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Passive leg raising–induced change in pulse pressure variation (PPV) may help identify preload responsiveness during pressure support ventilation (PSV), but its value appears greatest when inspiratory effort is low, as estimated by airway occlusion pressure at 100 ms (P0.1).
In this prospective ICU study, the PPV response to PLR outperformed baseline PPV and PLR-induced pulse pressure change.
The findings suggest a potentially simpler bedside approach to fluid decision-making in selected spontaneously breathing patients, though validation in larger cohorts is still needed.
Study background
Deciding whether to give intravenous fluids is one of the most consequential and frequent judgments in intensive care. The goal is not simply to raise blood pressure; it is to identify patients whose stroke volume will meaningfully rise after a preload increase. If fluids are given to a preload-responsive patient, perfusion may improve. If they are given indiscriminately, the downside can be substantial: pulmonary edema, impaired oxygenation, tissue edema, and venous congestion.
Passive leg raising (PLR) has become a favored reversible “self-volume challenge.” By shifting venous blood from the lower extremities and splanchnic circulation toward the central circulation, PLR transiently increases venous return and mimics the hemodynamic effect of a fluid bolus. The major advantage of PLR is that it is dynamic and reversible; the test can be abandoned without actually infusing fluid. The limitation is that, in standard practice, PLR must be interpreted using a direct cardiac output or stroke volume measurement, often by echocardiography or another flow monitor.
Pulse pressure variation is a classic dynamic index of fluid responsiveness in fully controlled mechanical ventilation. It depends on cyclic changes in intrathoracic pressure and the resultant changes in venous return and stroke volume. However, PPV becomes less dependable in patients who breathe spontaneously or receive pressure support ventilation, because inspiratory effort is variable and can distort the cardiopulmonary interaction that PPV depends on. That limitation has led investigators to ask whether a change in PPV during PLR might restore some utility in this setting.
This study asked a practical question: during PSV, can PLR-induced changes in PPV or pulse pressure predict whether a patient will respond to fluids, and does inspiratory effort influence the answer?
Study design
This was a prospective study performed in two ICUs of French university hospitals. The investigators enrolled critically ill patients receiving PSV who needed evaluation of preload responsiveness.
Hemodynamic measurements and transthoracic echocardiography were recorded immediately before PLR and within one minute after PLR. The main endpoints were the PLR-induced changes in PPV and pulse pressure (PP), assessed against a reference definition of preload responsiveness.
Preload responsiveness was defined as an increase of at least 12% in the velocity-time integral of subaortic flow during PLR. The cohort was also stratified by the median airway occlusion pressure at 100 ms (P0.1), used as a surrogate for inspiratory effort.
Key findings
Thirty-four patients were included. Their median Simplified Acute Physiology Score II was 52, indicating substantial illness severity. Fourteen patients (41%) were classified as preload responders.
Across the entire cohort, the most informative variable was PLR-induced change in PPV. It was associated with preload responsiveness, with an area under the receiver operating characteristic curve (AUROC) of 0.76 and a statistically significant p value of 0.026. The identified cutoff value was a decrease of 3% in PPV during PLR. In other words, a small fall in PPV after leg raising tended to identify patients whose stroke volume increased during the maneuver.
By contrast, baseline PPV and PLR-induced change in PP did not show comparable discriminative ability in the full sample. This is clinically relevant because it suggests that the information lies not in the single resting value, but in the physiologic response to a preload challenge.
The role of inspiratory effort was especially important. In patients with lower P0.1, defined as less than 2.3 cm H2O, PLR-induced change in PPV had excellent diagnostic performance with an AUROC of 0.90 and the same cutoff of -3%. In patients with higher P0.1, performance dropped markedly, with an AUROC of 0.61 and no statistically significant discrimination.
These results imply that respiratory drive is a major modifier of test accuracy. A strong inspiratory effort can create large and irregular swings in intrathoracic pressure, altering venous return and arterial pressure in ways that obscure the preload signal. When effort is modest, the relationship between PLR, stroke volume, and PPV may be sufficiently stable for the test to work.
Clinical interpretation
The study is attractive because it proposes a simplified bedside method for a common ICU problem. Clinicians already monitor arterial pulse pressure in many patients, and PPV is often available on standard monitors. If PLR-induced PPV change can reliably predict fluid responsiveness in the right physiologic context, it could reduce the need for direct cardiac output monitoring in selected PSV patients.
The physiologic logic is straightforward. PLR transiently increases venous return. If the heart operates on the ascending limb of the Frank-Starling curve, stroke volume should rise. That change may be reflected in arterial waveform behavior, but only when respiratory mechanics are not too noisy. P0.1, an estimate of inspiratory effort, may be the practical clue that helps distinguish when the signal is trustworthy.
However, the study should not be overinterpreted. The sample was small, and the confidence intervals around diagnostic performance are likely wide. The thresholds need prospective confirmation. Moreover, the study used transthoracic echocardiography as the reference, which is appropriate and noninvasive, but still operator dependent. The findings are best viewed as a promising physiologic proof-of-concept rather than a definitive bedside rule.
Generalizability is another concern. The population consisted of patients on PSV in two French university ICUs, and the range of ventilatory patterns, sedation practices, and disease states may not mirror those in other settings. The test may also be less reliable in the presence of arrhythmias, significant valvular disease, right ventricular failure, or marked hemodynamic instability. As with many dynamic indices, context matters.
Implications for practice
This study reinforces an important principle in hemodynamic monitoring: dynamic indices are not absolute. Their performance depends on the mechanical conditions under which they are measured. In spontaneously breathing or pressure-supported patients, inspiratory effort is a major source of variability. That does not make PPV useless, but it does mean clinicians should interpret it cautiously and ideally in conjunction with the respiratory pattern, sedation level, and overall clinical context.
For now, the most reasonable interpretation is that PLR-induced PPV change may be a useful adjunct in PSV patients with low inspiratory effort. It may help identify those likely to respond to a fluid challenge, potentially streamlining bedside decision-making. But it should not replace direct flow measurement in complex or ambiguous cases.
Conclusion
In critically ill patients receiving pressure support ventilation, passive leg raising–induced change in PPV appears to predict preload responsiveness, particularly when inspiratory effort is low. The method may offer a practical alternative to direct cardiac output measurement, but larger studies are needed before routine implementation.
Funding and clinicaltrials.gov
The abstract does not report funding details or a clinicaltrials.gov registration number.
References
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