Factors complicating interpretation of capnography during advanced life support in cardiac arrest—A clinical retrospective study in 575 patients

Początek formularza

• Bĺrd E. Heradstveit

, 

• Kjetil Sunde

, 

• Geir-Arne Sunde

, 

• Tore Wentzel-Larsen

, 

• Jon-Kenneth Heltne

Dół formularza

Received 21 November 2011; received in revised form 7 February 2012; accepted 15 February 2012. published online 27 February 2012.

Article Outline

1. Abstract

2. 1. Introduction

3. 2. Material and methods

1. 2.1. Ethics

2. 2.2. Organisation

3. 2.3. ALS treatment

4. 2.4. Capnography use

5. 2.5. Study design and data collection

6. 2.6. Statistics

2. 3. Results

1. 3.1. ETCO2 and different causes

2. 3.2. ETCO2 and different initial rhythms

3. 3.3. ETCO2 and bystander CPR

4. 3.4. ETCO2 and time of measurement

2. 4. Discussion

3. 5. Conclusion

4. Role of the funding source

5. Conflict of interest statement

6. Acknowledgements

7. References

8. Copyright

Abstract 

Background

End tidal carbon dioxide (ETCO₂) monitoring during advanced life support (ALS) using capnography, is recommended in the latest international guidelines. However, several factors might complicate capnography interpretation during ALS. How the cause of cardiac arrest, initial rhythm, bystander cardiopulmonary resuscitation (CPR) and time impact on the ETCO₂ values are not completely clear. Thus, we wanted to explore this in out-of-hospital cardiac arrested (OHCA) patients.

Methods

The study was carried out by the Emergency Medical Service of Haukeland University Hospital, Bergen, Norway. All non-traumatic OHCAs treated by our service between January 2004 and December 2009 were included. Capnography was routinely used in the study, and these data were retrospectively reviewed together with Utstein data and other clinical information.

Results

Our service treated 918 OHCA patients, and capnography data were present in 575 patients. Capnography distinguished well between patients with or without return of spontaneous circulation (ROSC) for any initial rhythm and cause of the arrest (p
<
0.001). Cardiac arrests with a respiratory cause had significantly higher levels of ETCO₂ compared to primary cardiac causes (p
<
0.001). Bystander CPR affected ETCO₂-recordings, and the ETCO₂ levels declined with time.

Conclusions

Capnography is a useful tool to optimise and individualise ALS in cardiac arrested patients. Confounding factors including cause of cardiac arrest, initial rhythm, bystander CPR and time from cardiac arrest until quantitative capnography had an impact on the ETCO₂ values, thereby complicating and limiting prognostic interpretation of capnography during ALS.

Keywords: Cardiac arrest, Outcome, Capnography, Capnometry, Advanced life support, Pulmonary embolism, Prognostics

 

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1. Introduction 

The partial pressure of end tidal carbon dioxide (ETCO₂) estimates alveolar carbon dioxide (CO₂) tension, and reflects its production, transport to, and elimination from the lungs; hence it generally reflects cardiac output.¹, ² Alteration in one of these factors will affect the measurement. The technique was first described during anaesthesia in the 1950s,³ in order to verify correct tube placement. Monitoring of ETCO₂ during cardiopulmonary resuscitation (CPR) was first described by Kalenda, who used ETCO₂ as a guide to the efficacy of CPR. A drop in ETCO₂ was an indicator for when to change the person providing chest compressions, due to inadequate compression efficacy.⁴ This was later followed by studies reporting its use during CPR in experimental models.¹, ⁵ The positive correlation between ETCO₂ and outcome of cardiac arrest in patients has been well described in several studies,⁵, ⁶, ⁷, ⁸, ⁹, ¹⁰, ¹¹ and a significant increase in ETCO₂ during CPR has been associated with return of spontaneous circulation (ROSC).¹², ¹³ The 2010 guidelines from European Resuscitation Council (ERC) now encourage the use of capnography to guide CPR during Advanced Life Support (ALS).¹⁴

Interpretation of ETCO₂ during resuscitation from cardiac arrest is still challenging and has several pitfalls. Especially the cause of the arrest seems to have impact on the ETCO₂, and recent studies have described higher ETCO₂ in asphyxial arrests compared with arrests of cardiac aetiology.¹⁵, ¹⁶ Further, the influence of bystander CPR may impact on ETCO₂ as well as variations over time, but this has not been documented in clinical studies.

Thus, the aims of the study were to document levels of ETCO₂ in patients with out-of-hospital cardiac arrest (OHCA). We hypothesised that although capnography will give valuable feedback to the ALS providers, initial heart rhythm, cause of the arrest, presence of bystander CPR and time dependency will limit and complicate its interpretation.

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2. Material and methods 

2.1. Ethics 

This retrospective study was carried out at the Emergency Medical Service (EMS), Haukeland University Hospital, Norway. The Privacy Protection Supervisor approved the study and the Regional Committees for Medical Research Ethics had no objections. The need of an informed consent from the patients or the families was waived.

2.2. Organisation 

Our region has a population of approximately 470,000 people (15,000
km²). Since 1988, the Helicopter Emergency Medical Service (HEMS) at Haukeland University Hospital has assisted the decentralised ambulances treating cardiac arrests. The paramedics are trained in ALS and are yearly certified. The HEMS is served by an anaesthesiologist by helicopter or rapid response car. Regarding cardiac arrest, the emergency dispatch centre provides telephone guided CPR to lay people if the patient is unconscious with abnormal breathing. In parallel, both the nearest ambulance and the HEMS are immediately despatched for initiation of ALS. Local first-responders providing basic life support with defibrillation (fire-fighters) are also despatched, who may arrive at the patient before the ambulance/HEMS.

2.3. ALS treatment 

All patients in the present study were treated according to the current international guidelines with our national adjustments.¹⁷, ¹⁸, ¹⁹ Both the ambulances and the HEMS were equipped with Lifepak^® 12 Defibrillator (Physio-Control Inc., Redmond, WA, USA), while the first responders used the fully automatic Lifepak CR^® (Physio-Control). To permit continuous chest compressions, the patients had airways secured with a supraglottic laryngeal tube (LTS-D, VBM Medizintechnik GmbH, Germany) by the paramedics, or endotracheal tube by the anaesthesiologists. The first responders used mouth-to-mouth ventilation with a pocket mask. All patients were manually ventilated according to the current guidelines.¹⁷, ¹⁸, ¹⁹ ALS drugs were used according to national guidelines,¹⁷, ¹⁸, ¹⁹ and no bicarbonate buffer was administered during the study period. If ROSC did not occur and the resuscitation attempt was deemed to be futile by the attending doctor, ALS was terminated on the scene. In the presence of profound hypothermia, or in other special circumstances, patients were transported with ongoing CPR to Haukeland University Hospital.

2.4. Capnography use 

The HEMS has routinely used waveform capnography in all intubated patients since 1999. Initially, the purpose of capnography was to verify correct tracheal tube placement. However, in cardiac arrest patients, we also used it as a surrogate marker of circulation.²⁰ ETCO₂-monitoring was performed using a mainstream sensor, using single beam, non-dispersive infrared absorption, ratiometric measurements (Tidal Wave^®, Philips Respironics, The Netherlands). Recording of ETCO₂-values were initiated upon the arrival of the HEMS, and after placement of a secured airway, and were continuously observed by the treating anaesthesiologist.

2.5. Study design and data collection 

All patients with ALS initiated non-traumatic cardiac arrest treated at our HEMS between January 2004 and December 2009 were included in the study. Pre-hospital data were recorded according to the Utstein model.²¹ Time records from the dispatch centre supplemented ambulance records regarding response times. In cases where the exact time of cardiac arrest was unknown, the time was estimated based on the current information available. In patients with unknown arrest time of over 60
min, all response times were increased by 60
min.

In patients with ROSC admitted to hospital, the cause of arrest was determined based on hospital records and all available information. Patients were classified in four categories; cardiac, respiratory, pulmonary embolism (PE) and unknown. Based on the initial heart rhythm, patients were classified in three groups; ventricular fibrillation/pulseless ventricular tachycardia (VF/VT), asystole (AS) or pulseless electric activity (PEA). For those pronounced dead at the scene, the anaesthesiologist stated the assumed cause of the arrest according to the Utstein-criteria. This assumption was based on previous medical history, comparative information from family, witnesses and bystanders and all available clinical or environmental data or signs.²¹ For example, a PE was decided as the cause of the arrest if a clinical suspicion of a deep vein thrombosis (presumably with initial AS or PEA) was present. Those patients with an unclear cause of the arrest were grouped as “unknown” in order to have as clean groups as possible.

Patients who gained ROSC before arrival of HEMS, patients transported to the hospital with ongoing resuscitation (hypothermic patients or other special circumstances), and patients with unknown initial heart rhythm were excluded from the study.

ETCO₂ were recorded after the HEMS crew arrived at the patient as previously described. After one minute of normal ventilation, the average, minimal and maximal values in the following 15
min of ALS (or until ROSC if it occurred before 15
min) were recorded manually by the anaesthesiologist. The Tidal Wave^® capnograph has no automatic recording of data, and the average value during these 15
min was not an average in a strict sense, but was based on the anaesthesiologist's judgement. ETCO₂ measurements were then analysed based upon the initial heart rhythm, cause of the arrest and presence of bystander CPR, and further classified depending on ROSC or no ROSC. Association of ETCO₂ related to bystander CPR, time of measurement, initial rhythms and cause of the arrest were also classified. Other factors that may influence ETCO₂ like epinephrine, quality of CPR and ventilation data were not available.

2.6. Statistics 

All numbers are presented as mean
±
SD. Continuous data were compared using independent samples t-tests. Linear regression analysis was used to determine the relationship of average measurement on ETCO₂ with bystander CPR, time of measurement, rhythm and cause of the arrest. Regression analysis used all observations where average ETCO₂ was known. Since some covariates from different patients were missing, the regression analysis was run using multiple imputation, a well described general procedure to use as much information as possible.²² In this procedure, several completed data sets (200 in our case) are constructed and analyses from these completed data sets are combined. Some continuous covariates were entered nonlinearly, when deviations from a linear relationship was suspected. A p-value <0.05 was considered significant. The R (The R Foundation for Statistical Computing, Vienna, Austria) packages rms and Hmisc were used for regression analysis, imputation and assessment of which covariates that should be entered nonlinearly. SPSS version 17-18 (IBM SPSS, Somers, NY, USA) was used for presentation of the data and for other statistical analyses.

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3. Results 

A total of 918 patients received ALS after OHCA during the study period. Patient flow chart with included and excluded patients is shown in Fig. 1. Of 724 eligible patients, ETCO₂ recordings were present in 575 (82%) patients who were included in the final study. Patients with ETCO₂ measurements did not differ from the missing/excluded group regarding gender, age, initial heart rhythm, response times or outcome. All baseline characteristics are presented in Table 1. Data only relates to patients in whom a clear airway and controlled ventilation were established and confirmed by capnography before data collection started. Additionally all tube placements were confirmed by signs of effective ventilation. Among the 575 included, 232 patients (40%) gained ROSC and were transported to the hospital. For all initial heart rhythms and different causes, ETCO₂ were significantly higher in those achieving ROSC compared to those not achieving ROSC (Table 2, Table 3).

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• Fig. 1. 

Included and excluded patients - flow chart.

Table 1. Baseline characteristics in study population (n
=
575).

Variable	Mean ± SD
Age (year)	60.7 ± 17.8
Female/male	145/430
Witnessed	414 (72%)
Bystander CPR	438 (76%)
Arrest-CPR (min)	8.6 ± 15.4
Arrest-ACLS (min)	14.7 ± 16.9
Arrest-CO2 recording (min)	22.5 ± 17.5
Admitted hospital with ROSC	232 (40%)
Any ROSC (%)	286 (50%)
Termination of resuscitation (min)^a	43.3 ± 22.3
Cause of the arrest
Cardiac	336 (58%)
Respiratory	117 (20%)
Pulmonary embolism	12 (2%)
Unknown/other	110 (19%)
Initial rhythm
Ventricular fibrillation	195 (34%)
Ventricular tachycardia	3 (1%)
Asystole	266 (46%)
Pulseless electrical activity	111 (19%)

CPR, cardio pulmonary resuscitation; ACLS, advanced cardiac life support.

aTime between arrest and termination of resuscitation.

Table 2. Average ETCO₂ (kPa) during CPR in patients with or without ROSC, regarding the cause of the arrest.

Cause	Overall ETCO2, mean ± SD	ROSC, mean ± SD	No-ROSC, mean ± SD	p-Value^a
Cardiac	2.8 ± 1.3	3.4 ± 1.2	2.4 ± 1.2	<0.001
Respiratory	3.5 ± 2.2	4.5 ± 2.2	2.3 ± 1.5	<0.001
Pulmonary embolism	1.7 ± 1.1	2.2 ± 1.0	0.9 ± 0.5	0.023
Unknown/Other	2.0 ± 1.2	2.7 ± 1.0	1.3 ± 1.1	<0.001
aContrast between ROSC and no-ROSC using independent samples t-test.

Table 3. ETCO₂ (kPa) in patients presenting asystole with respiratory and cardiac causes to the arrest.

ETCO2	Cardiac cause, mean ± SD	Respiratory cause, mean ± SD	p-Value^a
Average	2.3 ± 1.4	3.5 ± 2.3	<0.001
Min.	1.5 ± 1.0	2.4 ± 2.0	<0.001
Max.	3.4 ± 2.3	5.1 ± 3.5	<0.001
aContrast between cardiac and respiratory causes using independent samples t-test.

3.1. ETCO₂ and different causes 

There were significant differences in ETCO₂ depending on the cause of the arrest (p
<
0.001) (Table 2), with respiratory arrests having increased levels compared to primary cardiac caused arrests. Furthermore, a significantly lower level of ETCO₂ was present in patients with PE compared to patients with respiratory and cardiac causes, regardless of ROSC or not (Table 2). Patients with ROSC and PE, had similar values as patients without ROSC and all other causes (and actually tended to be even lower) (Table 2). In patients with initial asystole, the minimum, maximum and average ETCO₂ were characteristically higher among those patients with respiratory compared to cardiac causes (p
<
0.001) (Table 3). More patients gained ROSC in the respiratory compared to the cardiac group, 49% vs. 15%.

3.2. ETCO₂ and different initial rhythms 

Initial VF/VT was present in 198 patients (34%), AS in 266 patients (46%), and PEA in 111 (19%) patients (Table 4). Regression analysis did reveal differences in the ETCO₂ with respect to initial rhythms (p
=
0.004). Within each rhythm, there were significant contrasts between patients with and without ROSC (Table 4). In the presence of ROSC, patients with initial asystole had the highest ETCO₂, and PEA the lowest, whereas in absence of ROSC, patients with initial VF/VT had the highest levels (Table 4).

Table 4. Average ETCO₂ (kPa) during CPR in patients with or without ROSC, regarding the initial heart rhythm.

Initial heart rhythm	ETCO2	ROSC, mean ± SD	No-ROSC, mean ± SD	p-Value^a
VF/VT (n = 198)	Average	3.4 ± 1.1	2.8 ± 1.2	<0.001
		Min.	2.6 ± 1.0	1.8 ± 0.9	<0.001
		Max.	5.1 ± 2.2	4.3 ± 1.9	0.009
	AS (n = 266)	Average	4.1 ± 2.1	2.0 ± 1.3	<0.001
		Min.	2.9 ± 1.8	1.4 ± 1.0	<0.001
		Max.	5.9 ± 3.3	3.0 ± 2.1	<0.001
	PEA (n = 111)	Average	3.1 ± 1.5	2.2 ± 1.3	0.001
		Min.	2.2 ± 1.4	1.3 ± 1.0	<0.001
		Max.	4.4 ± 2.5	3.1 ± 1.9	0.003
aContrast between ROSC and No-ROSC using independent samples t-test.

3.3. ETCO₂ and bystander CPR 

The impact of bystander CPR affected the ETCO₂ significantly (p
=
0.003). Initiation of bystander CPR within four minutes after the cardiac arrest resulted in higher values of ETCO₂ while CPR started later resulted in lower values (Fig. 2a). Over time, the trend was decreasing values of ETCO₂.

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Fig. 2 (a) End tidal CO2 and time of onset bystander CPR after the arrest, adjusted for time of measurement, initial rhythms and cause of the arrest (estimated values with 95% CI). (b) Measurement of end tidal CO2 at different times after the arrest, adjusted for bystander CPR, initial rhythms and cause of the arrest (estimated values with 95% CI). © 2012 Elsevier Ireland Ltd

 

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• Fig. 2. 

(a) End tidal CO₂ and time of onset bystander CPR after the arrest, adjusted for time of measurement, initial rhythms and cause of the arrest (estimated values with 95% CI). (b) Measurement of end tidal CO₂ at different times after the arrest, adjusted for bystander CPR, initial rhythms and cause of the arrest (estimated values with 95% CI).

3.4. ETCO₂ and time of measurement 

The average ETCO₂ was significantly affected by the time of recording after the arrest (p
=
0.037), and the values declined with delayed measurement (Fig. 2b).

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4. Discussion 

In the present study we have documented that several factors complicate the interpretation of ETCO₂ during ALS. Although ETCO₂ differs well between patients with and without ROSC, there is no clear generalised cut-off value determining whether ROSC will be achieved or not. Several confounding factors such as cause of the arrest, initial rhythm, bystander CPR and changes over time from arrest until ETCO₂ recordings seem to influence this.

Patients with respiratory causes and initial AS had in general higher levels of ETCO₂ than those with a primary cardiac cause. Similarly, Grmec et al. have previously reported higher ETCO₂ immediately after intubation in patients with asphyxial compared to primary cardiac arrests.¹⁵ Lah et al. from the same group demonstrated that this difference normalised within three to five minutes after initiation of ALS.¹⁶ They also reported that the initial ETCO₂ could not be used as a prognostic factor due to these aetiology differences.¹⁶ We speculate that capnography for CPR guidance during ALS is easier to interpret in patients with cardiac causes than in patients with asphyxial arrests.

The higher ETCO₂ in patients with asphyxial arrests are presumably not due to better cardiac output, but due to CO₂accumulation in the tissue and venous blood due to asphyxia and absence of ventilation.¹⁵ This assumption introduces the possibility for confounding in the presence of bystander CPR, which affected the ETCO₂. First, we found increased ETCO₂with onset of CPR within the first four minutes after the cardiac arrest. Thereafter, the ETCO₂ seemed to decrease with delayed onset of CPR beyond four minutes. Survival after cardiac arrest depends on time from arrest until CPR and successful defibrillation,¹⁷, ¹⁸, ²³ and thereby reduces with later onset of bystander CPR.²⁴, ²⁵ Besides the hypoxic component, this can also be related to development of stone heart with thickening of the myocardium and decrease in left ventricular volume. This has been demonstrated in untreated cardiac arrest in pigs.²⁶ Our data confirm that delayed initiation of CPR leads to lower ETCO₂. This might be explained by less effective chest compressions due to development of stone heart. The reported delay between time of arrest and ETCO₂-recording may seem long, but can partly be explained by the fact that also unwitnessed arrests were included.

An interesting result in our study was the low levels of ETCO₂ in patients with PE. ETCO₂ in PE patients are characteristically lower because of diminished pulmonary perfusion and increased alveolar dead space, and consequently decreased CO₂elimination capability.²⁷, ²⁸ Low ETCO₂ and clinical suspicion of PE, might therefore be an indication for trombolysis during ongoing ALS, since individually adjusted treatment with fibrinolytics for these patients previously can be successful.²⁹ Only 12/575 patients in the present study had a PE confirmed as the cause of their arrest. This is far less than previously reported,³⁰ and emphasizes the fact that PE is difficult to diagnose in cardiac arrest. Low ETCO₂ combined with a non-shockable rhythm can be suspectible of PE.

In clinical studies, ETCO₂
>
2.4
kPa after 20
min has been shown to predict ROSC, and values <1.3
kPa have been associated with no ROSC.¹⁵, ¹⁶ Our data demonstrates that such cut-off values must be used with caution. Too many confounding factors impact on the actual ETCO₂. Importantly, cut-off values from observational studies are only based on the actual dataset, and cannot be generalised to other systems. Strict use of cut-off values in patient treatment will lead to treatment withdrawal based on self-fulfilling prophecy. Furthermore, the compression site on sternum might presumably affect haemodynamics and thereby cardiac output and ETCO₂, as recently shown in a clinical study.³¹ This fits well with our impression that levels of ETCO₂ in each patient varied depending on the rescuer performing chest compressions. Thus, since both compression site and quality of chest compressions impact on the ETCO₂, this should be acknowledged by ALS-providers during interpretation of capnography. With ETCO₂-guided resuscitation it is thereby possible to encourage the rescuers to maximise quality of CPR and to change the person providing compressions when the ETCO₂ drops, thereby optimising CPR for each patient.

The major limitation in the present study is the method used for ETCO₂ recordings. The anaesthesiologist on scene observed the ETCO₂ continuously during the first 15
min after arrival on scene, and registered manually the values without any further validation of these data. Since the Tidal Wave^® capnograph had no automatic recording, the registered minimum, maximum and average ETCO₂ from each patient were based on the anaesthesiologists' judgement. Such observation might lead to recording errors and bias, but since this was a non-interventional study, the registered data should only have been prone to recording error. Due to the interesting finding of the time variation and difference between causes and initial rhythms, future studies should link every ETCO₂ to time during the resuscitation procedure. The method used for ETCO₂recordings should be improved and optimised for better data management and scientific and valid interpretation. Further, the patients were manually ventilated, and although this was done or observed by an experienced anaesthesiologist we have no data on quality of ventilations. However, the impact of ventilation may be of minor importance in a low flow state like cardiac arrest.²⁰ Pulmonary flow, generated from cardiac output achieved through chest compressions, is more important in this situation. Another limitation is how cause of death was determined in the field in patients without ROSC. We have no autopsy data, and the uncertainty involved in these causes may also hide undiagnosed PE. Consequently, the number of unknown causes is high. Finally, epinephrine impacts on cardiac output and ETCO₂ during ALS,³² but unfortunately we have no data on epinephrine use in the present study. Our patients received epinephrine following guideline recommendations.¹⁷, ¹⁸, ¹⁹

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5. Conclusion 

Capnography is a useful tool to optimise and individualise ALS in cardiac arrested patients. However, confounding factors including cause of arrest, initial rhythm, bystander CPR and time from cardiac arrest until quantitative capnography had an impact on ETCO₂ values, thereby complicating and limiting prognostic interpretation of capnography during ALS.

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Role of the funding source 

Bård E. Heradstveit is a fellow research of The Regional Centre for Emergency Medical Research and Development (RAKOS, Stavanger/Norway). The RAKOS had no influence on the topic, study design or interpretation of the data.

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Conflict of interest statement 

There are no conflicts of interest.

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Acknowledgements 

The study was supported by a research grant from the Regional Centre for Emergency Medical Research and Development (RAKOS, Stavanger/Norway). MD Ivar Austlid provided supportive information to the registration, and MD Brian Burns made valuable comments to the manuscript.

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http://www.resuscitationjournal.com/article/S0300-9572(12)00116-5/fulltext

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