Cardiology

Chest compression release velocity: An independent determinant of end-tidal carbon dioxide in out-of-hospital cardiac arrest

a b s t r a c t

Background: chest compression depth, CC rate and ventilatory rate (VR) are known to have an impact on end-tidal carbon dioxide (ETCO2) values. Chest compression release velocity (CCRV) is increasingly acknowledged as a novel metric in cardiopulmonary resuscitation (CPR). The objective of this study was to analyze whether CCRV would have any effect on ETCO2 values.

Methods: In Out-of-hospital cardiac arrests , effects of CC depth, CC rate, CCRV and VR on ETCO2 were analyzed through linear mixed effect models. A stratification was made on a CCRV of 300, 400 and 500 mm/s. In these categories, mean ETCO2 values were corrected for CC depth and compared through a one-way ANOVA. Results: A 10 mm increase in CC depth was associated with a 1.5 mmHg increase in ETCO2 (p < 0.001), a 100 mm/s increase in CCRV with a 0.8 mmHg increase (p = 0.010) and a 5 breaths per minute increase in VR with a 2.0 mmHg decrease (p < 0.001). CC depth was strongly correlated with CCRV (Pearson’s r = 0.709, p < 0.001). After adjusting for CC depth, ETCO2 was on average 6.5 mmHg higher at a CCRV of 500 than at 400 mm/s (p = 0.005) and 5.3 mmHg higher than at 300 mm/s (p = 0.033).

Conclusions: In OHCA patients, higher CCRV values resulted in higher ETCO2 values. This effect is independent of CC depth, despite the strong correlation between CCRV and CC depth.

(C) 2022

  1. Introduction

Guidelines emphasize the importance of high-quality cardiopulmo- nary resuscitation (CPR), to improve survival following out-of-hospital cardiac arrest (OHCA) [1]. In OHCA, capnography has proven to be a practical method of monitoring CPR quality. Continuous end-tidal car- bon dioxide (ETCO2) measurement during resuscitation has been associated with higher rates of return of spontaneous circulation (ROSC) [2]. Still, the exact impact of alterations in CPR administration on ETCO2 is not fully understood.

Quality of CPR has traditionally been characterized by adequate chest compression depth, chest compression rate, ventilatory rate (VR) and ventilatory tidal volume (TV) [1]. Lately, chest compres- sion release or recoil velocity (CCRV) has also been acknowledged as a novel important metric in CPR [3-8].

CCRV is defined as the maximum velocity of the chest in the poste- rior to anterior direction after a compression of the chest [3]. Mean CCRV varies between 300 and 360 mm/s [3-8]. Animal studies have

* Corresponding author at: Department of Emergency Medicine, Ghent University Hospital, Corneel Heymanslaan 10, Ghent, Belgium.

E-mail address: [email protected] (E. De Roos).

concluded that mechanical high-impulse compressions and decom- pressions and thus higher CCRV values improve blood flow [9-11].

In humans, CCRV has been assessed as a predictor of survival and beneficial neurological outcome, with mixed results [3,7,8]. CCRV seems to be rescuer-dependent (fatigue and leaning), as well as influ- enced by patient factors [5].

A corroborative argument for the latter was made in a recent study of Beger et al., which suggested that CCRV is not solely rescuer- dependent. CCRV may also slightly decline in the first minutes of CPR, likely due to ongoing changes in chest compliance and elasticity. CCRV was also shown to vary by patient factors: male gender and younger age were associated with a higher CCRV. The female sex is associated with lower required compression forces and thus with more chest com- pliance, with a lower chest elasticity and consequently with a lower CCRV [5,12]. Increasing age is associated with lower required compres- sion forces and with a declining chest elasticity [5,12,13]. CCRV was ap- proximately 11 mm/s higher in males and was about 20 mm/s higher in the youngest subgroup [5].

Efficient CPR produces higher cardiac output and therefore higher concentrations of CO2 in expiratory gases [14,15]. In Sheak and Murphy et al.’s studies, changes in CC depth, CC rate and VR were asso- ciated with changes in ETCO2 [16,17]. The effect of CCRV on ETCO2 in humans was previously analyzed in only one study. Murphy et al.

https://doi.org/10.1016/j.ajem.2022.01.053

0735-6757/(C) 2022

showed a 2.8% increase in ETCO2 with a 100 mm/s increase in CCRV [17]. Importantly, as CCRV was observed to be correlated with CC depth, CC depth was excluded from their analysis when the effect of CCRV on ETCO2 was considered and CCRV was excluded when the effect of CC depth on ETCO2 was analyzed [17].

Indeed, as CC are deeper, the faster the recoil of the sternum might be. In other words, CCRV could be a surrogate marker of the depth of the CC. This could imply that the previously observed effect of CCRV on ETCO2 is associated with the effect of CC depth on ETCO2.

Recently, Gonzalez-Otero et al. found that CC at a fixed depth could have a variable CCRV and inversely, CC with different depths could have a similar CCRV, depending on the vigorousness and impulsiveness of the CC [4].

Therefore, we set up a study to further explore this phenomenon and to explore the possible relation between CCRV and the CC depth, as well as the effect of the CCRV on ETCO2.

  1. Material and methods
    1. Study design and patient population

A monocentric, prospective observational study was conducted at Ghent University Hospital, Belgium. This study had a prehospital scope and only included OHCA. Patients were prospectively enrolled from July 2013 to September 2020. Adult patients (>=18 years) suffering OHCA, resuscitated and intubated by the medical emergency team (MET) (staffed by an emergency physician, an emergency nurse and an emergency medical technician) were included. Only cases with at least one minute of simultaneous correct CPR data and a valid capnogram were included. Cases with missing files or faulty data (missing or disturbed) were excluded. Cases with a traumatic etiology were also excluded, as a trauma to the chest could influence CCRV.

The resuscitations were carried out in accordance with the current ERC guidelines applicable at that time. Approval from our ethical com- mittee was obtained (B670201941165).

The emergency services worked in two tiers. The paramedics were usually the first to arrive and performed basic life support (BLS). The second to arrive was the MET, they performed advanced life support and were therefore able to intubate the patient. Measurements of ETCO2 started after intubation. The analyzes in this study only include the data after this timepoint. Hence, the first part of CPR (with BLS) is not considered in this study.

The MET had instant feedback about CC depth and CC rate.

    1. Materials

Two types of data were collected for analysis: a clinical case report and a Zoll event file.

The clinical case report was filled out by the emergency physician member of the MET at the time of the case. This report contained the pa- tient’s information and the details of the intervention e.g. date and time of intervention, clinical findings, initial heart rhythm, presumed etiol- ogy, duration of resuscitation, therapies administered and ROSC.

The Zoll event file was created by the Zoll X Series defibrillator/mon- itor (Zoll medical company, USA) and included heart frequency, ECG, depth and frequency of CC and ETCO2. The Zoll event file was manually collected after every case.

The follow-up of patients was performed by emergency physicians.

Data about the survival to discharge was retrospectively collected.

    1. Data processing

Zoll event files were reviewed using RescueNet Code Review (Zoll medical company, USA).

The capnograms were manually minute-to-minute examined for a correct square waveform. If the waveform was disturbed due to

superimposing CC-induced oscillations, the automatically calculated ETCO2 values were verified. Only minutes containing simultaneous CPR data and valid ETCO2 values were extracted for each case.

Ventilations were marked in the capnogram, VR was subsequently calculated. The variables originating from the Zoll event file (CC depth, CC rate, CCRV and ETCO2 values) and the VR were averaged per minute.

ROSC was retrospectively identified through physician assessment (case report, ceasing of CC), ECG analysis and increase in ETCO2.

    1. Statistical analysis

CPR quality variables (CC depth, CC rate, CCRV and VR) and ETCO2 values were presented by mean and standard deviation (SD) for the overall study population and stratified by ROSC and non-ROSC. These subgroups were compared through independent samples t-tests.

The relationship between each CPR variable (CC depth, CC rate, CCRV and VR) and time in minutes and ETCO2 was graphically evaluated through scatter plots and locally weighted polynomial regressions (through fitting a Loess curve). A linear mixed effect model with a ran- dom intercept and an autoregressive heterogeneous covariance struc- ture was used to analyze the association between each CPR variable and ETCO2. The covariance structure was chosen to conform the best model fit. The model was corrected for time since the start of CPR.

To analyze the effect of each CPR variable, a model with all variables

included was fitted. To further analyze the independent effect of both CC depth and CCRV, extra models were fitted in which only one of both variables were included for collinearity. These models were per- formed on all cases, after stratification by shockable rhythm and after stratification by ROSC.

As most of the CCRV data was between 300 and 500 mm/s, CCRV was categorized to groups of 300, 400 and 500 mm/s. These categories in- cluded minutes with average measurements of [250;350], [350;450] and [450;550] mm/s respectively. In these categories, mean ETCO2 values were calculated and corrected for CC depth, according to the re- sults of the linear mixed effect models. These were subsequently com- pared through a one-way ANOVA with a Bonferroni post-hoc analysis.

All tests were conducted using SPSS Statistics 27 (IBM, USA) with ? set at 0.05.

  1. Results

Data of 272 OHCA patients, intubated during resuscitation was gath- ered. Of these cases, 153 (56%) had a missing Zoll event file, 23 (8%) had no ETCO2 measurements, 17 (6%) had no CC data, 12 (4%) had disturbed measurements, 12 (4%) had no overlapping compressions and ETCO2 measurement for at least 1 min and 6 (2%) had no clinical case report. 2 cases (1%) had a traumatic etiology. 47 cases (17%) met inclusion criteria, with 347 analyzable minutes in total.

The case and event characteristics of the included cases are summa- rized in Table 1. The time to the start of CPR (BLS by bystanders or para- medics) could not be determined, however the mean time to MET arrival is reported.

CPR quality variables (CC depth, CC rate, CCRV and VR) and ETCO2 values of the included cases are summarized in Table 2. On average, CC depth was 57.5 mm, CC rate was 115.6 compressions per minute (cpm), CCRV was 405.2 mm/s, VR was 14.3 breaths per minute (bpm) and ETCO2 was 29.2 mmHg. ETCO2 was significantly higher in ROSC cases than in non-ROSC cases. CC depth, CC rate, CCRV and VR did not significantly differ between the two groups (Table 2).

    1. Quantitative relationship between CPR variables and ETCO2

Scatter plots and locally weighted polynomial regressions suggested approximately linear relationships between each CPR variable and cor- responding ETCO2 values.

Table 1

Case and event characteristics.

Variable

Summary

(n = 47)

Age (years), mean (SD)

64

(16.1)

Gender

Male, n (%)

30

(64)

Witnessed Bystander CPR

Unknown, n (%)

14

(30)

Asystole, n (%)

27

(57)

Initial rhythm

PEA, n (%)

9

(19)

VF/VT, n (%)

11

(23)

Cardiac, n (%)

33

(70)

Presumed etiology

Asphyxial, n (%)

11

(23)

Other, n (%)

3

(6)

ROSC

Yes, n (%)

19

(40)

Survival to discharge

Yes, n (%)

5

(11)

Time to MET arrivala (minutes), mean (SD)

10.2

(4.0)

Time to initial measurementsb (minutes), mean (SD)

12.4

(7.4)

Analyzed minutes per case, mean (SD)

8.6

(9.2)

Yes, n (%)

29

(62)

Unknown, n (%)

7

(15)

Yes, n (%)

22

(47)

MET: medical emergency team, n: number, PEA: pulseless electrical activity, ROSC: return of spontaneous circulation, SD: standard deviation, VF: ventricular fibrillation, VT: ventric- ular tachycardia.

a The time between the emergency call and the arrival of the MET at the site.

b The time between the start of CPR (by the MET) and the start of measurements (after intubation).

The linear mixed effect model with all CPR variables included showed a 10 mm increase in CC depth to result in a 1.7 mmHg increase in ETCO2 (p = 0.043) and an increase in VR of 5 bpm to result in a de- crease in ETCO2 of 2.0 mmHg (p < 0.001). The association of CCRV and CC rate with ETCO2 was not statistically significant.

Yet, this model could be disturbed due to a strong correlation between CC depth and CCRV (Pearson’s r = 0.709, p < 0.001). (Fig. 1) This indi- cates that when CC are deeper, CCRV is higher and vice versa. No cor- relation was found between CC rate and CCRV (Pearson’s r = -0.073, p = 0.204) or between CCRV and VR (Pearson’s r = -0.103, p = 0.076).

    1. Independent effect of CCRV on ETCO2

In the extra models, which either included CC depth or CCRV, an in- crease of 10 mm in CC depth resulted in an increase in ETCO2 of

1.5 mmHg (p < 0.001) and an increase of 100 mm/s in CCRV in an in- crease in ETCO2 of 0.8 mmHg (p = 0.010). The results of the fitted models are summarized in Table 3. Tables 4 and 5 contain the results of the fitted models, after stratification by initial rhythm and after stratification by outcome.

The mean CCRV in this study was 405.2 (SD: 79.6) mm/s. Therefore, CCRV was categorized to rounded values of 300, 400 and 500 mm/s. These categories included 96, 107 and 70 analyzed minutes respectively. A CCRV of 500 mm/s reflected in ETCO2 of 34.7 mmHg on average, while a CCRV of 400 and 300 mm/s reflected in an average of

27.1 mmHg and 27.2 mmHg respectively.

After adjusting for CC depth, mean ETCO2 was 33.5, 27.0 and

28.2 mmHg respectively. The corrective factors applied in this adjustment were based on the results obtained using the linear mixed effect model.

Image of Fig. 1

Fig. 1. Scatterplot of CCRV by CC depth; CC: chest compression, CCRV: chest compression release velocity.

The Bonferroni post-hoc analysis showed that the 500 mm/s CCRV group had a 6.5 mmHg (95% CI: [1.6; 11.4], p = 0.005) higher ETCO2

than the 400 mm/s group and a 5.3 mmHg (95% CI: [0.3; 10.3], p = 0.033) higher ETCO2 than the 300 mm/s group. A CCRV of 400 and 300 mm/s resulted in no significantly different ETCO2 (1.2 mmHg, 95%

CI: [-3.3; 5.7], p = 1.000).

  1. Discussion

In our study, measured CC depth and CC rate were on average within the ranges recommended by guidelines. Mean VR was higher (14.3 bpm) than recommended (10 bpm). Mean CCRV was higher (405.2 mm/s) than CCRV reported in previous studies (300-360 mm/s) [3-8].

Our study found effects on ETCO2 of altering CC depth, CC rate, CCRV and VR.

CC depth, CCRV and VR had statistically significant effects, while CC rate had no effect when all cases were considered.

Of particular interest is that in ROSC cases, no variable had a signifi- cant impact on ETCO2 values. Moreover, the effects in non-ROSC cases were significant and larger. These findings are also reported in the study of Murphy et al., which had a larger study population [17]. The reason for this insignificances and differences in effect sizes is unknown. A plausible explanation is that changes in CPR administration in cases ultimately achieving ROSC do not have an impact as strong as in the non-ROSC cases. The patients ultimately achieving ROSC had a higher baseline ETCO2 (Table 2). Hence, they may be less dependent on the quality of CPR administration than the patients not achieving ROSC, be- cause of their better status. Another possible explanation is the acciden- tal inclusion of minutes with ROSC and ongoing CC in the analyzes.

The effects of an increase in CC depth and an increase of VR on ETCO2 are comparable with the effect previously reported by Sheak et al. In their study, each 10 mm increase in CC depth was associated with an ETCO2 increase of 1.3 mmHg on average. For each 10 bpm increase in

Table 2

CPR quality variables and ETCO2 values.

All

ROSC (n = 19)

Non-ROSC (n = 28)

p-value

CC depth (mm), mean (SD)

57.5

(10.3)

57.5

(11, 7)

57.5

(9.2)

0.997

CC rate (cpm), mean (SD)

115.6

(8.8)

117.7

(9, 2)

113.8

(8.3)

0.118

CCRV (mm/s), mean (SD)

405.2

(79.6)

410.1

(79, 3)

401.0

(81.2)

0.703

VR (bpm), mean (SD)

14.3

(4.3)

14.3

(4, 5)

14.4

(4.1)

0.961

ETCO2 (mmHg), mean (SD)

29.2

(13.1)

35.1

(11, 9)

24.3

(12.1)

0.003

bpm: breaths per minute, CC: chest compression, CCRV: chest compression release velocity, cpm: compressions per minute, ETCO2: end-tidal carbon dioxide, ROSC: return of spontaneous circulation, SD: standard deviation, VR: ventilation rate.

Table 3

Effect of changes in CPR variables on ETCO2 values.

Effecta on ETCO2 (mmHg) 95% CI p-value

+10 mm in CC depthb +1.5 +0.8; +2.1 < 0.001

+100 mm/s in CCRVc +0.8 +0.2; +1.4 0.010

+10 cpm in CC rated -0.7 -2.5; +1.0 0.210

+5 bpm in VRd -2.0 -2.6; -1.3 < 0.001

bpm: breaths per minute, CC: chest compression, CCRV: chest compression release veloc- ity, CI: confidence interval, cpm: compressions per minute, ETCO2: end-tidal carbon dioxide, VR: ventilation rate.

a Effect: absolute increase or decrease in ETCO2 values; Effects are presented with a 95% confidence interval (CI); p-values <0,05 were considered statistically significant.

b To analyze the effect of CC depth, a mixed model with all CPR variables except CCRV

was used.

c To analyze the effect of CCRV, a mixed model with all CPR variables except CC depth was used.

d To analyze the effect of CC rate and VR, a mixed model with all CPR variables was used.

VR, ETCO2 declined with 3.6 mmHg on average. Their study did not find a significant result for CC rate either. The relationship between CCRV and ETCO2 was not analyzed in their study [16].

The effects found in our study are also comparable with the effects previously reported by Murphy et al. In their study, a 10 mm increase in CC depth caused a 4% increase in ETCO2, a CC rate increase of 10 cpm caused a 1.7% increase in ETCO2, and a 10 bpm increase caused a 17.4% decrease in ETCO2. They reported a statistically significant effect of an increase in CC rate on ETCO2, which our study did not find.

It should be noted that the absolute effect sizes are modest. How-

ever, these effects are cumulative. For example, if a rescuer becomes tired, CC will be poor and less effective. For example, if CC are performed at a depth of +-40 mm with a CCRV of +-300 mm/s, ETCO2 would drop with +-4 mmHg (compared to 60 mm and 400 mm/s, which are the approximate means in our study). This change is fairly small, but noticeable. It should be the objective to reach a maximal ETCO2 during CPR, as ETCO2 is a marker for circulation and hence CPR effectiveness.

The study by Murphy et al. was the only study which examined the effect of CCRV on ETCO2 in humans. ETCO2 would increase with 2.8% with a 100 mm/s increase in CCRV. Yet, the effect of CCRV on ETCO2 was not corrected for the effect of CC depth in their study [17].

Our study showed CCRV to be strongly correlated with CC depth. This was reported in other studies as well [3,4,8,17]. The sternum recoils faster when pressed in deeper. The positive effect of a higher CCRV on ETCO2 could therefore be caused solely by an increase in CC depth rather than an independent effect caused by a higher CCRV. This hypothesis was not considered in the study of Murphy et al. [17].

Importantly, Gonzalez-Otero et al. reported CC of a fixed depth to have variable CCRV or inversely, CC with different depths to have a similar CCRV, depending on the vigorousness and impulsiveness of the CC [4].

The model with all cases considered and with all CPR variables in- cluded, showed no significant effect of CCRV. Yet, this analysis could be disturbed by the strong correlation between CC depth and CCRV. Therefore, extra models were fitted, in which only one of both variables were included for collinearity, to further analyze the independent effect of both CC depth and CCRV. Herein, CCRV did have a significant effect on ETCO2.

The question remained if CCRV could have been a surrogate marker of the CC depth and if the observed effect of CCRV on ETCO2 was therefore merely the effect of the correlated change in CC depth.

Therefore, CCRV was categorized at 300, 400 and 500 mm/s. A CCRV of 500 mm/s reflected in a significantly higher mean ETCO2 value than a CCRV of 300 mm/s or 400 mm/s, after adjusting for CC depth. A CCRV of 300 mm/s or 400 mm/s resulted in no different mean ETCO2. This indicates that the positive effect of higher CCRV values was possibly not linear (as suggested by the linear models above). Yet, both analyses suggest that higher CCRV values resulted in higher ETCO2 values. The effect of a CCRV rise had a much larger effect in the ANOVA than in the linear models, however this could be explained because the ANOVA did not correct for other CPR variables.

The independent positive effect of higher CCRV on ETCO2 observed in our study, is supported by animal studies which have shown mechanical high-impulse compressions and decompressions to improve blood flow [9,10]. In an animal model of mechanical CC, shorter release times for fixed depths (and therefore higher CCRV for fixed depths), resulted in increased blood flow and higher ETCO2 levels [11].

Our study corroborates that higher CCRV values are correlated with higher ETCO2 values in humans. The effect of CCRV on ETCO2 in humans has only been studied once before [17]. The effect of CCRV independent of CC depth however, had not yet been studied in humans.

Since higher ETCO2 values are associated with higher blood flow and chances of survival [18], an argument could be made for optimization of CCRV in CPR through releasing the chest as rapidly as possible and through not leaning on the chest after CC. Possible solutions to optimize CCRV in CPR are therefore paramount and include frequent changing of the rescuer and rescuer feedback. Active decompression devices and mechanical CC might also increase CCRV.

    1. Limitations

Several limitations existed in our study. Data was missing in a large number of cases, strict data collection in the prehospital envi- ronment proved to be difficult. Despite this, several important re- sults were found, which illustrates that the possible relationships are in fact relatively strong. Because of the rather small study popu- lation, these results must be interpreted with caution. The time to

Table 4

Effect of changes in CPR variables on ETCO2 values, stratified by shockable rhythm versus Non-shockable rhythm.

Effecta on ETCO2 (mmHg)

95% CI

p-value

+10 mm in CC depthb

Shockable

+2.2

+1.6; +2.7

<0.001

Non-shockable

+1,5

-1.0; +3.1

0.056

+100 mm/s CCRVc

Shockable

+1.8

+1,7; +1,9

<0.001

Non-shockable

+1.4

+0.5; +2.2

0.003

+10 cpm in CC rated

Shockable

+0.4

-1.4; +2.2

0.403

+5 bpm in VRd

Non-shockable

Shockable

-2.1

-5.1

-2.8; -1.3

-5.8; -4.5

<0.001

<0.001

Non-shockable

-2.5

-3.8; -1.3

<0.001

bpm: breaths per minute, CC: chest compression, CCRV: chest compression release velocity, CI: confidence interval, cpm: compressions per minute, ETCO2: end-tidal carbon dioxide, VR: ventilation rate.

a Effect: absolute increase or decrease in ETCO2 values; Effects are presented with a 95% confidence interval (CI); p-values <0,05 were considered statistically significant.

b To analyze the effect of CC depth, a mixed model with all CPR variables except CCRV was used.

c To analyze the effect of CCRV, a mixed model with all CPR variables except CC depth was used.

d To analyze the effect of CC rate and VR, a mixed model with all CPR variables was used.

Table 5

Effect of changes in CPR variables on EtCO2 values, stratified by ROSC versus non-ROSC.

Effecta on ETCO2 (mmHg)

95% CI

p-value

+10 mm in CC depthb

ROSC

+1.4

-0.6; +3.3

0.170

Non-ROSC

+1.5

-2.3; +5.3

0.140

+100 mm/s in CCRVc

ROSC

+0,8

-0.9; +2.5

0.322

Non-ROSC

+1.3

+0.6; +1.9

<0.001

+10 cpm in CC rated

ROSC

+0.6

-1.2; +2.4

0.520

Non-ROSC

-1.0

-1,8; -0.3

0.006

+5 bpm in VRd

ROSC

-1.4

-4.2; +1.4

0.322

Non-ROSC

-4.8

-6.1; -3.4

<0.001

bpm: breaths per minute, CC: chest compression, CCRV: chest compression release velocity, CI: confidence interval, cpm: compressions per minute, ETCO2: end-tidal carbon dioxide, VR: ventilation rate.

a Effect: absolute increase or decrease in ETCO2 values; Effects are presented with a 95% confidence interval (CI); p-values <0,05 were considered statistically significant.

b To analyze the effect of CC depth, a mixed model with all CPR variables except CCRV was used.

c To analyze the effect of CCRV, a mixed model with all CPR variables except CC depth was used.

d To analyze the effect of CC rate and VR, a mixed model with all CPR variables was used.

CPR after occurring of OHCA could not be accurately defined, as this was not always clear in the prehospital setting. Moreover, intubation is often postponed to a later stage of resuscitation, as a result, the first minutes of CPR were not analyzed in this study. Furthermore, the effect of changing tidal volumes on ETCO2 was not considered in this study. The CPR variables in this study were not fixed, but they were minute-averaged values. Epinephrine can influence ETCO2, but the exact moments of epinephrine administration were not adequately noted. Consequently, analyses were not corrected for epinephrine administration.

  1. Conclusion

In this monocentric, observational prospective study, changes in CPR quality variables (CC depth, CC rate, CCRV and VR) were independently associated with changes in ETCO2 values. Especially the individual effect of CCRV on ETCO2 is an important finding of this study, as this effect has not yet been proven independently from the effect of CC depth in OHCA patients. Our results hence support the optimization of CCRV during CPR to enhance ETCO2 values and chances of survival.

CrediT authorship contribution statement Egbert De Roos: Writing – review & editing, Writing – original draft,

Visualization, Validation, Supervision, Software, Project administration,

Methodology, Investigation, Formal analysis, Data curation, Conceptual- ization. Maxim Vanwulpen: Writing – review & editing, Supervision, Software, Project administration, Data curation, Conceptualization. Said Hachimi-Idrissi: Writing – review & editing, Validation, Supervi- sion, Resources, Project administration, Conceptualization.

Declaration of Competing Interest

All authors do not have any conflicts of interest to disclose. This re- search did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

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