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Increasing CPR duration prior to first defibrillation does not improve return of spontaneous circulation or survival in a swine model of prolonged ventricular fibrillation
Resuscitation 80 (2009) 382–388
Contents lists available at ScienceDirect
Resuscitation journal homepage: www.elsevier.com/locate/resuscitation
Letters to the Editor Sudhakar Sattur ∗ Karl B. Kern Sarver Heart Center, College of Medicine, University of Arizona, 1501 N Campbell Av., PO Box 245212, Tucson, AZ, 85721, United States
Increasing CPR duration prior to first defibrillation does not improve return of spontaneous circulation or survival in a swine model of prolonged ventricular fibrillation Sir, We read with interest the article by Rittenberger et al.1 evaluating the impact of increasing CPR duration prior to defibrillation on return of spontaneous circulation and survival in a porcine model. We would like to comment on a few aspects of the study. It was surprising to see the low percentages of survival and return of spontaneous circulation in all the groups of the study. Prior studies with even longer periods of ventricular fibrillation and CPR duration prior to defibrillation were associated with better outcomes. Aufderheide et al.2 demonstrated 86 percent survival in a porcine model after 6 min of ventricular fibrillation and follow up CPR with mechanical device at a ventilation rate of 12/min. Ewy et al.3 , in a comparative study of continuous chest compressions to 30:2 compressions to ventilation CPR in prolonged ventricular fibrillation upto 12 min before defibrillation have shown better survival, ROSC and neurological outcomes in the continuous chest compressions group. In the same study, more than fifty percent animals achieved ROSC and survival even in 30:2 compressions to ventilation CPR group. Hayes et al.4 evaluated ventilation scenarios in a swine model, and reported 25–41 percent ROSC and survival after 8 min of uninterrupted ventricular fibrillation followed by 3 cycles of 2 min continuous chest compressions prior to defibrillation. The authors alluded to some possible reasons for the low percentages of ROSC and survival. Certainly the low CPP pressures in all the groups could explain the poor outcomes. Our conclusion is that provision of poor CPR (poor CPP) prior to defibrillation does not improve outcomes. Conflict of interest None. References 1. Rittenberger JC, Suffoletto B, Salcido D, Logue E, Menegazzi JJ. Increasing CPR duration prior to first defibrillation does not improve return of spontaneous circulation or survival in a swine model of prolonged ventricular fibrillation. Resuscitation 2008;79(1, October):155–60 [Epub Jul 11, 2008]. 2. Aufderheide TP, Sigurdsson G, Pirrallo RG, et al. Hyperventilationinduced hypotension during cardiopulmonary resuscitation. Circulation 2004;109:1960–5. 3. Ewy GA, Zuercher M, Hilwig RW, et al. Improved neurological outcome with continuous chest compressions compared with 30:2 compressions-to-ventilations cardiopulmonary resuscitation in a realistic swine model of out-of-hospital cardiac arrest. Circulation 2007;16:2525–30. 4. Hayes MM, Ewy GA, Anavy ND, et al. Continuous passive oxygen insufflation results in a similar outcome to positive pressure ventilation in a swine model of out-of-hospital ventricular fibrillation. Resuscitation 2007;74:357–65.
0300-9572/$ – see front matter © 2008 Elsevier Ireland Ltd. All rights reserved.
∗ Corresponding author. E-mail address: [email protected] (S. Sattur)
4 November 2008 doi:10.1016/j.resuscitation.2008.11.005
Reply to letter: Increasing CPR duration prior to first defibrillation does not improve return of spontaneous circulation or survival in a swine model of prolonged ventricular fibrillation Sir, We appreciate the interest of our esteemed colleagues, Drs. Sattur and Kern, in our work. We believe this model to be realistic, for 8 min of untreated VF is common in North America.1 We demonstrated previously that one reason for the discrepancy between animal and clinical studies might be the difference in drug delivery timing.2,3 Recent studies have altered cardiac arrest protocols to expedite drug administration with excellent results.4 Survival in this study is lower than we have previously reported.5 We believe the discrepancy in outcomes between this study and our prior work is due to the vascular collapse that accompanies prolonged, untreated ventricular fibrillation (VF). Normally, we employ a drug cocktail including vasopressin (40 IU), epinephrine (0.1 mg/kg), propanolol (1.0 mg) and sodium bicarbonate (1.0 mEquiv./kg). In this study drugs were not administered because we intended to simulate first responder treatment with CPR and an AED. We also used a programmable resuscitation device that, at the time, did not allow us to do more than 15 chest compressions before a ventilatory pause. The more frequent interruptions of chest compressions in our study decreased mean CPP per epoch. Importantly, there are several differences between our study and those cited by our colleagues. The work by Aufderheide et al. employed a 6-min VF model.6 Despite the shorter duration of untreated VF, they also noted a progressive diminution of CPP between 8 and 11.5 min in Table 4. It is possible that earlier CPR may delay this vascular collapse. The work by Ewy et al. examined 3, 4, 5, or 6 min of untreated VF and administered drugs to 20 of the 31 swine in the 30:2 CPR group.7 As data on the 11 swine that did not receive drugs are not separately presented, we encourage the reader to consider only the perfusing rhythm after first shock (Table 2) results as comparable to those in this study. Our present rate of ROSC in the 5 min untreated VF group is higher than those reported by Dr. Ewy’s group. Physiologically, our CPP results in the 5 min VF group are similar, strengthening the validity of our model.
Contents lists available at ScienceDirect
Resuscitation journal homepage: www.elsevier.com/locate/resuscitation
Letters to the Editor Sudhakar Sattur ∗ Karl B. Kern Sarver Heart Center, College of Medicine, University of Arizona, 1501 N Campbell Av., PO Box 245212, Tucson, AZ, 85721, United States
Increasing CPR duration prior to first defibrillation does not improve return of spontaneous circulation or survival in a swine model of prolonged ventricular fibrillation Sir, We read with interest the article by Rittenberger et al.1 evaluating the impact of increasing CPR duration prior to defibrillation on return of spontaneous circulation and survival in a porcine model. We would like to comment on a few aspects of the study. It was surprising to see the low percentages of survival and return of spontaneous circulation in all the groups of the study. Prior studies with even longer periods of ventricular fibrillation and CPR duration prior to defibrillation were associated with better outcomes. Aufderheide et al.2 demonstrated 86 percent survival in a porcine model after 6 min of ventricular fibrillation and follow up CPR with mechanical device at a ventilation rate of 12/min. Ewy et al.3 , in a comparative study of continuous chest compressions to 30:2 compressions to ventilation CPR in prolonged ventricular fibrillation upto 12 min before defibrillation have shown better survival, ROSC and neurological outcomes in the continuous chest compressions group. In the same study, more than fifty percent animals achieved ROSC and survival even in 30:2 compressions to ventilation CPR group. Hayes et al.4 evaluated ventilation scenarios in a swine model, and reported 25–41 percent ROSC and survival after 8 min of uninterrupted ventricular fibrillation followed by 3 cycles of 2 min continuous chest compressions prior to defibrillation. The authors alluded to some possible reasons for the low percentages of ROSC and survival. Certainly the low CPP pressures in all the groups could explain the poor outcomes. Our conclusion is that provision of poor CPR (poor CPP) prior to defibrillation does not improve outcomes. Conflict of interest None. References 1. Rittenberger JC, Suffoletto B, Salcido D, Logue E, Menegazzi JJ. Increasing CPR duration prior to first defibrillation does not improve return of spontaneous circulation or survival in a swine model of prolonged ventricular fibrillation. Resuscitation 2008;79(1, October):155–60 [Epub Jul 11, 2008]. 2. Aufderheide TP, Sigurdsson G, Pirrallo RG, et al. Hyperventilationinduced hypotension during cardiopulmonary resuscitation. Circulation 2004;109:1960–5. 3. Ewy GA, Zuercher M, Hilwig RW, et al. Improved neurological outcome with continuous chest compressions compared with 30:2 compressions-to-ventilations cardiopulmonary resuscitation in a realistic swine model of out-of-hospital cardiac arrest. Circulation 2007;16:2525–30. 4. Hayes MM, Ewy GA, Anavy ND, et al. Continuous passive oxygen insufflation results in a similar outcome to positive pressure ventilation in a swine model of out-of-hospital ventricular fibrillation. Resuscitation 2007;74:357–65.
0300-9572/$ – see front matter © 2008 Elsevier Ireland Ltd. All rights reserved.
∗ Corresponding author. E-mail address: [email protected] (S. Sattur)
4 November 2008 doi:10.1016/j.resuscitation.2008.11.005
Reply to letter: Increasing CPR duration prior to first defibrillation does not improve return of spontaneous circulation or survival in a swine model of prolonged ventricular fibrillation Sir, We appreciate the interest of our esteemed colleagues, Drs. Sattur and Kern, in our work. We believe this model to be realistic, for 8 min of untreated VF is common in North America.1 We demonstrated previously that one reason for the discrepancy between animal and clinical studies might be the difference in drug delivery timing.2,3 Recent studies have altered cardiac arrest protocols to expedite drug administration with excellent results.4 Survival in this study is lower than we have previously reported.5 We believe the discrepancy in outcomes between this study and our prior work is due to the vascular collapse that accompanies prolonged, untreated ventricular fibrillation (VF). Normally, we employ a drug cocktail including vasopressin (40 IU), epinephrine (0.1 mg/kg), propanolol (1.0 mg) and sodium bicarbonate (1.0 mEquiv./kg). In this study drugs were not administered because we intended to simulate first responder treatment with CPR and an AED. We also used a programmable resuscitation device that, at the time, did not allow us to do more than 15 chest compressions before a ventilatory pause. The more frequent interruptions of chest compressions in our study decreased mean CPP per epoch. Importantly, there are several differences between our study and those cited by our colleagues. The work by Aufderheide et al. employed a 6-min VF model.6 Despite the shorter duration of untreated VF, they also noted a progressive diminution of CPP between 8 and 11.5 min in Table 4. It is possible that earlier CPR may delay this vascular collapse. The work by Ewy et al. examined 3, 4, 5, or 6 min of untreated VF and administered drugs to 20 of the 31 swine in the 30:2 CPR group.7 As data on the 11 swine that did not receive drugs are not separately presented, we encourage the reader to consider only the perfusing rhythm after first shock (Table 2) results as comparable to those in this study. Our present rate of ROSC in the 5 min untreated VF group is higher than those reported by Dr. Ewy’s group. Physiologically, our CPP results in the 5 min VF group are similar, strengthening the validity of our model.