Dear Editor,
Si and colleagues provide a carefully conducted, two-centre prospective study showing that intra-abdominal hypertension (IAH) substantially attenuates the cardiac-index response to passive leg raising (PLR), whereas the end-expiratory occlusion test and mini-fluid challenge retain useful diagnostic performance [1]. Their principal clinical conclusion—that a negative PLR result should not exclude fluid responsiveness in patients with IAH—is persuasive. We nevertheless believe that the proposed mechanism, namely persistence in abdominal vascular zone 2 when the central venous pressure–intra-abdominal pressure (CVP–IAP) difference remains negative, requires a more cautious physiological interpretation.
The classic abdominal vascular-zone model is defined by the relationship among upstream driving pressure, pressure within the inferior vena cava (IVC) near the diaphragm, surrounding abdominal pressure, and the critical closing pressure of the collapsible vessel [2]. In the study by Si et al., mean systemic filling pressure (Pmsf) was assumed to exceed both CVP and IAP, allowing only zones 2 and 3 to be considered, but Pmsf was neither measured nor estimated [1]. This assumption is central rather than incidental. A negative CVP–IAP difference indicates that the measured downstream pressure is below the measured abdominal pressure; it does not establish that Pmsf remains above IAP, as required to infer a classic zone-2 waterfall. In patients with vasoplegia, hypovolaemia, or both, the upstream pressure may approach the external closing pressure. Recent clinical data also show that PLR changes Pmsf, the pressure gradient for venous return, and resistance to venous return, and that these changes differ according to preload responsiveness [3]. Thus, the distinction between PLR true-positive and false-negative cases may depend not only on whether CVP crosses IAP, but also on how PLR alters the upstream pressure and venous-return resistance.
The physiological meaning of CVP–IAP also depends on whether its two components approximate intraluminal and extraluminal pressure at the same vascular segment. The original model used IVC pressure at the diaphragmatic level, not thoracic CVP, as the downstream pressure [2]. CVP is influenced by pleural-pressure transmission, positive end-expiratory pressure, right-heart function, and the pressure drop between the abdominal IVC and right atrium. Conversely, bladder-derived IAP is a clinically useful estimate of global abdominal pressure but may not equal the local pressure surrounding the subdiaphragmatic IVC. The authors appropriately acknowledge the absence of oesophageal-pressure measurement and the possibility that gastric pressure may better represent IVC extramural pressure [1]. For this reason, CVP–IAP may be better described as an exploratory intercompartmental pressure difference than as a directly measured IVC transmural pressure.
A further issue is the hydrostatic reference during the postural transition. CVP transducers were fixed to the upper arm at the mid-axillary level, whereas the abdominal transducer was fixed near the pelvis [1]. PLR changed the patient from a semi-recumbent position to a horizontal trunk with the legs elevated. Unless both pressure signals were continuously referenced to a common hydrostatic datum, their difference could change partly because the vertical relationship between the two measurement sites changed. This matters because the proposed zone transition in PLR true-positive responders depended on a mean CVP–IAP change of only 4.6 mmHg, from − 2.4 to + 2.2 mmHg [1]. In a prospective study of invasive pressure monitoring, changes in transducer level produced errors of at least 3 mmHg in 46% and at least 5 mmHg in 18.7% of observations [4]. This does not imply that the present finding is artefactual, but it makes clarification of levelling, zeroing, and positional correction essential.
Several analyses could strengthen the proposed mechanism without altering the main diagnostic conclusions. Using the available mean arterial pressure, CVP, cardiac index, and anthropometric data, the authors could estimate analogue Pmsf and examine Pmsf–IAP, Pmsf–CVP, and resistance to venous return before and during PLR. A sensitivity analysis shifting the CVP–IAP difference by ± 3 and ± 5 mmHg would show how robust the classification of zone transitions is to plausible levelling error. Future validation could combine a common hydrostatic reference with gastric or local pericaval pressure, direct or Doppler-based assessment of IVC flow, and measurements of intrathoracic pressure.
These considerations do not weaken the study’s important finding that PLR has limited rule-out value in mechanically ventilated patients with IAH. They do, however, suggest that the association between a persistently negative CVP–IAP difference and PLR false-negativity should remain hypothesis-generating. A pressure difference becomes a vascular zone only when the upstream pressure, local intravascular and extravascular pressures, and hydrostatic reference are defined together.
Abbreviations
- CI
Cardiac index
- CVP
Central venous pressure
- IAH
Intra-abdominal hypertension
- IAP
Intra-abdominal pressure
- IVC
Inferior vena cava
- PLR
Passive leg raising
- Pmsf
Mean systemic filling pressure
Author contributions
All authors made substantial contributions to the conception or interpretation of the work, approved the final version of the manuscript, and agree to be accountable for all aspects of the work in accordance with the International Committee of Medical Journal Editors authorship criteria.
Funding
This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Data availability
No datasets were generated or analysed during the current study.
Declarations
Ethics approval and consent to participate
Not applicable.
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
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References
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Data Availability Statement
No datasets were generated or analysed during the current study.
