is so challenging, and why ABG interpretation cannot be reduced to a single mechanistic schema. In the postoperative cardiac surgical patient, two distinct and frequently competing interests must be reconciled: those of the lungs and those of the heart. The lungs may benefit from continued positive-pressure support to maintain recruitment and optimize gas exchange, whereas the heart, depending on the specific anatomy and physiology, may benefit from prompt liberation or continued support. These interests are rarely aligned, and the intensivist must broker the optimal compromise for each patient. This is not an abstract concern. The well-documented variability in extubation failure rates across institutions and lesion types, together with the persistent 10–15% failure rate despite protocolized ERTs, reflects the difficulty of this balancing act.^1,4

Fourth, the recognition that extubation readiness in children with cardiac disease is inseparable from cardiopulmonary physiology is already driving the field forward. Hames and colleagues⁵ recently demonstrated that adding risk analytics algorithms quantifying the probability of inadequate oxygen delivery and inadequate ventilation to conventional extubation readiness assessments significantly improved the identification of neonates at risk of extubation failure, with a net reclassification index of 45%. Our own work has likewise examined candidate physiologic markers of cardiopulmonary status, including the dead-space-to-tidal-volume ratio (V_D/V_T), which is associated with duration of postextubation respiratory support on univariate analysis but loses its independent association after adjustment for age, weight, and cyanotic heart disease.⁶ The lesson from these efforts is two-fold. Physiologic signals that appear promising in isolation often attenuate or disappear once relevant patient-level covariates are accounted for, and no single biomarker, whether ABG, V_D/V_T, or a proprietary risk index, is likely to supplant the integrated clinical judgment of the experienced intensivist.²

Finally, although we share Wu and Zhu’s enthusiasm for multimodal prognostication, the specific variables they propose warrant pragmatic scrutiny. Peri-extubation BNP is unlikely to be informative within the narrow temporal window of an ERT: Its plasma half-life and the turnaround time of laboratory assays render it insensitive to the acute, minute-to-minute hemodynamic shifts that occur during and immediately after extubation. Point-of-care echocardiographic assessment of diastolic function during an ERT is similarly problematic. Probe placement and prolonged image acquisition can agitate the patient, alter respiratory mechanics through chest wall compression, and confound the very physiologic signals the ERT is designed to capture. ScvO₂ trends, by contrast, are more immediately responsive and are already incorporated, explicitly or implicitly, into the risk analytics platforms described above.⁵ Many centers also continuously monitor near-infrared spectroscopy during ERTs as a surrogate for ScvO₂.

In summary, we agree with Wu and Zhu that cardiopulmonary interactions are central to understanding postextubation physiology in children with congenital heart disease, and we welcome their call for multimodal prognostication. We would caution, however, against a unifying mechanistic framework that privileges afterload mismatch as the dominant driver of postextubation acidemia over other causes such as respiratory insufficiency, airway obstruction, or atelectasis. The PCICU cohort is heterogeneous, and the physiology of ventilator liberation depends on the specific lesion, the operation performed, and the postoperative state of both the pulmonary and systemic circulations. Postextubation ABG analysis remains a useful but imperfect tool, and its interpretation, like every other aspect of ventilator liberation in this population, requires the integration of cardiopulmonary interactions that are often in tension. The path forward lies not in reframing acidemia as adaptive or maladaptive a priori but in continuing to develop and validate analytic approaches that consider the complexity of the underlying physiology.