Perioperative Pulmonary Atelectasis: Comment

We read the review articles by Zeng et al.¹  and Lagier et al.²  with great interest, with their emphasis that atelectasis caused by peripheral airway closure is a common complication of mechanical positive pressure ventilation. This phenomenon was first detected during anesthesia by Hedenstierna et al.^3,4  and was reviewed by Milic-Emili et al.⁵  It is well known that negative pleural pressure resolves peripheral airway closure and subsequent atelectasis. This can be achieved by synchronizing ventilation with the patient’s efforts or by stimulating the phrenic nerve. However, a far simpler solution to avoid or treat atelectasis is to use negative pressure ventilation.

Before the polio pandemic in the 1950s, patients with atelectasis were treated with negative pressure ventilation in the iron lung. Its use was, however, abandoned for practical nursing reasons during and after the polio pandemic. After the introduction of positive pressure ventilation, the fight against ventilator-induced atelectasis started and is still going on.

A recent publication by Klassen et al.⁶  clearly shows the impact of peripheral airway closure in the context of positive and negative pressure ventilation. In an excised porcine lung, the driving pressure during positive pressure ventilation needed to be twice as large as during negative pressure ventilation to reach the same tidal volume. Moreover, the leakage from deliberate damage to the visceral pleura was five times larger during negative pressure ventilation. This demonstrates that positive pressure ventilation caused peripheral airway closure that reduced ventilation of the peripheral parts of the lung, while negative pressure ventilation did not.

It has also been demonstrated in ventilated and perfused isolated rat⁷  and human⁸  lungs that negative pressure ventilation provides a superior method of preserving these organs for transplantation as compared to positive pressure ventilation.

Recent interest in negative pressure ventilation led to the Exovent⁹  project (www.Exovent.org; accessed January 29, 2022), in which a lightweight torso-only device was developed. This device can deliver continuous negative extrathoracic pressure to increase the functional residual capacity. It can also provide full negative pressure ventilation, with the addition of negative end-expiratory extrathoracic pressure, the analog of positive end-expiratory pressure in positive pressure ventilation. It is to be expected that later versions will be leaner than the first prototype described by Coulthard.⁹  It remains unknown whether using negative pressure ventilatory support to patients with diseased lungs (such as those seen with COVID-19 pneumonia) may influence lung damage from atelectasis, but studies on animals with surfactant-depleted lungs by Grasso et al.¹⁰  suggest this may be a possibility. Clinical trials to investigate whether this also applies to patients are needed.

The authors declare no competing interests.