Worse arterial pressure reservoir capacity is associated with exacerbated hemodynamic response to capnogram changes and more labile intraoperative cardiopulmonary-metabolic coupling
Authors: Alan Y , Tas A , Bayhan M I , Koker S , Kara Tas I , Umman S , Parker K H , Sezer M 
Published: October 2024

Background

The apparent promise of capnography as a cardiac monitor based on the coupled cardiopulmonary response to metabolic changes remains hampered by inconsistent results in studies investigating previous correlations between hemodynamics (e.g.cardiac output) and end-tidal CO2 (EtCO2).(1,2,3) Excess pressure (Pexcess), a dynamic sub-component of pressure waveform representing pressure beyond buffering capacity (reservoir pressure) of elastic large arteries, strongly correlates with aortic flow in humans, suggesting the Pexcess as a promising tool for non-invasive hemodynamic monitoring.(4,5)

Purpose

We aimed to clarify potential cofounders and pathophysiological mechanisms modifying the EtCO2-arterial hemodynamic coupling, by analysing the intra-operative temporal relations of paired reservoir-excess and capnogram parameters

Methods

In 190 patients with normal pre-operative pulmonary function tests who underwent non-cardiac surgery, simultaneous capnogram and intra-arterial pressure signals were analysed off-line. Signal windows (&gt;2 minutes) of maximum and minimum mean arterial pressure were autoidentified, the capnogram and pressure signals were averaged into a single representative cycle, to extract reservoir-excess pressure and capnogram parameters (EtCO2, expiratory slope, alpha slope, and plateau slope) accordingly.(6,7) Arterial reservoir capacity (ARC) was defined as Preservoir/Pexcess, which was used to stratify patients into quartiles. Relationships between maximum changes in capnogram and pressure parameters were analysed (Figure 1).

Results

The ΔEtCO2 and ΔPa mean were correlated significantly in all groups. In patients with the highest ARC (Q4), Pexcess remained unaltered in response to ΔEtCO2 (r:0.095 p:0.545), unlike other subgroups with significant positive correlations. In Q4 (the highest ARC group), the increment in Preservoir was the main cause of ΔPa in relation to ΔEtCO2. In contrast, the ΔEtCO2 - ∆Pexcess relationship was most pronounced in the group with the poorest ARC (r:0.634 p:0.005), underlying the significance of the pressure reservoir behaviour as a determinant of metabolic oscillations in arterial hemodynamics, even though the changes in ΔEtCO2 were equivalent.(Figure 2)

Conclusion(s)

Worse arterial pressure reserve capacity is associated with an exacerbated hemodynamic response to capnogram changes and a more labile cardiopulmonary-metabolic coupling, characterised by a pronounced increase in excess pressure in response to increased EtCO2 in patients with low ARC. Substantial Pa alterations accompanying EtCO2 changes had opposite drivers in low and high ARC groups (predominant augmentation of Preservoir vs Pexcess). Utilisation of the capnogram for cardiac hemodynamic monitoring is substantially affected by ARC, hence it should be considered while developing capnogram-based monitoring indices.Figure 1.Methodology and example casesFigure 2.Main results