Key result
Volume loading is linked to a ~6 ms higher pulse pressure-normalized systolic descending AUC vs phenylephrine.
Why the study?
Arterial pressure waveform analysis assesses hemodynamic status, but investigations focusing specifically on waveform morphology remain limited.
Does volume loading via blood return alter arterial pressure waveform morphology differently than vasopressor administration in critically ill patients?
Observational (n=46)
No
Does volume loading via blood return alter arterial pressure waveform morphology differently than vasopressor administration in critically ill patients?
Volume loading and vasopressor administration produce distinct morphological changes in the arterial pressure waveform, suggesting that waveform analysis may provide complementary physiological insights into underlying hemodynamic states.
Waveform morphology differed after volume loading versus phenylephrine; hypothesis-generating for complementary hemodynamic monitoring in critically ill patients.
Arterial pressure waveform analysis has been used to assess hemodynamic status, however, investigations focusing on waveform morphology remain limited. In this study, we examined changes in selected morphological features of the arterial pressure waveform following volume loading versus vasopressor administration in critically ill patients. In this retrospective observational study, we analyzed adult patients admitted to an intensive care unit between April 2022 and June 2023. Participants were included if they exhibited increased mean arterial pressure (MAP) following either blood return during hemodiafiltration discontinuation (Volume group) or intravenous phenylephrine administration (Pressor group). Arterial waveforms were extracted from one minute before to four minutes after the intervention. We compared 21 waveform-derived features and their normalized parameters at peak MAP with baseline values. Pre- and post-intervention differences for each parameter were assessed using the Wilcoxon matched-pairs signed-rank test. The Volume group comprised 26 patients, and the Pressor group included 20 patients. Systolic angle, systolic dP/dt, and systolic area under the curve (AUC) increased in both groups following intervention. After pulse-pressure normalization, however, systolic AUC increased significantly in the Volume group (median paired difference 4.6 [-0.3-10.2] ms, 95% CI 1.9 to 7.9, P = 0.0038) but not in the Pressor group. This elevation in systolic AUC occurred mainly during the systolic descending phase (4.4 [1.1-9.5] ms, 95% CI 2.7 to 9.1, P = 0.00021). The systolic descending duration exhibited a significant prolongation in the Volume group, whereas no significant change was observed in the Pressor group. Arterial waveform morphology exhibited different patterns of change following blood return versus phenylephrine administration, particularly in the systolic descending phase. Waveform morphology analysis may provide complementary physiological information for monitoring the mechanisms underlying hemodynamic changes.
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Hara et al. (2026) conducted an observational in Hemodynamic instability in critically ill patients (n=46). Volume loading (blood return during hemodiafiltration discontinuation) vs. Vasopressor administration (intravenous phenylephrine) was evaluated on Change in pulse pressure-normalized systolic descending area under the curve (AUC) (HL median difference 5.80 ms, 95% CI 2.1-10.6, p=0.0062). Volume loading via blood return significantly increased the pulse pressure-normalized systolic descending area under the curve compared to phenylephrine administration (HL median difference 5.80 ms) in critically ill patients.
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