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Hemodynamic Effect of External Chest Compressions at the Lower End of the Sternum in Cardiac Arrest Patients
The Journal of Emergency Medicine, Vol. 44, No. 3, pp. 691–697, 2013 Copyright Ó 2013 Elsevier Inc. Printed in the USA. All rights reserved 0736-4679/$ - see front matter
http://dx.doi.org/10.1016/j.jemermed.2012.09.026
Brief Reports HEMODYNAMIC EFFECT OF EXTERNAL CHEST COMPRESSIONS AT THE LOWER END OF THE STERNUM IN CARDIAC ARREST PATIENTS Kyoung Chul Cha, MD,* Ho Jung Kim, MD,† Hyung Jin Shin, MD,* Hyun Kim, MD,* Kang Hyun Lee, MD,* and Sung Oh Hwang, MD* *Department of Emergency Medicine, Wonju College of Medicine, Yonsei University, Wonju, Republic of Korea and †Department of Emergency Medicine, University of Soonchunhyang, Bucheon, Republic of Korea Reprint Address: Sung Oh Hwang, MD, Department of Emergency Medicine, Wonju College of Medicine, Yonsei University,162 Ilsandong, Wonju 220-701, Republic of Korea
, Abstract—Background: Little is known about the hemodynamic effects of chest compression at different positions on the sternum during cardiopulmonary resuscitation (CPR). Objectives: This study aimed to test whether external chest compression at the lower end of the sternum as an alternative position (alternative compression) results in superior hemodynamic effects compared to standard external chest compression (standard compression). Methods: We enrolled 17 patients with non-traumatic cardiac arrest who failed to regain spontaneous circulation within 30 min after CPR initiation. Standard compression was begun when cardiac arrest was confirmed. Alternative compression was performed for 2 min if spontaneous circulation was not attained after 30 min of standard CPR. We compared hemodynamics and end-tidal CO2 pressure during the last 2 min of standard compression and during alternative compression. Results: Peak arterial pressure during compression systole (114 ± 51 vs. 95 ± 42 mm Hg, p < 0.001) and end-tidal CO2 pressure (11.0 ± 6.7 vs. 9.6 ± 6.9 mm Hg, p < 0.05) were higher with alternative than standard compression, whereas arterial pressure during compression diastole, peak right atrial pressure, and coronary perfusion pressure did not differ between standard and alternative compression. Conclusions: Compared to standard compression, alternative compression results in a higher peak arterial pressure and end-tidal CO2 pressure, but no change in coronary perfusion pressure. Ó 2013 Elsevier Inc.
, Keywords—cardiopulmonary resuscitation; external chest compressions; cardiac arrest; heart arrest
INTRODUCTION Since its introduction six decades ago, external chest compression (ECC) has become the standard method to provide artificial circulation and, in combination with artificial ventilation, has saved many lives from sudden cardiac arrest (1). Initially, the optimal location for hand placement for ECC was determined using a dog model of cardiac arrest and extrapolated to resuscitating humans (2,3). Although the results derived from dog studies cannot be generalized to humans due to the obvious interspecies differences in chest wall configuration, ECC position and method during cardiopulmonary resuscitation (CPR) remain mostly unchanged since 1960, except for a change in compression rate from 60 to 100 per minute. Despite the lack of scientific evidence in humans for optimal hand location for ECC, the 2010 International Consensus Conference on Cardiopulmonary Resuscitation and Emergency Cardiac Care Science with Treatment Recommendation recommended that the rescuer place his/her hands on the lower half of the victim’s sternum,
RECEIVED: 7 October 2011; FINAL SUBMISSION RECEIVED: 14 May 2012; ACCEPTED: 18 September 2012 691
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in the center of the chest, between the nipples, and depress the sternum at least 5 cm for the adult (4). Blood flow generated by ECC is about one-third of the normal cardiac output, which is insufficient for resuscitating cardiac arrest patients (5–7). Although several approaches to increase blood flow during resuscitation are being studied, whether ECC at the currently recommended position produces the most efficient hemodynamic effect has never been tested in humans. Recent studies analyzing chest computed tomography scans of patients demonstrated that intrathoracic structures just beneath the inter-nipple line include the root of the aorta, the ascending aorta, and the left ventricular outflow tract (8,9). Compressions of the sternum caudal to the current recommended position might produce a more effective hemodynamic effect by compressing the ventricles of the heart. However, no studies have addressed which hand placement location on the sternum would be most effective in generating blood flow during CPR. This study was aimed at comparing the hemodynamic effects of ECC at different compression positions on the sternum during CPR in humans. METHODS Study Setting and Subjects This study was a prospective, clinical trial performed in an Emergency Department (ED) of a university-based tertiary care hospital in Wonju, Republic of Korea. The study was approved by the Institutional Review Board (IRB) with a waiver of informed consent. Verbal instructions were given to the families of the patients. The patient was included in the study if the families of the patient provided a verbal acceptance to the study inclusion. Seventeen consecutive individuals included in this study were patients with non-traumatic cardiac arrest
who failed to gain spontaneous circulation after standard CPR for 30 min, including Advanced Cardiovascular Life Support (ACLS) in the ED. All patients were over 18 years old. Patients who regained spontaneous circulation during the first 30 min of the resuscitation attempt were excluded from the study. According to the Utstein-style definition, a cardiac arrest is presumed to be of cardiac etiology unless it is known or likely to be secondary to a definitive cause such as submersion, drug overdose, asphyxia, exsanguinations, or any other non-cardiac cause as determined by an attending physician (10). CPR CPR was instituted immediately upon arrival of a cardiac arrest patient. CPR was conducted by a team consisting of two doctors, two nurses, and two emergency medical technicians, according to previously defined guidelines (4). External chest compressions were done by emergency medical technicians who were certified by Basic Life Support provider courses and were blinded to the purpose of the study. Standard external chest compressions (standard compression) were performed by rhythmic applications of pressure over the lower half of the sternum in the center of the chest at a rate of 100 times/ min, keeping pace with the click of a metronome. Alternative external chest compressions (alternative compression) were performed by pressing the lower end of the sternum with the center of the heel of a dominant hand placed at the infrasternal notch, which is caudal to the position on the sternum that is currently recommended by the American Heart Association (Figure 1). Alternative compression was performed in the same way as standard compression in terms of the frequency and depth of the compressions. Artificial respiration was given by using a bag valve device at a rate of 10 times per minute. ACLS, including epinephrine administration and defibrillation as indicated, was given during resuscitation. If
Figure 1. Schematic illustrations of compression positions for external chest compressions. A dominant hand is placed over the lower half of the sternum in the center of the chest, between the nipples, for standard compression (A). Alternative compressions are performed by pressing the lower end of the sternum with the center of the heel of a dominant hand placing at the infrasternal notch (B).
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spontaneous circulation was not regained after 30 min of standard CPR, CPR with alternative compression was performed for 2 min. The last 2 min of standard compression and the 2 min of alternative compression during the additional CPR period for the study were performed by a single emergency medical technician. Epinephrine was given every 3 min during standard compression, but not during alternative compression.
catheter was inserted into the femoral artery. Once the catheters were inserted, the right atrial and arterial pressures were measured using a multi-function patient monitor (Solar 8000 Modular Patient Monitor, GE Medical Systems, Milwaukee, WI) and recorded on graph paper. Pressures from the right atrium and the femoral artery as well as end-tidal CO2 pressures were recorded and measured during the last 30 s of standard compression and alternative compression, and determined as the average of measurements during five consecutive cycles between ventilations.
Measurements Once endotracheal intubation was completed, a mainstream CO2 monitor (CAPNOSTAT mainstream CO2 module, GE Medical Systems, Milwaukee, WI) was connected to the endotracheal tube and the end-tidal CO2 pressure was monitored continuously. After the endotracheal intubation was completed and the external chest compressions had begun, a doctor who was not a member of the CPR team introduced a 5-MHz multi-plane transesophageal transducer (Ultramark-9, Advanced Technology Laboratories Inc, Bothell, WA or Sequoia C256 echocardiography system, Acuson Corp, Malvern, PA) into the esophagus. In our department, transesophageal echocardiography is a routine procedure of resuscitation to seek the potential cause of the cardiac arrest, guide the catheter insertion, and verify the position of the catheter. If spontaneous circulation was not regained after 25 min of the resuscitation attempt, catheterizations were performed. The right internal jugular vein was punctured by Seldinger method and a central venous catheter was introduced into the right atrium of the subject. The insertion and positioning of the catheter into the right atrium were done while maintaining transesophageal echocardiography to have the best right atrium-left atrium longitudinal view. In addition, the left or right femoral artery was punctured by the Seldinger method, and a central venous
Data Analysis Coronary perfusion pressures were obtained by calculating the difference between the arterial pressure and the right atrial pressure at the middle of the relaxation period. The arterial pressures, the right atrial pressures, the endtidal CO2 pressures, and the coronary perfusion pressures were collected and analyzed using paired t-tests and SPSS software (version 11.0; SPSS Inc., Chicago, IL). Data were presented as mean 6 SD. Any differences were regarded as significant if p-values were <0.05. RESULTS Characteristics of the Study Subjects The characteristics of 17 non-traumatic cardiac arrest patients are described in Table 1. The average age was 57 6 13 years, and 12 patients were male. In 15 cases, the cardiac arrest occurred outside the hospital, and in 2 cases, the arrest occurred in the ED. Of the patients who had their cardiac arrest outside the hospital, only one case underwent CPR that was started by a bystander. The average length of time from the occurrence of cardiac arrest
Table 1. A Summary of the Enrolled Patients Case No.
Sex/Age (Years)
Location of CA
Collapse-to-ED Arrival Interval (min)
First Monitored Rhythm
Presumed Etiology
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17
M/73 M/60 M/58 M/53 M/66 M/65 F/49 F/80 F/65 M/45 M/31 M/62 M/48 M/43 M/38 F/64 F/63
OH OH OH OH ED OH OH OH OH ED OH OH OH OH OH OH OH
20 30 25 15 1 30 25 16 35 1 30 10 18 10 25 20 30
Asystole Asystole Asystole Asystole Asystole Asystole Asystole Asystole Asystole Asystole Asystole Asystole Asystole Asystole Asystole Asystole Asystole
Cardiac Cardiac Unknown Cardiac Unknown Non-cardiac Cardiac Cardiac Unknown Unknown Unknown Unknown Non-cardiac Cardiac Unknown Unknown Cardiac
CA = cardiac arrest; ED = Emergency Department; OH = out-of-hospital.
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to the start of CPR was 20 6 10 min, and on arrival at the hospital, all of the subjects had a first presenting electrocardiographic rhythm of asystole. The presumed cause of arrest was cardiac in seven cases (41%), non-cardiac in two cases (12%), and unknown in eight cases (47%). None of the cases had restoration of spontaneous circulation after the resuscitation attempt. Hemodynamic Results during CPR Alternative compression raised the peak arterial pressure in 15 cases (88%) (Figure 2). The peak arterial pressure during compression systole and mean arterial pressure were higher during the alternative than the standard compression (peak arterial pressure: 114 6 51 vs. 95 6 42 mm Hg, p < 0.001; mean arterial pressure: 56 6 27 vs. 50 6 23 mm Hg, p = 0.010) (Figure 3). The end-tidal CO2 pressure was higher during alternative than standard compression (11.0 6 6.7 vs. 9.6 6 6.9 mm Hg, p = 0.020). We found no significant difference in the arterial pressure at the end of compression diastole. The right atrial pressures at the end of compression systole and compression diastole during standard compression and alternative compression were not significantly different (77 6 30 vs. 79 6 27 mm Hg, p = 0.703; 13 6 8 vs. 13 6 9 mm Hg, respectively, p = 0.090). Finally, the coronary perfusion pressure was 14 6 14 mm Hg with alternative compression and 16 6 12 mm Hg with standard compression, which was not statistically significant (p = 0.398) (Table 2). DISCUSSION Our study demonstrates that compression of the sternum caudal to the position recommended by the current guidelines produces better hemodynamic effects than standard chest compression in humans. External chest compression
encompasses five determinants for generating artificial circulation, including the hand placement on the sternum, the compression force (depth), the rate of compression, the ratio of compression and relaxation, and the completeness of relaxation. Several reports on the hemodynamic effects of changes in these determinants have been published (11–15). However, the compression position in external chest compressions has never been evaluated in terms of hemodynamic effectiveness since the current CPR method was introduced. To the best of our knowledge, our study is one of few human trials to test the hemodynamic effect of chest compressions at a location other than the standard recommended location. Considering the anatomic configuration of the heart in the thoracic cavity, it is easy to understand that hand placement in standard compression is just above the base of the heart. Accordingly, because the left ventricle is located behind the lower part of the sternum, standard compression might cause the compression of the outflow tracts of the ventricle instead of that of the ventricle itself (16). A higher peak arterial pressure and end-tidal CO2 pressure during alternative compression in our study suggest that alternative compression presumably produces a higher degree of compression of the left ventricle, with consequent increase in arterial pressure during compression systole. Because peak arterial pressure is positively correlated with cerebral perfusion pressure and systemic blood flow, an increase in peak arterial pressure with alternative compression might result in a higher cerebral and systemic perfusion (17,18). Even though the peak arterial pressure was higher with alternative compression, the arterial pressure during diastole and coronary perfusion pressure were not different between the two methods. This might be because the vascular resistance became low as the resuscitation time was prolonged or the hemodynamic effect with alternative compression was not as strong
Figure 2. Pressure tracings during standard compression and alternative compression in a patient. Peak femoral arterial pressure (FAP) during standard compression (A) is about 90 mm Hg. (B) It increases to 150 mm Hg when alternative compressions are performed. Peak right atrial pressure (RAP) and end-tidal carbon dioxide pressure (ETCO2) also increase during alternative compression compared to during standard compression. Units of number in the tracings are mm Hg.
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pressure will be associated with a better hemodynamic effect and clinical outcome. Unmeasured tidal volume during resuscitation might limit an interpretation on the significance of increased end-tidal CO2 pressure. Several alternative CPR techniques have been sought to increase blood flow during resuscitation. Many of the alternative techniques have some disadvantages over standard CPR because they require additional personnel or equipment (22–24). The alternative compression used in this study is a modification of the standard compression method, including a simple shift of the hand position for chest compressions. It can be easily implemented in clinical practice with little training. Figure 3. Peak femoral arterial pressure during standard compression and alternative compression in an individual patient.
as to increase the diastolic pressure. Coronary perfusion pressure, which is a key correlate to restoration of spontaneous circulation, is calculated by subtracting the right atrial pressure from the aortic diastolic pressure (19). It is likely that a substantial increase in cardiac output will be needed to raise the diastolic arterial pressure during resuscitation. Failure to increase the coronary pressure suggests that alternative compression might not generate a substantial increase in cardiac output in this study setting. End-tidal CO2 pressure was measured as an indirect surrogate of cardiac output in this study. Direct measurement of cardiac output is not feasible during CPR. Endtidal CO2 pressure is a reliable indicator of cardiac output and systemic perfusion during CPR (20,21). The result of our study revealed that end-tidal CO2 pressure was significantly higher with alternative compression than with standard compression. Higher end-tidal CO2 pressure indicates that alternative compressions generate higher cardiac output and pulmonary perfusion. However, it is not clear whether this small difference in end-tidal CO2
Limitations Our study has several limitations. The depth of compressions could not be measured due to lack of equipment. Differences in the depth of compressions between the two methods could change the hemodynamic result, which in turn could make the research invalid. Such a difference can take place, particularly if those who perform chest compressions know the purpose of the research. Emergency medical technicians involved in chest compressions were certified Basic Life Support providers and were blinded to this research. Tidal volume could not be measured during CPR, which might affect the result of end-tidal CO2 pressure. However, ventilation with two hands using a 2-L bag was given in a consistent manner by a doctor to reduce the possibility of bias from tidal volume given during resuscitation. Another limitation was that alternative chest compressions were not used from CPR initiation for ethical reasons. The long interval from the onset of cardiac arrest to CPR initiation while transporting the cardiac arrest victim to the ED in Korea and prolonged CPR administration might have influenced (favorably or unfavorably) the hemodynamic effects that were induced by a change in compression position. Another concern resides in the comparison of
Table 2. Hemodynamic Data during Standard Compression and Alternative Compression Pressure (mm Hg)
Standard Compression
Alternative Compression
95% Confidence Interval for the Difference*
p-Value
Peak arterial pressure during compression systole Arterial pressure at the end of compression diastole Mean arterial pressure Right atrial pressure at the end of compression systole Right atrial pressure at the end of compression diastole Coronary perfusion pressure End-tidal CO2 pressure
95 6 42
114 6 51
28.8–9.0
<0.001
28 6 17
28 6 18
3.1 to
50 6 23 77 6 30
56 6 27 79 6 27
10.6 to 1.7 12.9 to 8.9
0.010 0.703
13 6 8
13 6 9
0.9 to
0.1
0.090
16 6 12 9.6 6 6.9
14 6 14 11.0 6 6.7
2.1 to 5.1 2.9–0.3
0.398 0.020
* Alternative compression minus standard compression.
3.6
0.883
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complications between the standard and alternative chest compressions. In our study, we could not examine possible new complications from pressing the lower end of the sternum instead of compressing the lower one-third of the sternum, even though there was no case with a definitive fracture of the xiphoid process on palpation after alternative compression. Thus, we could not distinguish differential complications between alternative and standard compression because the study was conducted only after the patients had 30 min of standard CPR. However, because the sternum is pressed against the epigastric area during alternative compression, the latter would not be expected to be much different from standard compression in terms of complications. Future research is needed to compare complications between compression methods. We did not give epinephrine during alternative compression because our IRB did not allow giving additional epinephrine to the patient who did not respond for 30 min of ACLS in the hospital. This could bias study results in favor of standard compressions, because they had more benefit of epinephrine. Finally, our study includes a small number of subjects, and the clinical effect of hemodynamic changes could not be evaluated due to the study design. Further study is warranted to validate the findings of this exploratory trial. CONCLUSION Compared to standard compression, alternative compression results in a higher peak arterial pressure and endtidal CO2 pressure, but no change in coronary perfusion pressure. Acknowledgment—This work was supported by a research grant (YUWCM 2012-53) from Yonsei University Wonju College of Medicine.
REFERENCES 1. Safar P, Brown TC, Holtey WJ, Wilder RJ. Ventilation and circulation with closed-chest cardiac massage in man. JAMA 1961;176: 574–6. 2. Kouwenhoven WB, Jude JR, Knickerbocker GG. Closed-chest cardiac massage. JAMA 1960;173:1064–7. 3. Jude JR. Personal reminiscences of the origin and history of cardiopulmonary resuscitation (CPR). Am J Cardiol 2003;92:956–63. 4. Berg RA, Hemphill R, Abella BS, et al. Part 5: adult basic life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010;122(18 Suppl 3):S685–705. 5. Fitzgerald KR, Babbs CF, Frissora HA, Davis RW, Silver DI. Cardiac output during cardiopulmonary resuscitation at various compression rates and durations. Am J Physiol 1981;241:H442–8.
6. Klouche K, Weil MH, Sun S, Tang W, Povoas H, Bisera J. Stroke volumes generated by precordial compression during cardiac resuscitation. Crit Care Med 2002;30:2626–31. 7. Voorhees WD, Babbs CF, Tacker WA Jr. Regional blood flow during cardiopulmonary resuscitation in dogs. Crit Care Med 1980;8:134–6. 8. Pickard A, Darby M, Soar J. Radiological assessment of the adult chest: implications for chest compressions. Resuscitation 2006; 71:387–90. 9. Shin J, Rhee JE, Kim K. Is the inter-nipple line the correct hand position for effective chest compression in adult cardiopulmonary resuscitation? Resuscitation 2007;75:305–10. 10. Jacobs I, Nadkarni V, Bahr J, et al. Cardiac arrest and cardiopulmonary resuscitation outcome reports: update and simplification of the Utstein templates for resuscitation registries: a statement for healthcare professionals from a task force of the International Liaison Committee on Resuscitation (American Heart Association, European Resuscitation Council, Australian Resuscitation Council, New Zealand Resuscitation Council, Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation, Resuscitation Councils of Southern Africa). Circulation 2004;110:3385–97. 11. Aufderheide TP, Pirrallo RG, Yannopoulos D, et al. Incomplete chest wall decompression: a clinical evaluation of CPR performance by EMS personnel and assessment of alternative manual chest compression-decompression techniques. Resuscitation 2005; 64:353–62. 12. Handley AJ, Handley JA. The relationship between rate of chest compression and compression: relaxation ratio. Resuscitation 1995;30:237–41. 13. Kern KB, Sanders AB, Raife J, Milander MM, Otto CW, Ewy GA. A study of chest compression rates during cardiopulmonary resuscitation in humans. The importance of rate-directed chest compressions. Arch Intern Med 1992;152:145–9. 14. Ornato JP, Levine RL, Young DS, Racht EM, Garnett AR, Gonzalez ER. The effect of applied chest compression force on systemic arterial pressure and end-tidal carbon dioxide concentration during CPR in human beings. Ann Emerg Med 1989;18:732–7. 15. Yannopoulos D, McKnite S, Aufderheide TP, et al. Effects of incomplete chest wall decompression during cardiopulmonary resuscitation on coronary and cerebral perfusion pressures in a porcine model of cardiac arrest. Resuscitation 2005;64:363–72. 16. Hwang SO, Zhao PG, Choi HJ, et al. Compression of the left ventricular outflow tract during cardiopulmonary resuscitation. Acad Emerg Med 2009;16:928–33. 17. Arai T, Dote K, Tsukahara I, Nitta K, Nagaro T. Cerebral blood flow during conventional, new and open-chest cardio-pulmonary resuscitation in dogs. Resuscitation 1984;12:147–54. 18. White BC, Winegar CD, Jackson RE, et al. Cerebral cortical perfusion during and following resuscitation from cardiac arrest in dogs. Am J Emerg Med 1983;1:128–38. 19. 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. 20. Garnett AR, Ornato JP, Gonzalez ER, Johnson EB. End-tidal carbon dioxide monitoring during cardiopulmonary resuscitation. JAMA 1987;257:512–5. 21. Gudipati CV, Weil MH, Bisera J, Deshmukh HG, Rackow EC. Expired carbon dioxide: a noninvasive monitor of cardiopulmonary resuscitation. Circulation 1988;77:234–9. 22. Babbs CF. Interposed abdominal compression CPR: a comprehensive evidence based review. Resuscitation 2003;59:71–82. 23. Timerman S, Cardoso LF, Ramires JA, Halperin H. Improved hemodynamic performance with a novel chest compression device during treatment of in-hospital cardiac arrest. Resuscitation 2004;61:273–80. 24. Lurie KG, Shultz JJ, Callaham ML, et al. Evaluation of active compression-decompression CPR in victims of out-of-hospital cardiac arrest. JAMA 1994;271:1405–11.
Hemodynamic Effect of Alternative CPR
ARTICLE SUMMARY 1. Why is this topic important? The optimal position for external chest compression, which is one of the most important determinants for generating an effective hemodynamic effect, has never been investigated in humans. 2. What does this study attempt to show? This study aimed to assess hemodynamic effects of chest compression at different positions on the sternum. 3. What are the key findings? This study reveals that chest compressions at the lower end of the sternum produce a higher peak arterial pressure during compression systole compared to standard compressions. 4. How is patient care impacted? Improving the hemodynamic effect by using an optimal position for chest compression can contribute to increasing the survival rate of cardiac arrest patients.
697
http://dx.doi.org/10.1016/j.jemermed.2012.09.026
Brief Reports HEMODYNAMIC EFFECT OF EXTERNAL CHEST COMPRESSIONS AT THE LOWER END OF THE STERNUM IN CARDIAC ARREST PATIENTS Kyoung Chul Cha, MD,* Ho Jung Kim, MD,† Hyung Jin Shin, MD,* Hyun Kim, MD,* Kang Hyun Lee, MD,* and Sung Oh Hwang, MD* *Department of Emergency Medicine, Wonju College of Medicine, Yonsei University, Wonju, Republic of Korea and †Department of Emergency Medicine, University of Soonchunhyang, Bucheon, Republic of Korea Reprint Address: Sung Oh Hwang, MD, Department of Emergency Medicine, Wonju College of Medicine, Yonsei University,162 Ilsandong, Wonju 220-701, Republic of Korea
, Abstract—Background: Little is known about the hemodynamic effects of chest compression at different positions on the sternum during cardiopulmonary resuscitation (CPR). Objectives: This study aimed to test whether external chest compression at the lower end of the sternum as an alternative position (alternative compression) results in superior hemodynamic effects compared to standard external chest compression (standard compression). Methods: We enrolled 17 patients with non-traumatic cardiac arrest who failed to regain spontaneous circulation within 30 min after CPR initiation. Standard compression was begun when cardiac arrest was confirmed. Alternative compression was performed for 2 min if spontaneous circulation was not attained after 30 min of standard CPR. We compared hemodynamics and end-tidal CO2 pressure during the last 2 min of standard compression and during alternative compression. Results: Peak arterial pressure during compression systole (114 ± 51 vs. 95 ± 42 mm Hg, p < 0.001) and end-tidal CO2 pressure (11.0 ± 6.7 vs. 9.6 ± 6.9 mm Hg, p < 0.05) were higher with alternative than standard compression, whereas arterial pressure during compression diastole, peak right atrial pressure, and coronary perfusion pressure did not differ between standard and alternative compression. Conclusions: Compared to standard compression, alternative compression results in a higher peak arterial pressure and end-tidal CO2 pressure, but no change in coronary perfusion pressure. Ó 2013 Elsevier Inc.
, Keywords—cardiopulmonary resuscitation; external chest compressions; cardiac arrest; heart arrest
INTRODUCTION Since its introduction six decades ago, external chest compression (ECC) has become the standard method to provide artificial circulation and, in combination with artificial ventilation, has saved many lives from sudden cardiac arrest (1). Initially, the optimal location for hand placement for ECC was determined using a dog model of cardiac arrest and extrapolated to resuscitating humans (2,3). Although the results derived from dog studies cannot be generalized to humans due to the obvious interspecies differences in chest wall configuration, ECC position and method during cardiopulmonary resuscitation (CPR) remain mostly unchanged since 1960, except for a change in compression rate from 60 to 100 per minute. Despite the lack of scientific evidence in humans for optimal hand location for ECC, the 2010 International Consensus Conference on Cardiopulmonary Resuscitation and Emergency Cardiac Care Science with Treatment Recommendation recommended that the rescuer place his/her hands on the lower half of the victim’s sternum,
RECEIVED: 7 October 2011; FINAL SUBMISSION RECEIVED: 14 May 2012; ACCEPTED: 18 September 2012 691
692
K. C. Cha et al.
in the center of the chest, between the nipples, and depress the sternum at least 5 cm for the adult (4). Blood flow generated by ECC is about one-third of the normal cardiac output, which is insufficient for resuscitating cardiac arrest patients (5–7). Although several approaches to increase blood flow during resuscitation are being studied, whether ECC at the currently recommended position produces the most efficient hemodynamic effect has never been tested in humans. Recent studies analyzing chest computed tomography scans of patients demonstrated that intrathoracic structures just beneath the inter-nipple line include the root of the aorta, the ascending aorta, and the left ventricular outflow tract (8,9). Compressions of the sternum caudal to the current recommended position might produce a more effective hemodynamic effect by compressing the ventricles of the heart. However, no studies have addressed which hand placement location on the sternum would be most effective in generating blood flow during CPR. This study was aimed at comparing the hemodynamic effects of ECC at different compression positions on the sternum during CPR in humans. METHODS Study Setting and Subjects This study was a prospective, clinical trial performed in an Emergency Department (ED) of a university-based tertiary care hospital in Wonju, Republic of Korea. The study was approved by the Institutional Review Board (IRB) with a waiver of informed consent. Verbal instructions were given to the families of the patients. The patient was included in the study if the families of the patient provided a verbal acceptance to the study inclusion. Seventeen consecutive individuals included in this study were patients with non-traumatic cardiac arrest
who failed to gain spontaneous circulation after standard CPR for 30 min, including Advanced Cardiovascular Life Support (ACLS) in the ED. All patients were over 18 years old. Patients who regained spontaneous circulation during the first 30 min of the resuscitation attempt were excluded from the study. According to the Utstein-style definition, a cardiac arrest is presumed to be of cardiac etiology unless it is known or likely to be secondary to a definitive cause such as submersion, drug overdose, asphyxia, exsanguinations, or any other non-cardiac cause as determined by an attending physician (10). CPR CPR was instituted immediately upon arrival of a cardiac arrest patient. CPR was conducted by a team consisting of two doctors, two nurses, and two emergency medical technicians, according to previously defined guidelines (4). External chest compressions were done by emergency medical technicians who were certified by Basic Life Support provider courses and were blinded to the purpose of the study. Standard external chest compressions (standard compression) were performed by rhythmic applications of pressure over the lower half of the sternum in the center of the chest at a rate of 100 times/ min, keeping pace with the click of a metronome. Alternative external chest compressions (alternative compression) were performed by pressing the lower end of the sternum with the center of the heel of a dominant hand placed at the infrasternal notch, which is caudal to the position on the sternum that is currently recommended by the American Heart Association (Figure 1). Alternative compression was performed in the same way as standard compression in terms of the frequency and depth of the compressions. Artificial respiration was given by using a bag valve device at a rate of 10 times per minute. ACLS, including epinephrine administration and defibrillation as indicated, was given during resuscitation. If
Figure 1. Schematic illustrations of compression positions for external chest compressions. A dominant hand is placed over the lower half of the sternum in the center of the chest, between the nipples, for standard compression (A). Alternative compressions are performed by pressing the lower end of the sternum with the center of the heel of a dominant hand placing at the infrasternal notch (B).
Hemodynamic Effect of Alternative CPR
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spontaneous circulation was not regained after 30 min of standard CPR, CPR with alternative compression was performed for 2 min. The last 2 min of standard compression and the 2 min of alternative compression during the additional CPR period for the study were performed by a single emergency medical technician. Epinephrine was given every 3 min during standard compression, but not during alternative compression.
catheter was inserted into the femoral artery. Once the catheters were inserted, the right atrial and arterial pressures were measured using a multi-function patient monitor (Solar 8000 Modular Patient Monitor, GE Medical Systems, Milwaukee, WI) and recorded on graph paper. Pressures from the right atrium and the femoral artery as well as end-tidal CO2 pressures were recorded and measured during the last 30 s of standard compression and alternative compression, and determined as the average of measurements during five consecutive cycles between ventilations.
Measurements Once endotracheal intubation was completed, a mainstream CO2 monitor (CAPNOSTAT mainstream CO2 module, GE Medical Systems, Milwaukee, WI) was connected to the endotracheal tube and the end-tidal CO2 pressure was monitored continuously. After the endotracheal intubation was completed and the external chest compressions had begun, a doctor who was not a member of the CPR team introduced a 5-MHz multi-plane transesophageal transducer (Ultramark-9, Advanced Technology Laboratories Inc, Bothell, WA or Sequoia C256 echocardiography system, Acuson Corp, Malvern, PA) into the esophagus. In our department, transesophageal echocardiography is a routine procedure of resuscitation to seek the potential cause of the cardiac arrest, guide the catheter insertion, and verify the position of the catheter. If spontaneous circulation was not regained after 25 min of the resuscitation attempt, catheterizations were performed. The right internal jugular vein was punctured by Seldinger method and a central venous catheter was introduced into the right atrium of the subject. The insertion and positioning of the catheter into the right atrium were done while maintaining transesophageal echocardiography to have the best right atrium-left atrium longitudinal view. In addition, the left or right femoral artery was punctured by the Seldinger method, and a central venous
Data Analysis Coronary perfusion pressures were obtained by calculating the difference between the arterial pressure and the right atrial pressure at the middle of the relaxation period. The arterial pressures, the right atrial pressures, the endtidal CO2 pressures, and the coronary perfusion pressures were collected and analyzed using paired t-tests and SPSS software (version 11.0; SPSS Inc., Chicago, IL). Data were presented as mean 6 SD. Any differences were regarded as significant if p-values were <0.05. RESULTS Characteristics of the Study Subjects The characteristics of 17 non-traumatic cardiac arrest patients are described in Table 1. The average age was 57 6 13 years, and 12 patients were male. In 15 cases, the cardiac arrest occurred outside the hospital, and in 2 cases, the arrest occurred in the ED. Of the patients who had their cardiac arrest outside the hospital, only one case underwent CPR that was started by a bystander. The average length of time from the occurrence of cardiac arrest
Table 1. A Summary of the Enrolled Patients Case No.
Sex/Age (Years)
Location of CA
Collapse-to-ED Arrival Interval (min)
First Monitored Rhythm
Presumed Etiology
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17
M/73 M/60 M/58 M/53 M/66 M/65 F/49 F/80 F/65 M/45 M/31 M/62 M/48 M/43 M/38 F/64 F/63
OH OH OH OH ED OH OH OH OH ED OH OH OH OH OH OH OH
20 30 25 15 1 30 25 16 35 1 30 10 18 10 25 20 30
Asystole Asystole Asystole Asystole Asystole Asystole Asystole Asystole Asystole Asystole Asystole Asystole Asystole Asystole Asystole Asystole Asystole
Cardiac Cardiac Unknown Cardiac Unknown Non-cardiac Cardiac Cardiac Unknown Unknown Unknown Unknown Non-cardiac Cardiac Unknown Unknown Cardiac
CA = cardiac arrest; ED = Emergency Department; OH = out-of-hospital.
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to the start of CPR was 20 6 10 min, and on arrival at the hospital, all of the subjects had a first presenting electrocardiographic rhythm of asystole. The presumed cause of arrest was cardiac in seven cases (41%), non-cardiac in two cases (12%), and unknown in eight cases (47%). None of the cases had restoration of spontaneous circulation after the resuscitation attempt. Hemodynamic Results during CPR Alternative compression raised the peak arterial pressure in 15 cases (88%) (Figure 2). The peak arterial pressure during compression systole and mean arterial pressure were higher during the alternative than the standard compression (peak arterial pressure: 114 6 51 vs. 95 6 42 mm Hg, p < 0.001; mean arterial pressure: 56 6 27 vs. 50 6 23 mm Hg, p = 0.010) (Figure 3). The end-tidal CO2 pressure was higher during alternative than standard compression (11.0 6 6.7 vs. 9.6 6 6.9 mm Hg, p = 0.020). We found no significant difference in the arterial pressure at the end of compression diastole. The right atrial pressures at the end of compression systole and compression diastole during standard compression and alternative compression were not significantly different (77 6 30 vs. 79 6 27 mm Hg, p = 0.703; 13 6 8 vs. 13 6 9 mm Hg, respectively, p = 0.090). Finally, the coronary perfusion pressure was 14 6 14 mm Hg with alternative compression and 16 6 12 mm Hg with standard compression, which was not statistically significant (p = 0.398) (Table 2). DISCUSSION Our study demonstrates that compression of the sternum caudal to the position recommended by the current guidelines produces better hemodynamic effects than standard chest compression in humans. External chest compression
encompasses five determinants for generating artificial circulation, including the hand placement on the sternum, the compression force (depth), the rate of compression, the ratio of compression and relaxation, and the completeness of relaxation. Several reports on the hemodynamic effects of changes in these determinants have been published (11–15). However, the compression position in external chest compressions has never been evaluated in terms of hemodynamic effectiveness since the current CPR method was introduced. To the best of our knowledge, our study is one of few human trials to test the hemodynamic effect of chest compressions at a location other than the standard recommended location. Considering the anatomic configuration of the heart in the thoracic cavity, it is easy to understand that hand placement in standard compression is just above the base of the heart. Accordingly, because the left ventricle is located behind the lower part of the sternum, standard compression might cause the compression of the outflow tracts of the ventricle instead of that of the ventricle itself (16). A higher peak arterial pressure and end-tidal CO2 pressure during alternative compression in our study suggest that alternative compression presumably produces a higher degree of compression of the left ventricle, with consequent increase in arterial pressure during compression systole. Because peak arterial pressure is positively correlated with cerebral perfusion pressure and systemic blood flow, an increase in peak arterial pressure with alternative compression might result in a higher cerebral and systemic perfusion (17,18). Even though the peak arterial pressure was higher with alternative compression, the arterial pressure during diastole and coronary perfusion pressure were not different between the two methods. This might be because the vascular resistance became low as the resuscitation time was prolonged or the hemodynamic effect with alternative compression was not as strong
Figure 2. Pressure tracings during standard compression and alternative compression in a patient. Peak femoral arterial pressure (FAP) during standard compression (A) is about 90 mm Hg. (B) It increases to 150 mm Hg when alternative compressions are performed. Peak right atrial pressure (RAP) and end-tidal carbon dioxide pressure (ETCO2) also increase during alternative compression compared to during standard compression. Units of number in the tracings are mm Hg.
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pressure will be associated with a better hemodynamic effect and clinical outcome. Unmeasured tidal volume during resuscitation might limit an interpretation on the significance of increased end-tidal CO2 pressure. Several alternative CPR techniques have been sought to increase blood flow during resuscitation. Many of the alternative techniques have some disadvantages over standard CPR because they require additional personnel or equipment (22–24). The alternative compression used in this study is a modification of the standard compression method, including a simple shift of the hand position for chest compressions. It can be easily implemented in clinical practice with little training. Figure 3. Peak femoral arterial pressure during standard compression and alternative compression in an individual patient.
as to increase the diastolic pressure. Coronary perfusion pressure, which is a key correlate to restoration of spontaneous circulation, is calculated by subtracting the right atrial pressure from the aortic diastolic pressure (19). It is likely that a substantial increase in cardiac output will be needed to raise the diastolic arterial pressure during resuscitation. Failure to increase the coronary pressure suggests that alternative compression might not generate a substantial increase in cardiac output in this study setting. End-tidal CO2 pressure was measured as an indirect surrogate of cardiac output in this study. Direct measurement of cardiac output is not feasible during CPR. Endtidal CO2 pressure is a reliable indicator of cardiac output and systemic perfusion during CPR (20,21). The result of our study revealed that end-tidal CO2 pressure was significantly higher with alternative compression than with standard compression. Higher end-tidal CO2 pressure indicates that alternative compressions generate higher cardiac output and pulmonary perfusion. However, it is not clear whether this small difference in end-tidal CO2
Limitations Our study has several limitations. The depth of compressions could not be measured due to lack of equipment. Differences in the depth of compressions between the two methods could change the hemodynamic result, which in turn could make the research invalid. Such a difference can take place, particularly if those who perform chest compressions know the purpose of the research. Emergency medical technicians involved in chest compressions were certified Basic Life Support providers and were blinded to this research. Tidal volume could not be measured during CPR, which might affect the result of end-tidal CO2 pressure. However, ventilation with two hands using a 2-L bag was given in a consistent manner by a doctor to reduce the possibility of bias from tidal volume given during resuscitation. Another limitation was that alternative chest compressions were not used from CPR initiation for ethical reasons. The long interval from the onset of cardiac arrest to CPR initiation while transporting the cardiac arrest victim to the ED in Korea and prolonged CPR administration might have influenced (favorably or unfavorably) the hemodynamic effects that were induced by a change in compression position. Another concern resides in the comparison of
Table 2. Hemodynamic Data during Standard Compression and Alternative Compression Pressure (mm Hg)
Standard Compression
Alternative Compression
95% Confidence Interval for the Difference*
p-Value
Peak arterial pressure during compression systole Arterial pressure at the end of compression diastole Mean arterial pressure Right atrial pressure at the end of compression systole Right atrial pressure at the end of compression diastole Coronary perfusion pressure End-tidal CO2 pressure
95 6 42
114 6 51
28.8–9.0
<0.001
28 6 17
28 6 18
3.1 to
50 6 23 77 6 30
56 6 27 79 6 27
10.6 to 1.7 12.9 to 8.9
0.010 0.703
13 6 8
13 6 9
0.9 to
0.1
0.090
16 6 12 9.6 6 6.9
14 6 14 11.0 6 6.7
2.1 to 5.1 2.9–0.3
0.398 0.020
* Alternative compression minus standard compression.
3.6
0.883
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complications between the standard and alternative chest compressions. In our study, we could not examine possible new complications from pressing the lower end of the sternum instead of compressing the lower one-third of the sternum, even though there was no case with a definitive fracture of the xiphoid process on palpation after alternative compression. Thus, we could not distinguish differential complications between alternative and standard compression because the study was conducted only after the patients had 30 min of standard CPR. However, because the sternum is pressed against the epigastric area during alternative compression, the latter would not be expected to be much different from standard compression in terms of complications. Future research is needed to compare complications between compression methods. We did not give epinephrine during alternative compression because our IRB did not allow giving additional epinephrine to the patient who did not respond for 30 min of ACLS in the hospital. This could bias study results in favor of standard compressions, because they had more benefit of epinephrine. Finally, our study includes a small number of subjects, and the clinical effect of hemodynamic changes could not be evaluated due to the study design. Further study is warranted to validate the findings of this exploratory trial. CONCLUSION Compared to standard compression, alternative compression results in a higher peak arterial pressure and endtidal CO2 pressure, but no change in coronary perfusion pressure. Acknowledgment—This work was supported by a research grant (YUWCM 2012-53) from Yonsei University Wonju College of Medicine.
REFERENCES 1. Safar P, Brown TC, Holtey WJ, Wilder RJ. Ventilation and circulation with closed-chest cardiac massage in man. JAMA 1961;176: 574–6. 2. Kouwenhoven WB, Jude JR, Knickerbocker GG. Closed-chest cardiac massage. JAMA 1960;173:1064–7. 3. Jude JR. Personal reminiscences of the origin and history of cardiopulmonary resuscitation (CPR). Am J Cardiol 2003;92:956–63. 4. Berg RA, Hemphill R, Abella BS, et al. Part 5: adult basic life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010;122(18 Suppl 3):S685–705. 5. Fitzgerald KR, Babbs CF, Frissora HA, Davis RW, Silver DI. Cardiac output during cardiopulmonary resuscitation at various compression rates and durations. Am J Physiol 1981;241:H442–8.
6. Klouche K, Weil MH, Sun S, Tang W, Povoas H, Bisera J. Stroke volumes generated by precordial compression during cardiac resuscitation. Crit Care Med 2002;30:2626–31. 7. Voorhees WD, Babbs CF, Tacker WA Jr. Regional blood flow during cardiopulmonary resuscitation in dogs. Crit Care Med 1980;8:134–6. 8. Pickard A, Darby M, Soar J. Radiological assessment of the adult chest: implications for chest compressions. Resuscitation 2006; 71:387–90. 9. Shin J, Rhee JE, Kim K. Is the inter-nipple line the correct hand position for effective chest compression in adult cardiopulmonary resuscitation? Resuscitation 2007;75:305–10. 10. Jacobs I, Nadkarni V, Bahr J, et al. Cardiac arrest and cardiopulmonary resuscitation outcome reports: update and simplification of the Utstein templates for resuscitation registries: a statement for healthcare professionals from a task force of the International Liaison Committee on Resuscitation (American Heart Association, European Resuscitation Council, Australian Resuscitation Council, New Zealand Resuscitation Council, Heart and Stroke Foundation of Canada, InterAmerican Heart Foundation, Resuscitation Councils of Southern Africa). Circulation 2004;110:3385–97. 11. Aufderheide TP, Pirrallo RG, Yannopoulos D, et al. Incomplete chest wall decompression: a clinical evaluation of CPR performance by EMS personnel and assessment of alternative manual chest compression-decompression techniques. Resuscitation 2005; 64:353–62. 12. Handley AJ, Handley JA. The relationship between rate of chest compression and compression: relaxation ratio. Resuscitation 1995;30:237–41. 13. Kern KB, Sanders AB, Raife J, Milander MM, Otto CW, Ewy GA. A study of chest compression rates during cardiopulmonary resuscitation in humans. The importance of rate-directed chest compressions. Arch Intern Med 1992;152:145–9. 14. Ornato JP, Levine RL, Young DS, Racht EM, Garnett AR, Gonzalez ER. The effect of applied chest compression force on systemic arterial pressure and end-tidal carbon dioxide concentration during CPR in human beings. Ann Emerg Med 1989;18:732–7. 15. Yannopoulos D, McKnite S, Aufderheide TP, et al. Effects of incomplete chest wall decompression during cardiopulmonary resuscitation on coronary and cerebral perfusion pressures in a porcine model of cardiac arrest. Resuscitation 2005;64:363–72. 16. Hwang SO, Zhao PG, Choi HJ, et al. Compression of the left ventricular outflow tract during cardiopulmonary resuscitation. Acad Emerg Med 2009;16:928–33. 17. Arai T, Dote K, Tsukahara I, Nitta K, Nagaro T. Cerebral blood flow during conventional, new and open-chest cardio-pulmonary resuscitation in dogs. Resuscitation 1984;12:147–54. 18. White BC, Winegar CD, Jackson RE, et al. Cerebral cortical perfusion during and following resuscitation from cardiac arrest in dogs. Am J Emerg Med 1983;1:128–38. 19. 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. 20. Garnett AR, Ornato JP, Gonzalez ER, Johnson EB. End-tidal carbon dioxide monitoring during cardiopulmonary resuscitation. JAMA 1987;257:512–5. 21. Gudipati CV, Weil MH, Bisera J, Deshmukh HG, Rackow EC. Expired carbon dioxide: a noninvasive monitor of cardiopulmonary resuscitation. Circulation 1988;77:234–9. 22. Babbs CF. Interposed abdominal compression CPR: a comprehensive evidence based review. Resuscitation 2003;59:71–82. 23. Timerman S, Cardoso LF, Ramires JA, Halperin H. Improved hemodynamic performance with a novel chest compression device during treatment of in-hospital cardiac arrest. Resuscitation 2004;61:273–80. 24. Lurie KG, Shultz JJ, Callaham ML, et al. Evaluation of active compression-decompression CPR in victims of out-of-hospital cardiac arrest. JAMA 1994;271:1405–11.
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ARTICLE SUMMARY 1. Why is this topic important? The optimal position for external chest compression, which is one of the most important determinants for generating an effective hemodynamic effect, has never been investigated in humans. 2. What does this study attempt to show? This study aimed to assess hemodynamic effects of chest compression at different positions on the sternum. 3. What are the key findings? This study reveals that chest compressions at the lower end of the sternum produce a higher peak arterial pressure during compression systole compared to standard compressions. 4. How is patient care impacted? Improving the hemodynamic effect by using an optimal position for chest compression can contribute to increasing the survival rate of cardiac arrest patients.
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