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Mechanical active compression–decompression cardiopulmonary resuscitation (ACD-CPR) versus manual CPR according to pressure of end tidal carbon dioxide (PETCO2) during CPR in out-of-hospital cardiac arrest (OHCA)
Resuscitation 80 (2009) 1099–1103
Contents lists available at ScienceDirect
Resuscitation journal homepage: www.elsevier.com/locate/resuscitation
Clinical paper
Mechanical active compression–decompression cardiopulmonary resuscitation (ACD-CPR) versus manual CPR according to pressure of end tidal carbon dioxide (PET CO2 ) during CPR in out-of-hospital cardiac arrest (OHCA)夽 C. Axelsson a , T. Karlsson b , Å.B. Axelsson c , J. Herlitz b,∗ a
Göteborg EMS System, Göteborg, Sweden Institute of Medicine, Department of Molecular and Clinical Medicine, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden c Institute of Health and Caring Science, Sahlgrenska Academy at Gothenburg University, Göteborg, Sweden b
a r t i c l e
i n f o
Article history: Received 17 April 2009 Received in revised form 10 July 2009 Accepted 6 August 2009
Keywords: Out-of-hospital cardiac arrest Mechanical compression End tidal carbon dioxide
a b s t r a c t Aim: In animal and human studies, measuring the pressure of end tidal carbon dioxide (PET CO2 ) has been shown to be a practical non-invasive method that correlates well with the pulmonary blood flow and cardiac output (CO) generated during cardiopulmonary resuscitation (CPR). This study aims to compare mechanical active compression–decompression (ACD) CPR with standard CPR according to PET CO2 among patients with out-of-hospital cardiac arrest (OHCA), during CPR and with standardised ventilation. Methods: This prospective, on a cluster level, pseudo-randomised pilot trial took place in the Municipality of Göteborg. During a 2-year period, all patients aged >18 years suffering an out-of-hospital cardiac arrest (OHCA) of presumed cardiac etiology were enrolled. The present analysis included only tracheally intubated patients in whom PET CO2 was measured for 15 min or until the detection of a pulse-giving rhythm. Results: In all, 126 patients participated in the evaluation, 64 patients in the mechanical chest compression group and 62 patients in the control group. The group receiving mechanical ACD-CPR obtained the significantly highest PET CO2 values according to the average (p = 0.04), initial (p = 0.01) and minimum (p = 0.01) values. We found no significant difference according to the maximum value between groups. Conclusion: In this hypothesis generating study mechanical ACD-CPR compared with manual CPR generated the highest initial, minimum and average value of PET CO2 . Whether these data can be repeated and furthermore be associated with an improved outcome after OHCA need to be confirmed in a large prospective randomised trial. © 2009 Elsevier Ireland Ltd. All rights reserved.
1. Introduction Success in the resuscitation of patients with out-of-hospital cardiac arrest (OHCA) is dependent on several factors, such as the patient’s general condition, the character and severity of the insult, the time interval from cardiac arrest (CA) to the start of bystander cardiopulmonary resuscitation (B-CPR), the quality of B-CPR and the subsequent quality of advanced cardiac life support (ACLS). In patients with OHCA, survival with a good neurological outcome is dependent upon the generation of blood flow to the heart and brain during resuscitation.1 A coronary perfusion pressure (CPP) of 15 mmHg, at defibrillation, also appears to be necessary for the return of spontaneous circulation (ROSC).2 Blood flow and CPP
夽 A Spanish translated version of the abstract of this article appears as Appendix in the final online version at doi:10.1016/j.resuscitation.2009.08.006. ∗ Corresponding author. Tel.: +46 31 342 1000. E-mail addresses: [email protected], [email protected] (J. Herlitz). 0300-9572/$ – see front matter © 2009 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.resuscitation.2009.08.006
during cardiac arrest are related to the quality and continuity of chest compressions during CPR.3 The direct measurement of blood flow and CPP requires time-consuming invasive methods that are impossible to perform in the pre-hospital setting. Measuring pressure of end tidal carbon dioxide (PET CO2 ) has in animal and human studies shown to be a practical non-invasive method to detect pulmonary blood flow, in reality cardiac output (CO), generated during CPR and as an almost immediate indicator for return of spontaneous circulation (ROSC). Previous reports have also presented threshold values under which no resuscitation succeeded.4–17 LUCASTM is a gas-driven device performing mechanical active compression–decompression (ACD) CPR. Active decompression increases the naturally occurring negative intrathoracic pressure by physically expanding the chest wall. During manual CPR, incomplete chest wall recoil is a common error, resulting in significantly less blood flow back to the heart.18 A randomised animal study showed significantly higher cardiac output, carotid artery blood flow, PET CO2 levels and CPP with the LUCAS device compared with manual CPR.19 However, in clinical studies of OHCA, mechanical
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chest compressions have not yet shown any improvement in survival rates. This study aimed to compare mechanical ACD-CPR with standard CPR according to PET CO2 , among patients with OHCA, during CPR and with standardised ventilation. 2. Methods 2.1. Design This prospective, on a cluster level, pseudo-randomised pilot study in Göteborg, Sweden, was approved by the local ethical vetting board at Göteborg University, Sweden, on 27 March 2003. During a limited period of about 2 years (22/5/2003 to 25/5/2005), LUCASTM was exchanged between the three advanced life support (ALS) units for approximate 6-month periods. The cluster method is in reality a non-randomised method but since the CA appears unpredictably and was included by the nearest, available ALS unit, this study can be described as pseudo-randomised. In the present analysis, only tracheally intubated patients with OHCA of presumed cardiac etiology were enrolled. The exclusion criteria were age <18 years, trauma, pregnancy, hypothermia, intoxication, hanging and drowning, as the judged etiologies behind OHCA, the return of spontaneous circulation (ROSC) before the arrival of the second tier and other reasons, such as terminal illness. 2.2. Organisation The emergency medical services (EMS) system in Göteborg serves about 450,000 inhabitants in an area of 445 km2 . The ambulances were dispatched according to a two-tier system—i.e. for each call judged to relate to a life-threatening state of health, an ALS unit, if available, and the nearest basic life support (BLS) unit were dispatched simultaneously. The BLS-units were staffed by at least one nurse and the ALS units by a paramedic and a well-trained anaesthesia nurse. In the Göteborg EMS system, three ALS units were available for 24 h every day. All OHCAs were treated according to American Heart Association and European Resuscitation Council guidelines. The criterion for ceasing resuscitation “in the field” is asystole for more than 30 min and this can only be assessed by the nurse in the ALS unit. 2.3. Intervention Before starting the study, 35 ALS personnel (paramedics and anaesthesia nurses) were trained to perform mechanical ACD-CPR and re-trained in manual chest compression. The instructor was an anaesthesia nurse educated as a LUCASTM instructor by Jolife AB. Each training session lasted 3 h and ended with a practical and a theoretical test. To pass the test, the participants had to minimise the hands-off time between manual and mechanical chest compressions to less than 20 s. When adapting the training, they were informed about the importance of minimising hands-off situations and preparing for fatigue by rotating the rescuers during manual CPR. In the intervention group, they were told to attach LUCAS to the patient as soon as possible after arriving and before tracheal intubation. In the upstart of the study we randomised, by drawing lots, which two (of three) ALS units to start include patients to the intervention group. The LUCAS device was subsequently exchanged between the three ALS units for approximate 6-month periods during the 2-year study period. Before every half-year period in which the device was used, the EMS personnel took part in a re-training session lasting 2 h. PET CO2 was measured during CPR, according to a pre-designed protocol and after the patient was tracheally intubated. Standardised ventilation (7 l/min, 100% O2 ) was used and, if PET CO2
exceeded 6 kPa, the ALS personnel were instructed to increase the ventilation to 8 l/min. PET CO2 was continuously measured during at least 15 min of CPR or until ROSC was detected. If ROSC was detected, the ALS personal had to note the exact time they detected a pulse-generating rhythm by pressing the “event button” on the Life Pak 12 (LP 12). One milligram of epinephrine was given every second minute up to 5 mg during the measurement period in both groups. The PET CO2 was measured continuously and automatically recorded twice a minute and for each patient it was categorised as the initial (first obtained value), maximum (highest value), minimum (lowest value) and average value. Since the LUCAS device was applied before intubation, the initial value in the intervention group was recorded during mechanical chest compression. 2.4. Equipment 1. The LUCASTM -device is gas-driven and performs 100 noninterrupted compressions per minute. To run LUCAS, we used compressed air in double tubes that runs LUCAS for approximately 25 min. 2. AmbumaticTM is a volume controlled ventilator with a settable tidal volume from 2 to 12 l/min. The selected tidal volume emanates automatically a breathing frequency. 3. Medtronic “LIFEPAK 12” (LP 12) is equipped with Microstream® Capnography which is a PET CO2 sensor that continuously monitors CO2. The configuration curve and two values of PET CO2 /min are automatically recorded. 2.5. Unit In previous reports, PET CO2 was specified in either mm (millimetre mercury) or kPa (kilo Pascal). This article deals with kPa converted, 1 mmHg = 0.133 kPa.20 2.6. Data collection Data relating to the cardiac arrest cohort were obtained from the Göteborg EMS medical records and computer printouts (PET CO2 ). Data were also collected from the dispatch centre and National Registry for Out-of-hospital Cardiac Arrest in Sweden. Further medical data relating to patients admitted alive to hospital were obtained from hospital records. The end-point in the present analysis was PET CO2 , measured after tracheal intubation, during 15 min of CPR or until the detection of ROSC. Additional major clinical study endpoints, analysed for all enrolled patients, were survival to hospital admission and to hospital discharge. Data were collected according to the Utstein criteria.21 2.7. Statistical methods 2.7.1. Descriptive statistics The distribution of variables is given as means, medians or percentages. 2.7.2. Statistical analysis Comparisons between groups were performed using Fisher’s exact test and the Mann–Whitney U test for dichotomous and continuous variables, respectively. End tidal carbon dioxide values for each patient were defined as follows: average as mean of all values obtained during the first 15 min, initial value as the first PET CO2 value obtained, maximum and minimum value as the highest and lowest value, respectively, obtained during the first 15 min. All p-values are two tailed and considered significant if below 0.05.
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Fig. 1. Flow scheme on recruitment of patients for this study.
3. Results In all, 508 patients who suffered an OHCA and in whom CPR was started were available for inclusion in the trial. Of them, 291 patients fulfilled the inclusion criteria for OHCA with a presumed cardiac etiology (Fig. 1). Among these 291 patients, EtCO2 was not measured in 149 CA patients. The main reasons for drop-out were patients who were not intubated, early ROSC, severe field conditions and unfamiliarity with measuring PET CO2 . One hundred and forty-two patients were included in the survey and in 16 cases the measurement was interrupted for various reasons, such as mucus/aspiration (seven), technical errors (two) and unclear reasons (seven). As a result, 126 patients participated in the evaluation, 64 patients in the mechanical chest compression group and 62 patients in the control group. From now on, these two groups will be compared. Baseline data and mean values of PET CO2 among patients in whom EtCo2 was measured during CPR with either LUCAS or manual chest compressions are given in Table 1. The patients were relatively old (mean age 70 years in both groups) and about one third were women. The vast majority of the CA was witnessed and treated with epinephrine (1 mg every
Fig. 2. Mean EtCO2 values recorded at 30 s intervals for LUCAS and standard CPR arms. Note that the LUCAS device was applied prior to the first reading of EtCO2 .
second minute up to 5 mg). We found no differences between the two groups. About one third of the patients were found in VF/VT. According to outcome we found, in both groups, a very low percentage of patients discharged alive. There was a long time interval from CA to start of CPR and to ROSC in both groups. According to the average, initial and minimum values of PET CO2 there were significantly higher values among patients receiving mechanical ACD-CPR. However, there was no significant difference according to the maximum value of PET CO2 (Table 1 and Fig. 2). 4. Discussion In 1978, Kalenda22 found expired CO2 levels helpful in assessing rescuer fatigue. The replacement of an exhausted rescuer resulted in improvements in PET CO2 levels. He also found that a sudden increase in PET CO2 was a predictor of ROSC. These findings and the fact that a high concentration of PET CO2 is related to a better outcome are described in subsequently published reports.4–17,22–28 The explanation is the correlation between PET CO2 and pulmonary blood flow. However, many factors, such as the alveolar ventilation equation, affect the PET CO2 value during CPR. Therefore standardised ventilation (7 l/min) was used, so that the excretion of CO2 through the lungs was dependent on lung perfusion and related to PET CO2 .12,23 If PET CO2 exceed 6 kPa, the ALS personnel were instructed to increase the ventilation to 8 l/min but this was not necessary in any case. In the present analysis, we aimed to compare two different groups with two different kinds of chest compression. Within the studied population, we found no difference according to baseline data, but, compared with the whole population (n = 508), we found extremely low figures for survival to hospital discharge (3.0% vs. 8.5%) and a very long delay from CA to the start of CPR (6–7 min vs. 3 min).29 These findings are probably due to the inclusion criterion, tracheal intubation. The majority of survivors have already been resuscitated at the time of intubation, mostly by immediate defibrillation; tracheal intubation appears to be associated with prolonged resuscitation and therefore lower survival rates.30 The present analysis resulted in the highest mean values for initial, minimum and average PET CO2 among patients receiving mechanical ACD-CPR. Similar results were found in animal studies
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Table 1 Baseline data and mean values of PET CO2 among patients in whom ETCo2 was measured during CPR with either LUCAS or manual chest compressions. Data is presented as percent, median and mean with (95% CI), , 1 missing. Chest compressions
Manual n = 62
LUCAS n = 64
p-Value
Age, years, mean ± SD
70 ± 13 (67–74)
71 ± 14 (68–75)
0.75
Gender (%) Female
29 (19.1–41.3)
34 (24–46.6)
0.57
Witnessed (%) Bystander CPR (%) Treatment: Adrenalin (%) VF/VT (%)
87 (76.3–93.6) 44 (31.9–55.9) 100 (93–100) 34 (23.3–46.3)
86 (75.2–92.6) 44 (32.3–55.9) 100 (93–100) 31 (21.2–43.4)
1.0 1.0 1.0 0.85
Outcome (%) ROSC Admitted alive Discharged alive
52 (39.5–63.3) 32 (21.9–44.7) 3 (0.2–11.7)
44 (32.3–55.9) 31 (21.2–43.4) 3 (0.3–11.3)
0.47 1.0 1.0
Time from CA to: median, minutes n/na Start CPR, 54/57 ROSC, 28/25 Start measuring EtCO2 , 55/59
6 (2–8) 25 (23–30) 19 (16–20)
7 (4–10) 30 (23–35) 20 (17–22)
0.61 0.18 0.21
No. of measurements, mean ± SD
19.9 ± 8.8 (17.7–22.1)
20.4 ± 8.1 (18.4–22.4)
0.98
Mean values of PET CO2 ± SD Average Initial value Maximum value Minimum value
2.69 ± 1.41 (2.33–3.05) 2.71 ± 1.81 (2.25–3.17) 4.48 ± 2.39 (3.87–5.08) 1.69 ± 1.32 (1.35–2.03)
3.26 ± 1.68 (2.85–3.68) 3.38 ± 1.79 (2.93–3.82) 4.88 ± 2.16 (4.34–5.41) 2.24 ± 1.73 (1.8–2.67)
0.04 0.01 0.23 0.01
a
Number of patients.
conducted by Steen et al.19 . The result was explained by the explosivity of the gas-driven pneumatics that creates an instant increase and decrease (decompression) in pressure, with a 50% duty cycle regarding both time and flow. According to the findings of Rubertsson and Karlsten,31 the present result could indicate a higher cerebral blood flow among patients receiving mechanical ACD-CPR than in the group receiving manual chest compressions. We found no difference in outcome, but, as previously mentioned, we studied a high-risk group with a low chance of survival. The present study started about 20 min after CA and lasted to minute 35 (or to ROSC). In an earlier report from Göteborg,32 we found no difference in survival rates and LUCAS was started a median of 18 min after CA. LUCAS was placed in the second tier, arriving (at the patient’s side) a median of 12 min after CA and at a median of 2 min after the first tear (BLS-unit).32 Gradually and following the training of the EMS staff, we found a reduction in the delay to the start of mechanical compressions from 18 to 15 min. However, if the device arrives with a first tier, the delay will probably be reduced by a few more minutes. However, we do not know whether more rapid application of the LUCAS device will increase survival and if so whether it is possible to reach the vast majority of OHCAs early enough. The present results suggest that mechanical chest compression produces compressions associated with higher PET CO2 than manual compressions which might indicate an improved CO. It is also possible to maintain mechanical chest compressions during transport. Recently, the Swedish OHCA register.33 has reported an increase from 10% to 16% for crewwitnessed CA. We also know that a further 8% occur after ambulance dispatch but prior to the arrival of ambulance staff at the patient’s side (unpublished). It appears that the general public are calling 112 earlier. Among crew-witnessed patients, or patients with an extremely short delay from CA to the arrival of the EMS (at the patient’s side), mechanical chest compressions might give the CA patient a better chance by practising the “load and go” principle, i.e. if immediate resuscitation (defibrillation) fails, start mechanical chest compressions and go for hospital. Successful cases are described in the literature.34–36 A practice of this kind calls for a new pre-hospital treatment algorithm, ethical considerations and
direct co-operation with a responding hospital performing treatment with hypothermia and rescue PCI. During the 2-year study in Göteborg, 49 of 508 CA patients (16%) were crew-witnessed and eight of them survived to hospital discharge. 5. Conclusion Mechanical ACD-CPR resulted in the highest mean of initial, minimum and average value of PET CO2 , which suggests that mechanical ACD-CPR perform compressions with higher cardiac output than manual chest compressions. However, since this was a pilot study our data are hypothesis generating and need to be confirmed in a further study. Furthermore, we need to know whether early treatment with mechanical chest compression can improve survival after OHCA. Conflict of interest statement The authors, hereby certify that we have all seen and approved the paper and that the work has not been, and will not be, published elsewhere. There are no financial or other relations that might pose a conflict of interest. Acknowledgements The authors would like to acknowledge the support of the Laerdal Foundation in Norway, the OLA Foundation, the Heart and Lung Foundation and the Royal and Hvitfeldtska Foundation. References 1. Berg RA, Sanders AB, Kern KB, et al. Adverse hemodynamic effects of interrupting chest compressions for rescue breathing during cardiopulmonary resuscitation for ventricular fibrillation cardiac arrest. Circulation 2001;104: 2465–70. 2. Paradis NA, Martin GB, Rivers EP, et al. Coronary perfusion pressure and the return of spontaneous circulation in human cardiopulmonary resuscitation. JAMA 1990;263:1106–13.
C. Axelsson et al. / Resuscitation 80 (2009) 1099–1103 3. Steen S, Liao Q, Pierre L, Paskevicius A, Sjoberg T. The critical importance of minimal delay between chest compressions and subsequent defibrillation: a haemodynamic explanation. Resuscitation 2003;58:249–58. 4. Ahrens T, Schallom L, Bettorf K, et al. End-tidal carbon dioxide measurements as a prognostic indicator of outcome in cardiac arrest. Am J Crit Care 2001;10:391–8. 5. Deakin CD, Sado DM, Coats TJ, Davies G. Prehospital end-tidal carbon dioxide concentration and outcome in major trauma. J Trauma 2004;57:65–8. 6. Dubin A, Murias G, Estenssoro E, et al. End-tidal CO2 pressure determinants during hemorrhagic shock. Intensive Care Med 2000;26:1619–23. 7. Grmec S, Klemen P. Does the end-tidal carbon dioxide (EtCO2 ) concentration have prognostic value during out-of-hospital cardiac arrest? Eur J Emerg Med 2001;8:263–9. 8. Grmec S, Krizmaric M, Mally S, Kozelj A, Spindler M, Lesnik B. Utstein style analysis of out-of-hospital cardiac arrest—bystander CPR and end expired carbon dioxide. Resuscitation 2007;72:404–14. 9. Jin X, Weil MH, Tang W, et al. End-tidal carbon dioxide as a noninvasive indicator of cardiac index during circulatory shock. Crit Care Med 2000;28:2415–9. 10. Kolar M, Krizmaric M, Klemen P, Grmec S. Partial pressure of end-tidal carbon dioxide successful predicts cardiopulmonary resuscitation in the field: a prospective observational study. Crit Care 2008;12:R115. 11. Pernat A, Weil MH, Sun S, Tang W. Stroke volumes and end-tidal carbon dioxide generated by precordial compression during ventricular fibrillation. Crit Care Med 2003;31:1819–23. 12. Pokorna M, Andrlik M, Necas E. End tidal CO2 monitoring in condition of constant ventilation: a useful guide during advanced cardiac life support. Prague Med Rep 2006;107:317–26. 13. Salen P, O’Connor R, Sierzenski P, et al. Can cardiac sonography and capnography be used independently and in combination to predict resuscitation outcomes? Acad Emerg Med 2001;8:610–5. 14. Sanders AB, Ewy GA, Bragg S, Atlas M, Kern KB. Expired PCO2 as a prognostic indicator of successful resuscitation from cardiac arrest. Ann Emerg Med 1985;14:948–52. 15. Sanders AB, Kern KB, Otto CW, Milander MM, Ewy GA. End-tidal carbon dioxide monitoring during cardiopulmonary resuscitation. A prognostic indicator for survival. JAMA 1989;262:1347–51. 16. Tyburski JG, Collinge JD, Wilson RF, Carlin AM, Albaran RG, Steffes CP. End-tidal CO2 -derived values during emergency trauma surgery correlated with outcome: a prospective study. J Trauma 2002;53:738–43. 17. von Planta M, von Planta I, Weil MH, Bruno S, Bisera J, Rackow EC. End tidal carbon dioxide as an haemodynamic determinant of cardiopulmonary resuscitation in the rat. Cardiovasc Res 1989;23:364–8. 18. Frascone RJ, Bitz D, Lurie K. Combination of active compression decompression cardiopulmonary resuscitation and the inspiratory impedance threshold device: state of the art. Curr Opin Crit Care 2004;10:193–201. 19. Steen S, Liao Q, Pierre L, Paskevicius A, Sjoberg T. Evaluation of LUCAS, a new device for automatic mechanical compression and active decompression resuscitation. Resuscitation 2002;55:285–99.
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20. Wikipedia S. Pascal In; 2008. http://sv.wikipedia.org/wiki/KPa. 21. Nolan J. European Resuscitation Council guidelines for resuscitation 2005. Section 1. Introduction. Resuscitation 2005;67(Suppl. 1):S3–6. 22. Kalenda Z. The capnogram as a guide to the efficacy of cardiac massage. Resuscitation 1978;6:259–63. 23. Falk JL, Rackow EC, Weil MH. End-tidal carbon dioxide concentration during cardiopulmonary resuscitation. N Engl J Med 1988;318:607–11. 24. Garnett AR, Ornato JP, Gonzalez ER, Johnson EB. End-tidal carbon dioxide monitoring during cardiopulmonary resuscitation. JAMA 1987;257:512–5. 25. Kern KB, Sanders AB, Voorhees WD, Babbs CF, Tacker WA, Ewy GA. Changes in expired end-tidal carbon dioxide during cardiopulmonary resuscitation in dogs: a prognostic guide for resuscitation efforts. J Am Coll Cardiol 1989;13: 1184–9. 26. Levine RL, Wayne MA, Miller CC. End-tidal carbon dioxide and outcome of outof-hospital cardiac arrest. N Engl J Med 1997;337:301–6. 27. Morimoto Y, Kemmotsu O, Morimoto Y, Gando S. End-tidal carbon dioxide and resuscitation. Curr Opin Anaesthesiol 1999;12:173–7. 28. Sanders AB, Atlas M, Ewy GA, Kern KB, Bragg S. Expired PCO2 as an index of coronary perfusion pressure. Am J Emerg Med 1985;3:147–9. 29. Axelsson C, Axelsson AB, Svensson L, Herlitz J. Characteristics and outcome among patients suffering from out-of-hospital cardiac arrest with the emphasis on availability for intervention trials. Resuscitation 2007;75:460–8. 30. Holmberg M, Holmberg S, Herlitz J. Low chance of survival among patients requiring adrenaline (epinephrine) or intubation after out-of-hospital cardiac arrest in Sweden. Resuscitation 2002;54:37–45. 31. Rubertsson S, Karlsten R. Increased cortical cerebral blood flow with LUCAS: a new device for mechanical chest compressions compared to standard external compressions during experimental cardiopulmonary resuscitation. Resuscitation 2005;65:357–63. 32. Axelsson C, Nestin J, Svensson L, Axelsson AB, Herlitz J. Clinical consequences of the introduction of mechanical chest compression in the EMS system for treatment of out-of-hospital cardiac arrest—a pilot study. Resuscitation 2006;71:47–55. 33. Herlitz J. Swedish national registry of outside-hospital cardiac arrest. http://www.hlr.nu/index.php?q=node/163. 34. Holmstrom P, Boyd J, Sorsa M, Kuisma M. A case of hypothermic cardiac arrest treated with an external chest compression device (LUCAS) during transport to re-warming. Resuscitation 2005;67:139–41. 35. Vatsgar TT, Ingebrigtsen O, Fjose LO, Wikstrom B, Nilsen JE, Wik L. Cardiac arrest and resuscitation with an automatic mechanical chest compression device (LUCAS) due to anaphylaxis of a woman receiving caesarean section because of pre-eclampsia. Resuscitation 2006;68:155–9. 36. Wik L, Kiil S. Use of an automatic mechanical chest compression device (LUCAS) as a bridge to establishing cardiopulmonary bypass for a patient with hypothermic cardiac arrest. Resuscitation 2005;66:391–4.
Contents lists available at ScienceDirect
Resuscitation journal homepage: www.elsevier.com/locate/resuscitation
Clinical paper
Mechanical active compression–decompression cardiopulmonary resuscitation (ACD-CPR) versus manual CPR according to pressure of end tidal carbon dioxide (PET CO2 ) during CPR in out-of-hospital cardiac arrest (OHCA)夽 C. Axelsson a , T. Karlsson b , Å.B. Axelsson c , J. Herlitz b,∗ a
Göteborg EMS System, Göteborg, Sweden Institute of Medicine, Department of Molecular and Clinical Medicine, Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden c Institute of Health and Caring Science, Sahlgrenska Academy at Gothenburg University, Göteborg, Sweden b
a r t i c l e
i n f o
Article history: Received 17 April 2009 Received in revised form 10 July 2009 Accepted 6 August 2009
Keywords: Out-of-hospital cardiac arrest Mechanical compression End tidal carbon dioxide
a b s t r a c t Aim: In animal and human studies, measuring the pressure of end tidal carbon dioxide (PET CO2 ) has been shown to be a practical non-invasive method that correlates well with the pulmonary blood flow and cardiac output (CO) generated during cardiopulmonary resuscitation (CPR). This study aims to compare mechanical active compression–decompression (ACD) CPR with standard CPR according to PET CO2 among patients with out-of-hospital cardiac arrest (OHCA), during CPR and with standardised ventilation. Methods: This prospective, on a cluster level, pseudo-randomised pilot trial took place in the Municipality of Göteborg. During a 2-year period, all patients aged >18 years suffering an out-of-hospital cardiac arrest (OHCA) of presumed cardiac etiology were enrolled. The present analysis included only tracheally intubated patients in whom PET CO2 was measured for 15 min or until the detection of a pulse-giving rhythm. Results: In all, 126 patients participated in the evaluation, 64 patients in the mechanical chest compression group and 62 patients in the control group. The group receiving mechanical ACD-CPR obtained the significantly highest PET CO2 values according to the average (p = 0.04), initial (p = 0.01) and minimum (p = 0.01) values. We found no significant difference according to the maximum value between groups. Conclusion: In this hypothesis generating study mechanical ACD-CPR compared with manual CPR generated the highest initial, minimum and average value of PET CO2 . Whether these data can be repeated and furthermore be associated with an improved outcome after OHCA need to be confirmed in a large prospective randomised trial. © 2009 Elsevier Ireland Ltd. All rights reserved.
1. Introduction Success in the resuscitation of patients with out-of-hospital cardiac arrest (OHCA) is dependent on several factors, such as the patient’s general condition, the character and severity of the insult, the time interval from cardiac arrest (CA) to the start of bystander cardiopulmonary resuscitation (B-CPR), the quality of B-CPR and the subsequent quality of advanced cardiac life support (ACLS). In patients with OHCA, survival with a good neurological outcome is dependent upon the generation of blood flow to the heart and brain during resuscitation.1 A coronary perfusion pressure (CPP) of 15 mmHg, at defibrillation, also appears to be necessary for the return of spontaneous circulation (ROSC).2 Blood flow and CPP
夽 A Spanish translated version of the abstract of this article appears as Appendix in the final online version at doi:10.1016/j.resuscitation.2009.08.006. ∗ Corresponding author. Tel.: +46 31 342 1000. E-mail addresses: [email protected], [email protected] (J. Herlitz). 0300-9572/$ – see front matter © 2009 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.resuscitation.2009.08.006
during cardiac arrest are related to the quality and continuity of chest compressions during CPR.3 The direct measurement of blood flow and CPP requires time-consuming invasive methods that are impossible to perform in the pre-hospital setting. Measuring pressure of end tidal carbon dioxide (PET CO2 ) has in animal and human studies shown to be a practical non-invasive method to detect pulmonary blood flow, in reality cardiac output (CO), generated during CPR and as an almost immediate indicator for return of spontaneous circulation (ROSC). Previous reports have also presented threshold values under which no resuscitation succeeded.4–17 LUCASTM is a gas-driven device performing mechanical active compression–decompression (ACD) CPR. Active decompression increases the naturally occurring negative intrathoracic pressure by physically expanding the chest wall. During manual CPR, incomplete chest wall recoil is a common error, resulting in significantly less blood flow back to the heart.18 A randomised animal study showed significantly higher cardiac output, carotid artery blood flow, PET CO2 levels and CPP with the LUCAS device compared with manual CPR.19 However, in clinical studies of OHCA, mechanical
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chest compressions have not yet shown any improvement in survival rates. This study aimed to compare mechanical ACD-CPR with standard CPR according to PET CO2 , among patients with OHCA, during CPR and with standardised ventilation. 2. Methods 2.1. Design This prospective, on a cluster level, pseudo-randomised pilot study in Göteborg, Sweden, was approved by the local ethical vetting board at Göteborg University, Sweden, on 27 March 2003. During a limited period of about 2 years (22/5/2003 to 25/5/2005), LUCASTM was exchanged between the three advanced life support (ALS) units for approximate 6-month periods. The cluster method is in reality a non-randomised method but since the CA appears unpredictably and was included by the nearest, available ALS unit, this study can be described as pseudo-randomised. In the present analysis, only tracheally intubated patients with OHCA of presumed cardiac etiology were enrolled. The exclusion criteria were age <18 years, trauma, pregnancy, hypothermia, intoxication, hanging and drowning, as the judged etiologies behind OHCA, the return of spontaneous circulation (ROSC) before the arrival of the second tier and other reasons, such as terminal illness. 2.2. Organisation The emergency medical services (EMS) system in Göteborg serves about 450,000 inhabitants in an area of 445 km2 . The ambulances were dispatched according to a two-tier system—i.e. for each call judged to relate to a life-threatening state of health, an ALS unit, if available, and the nearest basic life support (BLS) unit were dispatched simultaneously. The BLS-units were staffed by at least one nurse and the ALS units by a paramedic and a well-trained anaesthesia nurse. In the Göteborg EMS system, three ALS units were available for 24 h every day. All OHCAs were treated according to American Heart Association and European Resuscitation Council guidelines. The criterion for ceasing resuscitation “in the field” is asystole for more than 30 min and this can only be assessed by the nurse in the ALS unit. 2.3. Intervention Before starting the study, 35 ALS personnel (paramedics and anaesthesia nurses) were trained to perform mechanical ACD-CPR and re-trained in manual chest compression. The instructor was an anaesthesia nurse educated as a LUCASTM instructor by Jolife AB. Each training session lasted 3 h and ended with a practical and a theoretical test. To pass the test, the participants had to minimise the hands-off time between manual and mechanical chest compressions to less than 20 s. When adapting the training, they were informed about the importance of minimising hands-off situations and preparing for fatigue by rotating the rescuers during manual CPR. In the intervention group, they were told to attach LUCAS to the patient as soon as possible after arriving and before tracheal intubation. In the upstart of the study we randomised, by drawing lots, which two (of three) ALS units to start include patients to the intervention group. The LUCAS device was subsequently exchanged between the three ALS units for approximate 6-month periods during the 2-year study period. Before every half-year period in which the device was used, the EMS personnel took part in a re-training session lasting 2 h. PET CO2 was measured during CPR, according to a pre-designed protocol and after the patient was tracheally intubated. Standardised ventilation (7 l/min, 100% O2 ) was used and, if PET CO2
exceeded 6 kPa, the ALS personnel were instructed to increase the ventilation to 8 l/min. PET CO2 was continuously measured during at least 15 min of CPR or until ROSC was detected. If ROSC was detected, the ALS personal had to note the exact time they detected a pulse-generating rhythm by pressing the “event button” on the Life Pak 12 (LP 12). One milligram of epinephrine was given every second minute up to 5 mg during the measurement period in both groups. The PET CO2 was measured continuously and automatically recorded twice a minute and for each patient it was categorised as the initial (first obtained value), maximum (highest value), minimum (lowest value) and average value. Since the LUCAS device was applied before intubation, the initial value in the intervention group was recorded during mechanical chest compression. 2.4. Equipment 1. The LUCASTM -device is gas-driven and performs 100 noninterrupted compressions per minute. To run LUCAS, we used compressed air in double tubes that runs LUCAS for approximately 25 min. 2. AmbumaticTM is a volume controlled ventilator with a settable tidal volume from 2 to 12 l/min. The selected tidal volume emanates automatically a breathing frequency. 3. Medtronic “LIFEPAK 12” (LP 12) is equipped with Microstream® Capnography which is a PET CO2 sensor that continuously monitors CO2. The configuration curve and two values of PET CO2 /min are automatically recorded. 2.5. Unit In previous reports, PET CO2 was specified in either mm (millimetre mercury) or kPa (kilo Pascal). This article deals with kPa converted, 1 mmHg = 0.133 kPa.20 2.6. Data collection Data relating to the cardiac arrest cohort were obtained from the Göteborg EMS medical records and computer printouts (PET CO2 ). Data were also collected from the dispatch centre and National Registry for Out-of-hospital Cardiac Arrest in Sweden. Further medical data relating to patients admitted alive to hospital were obtained from hospital records. The end-point in the present analysis was PET CO2 , measured after tracheal intubation, during 15 min of CPR or until the detection of ROSC. Additional major clinical study endpoints, analysed for all enrolled patients, were survival to hospital admission and to hospital discharge. Data were collected according to the Utstein criteria.21 2.7. Statistical methods 2.7.1. Descriptive statistics The distribution of variables is given as means, medians or percentages. 2.7.2. Statistical analysis Comparisons between groups were performed using Fisher’s exact test and the Mann–Whitney U test for dichotomous and continuous variables, respectively. End tidal carbon dioxide values for each patient were defined as follows: average as mean of all values obtained during the first 15 min, initial value as the first PET CO2 value obtained, maximum and minimum value as the highest and lowest value, respectively, obtained during the first 15 min. All p-values are two tailed and considered significant if below 0.05.
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Fig. 1. Flow scheme on recruitment of patients for this study.
3. Results In all, 508 patients who suffered an OHCA and in whom CPR was started were available for inclusion in the trial. Of them, 291 patients fulfilled the inclusion criteria for OHCA with a presumed cardiac etiology (Fig. 1). Among these 291 patients, EtCO2 was not measured in 149 CA patients. The main reasons for drop-out were patients who were not intubated, early ROSC, severe field conditions and unfamiliarity with measuring PET CO2 . One hundred and forty-two patients were included in the survey and in 16 cases the measurement was interrupted for various reasons, such as mucus/aspiration (seven), technical errors (two) and unclear reasons (seven). As a result, 126 patients participated in the evaluation, 64 patients in the mechanical chest compression group and 62 patients in the control group. From now on, these two groups will be compared. Baseline data and mean values of PET CO2 among patients in whom EtCo2 was measured during CPR with either LUCAS or manual chest compressions are given in Table 1. The patients were relatively old (mean age 70 years in both groups) and about one third were women. The vast majority of the CA was witnessed and treated with epinephrine (1 mg every
Fig. 2. Mean EtCO2 values recorded at 30 s intervals for LUCAS and standard CPR arms. Note that the LUCAS device was applied prior to the first reading of EtCO2 .
second minute up to 5 mg). We found no differences between the two groups. About one third of the patients were found in VF/VT. According to outcome we found, in both groups, a very low percentage of patients discharged alive. There was a long time interval from CA to start of CPR and to ROSC in both groups. According to the average, initial and minimum values of PET CO2 there were significantly higher values among patients receiving mechanical ACD-CPR. However, there was no significant difference according to the maximum value of PET CO2 (Table 1 and Fig. 2). 4. Discussion In 1978, Kalenda22 found expired CO2 levels helpful in assessing rescuer fatigue. The replacement of an exhausted rescuer resulted in improvements in PET CO2 levels. He also found that a sudden increase in PET CO2 was a predictor of ROSC. These findings and the fact that a high concentration of PET CO2 is related to a better outcome are described in subsequently published reports.4–17,22–28 The explanation is the correlation between PET CO2 and pulmonary blood flow. However, many factors, such as the alveolar ventilation equation, affect the PET CO2 value during CPR. Therefore standardised ventilation (7 l/min) was used, so that the excretion of CO2 through the lungs was dependent on lung perfusion and related to PET CO2 .12,23 If PET CO2 exceed 6 kPa, the ALS personnel were instructed to increase the ventilation to 8 l/min but this was not necessary in any case. In the present analysis, we aimed to compare two different groups with two different kinds of chest compression. Within the studied population, we found no difference according to baseline data, but, compared with the whole population (n = 508), we found extremely low figures for survival to hospital discharge (3.0% vs. 8.5%) and a very long delay from CA to the start of CPR (6–7 min vs. 3 min).29 These findings are probably due to the inclusion criterion, tracheal intubation. The majority of survivors have already been resuscitated at the time of intubation, mostly by immediate defibrillation; tracheal intubation appears to be associated with prolonged resuscitation and therefore lower survival rates.30 The present analysis resulted in the highest mean values for initial, minimum and average PET CO2 among patients receiving mechanical ACD-CPR. Similar results were found in animal studies
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Table 1 Baseline data and mean values of PET CO2 among patients in whom ETCo2 was measured during CPR with either LUCAS or manual chest compressions. Data is presented as percent, median and mean with (95% CI), , 1 missing. Chest compressions
Manual n = 62
LUCAS n = 64
p-Value
Age, years, mean ± SD
70 ± 13 (67–74)
71 ± 14 (68–75)
0.75
Gender (%) Female
29 (19.1–41.3)
34 (24–46.6)
0.57
Witnessed (%) Bystander CPR (%) Treatment: Adrenalin (%) VF/VT (%)
87 (76.3–93.6) 44 (31.9–55.9) 100 (93–100) 34 (23.3–46.3)
86 (75.2–92.6) 44 (32.3–55.9) 100 (93–100) 31 (21.2–43.4)
1.0 1.0 1.0 0.85
Outcome (%) ROSC Admitted alive Discharged alive
52 (39.5–63.3) 32 (21.9–44.7) 3 (0.2–11.7)
44 (32.3–55.9) 31 (21.2–43.4) 3 (0.3–11.3)
0.47 1.0 1.0
Time from CA to: median, minutes n/na Start CPR, 54/57 ROSC, 28/25 Start measuring EtCO2 , 55/59
6 (2–8) 25 (23–30) 19 (16–20)
7 (4–10) 30 (23–35) 20 (17–22)
0.61 0.18 0.21
No. of measurements, mean ± SD
19.9 ± 8.8 (17.7–22.1)
20.4 ± 8.1 (18.4–22.4)
0.98
Mean values of PET CO2 ± SD Average Initial value Maximum value Minimum value
2.69 ± 1.41 (2.33–3.05) 2.71 ± 1.81 (2.25–3.17) 4.48 ± 2.39 (3.87–5.08) 1.69 ± 1.32 (1.35–2.03)
3.26 ± 1.68 (2.85–3.68) 3.38 ± 1.79 (2.93–3.82) 4.88 ± 2.16 (4.34–5.41) 2.24 ± 1.73 (1.8–2.67)
0.04 0.01 0.23 0.01
a
Number of patients.
conducted by Steen et al.19 . The result was explained by the explosivity of the gas-driven pneumatics that creates an instant increase and decrease (decompression) in pressure, with a 50% duty cycle regarding both time and flow. According to the findings of Rubertsson and Karlsten,31 the present result could indicate a higher cerebral blood flow among patients receiving mechanical ACD-CPR than in the group receiving manual chest compressions. We found no difference in outcome, but, as previously mentioned, we studied a high-risk group with a low chance of survival. The present study started about 20 min after CA and lasted to minute 35 (or to ROSC). In an earlier report from Göteborg,32 we found no difference in survival rates and LUCAS was started a median of 18 min after CA. LUCAS was placed in the second tier, arriving (at the patient’s side) a median of 12 min after CA and at a median of 2 min after the first tear (BLS-unit).32 Gradually and following the training of the EMS staff, we found a reduction in the delay to the start of mechanical compressions from 18 to 15 min. However, if the device arrives with a first tier, the delay will probably be reduced by a few more minutes. However, we do not know whether more rapid application of the LUCAS device will increase survival and if so whether it is possible to reach the vast majority of OHCAs early enough. The present results suggest that mechanical chest compression produces compressions associated with higher PET CO2 than manual compressions which might indicate an improved CO. It is also possible to maintain mechanical chest compressions during transport. Recently, the Swedish OHCA register.33 has reported an increase from 10% to 16% for crewwitnessed CA. We also know that a further 8% occur after ambulance dispatch but prior to the arrival of ambulance staff at the patient’s side (unpublished). It appears that the general public are calling 112 earlier. Among crew-witnessed patients, or patients with an extremely short delay from CA to the arrival of the EMS (at the patient’s side), mechanical chest compressions might give the CA patient a better chance by practising the “load and go” principle, i.e. if immediate resuscitation (defibrillation) fails, start mechanical chest compressions and go for hospital. Successful cases are described in the literature.34–36 A practice of this kind calls for a new pre-hospital treatment algorithm, ethical considerations and
direct co-operation with a responding hospital performing treatment with hypothermia and rescue PCI. During the 2-year study in Göteborg, 49 of 508 CA patients (16%) were crew-witnessed and eight of them survived to hospital discharge. 5. Conclusion Mechanical ACD-CPR resulted in the highest mean of initial, minimum and average value of PET CO2 , which suggests that mechanical ACD-CPR perform compressions with higher cardiac output than manual chest compressions. However, since this was a pilot study our data are hypothesis generating and need to be confirmed in a further study. Furthermore, we need to know whether early treatment with mechanical chest compression can improve survival after OHCA. Conflict of interest statement The authors, hereby certify that we have all seen and approved the paper and that the work has not been, and will not be, published elsewhere. There are no financial or other relations that might pose a conflict of interest. Acknowledgements The authors would like to acknowledge the support of the Laerdal Foundation in Norway, the OLA Foundation, the Heart and Lung Foundation and the Royal and Hvitfeldtska Foundation. References 1. Berg RA, Sanders AB, Kern KB, et al. Adverse hemodynamic effects of interrupting chest compressions for rescue breathing during cardiopulmonary resuscitation for ventricular fibrillation cardiac arrest. Circulation 2001;104: 2465–70. 2. Paradis NA, Martin GB, Rivers EP, et al. Coronary perfusion pressure and the return of spontaneous circulation in human cardiopulmonary resuscitation. JAMA 1990;263:1106–13.
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