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Comment
. 2025 Jul 1;29(1):262.
doi: 10.1186/s13054-025-05440-5.

Co-existence of congestion and preload-dependence identified by pulse pressure respiratory variations: right ventricular afterload might be the key

David Bussy  1 , Guillaume Deniel  2   3   4 , Laurent Bitker  2   3   4 , Jean-Christophe Richard  2   3   4
Affiliations
Comment

Co-existence of congestion and preload-dependence identified by pulse pressure respiratory variations: right ventricular afterload might be the key

David Bussy et al. Crit Care. .
No abstract available

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Conflict of interest statement

Declarations. Ethics approval and consent to participate: Not applicable. Consent for publication: Not applicable. Competing interests: The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
Transmural RAP patterns reveal distinct mechanisms behind PPV changes. Pulse pressure variation (PPV) may result from the presence of a delta-up component, a delta-down component, or both. The delta-down component, typically observed a few heartbeats after insufflation, reflects a decrease in cardiac output subsequent to cardio-respiratory interactions. This reduction may be driven by two distinct mechanisms, described in the figure using varying tidal volumes and their effects on right ventricular preload and afterload. First, an increase in pleural pressure during insufflation is transmitted to the pericardial space, resulting in an elevation of intra-luminal right atrial pressure but a reduction in transmural right atrial pressure (RAPtm). This rise in intra-luminal right atrial pressure impairs the venous return gradient, thereby contributing to the drop in RAPtm. Additionally, the increase in pleural pressure reduces the transmural pressure of the superior vena cava via a “waterfall” effect, further reducing RAPtm. As a result, end-systolic right atrial volume and venous return are reduced, accentuating the decrease in right ventricular preload during insufflation, being indicative of a preload responsive state. Oppositely, an increase in transpulmonary pressure during tidal volume insufflation may elevate pulmonary vascular resistance of non-zone 3 West zones and right ventricular afterload, thereby opposing right ventricular outflow. This backward pressure is transmitted to the right atrium, leading to an increase in both intra-luminal and transmural RAP and a decrease in venous return [4]. These conditions would correspond to a preload unresponsive state, despite significant PPV. Finally, these two patterns of cardio-respiratory interactions may probably coexist in a ventilated patient, with the predominance of one or the other being only detectable if RAPtm is measured while tidal volumes are modified. CO: Cardiac output; PAW: Airway pressure; PPL: Pleural pressure; PTP: Transpulmonary pressure; RAP: Right atrial pressure; RPATM: Transmural right atrial pressure; RV: Right ventricle; RVEDP: Right ventricular end-diastolic pressure; RVESP: Right ventricular end-systolic pressure; VR: Venous return; VT: Tidal volume
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Comment on

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