- Email: [email protected]
AS06 Mechanisms involved in post resuscitation myocardial dysfunction in a rat model of cardiac arrest and resuscitation
S2
Abstracts, Resuscitation 2011 – Implementation / Resuscitation 82S1 (2011) S1–S34
survival with favorable neurologic outcome following out-of-hospital cardiac arrest (OOHCA) of cardiac etiology. We hypothesized that ITD+ACD-CPR would also increase survival with good neurologic function from all non-traumatic etiologies compared to standard CPR (S-CPR). Methods: This prospective, randomized trial evaluated adults with OOHCA in seven US study sites. Patients were randomized to ITD+ACD-CPR or S-CPR on a 1:1 proportional basis. CPR was initiated by the first arriving EMS provider. A run-in phase preceded the pivotal phase to assure study logistics were well-coordinated. A pre-planned analysis was conducted on data from all non-traumatic arrest patients with known outcomes, prospectively randomized into the run-in and pivotal phases (combined), on an intention-to-treat basis. The primary endpoint was survival to hospital discharge (HD) with good neurologic function, defined as a modified Rankin Score (MRS) ≤3; and at one year, a Cerebral Performance Category (CPC) score ≤2. Statistical analysis was performed using a 2-sided Fischer’s Exact Test. Results: Both groups had similar clinical profiles, baseline demographics and resuscitative efforts. Survival to HD with MRS ≤3 was achieved in 5.69% (75/1318) in the S-CPR group, and 7.88% (110/1396) in the ITD+ACD-CPR group, p=0.027 [Odds ratio = 1.42 (95% confidence interval = 1.04, 1.95)]. Survival to one year with CPC ≤2 was achieved in 4.71% (61/1296) in the S-CPR group, and 6.38% (86/1349) in the ITD+ACDCPR group, p=0.062 [Odds ratio = 1.38 (95% confidence interval = 0.97, 1.96)]. Conclusion: Compared to S-CPR, ITD+ACD-CPR resulted in a 38.5% increase in survival to hospital discharge with favorable neurologic function (p=0.027), and a 35.4% increase in survival at one year with favorable neurologic function (not significant). These findings support the use of ITD+ACD-CPR for treatment of adults with OOHCA from a variety of non-traumatic etiologies.
diopulmonary resuscitation (CPR), knowledge on the effectiveness of in-hospital CPR is not yet sufficient in Brazil. Methods: This cross-sectional study included, prospectively, 763 patients who presented in-hospital cardiac arrest (CA) from 2007 to 2010, in 17 hospitals (CPR in 575 patientes). Results: Asystole was the CA modality most frequently found (40.7%), followed by pulseless electrical activity (39.3%). Immediate survival (recovery of spontaneous circulation – ROSC up to 24 h) was 48.8%, survival until hospital discharge was 13%, 4.3% in 6 and 3.8% in 12 months. Independent predictors associated with higher immediate survival were: ventricular fibrillation (VF) or ventricular tachycardia (VT) without pulse as the initial rhythm of CA (RR1.31; IC95% 1.10 to 1.55; p=0.002); presence of victim consciousness signs when the emergency staff arrived (RR1.37; IC95% 1.16 to 1.61; p<0.001); use of epinephrine (RR1.61; IC95% 1.32 to 1.98; p<0.001); hypoglycemia as cause of CA (RR1.68; IC95% 1.11 to 2.55; p=0.014). Independent predictors associated with lower immediate survival were: hypotension as cause of CA (RR0.74; IC95% 0.61 to 0.90; p=0.003); sedentary lifestyle (RR0.76; IC95% 0.66 to 0.88; p<0.001) and duration of the CPR. Independent predictors associated with hospital discharge survival were: the emergency team trained in ACLS and/or BLS (HR 3.07; IC 95% 1.39 to 6.78; p=0.006), sinus rhythm after ROSC (HR 1.44; IC 95% 1.26 to 1.75; p=0.002). Conclusion: As independent predictors for immediate survival we identified: VF or VT without pulse as the initial rhythm, presence of signs of awareness of the victim, use of epinephrine, hypoglycemia as cause of PCR. As independent predictors associated survival until discharged: training in ACLS/BLS and the sinus rhythm after ROSC. These findings suggest a national resuscitation profile, providing relevant information, potentially representative of the in-hospital CPR in Brazil.
AS04 Passive leg raising rapidly elevates coronary perfusion pressure in a swine model of prolonged ventricular fibrillation and results in improved neurological outcomes: Preliminary results Vasilios Dragoumanos 1 , Nicoletta Iacovidou 1 , Athanasios Chalkias 1 , Pavlos Lelovas 1 , Apostolos Papalois 2 , Theodoros Xanthos 1 1 2
University of Athens, Athens, Greece Experimental-Research Center “ELPEN” Pharmaceutical Co, Athens, Greece
Objectives: Optimal positioning of cardiac arrest patients during cardiopulmonary resuscitation (CPR) is still questionable. Passive leg raising (PLR) causes a redirection of venous blood from the legs toward the thorax which, in turn, causes an increase in systemic venous return, right ventricular preload, and in the left ventricular end-diastolic volume. The aim of this study was to evaluate whether PLR during CPR in a porcine model of prolonged VF, would improve hemodynamics, ROSC, 24 hour survival and neurological outcome. Methods: Ventricular fibrillation was induced in 20 healthy Landrace/Large White piglets, which were left untreated for 8 minutes before attempted resuscitation with mechanical compressions, ventilation, and electrical defibrillation. Ten animals were randomly assigned into a control group resuscitated with the 2005 European Resuscitation Guidelines (ERC) and 10 animals into PLR group resuscitated with the 2005 ERC guidelines at 45º PLR with the use of a special metalic device. End points were either ROSC or asystole. Results: ROSC was observed in 6 and 9 animals from control and PLR group respectively (p=0.121, HR=0.16 95% CI: 0.01–1.87). Just before the first defibrillation attempt coronary perfusion pressure (CPP) was significantly higher in PLR group (22.8±9.5 vs. 10.6±6.5, p<0.004) but no significant difference was observed afterwards. All animals that achieved ROSC survived for 24 hours. Neurologic alertness score was significantly better in animals treated with PLR (88.8±10.5 vs. 70±20, p=0.032). Conclusions: PLR during cardiopulmonary resuscitation significantly increases CPP the minute before the first defibrillation attempt but has no significant effect afterwards. ROSC or 24 hour survival rate are comparable between groups. However animals in the PRL group exhibited significantly higher neurological scores.
AS05 Cardiac arrest Outcomes Data Evaluation – CODE registry: Brazilian registry of in-hospital cardiopulmonary resuscitation Helio Penna Guimarães 1 , Alvaro Avezum Junior 1 , Mariana Teixeira Carballo 2 , Ligia Nasi Laranjeira 2, José Roberto Zapiello Mendes 1 , Helder Jose de Lima Reis 5 , José Antonio Manetta 6 , Fernanda Gazoni 4 , Otavio Berwanger 2 , Alexandre Biasi Cavalcanti 2 , Renato Delascio Lopes 3
AS06 Mechanisms involved in post resuscitation myocardial dysfunction in a rat model of cardiac arrest and resuscitation Giuseppe Ristagno 1 , Giovanni Li Volti 2 , Francesca Fumagalli 1 , Valeria Sorrenti 2 , Rosa Santangelo 2 , Claudia Di Giacomo 2 , Antonino Gullo 2 1 2
Mario Negri Institute, Milan, Italy University of Catania, Catania, Italy
Myocardial dysfunction is cause of death after return of spontaneous circulation (ROSC). Impairment in myofilament cross-bridge cycling and degradation of cardiac troponins (cTn) accounts for the depressed function. Moreover, reperfusion leads to endothelial dysfunction and inhibition of nitric oxide synthase (NOS) due to oxidative stress. Hypotheses: Post ROSC myocardial dysfunction is associated with plasmatic cTn level and oxidative stress injury. Methods: Ventricular fibrillation was induced in 17 rats and untreated for 6 min. CPR was then performed for additional 6 min prior to defibrillations. Two, 4 and 72 hrs following ROSC, left ventricle ejection fraction (LVEF) was echocardiographically assessed. At sacrifice, plasma was collected for high sensitive-cTnT (hs-cTnT) assessment together with plasmatic asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NOS and thereby NO modulator. Hearts were harvested for lipid hydroxides (LOOH) measurement, markers of oxidative stress. Additional 5 control rats were not subjected to cardiac. Hs-cTnT and ADMA were assessed by ELISA. LOOH were evaluated following oxidation of Fe2+ . Results: LVEF decreased compared to that in controls (p<0.0001) at 2 and 4 hr following ROSC, while was similar 72 hr later. Plasmatic hs-cTnT increased compared to controls, at 2 and 4 hr post ROSC (p<0.01). However, at 72 hr, hs-cTnTs were similar to those in controls. LVEF correlated with hs-cTnT (r2 =0.80, p<0.0001). Similarly to LVEF and hs-cTNT, plasmatic ADMA significantly decreased following ROSC (p<0.05) and was restored 72 hr later. Similarly, myocardial LOOH in heart doubled at 2 and 4 hrs following ROSC, from 0.06 to 0.11 and 0.12 nmol/μg, respectively. LOOH returned to normal at 72 hrs. Conclusions: LVEF was related to circulating hs-cTNT. Plasmatic ADMA and heart LOOH were altered following ROSC, similarly to myocardial dysfunction. Decreases in plasmatic ADMA may reflect adaptative changes aimed to enhance NO release, under the condition of increased oxidative stress.
AS07 The effect of chest compressions and intrathoracic pressure differences on end-tidal CO2 tension in cardiac arrest patients: A pilot study
1
Jan Fierens 1 , Alain F. Kalmar 2 , Koenraad G. Monsieurs 1
2
1
Instituto Dante Pazzanese de Cardiologia, São Paulo - SP, Brazil Hospital do Coração - HCor, São Paulo - SP, Brazil 3 Instituto Brasileiro de Pesquisa Clínica (BCRI), São Paulo - SP, Brazil 4 Hospital São Paulo- Hospital de Ensino da UNIFESP, Disciplina de Clínica Médica, São Paulo - SP, Brazil 5 Hospital de Clínicas Gaspar Viana, Belém - PA, Brazil 6 Hospital Maria Braido, São Caetano do Sul - SP, Brazil Introduction: In spite of the advances and worldwide standardization for car-
Ghent University Hospital, Emergency Department, Ghent, Belgium University Medical Centre Groningen, Anaesthesia Department, Groningen, The Netherlands
2
Introduction: We aimed to quantify the effects of chest compression and intrathoracic pressure parameters on end-tidal carbon dioxide tension (Pet CO2 ) in individual out-of-hospital cardiac arrest (OHCA) patients. Material and Methods: Prospective observational study of 27 OHCA patients.
Abstracts, Resuscitation 2011 – Implementation / Resuscitation 82S1 (2011) S1–S34
survival with favorable neurologic outcome following out-of-hospital cardiac arrest (OOHCA) of cardiac etiology. We hypothesized that ITD+ACD-CPR would also increase survival with good neurologic function from all non-traumatic etiologies compared to standard CPR (S-CPR). Methods: This prospective, randomized trial evaluated adults with OOHCA in seven US study sites. Patients were randomized to ITD+ACD-CPR or S-CPR on a 1:1 proportional basis. CPR was initiated by the first arriving EMS provider. A run-in phase preceded the pivotal phase to assure study logistics were well-coordinated. A pre-planned analysis was conducted on data from all non-traumatic arrest patients with known outcomes, prospectively randomized into the run-in and pivotal phases (combined), on an intention-to-treat basis. The primary endpoint was survival to hospital discharge (HD) with good neurologic function, defined as a modified Rankin Score (MRS) ≤3; and at one year, a Cerebral Performance Category (CPC) score ≤2. Statistical analysis was performed using a 2-sided Fischer’s Exact Test. Results: Both groups had similar clinical profiles, baseline demographics and resuscitative efforts. Survival to HD with MRS ≤3 was achieved in 5.69% (75/1318) in the S-CPR group, and 7.88% (110/1396) in the ITD+ACD-CPR group, p=0.027 [Odds ratio = 1.42 (95% confidence interval = 1.04, 1.95)]. Survival to one year with CPC ≤2 was achieved in 4.71% (61/1296) in the S-CPR group, and 6.38% (86/1349) in the ITD+ACDCPR group, p=0.062 [Odds ratio = 1.38 (95% confidence interval = 0.97, 1.96)]. Conclusion: Compared to S-CPR, ITD+ACD-CPR resulted in a 38.5% increase in survival to hospital discharge with favorable neurologic function (p=0.027), and a 35.4% increase in survival at one year with favorable neurologic function (not significant). These findings support the use of ITD+ACD-CPR for treatment of adults with OOHCA from a variety of non-traumatic etiologies.
diopulmonary resuscitation (CPR), knowledge on the effectiveness of in-hospital CPR is not yet sufficient in Brazil. Methods: This cross-sectional study included, prospectively, 763 patients who presented in-hospital cardiac arrest (CA) from 2007 to 2010, in 17 hospitals (CPR in 575 patientes). Results: Asystole was the CA modality most frequently found (40.7%), followed by pulseless electrical activity (39.3%). Immediate survival (recovery of spontaneous circulation – ROSC up to 24 h) was 48.8%, survival until hospital discharge was 13%, 4.3% in 6 and 3.8% in 12 months. Independent predictors associated with higher immediate survival were: ventricular fibrillation (VF) or ventricular tachycardia (VT) without pulse as the initial rhythm of CA (RR1.31; IC95% 1.10 to 1.55; p=0.002); presence of victim consciousness signs when the emergency staff arrived (RR1.37; IC95% 1.16 to 1.61; p<0.001); use of epinephrine (RR1.61; IC95% 1.32 to 1.98; p<0.001); hypoglycemia as cause of CA (RR1.68; IC95% 1.11 to 2.55; p=0.014). Independent predictors associated with lower immediate survival were: hypotension as cause of CA (RR0.74; IC95% 0.61 to 0.90; p=0.003); sedentary lifestyle (RR0.76; IC95% 0.66 to 0.88; p<0.001) and duration of the CPR. Independent predictors associated with hospital discharge survival were: the emergency team trained in ACLS and/or BLS (HR 3.07; IC 95% 1.39 to 6.78; p=0.006), sinus rhythm after ROSC (HR 1.44; IC 95% 1.26 to 1.75; p=0.002). Conclusion: As independent predictors for immediate survival we identified: VF or VT without pulse as the initial rhythm, presence of signs of awareness of the victim, use of epinephrine, hypoglycemia as cause of PCR. As independent predictors associated survival until discharged: training in ACLS/BLS and the sinus rhythm after ROSC. These findings suggest a national resuscitation profile, providing relevant information, potentially representative of the in-hospital CPR in Brazil.
AS04 Passive leg raising rapidly elevates coronary perfusion pressure in a swine model of prolonged ventricular fibrillation and results in improved neurological outcomes: Preliminary results Vasilios Dragoumanos 1 , Nicoletta Iacovidou 1 , Athanasios Chalkias 1 , Pavlos Lelovas 1 , Apostolos Papalois 2 , Theodoros Xanthos 1 1 2
University of Athens, Athens, Greece Experimental-Research Center “ELPEN” Pharmaceutical Co, Athens, Greece
Objectives: Optimal positioning of cardiac arrest patients during cardiopulmonary resuscitation (CPR) is still questionable. Passive leg raising (PLR) causes a redirection of venous blood from the legs toward the thorax which, in turn, causes an increase in systemic venous return, right ventricular preload, and in the left ventricular end-diastolic volume. The aim of this study was to evaluate whether PLR during CPR in a porcine model of prolonged VF, would improve hemodynamics, ROSC, 24 hour survival and neurological outcome. Methods: Ventricular fibrillation was induced in 20 healthy Landrace/Large White piglets, which were left untreated for 8 minutes before attempted resuscitation with mechanical compressions, ventilation, and electrical defibrillation. Ten animals were randomly assigned into a control group resuscitated with the 2005 European Resuscitation Guidelines (ERC) and 10 animals into PLR group resuscitated with the 2005 ERC guidelines at 45º PLR with the use of a special metalic device. End points were either ROSC or asystole. Results: ROSC was observed in 6 and 9 animals from control and PLR group respectively (p=0.121, HR=0.16 95% CI: 0.01–1.87). Just before the first defibrillation attempt coronary perfusion pressure (CPP) was significantly higher in PLR group (22.8±9.5 vs. 10.6±6.5, p<0.004) but no significant difference was observed afterwards. All animals that achieved ROSC survived for 24 hours. Neurologic alertness score was significantly better in animals treated with PLR (88.8±10.5 vs. 70±20, p=0.032). Conclusions: PLR during cardiopulmonary resuscitation significantly increases CPP the minute before the first defibrillation attempt but has no significant effect afterwards. ROSC or 24 hour survival rate are comparable between groups. However animals in the PRL group exhibited significantly higher neurological scores.
AS05 Cardiac arrest Outcomes Data Evaluation – CODE registry: Brazilian registry of in-hospital cardiopulmonary resuscitation Helio Penna Guimarães 1 , Alvaro Avezum Junior 1 , Mariana Teixeira Carballo 2 , Ligia Nasi Laranjeira 2, José Roberto Zapiello Mendes 1 , Helder Jose de Lima Reis 5 , José Antonio Manetta 6 , Fernanda Gazoni 4 , Otavio Berwanger 2 , Alexandre Biasi Cavalcanti 2 , Renato Delascio Lopes 3
AS06 Mechanisms involved in post resuscitation myocardial dysfunction in a rat model of cardiac arrest and resuscitation Giuseppe Ristagno 1 , Giovanni Li Volti 2 , Francesca Fumagalli 1 , Valeria Sorrenti 2 , Rosa Santangelo 2 , Claudia Di Giacomo 2 , Antonino Gullo 2 1 2
Mario Negri Institute, Milan, Italy University of Catania, Catania, Italy
Myocardial dysfunction is cause of death after return of spontaneous circulation (ROSC). Impairment in myofilament cross-bridge cycling and degradation of cardiac troponins (cTn) accounts for the depressed function. Moreover, reperfusion leads to endothelial dysfunction and inhibition of nitric oxide synthase (NOS) due to oxidative stress. Hypotheses: Post ROSC myocardial dysfunction is associated with plasmatic cTn level and oxidative stress injury. Methods: Ventricular fibrillation was induced in 17 rats and untreated for 6 min. CPR was then performed for additional 6 min prior to defibrillations. Two, 4 and 72 hrs following ROSC, left ventricle ejection fraction (LVEF) was echocardiographically assessed. At sacrifice, plasma was collected for high sensitive-cTnT (hs-cTnT) assessment together with plasmatic asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NOS and thereby NO modulator. Hearts were harvested for lipid hydroxides (LOOH) measurement, markers of oxidative stress. Additional 5 control rats were not subjected to cardiac. Hs-cTnT and ADMA were assessed by ELISA. LOOH were evaluated following oxidation of Fe2+ . Results: LVEF decreased compared to that in controls (p<0.0001) at 2 and 4 hr following ROSC, while was similar 72 hr later. Plasmatic hs-cTnT increased compared to controls, at 2 and 4 hr post ROSC (p<0.01). However, at 72 hr, hs-cTnTs were similar to those in controls. LVEF correlated with hs-cTnT (r2 =0.80, p<0.0001). Similarly to LVEF and hs-cTNT, plasmatic ADMA significantly decreased following ROSC (p<0.05) and was restored 72 hr later. Similarly, myocardial LOOH in heart doubled at 2 and 4 hrs following ROSC, from 0.06 to 0.11 and 0.12 nmol/μg, respectively. LOOH returned to normal at 72 hrs. Conclusions: LVEF was related to circulating hs-cTNT. Plasmatic ADMA and heart LOOH were altered following ROSC, similarly to myocardial dysfunction. Decreases in plasmatic ADMA may reflect adaptative changes aimed to enhance NO release, under the condition of increased oxidative stress.
AS07 The effect of chest compressions and intrathoracic pressure differences on end-tidal CO2 tension in cardiac arrest patients: A pilot study
1
Jan Fierens 1 , Alain F. Kalmar 2 , Koenraad G. Monsieurs 1
2
1
Instituto Dante Pazzanese de Cardiologia, São Paulo - SP, Brazil Hospital do Coração - HCor, São Paulo - SP, Brazil 3 Instituto Brasileiro de Pesquisa Clínica (BCRI), São Paulo - SP, Brazil 4 Hospital São Paulo- Hospital de Ensino da UNIFESP, Disciplina de Clínica Médica, São Paulo - SP, Brazil 5 Hospital de Clínicas Gaspar Viana, Belém - PA, Brazil 6 Hospital Maria Braido, São Caetano do Sul - SP, Brazil Introduction: In spite of the advances and worldwide standardization for car-
Ghent University Hospital, Emergency Department, Ghent, Belgium University Medical Centre Groningen, Anaesthesia Department, Groningen, The Netherlands
2
Introduction: We aimed to quantify the effects of chest compression and intrathoracic pressure parameters on end-tidal carbon dioxide tension (Pet CO2 ) in individual out-of-hospital cardiac arrest (OHCA) patients. Material and Methods: Prospective observational study of 27 OHCA patients.