Beyond ventriculo-arterial coupling: can arterial waveform-derived profiling refine prediction of post-induction hypotension?

Dear editor-in-chief,

We read with great interest the prospective observational cohort study by Le et al., which evaluated the predictive value of ventriculo-arterial coupling (VAC) for post-induction hypotension (PIH) in patients undergoing elective non-cardiac surgery [1]. The study makes an important physiological contribution by showing that impaired VAC, expressed as an Ea/Ees ratio > 1, was independently associated with PIH and improved risk reclassification when added to clinical and echocardiographic variables. These findings support the concept that PIH is not merely a pressure-threshold phenomenon or an isolated pharmacological consequence of anaesthetic induction but may reflect a pre-existing mismatch between ventricular performance and arterial load.

The work by Le et al.. also raises a relevant question for future research: can pre-induction cardiovascular vulnerability be captured using continuous arterial waveform-derived variables immediately before induction?

Echocardiography-derived Ea/Ees offers a robust physiological framework, but its implementation requires transthoracic echocardiography, non-invasive blood pressure measurement, and estimates of effective arterial elastance and end-systolic elastance. In contrast, pulse contour and pressure-recording analytical methods may provide continuous, minimally invasive information for patients who already require invasive arterial monitoring for clinical reasons.

This question is supported by the work of Aktas Yildirim et al., who reported that pre-induction arterial elastance, measured with MostCare/PRAM, was associated with hypotension after induction of anaesthesia [2].

In a related PRAM-monitored study, Aktas Yildirim and colleagues also suggested that stroke volume index and cardiac power output may contribute to post-induction hemodynamic risk [3].

Taken together, these findings suggest that arterial load, flow generation, and cardiovascular power may all contribute to susceptibility to PIH. However, the available evidence remains fragmented, as most studies have evaluated single predictors or limited sets of variables in relatively small cohorts.

To date, no prospective study has integrated VAC-informed concepts with arterial waveform-derived indices of arterial load, cardiac performance, cardiovascular efficiency, and preload sensitivity in the immediate pre-induction window.

The need for an integrated approach is further supported by the literature on endotypes of intraoperative hypotension. Kouz et al. used hierarchical clustering in patients undergoing major abdominal surgery who were monitored with invasive pulse wave analysis and identified six distinct hypotension endotypes: myocardial depression, bradycardia, vasodilation with an increased cardiac index, vasodilation without an increased cardiac index, hypovolemia, and mixed type [4].

More recently, Zhu et al. applied a temporal deep learning approach to high-resolution intraoperative hemodynamic data and identified five hypotension endotypes, suggesting that hypotensive episodes may evolve dynamically over time [5].

These studies reinforce the view that similar reductions in arterial pressure may arise from different hemodynamic mechanisms.

However, these studies primarily classified hypotension after it had already occurred. The immediate pre-induction period remains underexplored. This distinction is clinically relevant because anaesthesia induction represents a short, relatively standardized window before later intraoperative confounders emerge, including bleeding, pneumoperitoneum, positional changes, neuraxial analgesia, cumulative fluid administration, and prolonged vasopressor exposure.

Future prospective studies should therefore assess whether pre-induction hemodynamic vulnerability profiles can be identified before the onset of PIH. Such studies could enroll adult patients undergoing elective major noncardiac surgery for whom invasive arterial monitoring is already indicated as part of routine care. Baseline variables obtained immediately before induction could include arterial pressure, heart rate, stroke volume, stroke volume index, cardiac output, cardiac index, systemic vascular resistance, systemic vascular resistance index, arterial elastance, dynamic arterial elastance, cardiac power output, cardiac cycle efficiency, dP/dt max, stroke volume variation, and pulse pressure variation.

Rather than aiming immediately to validate a definitive prediction model, these studies should first be framed as hypothesis-generating. Their purpose would be to determine whether distinct pre-induction profiles, such as high arterial load, reduced cardiovascular performance, preload-sensitive, compensated/low-risk, or mixed profiles, are associated with the incidence, timing, severity, and treatment requirements of early PIH. A standardized endpoint, such as MAP < 65 mmHg for at least 1 min, would improve comparability with the broader PIH literature, whereas relative definitions, such as a MAP decrease > 30% from baseline and/or systolic arterial pressure < 90 mmHg, may capture clinically relevant, patient-specific hypotension.

This physiology-driven approach may complement the VAC framework proposed by Le et al. Echocardiography-derived Ea/Ees provides a structured estimate of ventriculo-arterial interaction before induction, whereas arterial waveform-derived profiling may offer continuous, immediate peri-induction information on arterial load, cardiac performance, cardiovascular efficiency, and preload sensitivity. These strategies should therefore be viewed as complementary rather than competing approaches to perioperative hemodynamic risk stratification.

In conclusion, Le et al. provide compelling evidence that impaired ventriculo-arterial coupling is associated with PIH. Future studies should determine whether integrated pre-induction hemodynamic profiles derived from advanced arterial waveform analysis can further characterize individual vulnerability to PIH and support more mechanism-oriented perioperative blood pressure management.

Abbreviations

CCE

Cardiac cycle efficiency

CI

Cardiac index

CO

Cardiac output

CPO

Cardiac power output

Ea

Effective arterial elastance

Eadyn

Dynamic arterial elastance

Ea/Ees

Ventriculo-arterial coupling ratio

Ees

End-systolic elastance

MAP

Mean arterial pressure

PIH

Post-induction hypotension

PPV

Pulse pressure variation

PRAM

Pressure recording analytical method

SAP

Systolic arterial pressure

SV

Stroke volume

SVI

Stroke volume index

SVR

Systemic vascular resistance

SVRI

Systemic vascular resistance index

SVV

Stroke volume variation

VAC

Ventriculo-arterial coupling

Author contributions

[AC, CA] conceived the correspondence, drafted the manuscript, critically revised it, and approved the final version.

Funding

No funding was received.

Data availability

Data sharing is not applicable to this article as no datasets were generated or analysed.

Declarations

Ethics approval and consent to participate

Not applicable.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.