Positive and Negative-Pressure Ventilation: Time to Reconsider Physiological Equivalence: A Narrative Review of History

Positive- and Negative-Pressure Ventilation (PPV and NPV) have long been considered physiologically equivalent when they generate the same transpulmonary pressure. This concept became deeply embedded in respiratory physiology during the transition from NPV to PPV in the poliomyelitis era and has continued to influence the interpretation of mechanical ventilation. However, equivalent transpulmonary pressure does not imply equivalent absolute pleural pressure. PPV generates lung inflation by increasing airway pressure, accompanied by an increase in pleural pressure, whereas NPV generates it by decreasing pressure surrounding the thorax and thereby pleural pressure. This distinction has important consequences beyond haemodynamics. Intrathoracic airways are exposed to pleural and surrounding parenchymal pressure; increasing this external pressure reduces airway transmural pressure and will increase resistance, promote expiratory flow limitation and ultimately cause airway closure, particularly in dependent lung regions where pleural pressure is already highest. Progressive exclusion of these regions from tidal ventilation may contribute to atelectasis and concentrate ventilation in a progressively smaller functional “baby lung”. Experimental comparisons of PPV and NPV and studies using continuous negative abdominal pressure support the physiological relevance of the direction in which pleural pressure is changed. This narrative review re-examines the historical and physiological basis of PPV-NPV equivalence in light of contemporary evidence and renewed technological development of NPV. We propose that transpulmonary pressure alone is insufficient to establish physiological equivalence and that absolute pleural pressure and airway pressure should be considered an independent determinants of airway patency, regional ventilation, perfusion, haemodynamics and potentially ventilator-induced lung injury. Direct comparison of PPV and NPV at matched tidal volume and transpulmonary pressure offers a testable approach to this hypothesis.