A plea for better understanding and appropriate use of dynamic arterial elastance

The pursuit of individualised haemodynamic management has become a cornerstone of modern perioperative care, promising to optimise patient outcomes through personalised therapeutic interventions.1 However, the concept of ‘individualised’ therapy loses its meaning when built upon haemodynamic algorithms that simplifies the physiological basis of the parameters they seek to optimise. Recent published randomised controlled trials investigating advanced haemodynamic monitoring technologies have yielded disappointing results, raising questions about the validity of the monitoring tools themselves, but not about the challenges in our understanding of how to apply them clinically.2 The randomised clinical trial by Russo and colleagues3 investigating a dynamic elastance-based protocol, which guides intra-operative fluid management in major abdominal surgery, exemplifies this challenge. This study represents a significant contribution to perioperative haemodynamic research, yet provides compelling evidence that negative results may stem not from technological limitations but from fundamental oversimplifications of how physicians interpret and apply dynamic arterial elastance (Eadyn) clinically. A critical physiological principle often omitted is that arterial pressure is a regulated parameter, while cardiac output is a dependent variable, adjusted to tissue physiological demands.4 This fundamental relationship challenges simplistic linear interpretations of pressure-flow dynamics, and thus Eadyn objectives. For decades, investigators have simplistically positioned Eadyn as an indicator of vasomotor tone to differentiate patients requiring fluid versus vasopressor therapy.5 This interpretation ignores the contextual limitations of Eadyn application. While many authors assume that Eadyn serves as an indicator of vasomotor tone,5 several published studies have demonstrated that the meaning of Eadyn is far more complex.6 Eadyn, which is the ratio of the respiratory pulse pressure variation to the respiratory stroke volume variation, is mainly dependent on cardiac factors (stroke volume, heart rate) and vascular factors (arterial compliance, systemic vascular resistance, aortic impedance, and blood pressure).7,8 Typically observed values are close to 1 ± 0.3 units. Given these observations, some authors have suggested that Eadyn may be understood as an index reflecting ventriculo-arterial coupling and tissue perfusion, or in other words the balance between cardiac and vascular systems9,10 (Fig. 1). Nevertheless, clinical reality is far more complex as the behaviour of Eadyn is affected by disease (e.g. sepsis, vasoplegia) and therapeutics (fluid expansion, norepinephrine, dobutamine), which also affect the cardiac and/or vascular factors associated with Eadyn differently, and sometimes in contradictory ways.11 During sepsis (and vasoplegia), Eadyn increases because of an increase in the respiratory pulse pressure variation relative to the respiratory stroke volume variation.8 However, subsequent administration of norepinephrine decreases Eadyn values because of a decrease in the respiratory pulse pressure variation relative to the respiratory stroke volume variation. Interestingly, recovery from vasoplegia is associated with a gradual increase in Eadyn.12 The response of the arterial load and its determinants to fluid expansion is mainly affected by disease and vasopressor treatment.13 When patients are treated with norepinephrine, changes in arterial load following fluid expansion are more dependent on the resistive component because the arterial compliance does not change.13 In contrast, in patients not receiving norepinephrine, fluid expansion alters both the resistive and pulsatile components of arterial load. Thus, the effects of fluid expansion on Eadyn depend on the presence or absence of vasopressor support.Fig. 1: Factors associated with dynamic arterial elastance, and algorithm in patients supported by norepinephrine.As demonstrated by studies, and confirmed later by meta-analyses, Eadyn performs well for vasopressor weaning but shows limited predictability for pressure response following fluid expansion.12,14 Importantly, Eadyn performance is context-dependent (operating theatre vs. ICU, sepsis vs. nonsepsis patients) and shows different predictive abilities between these settings. The meta-analysis performed by Alvarado-Sánchez et al. demonstrated good Eadyn performance for vasopressor weaning in critically ill patients primarily supported with norepinephrine.14 Conversely, the meta-analysis by Zhou et al. specifically noted that Eadyn performance, in predicting pressure response following fluid expansion, is significantly lower in surgical patients in the operating room compared to ICU patients.15 The physiological distinction lies in how norepinephrine and disease (i.e., sepsis) affect Eadyn determinants. As previously shown, arterial compliance becomes fixed and decreases with norepinephrine use and in sepsis, rendering Eadyn primarily dependent on the resistive component.13 In contrast, surgical patients without vasopressor support exhibit variable influences from both pulsatile and resistive vascular components, fundamentally altering its interpretive value. These observations align with recent findings from Ripollés-Melchor et al., who applied the concept of Eadyn as a vasomotor tone indicator in haemodynamic management when guided by the hypotension prediction index in abdominal surgery.2 This well conducted multicentre randomised study assessed the clinical benefit of using the ‘hypotension prediction index’ (HPI) to reduce the occurrence of acute kidney injury. When reading their findings, one could understand that HPI, which has been demonstrated to predict arterial hypotension,16 may not be of clinical benefit. However, given that the haemodynamic algorithm used Eadyn as an indicator of vasomotor tone to anticipate and treat arterial hypotension, the authors demonstrated a significant increase in vasopressor use but no improvement in outcomes. Both trials demonstrate how haemodynamic algorithms, based on oversimplified physiological basic underlying haemodynamic parameters, produce negative results. A consistent pattern emerges; rigorous methodology and sophisticated monitoring technology, but with algorithms based on oversimplified interpretation of the existing literature, which has clearly demonstrated positive and negative results across different clinical contexts. The evidence from these randomised trials confirms that using Eadyn as a vasomotor tone marker, particularly in the operating theatre (i.e. patients without vasopressor support), leads to vasopressor over-utilisation with potentially deleterious effects on tissue perfusion and clinical outcomes.2,3 Conversely, when applied to vasopressor weaning, studies suggest improved outcomes.17 Introduction of vasopressors should rely on comprehensive haemodynamic assessment incorporating evaluation of heart rate, preload, contractility and afterload, not on oversimplified interpretations of complex haemodynamic indices.18 Nevertheless, when considering Eadyn as an indicator of the balance between the pressure aspect and the flow aspect of the cardiovascular system,7,8 Eadyn can be used to adjust vasopressor support only when a patient is supported by norepinephrine (Fig. 1). Because studies demonstrated an association between norepinephrine use and acute kidney injury (AKI)19 and that restoring blood pressure with norepinephrine may not always translate into tissue perfusion improvement,20 we can suppose that excessive use of vasopressors when using Eadyn may mask the benefit of reducing exposure to arterial hypotension. These results emphasise the critical importance of appropriate physiological understanding when implementing haemodynamic algorithms in RCTs and the necessity of considering the complete spectrum of available evidence (both negative and positive results). Future research should focus on developing haemodynamic protocols that respect the physiological principles underlying each haemodynamic parameter, acknowledge the full spectrum of positive and negative evidence, take into account context-specific clinical applicability,21 and validate their application in appropriate clinical contexts. Only through such physiologically informed and evidence-comprehensive approaches can we translate technological advances into meaningful clinical improvements.