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Editorial
. 2024 Jul 15;210(2):139-141.
doi: 10.1164/rccm.202402-0384ED.

Airway Occlusion Pressure and Dyspnea during Mechanical Ventilation: Giving Words to the Pleas of the Respiratory Centers

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Editorial

Airway Occlusion Pressure and Dyspnea during Mechanical Ventilation: Giving Words to the Pleas of the Respiratory Centers

Joaquin Pérez et al. Am J Respir Crit Care Med. .
No abstract available

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Figures

Figure 1.
Figure 1.
Relationship between airway occlusion pressure (P0.1), dyspnea, and clinical outcomes. On the left, the relationship between P0.1 and increased mortality is displayed, offering a series of possible mediators. On the right, the relationship between P0.1 and pathophysiology of dyspnea is displayed. P0.1 is a measure of respiratory centers’ output in the brainstem (i.e., respiratory drive) that, through specific neural pathways, stimulates the contraction of respiratory muscles aiming to achieve adequate ventilation and gas exchange to meet patients’ metabolic demands. Brains’ output and, therefore, expected input in terms of respiratory muscle contraction, ventilation, and gas exchange are schematically represented by “a” in black. In the context of neuromuscular dysfunction, abnormal respiratory mechanics, and impairment in gas exchange, frequently present in critically ill patients, real output of the respiratory system and, therefore, input received by the brain (schematically represented by “b” in blue) differs from what was expected by the brain (“a”). The difference between expected (“a”) and received (“b”) input is integrated in upper neural structures and perceived as “dyspnea.” The presence of dyspnea (red) can further stimulate (+++) the respiratory centers in the brainstem to increase their output to achieve “a,” often resulting in a higher P0.1. MV = mechanical ventilation; PaCO2 = arterial pressure of carbon dioxide; PACO2 = alveolar pressure of carbon dioxide; PaO2 = arterial pressure of oxygen; PAO2 = alveolar pressure of oxygen; Paw = airway pressure. ΔV/Δt = inspiratory flow rate.

Comment on

References

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