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Background: Annually 15,200 children suffer an in-hospital cardiac arrest (IHCA) in the US. Ventricular fibrillation or pulseless ventricular tachycardia (VF/pVT) is the initial rhythm in 10-15% of these arrests. We sought to evaluate the association of number of shocks and early dose escalation with survival for initial VF/pVT in pediatric IHCA., Methods: Using 2000-2020 data from the American Heart Association's (AHA) Get with the Guidelines®-Resuscitation (GWTG-R) registry, we identified children >48 hours of life and ≤18 years who had an IHCA from initial VF/pVT and received defibrillation., Results: There were 251 subjects (37.7%) who received a single shock and 415 subjects (62.3%) who received multiple shocks. Baseline and cardiac arrest characteristics did not differ between those who received a single shock versus multiple shocks except for duration of arrest and calendar year. The median first shock dose was consistent with AHA dosing recommendations and not different between those who received a single shock versus multiple shocks. Survival was improved for those who received a single shock compared to multiple shocks. However, no difference in survival was noted between those who received 2, 3, or ≥4 shocks. Of those receiving multiple shocks, no difference was observed with early dose escalation., Conclusions: In pediatric IHCA, most patients with initial VF/pVT require more than one shock. No distinctions in patient or pre-arrest characteristics were identified between those who received a single shock versus multiple shocks. Subjects who received a single shock were more likely to survive to hospital discharge even after adjusting for duration of resuscitation., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: ‘Tia Raymond reports she is a paid consultant of New England Research Institutes, Inc., as a member of the adjudication committee for the COMPASS Trial (Comparison of Methods for Pulmonary Blood Flow Augmentation in Neonates: Shunt versus Stent. Dianne Atkins reports she is a paid member of the Data Monitoring Safety Board for the Pediatric Heart Network, a multicenter study funded by NHLBI’., (Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved.)

During paediatric cardiopulmonary resuscitation (CPR), patients may transition between pulseless electrical activity (PEA), asystole, ventricular fibrillation/tachycardia (VF/VT), and return of spontaneous circulation (ROSC). The aim of this study was to quantify the dynamic characteristics of this process., Methods: ECG recordings were collected in patients who received CPR at the Children's Hospital of Philadelphia (CHOP) between 2006 and 2013. Transitions between PEA (including bradycardia with poor perfusion), VF/VT, asystole, and ROSC were quantified by applying a multi-state statistical model with competing risks, and by smoothing the Nelson-Aalen estimator of cumulative hazard., Results: Seventy-four episodes of cardiac arrest were included. Median age of patients was 15 years [IQR 11-17], 50% were female and 62% had a respiratory aetiology of arrest. Presenting cardiac arrest rhythms were PEA (60%), VF/VT (24%) and asystole (16%). A temporary surge of PEA was observed between 10 and 15 min due to a doubling of the transition rate from ROSC to PEA (i.e. 're-arrests'). The prevalence of sustained ROSC reached an asymptotic value of 30% at 20 min. Simulation suggests that doubling the transition rate from PEA to ROSC and halving the relapse rate might increase the prevalence of sustained ROSC to 50%., Conclusion: Children and adolescents who received CPR were prone to re-arrest between 10 and 15 min after start of CPR efforts. If the rate of PEA to ROSC transition could be increased and the rate of re-arrests reduced, the overall survival rate may improve., (Copyright © 2019. Published by Elsevier B.V.)

Background: In-hospital cardiac arrest (IHCA) is a major public health problem with significant mortality. A better understanding of where IHCA occurs in hospitals (intensive care unit [ICU] versus monitored ward [telemetry] versus unmonitored ward) could inform strategies for reducing preventable deaths., Methods and Results: This is a retrospective study of adult IHCA events in the Get with the Guidelines-Resuscitation database from January 2003 to September 2010. Unadjusted analyses were used to characterize patient, arrest, and hospital-level characteristics by hospital location of arrest (ICU versus inpatient ward). IHCA event rates and outcomes were plotted over time by arrest location. Among 85 201 IHCA events at 445 hospitals, 59% (50 514) occurred in the ICU compared to 41% (34 687) on the inpatient wards. Compared to ward patients, ICU patients were younger (64±16 years versus 69±14; P<0.001) and more likely to have a presenting rhythm of ventricular tachycardia/ventricular fibrillation (21% versus 17%; P<0.001). In the ICU, mean event rate/1000 bed-days was 0.337 (±0.215) compared with 0.109 (±0.079) for telemetry wards and 0.134 (±0.098) for unmonitored wards. Of patients with an arrest in the ICU, the adjusted mean survival to discharge was 0.140 (0.037) compared with the unmonitored wards 0.106 (0.037) and telemetry wards 0.193 (0.074). More IHCA events occurred in the ICU compared to the inpatient wards and there was a slight increase in events/1000 patient bed-days in both locations., Conclusions: Survival rates vary based on location of IHCA. Optimizing patient assignment to unmonitored wards versus telemetry wards may contribute to improved survival after IHCA., (© 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.)

Aim: To determine the association between amiodarone and lidocaine and outcomes in children with cardiac arrest with pulseless ventricular tachycardia (pVT) and ventricular fibrillation (VF)., Background: Current AHA guidelines for CPR and emergency cardiovascular care recommend amiodarone for cardiac arrest in children associated with shock refractory pVT/VF, based on a single pediatric study and extrapolation from adult data., Methods: Retrospective cohort study from the Get With the Guidelines-Resuscitation database for in-patient cardiac arrest. Patients<18 years old with pVT/VF cardiac arrest were included. Patients receiving amiodarone or lidocaine prior to arrest or whose initial arrest rhythm was unknown were excluded. Univariate analysis was performed to assess the association between patient and event factors and clinical outcomes. Multivariate analysis was performed to address independent association between lidocaine and amiodarone use and outcomes., Results: Of 889 patients, 171 (19%) received amiodarone, 295 (33%) received lidocaine, and 82 (10%) received both. Return of spontaneous circulation (ROSC) occurred in 484/889 (54%), 24-h survival in 342/874 (39%), and survival to hospital discharge in 194/889 (22%). Lidocaine was associated with improved ROSC (adjusted OR 2.02, 95% CI 1.36-3), and 24-h survival (adjusted OR 1.66, 95% CI 1.11-2.49), but not hospital discharge. Amiodarone use was not associated with ROSC, 24h survival, or survival to discharge., Conclusions: For children with in-hospital pVT/VF, lidocaine use was independently associated with improved ROSC and 24-h survival. Amiodarone use was not associated with superior rates of ROSC, survival at 24h. Neither drug was associated with survival to hospital discharge., (Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.)

Aim: To determine whether the residual weight of a 260 g sternal accelerometer/force feedback device (AFFD) adversely affects hemodynamics during cardiopulmonary resuscitation in a piglet model of ventricular fibrillation cardiac arrest., Methods: After induction of ventricular fibrillation, cardiopulmonary resuscitation was provided to ten piglets (10.8 ± 1.9 kg) for 12 min while maintaining aortic systolic pressure of 80-90 mm Hg during four 3-min periods with or without an AFFD on the chest. Cardiac output and left ventricular myocardial blood flow were determined by neutron-microsphere technique., Results: Using a linear mixed-effect model with residual maximum likelihood estimation to control for changes in cardiopulmonary resuscitation hemodynamics over time, cardiac output and myocardial blood flow did not differ with AFFD versus without AFFD. During the first 6 min, mean (± SEM) cardiac outputs were 0.42 (± 0.05)L/min with AFFD versus 0.31 (± 0.04)L/min without AFFD, and median left ventricular myocardial blood flows were 40.5 (± 7.3)mL/min/100g with AFFD versus 40.4 (± 5.0)mL/min/100g without AFFD. The mean right atrial diastolic pressures and coronary perfusion pressures were also not different (8 ± 0.7 mm Hg versus 8 ± 0.9 mm Hg and 16 ± 2 mm Hg versus 16 ± 2 mm Hg, respectively, during the first 6 min of CPR)., Conclusion: The use of a 260 g accelerometer/force feedback device designed for real-time feedback to the rescuer during resuscitation efforts did not adversely affect cardiac output or left ventricular myocardial blood flow during 12 min of chest compressions in a piglet model of ventricular fibrillation cardiac arrest., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

Background: Vasopressors administered IV late during resuscitation efforts fail to improve survival. Intraosseous (IO) access can provide a route for earlier administration. We hypothesized that IO epinephrine after 1 minute of cardiopulmonary resuscitation (CPR) (an "optimal" IO scenario) after 10 minutes of untreated ventricular fibrillation (VF) cardiac arrest would improve outcome in comparison with either IV epinephrine after 8 minutes of CPR (a "realistic" IV scenario) or placebo controls with no epinephrine., Methods: Thirty swine were randomized to IO epinephrine, IV epinephrine, or placebo. Important outcomes included return of spontaneous circulation (ROSC), 24-hour survival, and 24-hour survival with good neurological outcome (cerebral performance category 1)., Results: ROSC after 10 minutes of untreated VF was uncommon without administration of epinephrine (1 of 10), whereas ROSC was nearly universal with IO epinephrine or delayed IV epinephrine (10 of 10 and 9 of 10, respectively; P = 0.001 for either versus placebo). Twenty-four hour survival was substantially more likely after IO epinephrine than after delayed IV epinephrine (10 of 10 vs. 4 of 10, P = 0.001). None of the placebo group survived at 24 hours. Survival with good neurological outcome was more likely after IO epinephrine than after placebo (6 of 10 vs. 0 of 10, P = 0.011), and only 3 of 10 survived with good neurological outcome in the delayed IV epinephrine group (not significant versus either IO or placebo)., Conclusion: In this swine model of prolonged VF cardiac arrest, epinephrine administration during CPR improved outcomes. In addition, early IO epinephrine improved outcomes in comparison with delayed IV epinephrine.

Background: 'Stone heart' resulting from ischemic contracture of the myocardium, precludes successful resuscitation from ventricular fibrillation (VF). We hypothesized that mild hypothermia might slow the progression to stone heart., Methods: Fourteen swine (27 ± 1 kg) were randomized to normothermia (group I; n=6) or hypothermia groups (group II; n=8). Mild hypothermia (34 ± 2 °C) was induced with ice packs prior to VF induction. The LV and right ventricular (RV) cross-sectional areas were followed by cardiovascular magnetic resonance until the development of stone heart. A commercial 1.5T GE Signa NV-CV/i scanner was used. Complete anatomic coverage of the heart was acquired using a steady-state free precession (SSFP) pulse sequence gated at baseline prior to VF onset. Un-gated SSFP images were obtained serially after VF induction. The ventricular endocardium was manually traced and LV and RV volumes were calculated at each time point., Results: In group I, the LV was dilated compared to baseline at 5 minutes after VF and this remained for 20 minutes. Stone heart, arbitrarily defined as LV volume <1/3 of baseline at the onset of VF, occurred at 29 ± 3 minutes. In group II, there was less early dilation of the LV (p<0.05) and the development of stone heart was delayed to 52 ± 4 minutes after onset of VF (P<0.001)., Conclusions: In this closed-chest swine model of prolonged untreated VF, hypothermia reduced the early LV dilatation and importantly, delayed the onset of stone heart thereby extending a known, morphologic limit of resuscitability., (© 2011 Sorrell et al; licensee BioMed Central Ltd.)

Objective: We have demonstrated that a return of spontaneous circulation in the first 3 mins of resuscitation in swine is predicted by ventricular fibrillation waveform (amplitude spectral area or slope) when untreated ventricular fibrillation duration or presence of acute myocardial infarction is unknown. We hypothesized that in prolonged resuscitation efforts that return of spontaneous circulation immediately after a second or later shock with postshock chest compression is independently predicted by end-tidal CO2, coronary perfusion pressure, and ventricular fibrillation waveform measured before that shock in a swine model of ischemic and nonischemic ventricular fibrillation arrest., Design: Animal intervention study with comparison to a control group., Setting: University animal laboratory., Subjects: Twenty swine., Interventions: Myocardial infarction was induced by steel plug occlusion of the left anterior descending coronary artery. Ventricular fibrillation was untreated for 8 mins in normal swine (n=10) and acute myocardial infarction swine (n=10)., Measurements and Main Results: End-tidal CO2, coronary perfusion pressure, and ventricular fibrillation waveform characteristics of amplitude spectral area and slope were analyzed before second or later shocks. For an amplitude spectral area>35 mV-Hz, the odds ratio for achieving return of spontaneous circulation after that shock was 72 (95% confidence interval, 3.8-1300; p=.004) compared with an amplitude spectral area<28 mV-Hz and with an area under the receiver operator characteristic curve of 0.86. For slope>3.6 mV/s, the odds ratio for achieving return of spontaneous circulation was 36 (95% confidence interval, 2.7-480; p=.007) compared with slope<2.72 mV/s with an area under the curve of 0.86. End-tidal CO2 and coronary perfusion pressure were not predictive of return of spontaneous circulation after a shock, although coronary perfusion pressure was significantly related to both amplitude spectral area (p<.001) and slope (p<.001)., Conclusions: : In prolonged untreated ventricular fibrillation arrest, the waveform characteristics of amplitude spectral area and slope predict the attainment of return of spontaneous circulation with a second or later shock. This has implications for the ideal means to customize the timing of shocks and chest compressions when return of spontaneous circulation is not promptly obtained.

Background: In 2005, the AHA changed the treatment recommendation for shockable rhythms from 3 transthoracic stacked-shocks to a single shock followed by immediate chest compressions. The stacked-shock recommendation was based on low first-shock efficacy of monophasic waveforms and the theoretical decrease in transthoracic impedance (TTI) following each shock. The objective of this study was to characterize TTI following biphasic defibrillation attempts in children ≥ 8 yrs during cardiac arrest to assess whether a stacked-shock approach may be appropriate to improve defibrillation success., Methods: TTI (Ohms (Ω)) was collected via standard anterior-apical defibrillator electrode pads during consecutive in-hospital cardiac arrest biphasic defibrillation attempts in children ≥ 8 yrs. Analytic data points for TTI were: 0.1s pre-shock (baseline); post-shock at 0.1, 0.5, 1.0, 1.5, and 2.0 s. TTI variables analyzed with descriptive summaries/paired t-test. p values < 0.05 considered statistically significant after correction for multiple comparisons., Results: Analysis yielded 13 evaluable shock events during 5 cardiac arrests (mean age 14.3 ± 5 yrs, weight 47.4 ± 7.3 kg) between September 2006 and May 2009. Compared to 0.1s pre-shock baseline values (56.8 ± 23.4 Ω), TTI was significantly lower immediately 0.1s post-shock (55.2 ± 22.2 Ω, p = 0.003). Post-shock mean difference from baseline was 1.6 Ω at 0.1s (p = 0.015), 1.4 Ω at 0.5s (p = 0.019) 1.4 Ω at 1.0 s (p = 0.023), 1.1 Ω at 1.5 s (p = 0.028), and 0.95 Ω at 2.0 s (p = 0.096). Time to recharge our clinical defibrillators to standard biphasic shock dose was 2.80 ± 0.05 s., Conclusions: During cardiac arrests in children ≥ 8 yrs, TTI decreased after biphasic shocks, but the limited magnitude and duration of TTI changes suggest that stacked-shocks would not improve defibrillation success., (Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.)

Background: Continued breathing following ventricular fibrillation has here-to-fore not been described., Methods: We analyzed the spontaneous ventilatory activity during the first several minutes of ventricular fibrillation (VF) in our isoflurane anesthesized swine model of out-of-hospital cardiac arrest. The frequency and type of ventilatory activity was monitored by pneumotachometer and main stream infrared capnometer and analyzed in 61 swine during the first 3 to 6 minutes of untreated VF., Results: During the first minute of VF, the air flow pattern in all 61 swine was similar to those recorded during regular spontaneous breathing during anesthesia and was clearly different from the patterns of gasping. The average rate of continued breathing during the first minute of untreated VF was 10 breaths per minute. During the second minute of untreated VF, spontaneous breathing activity either stopped or became typical of gasping. During minutes 2 to 5 of untreated VF, most animals exhibited very slow spontaneous ventilatory activity with a pattern typical of gasping; and the pattern of gasping was crescendo-decrescendo, as has been previously reported. In the absence of therapy, all ventilatory activity stopped 6 minutes after VF cardiac arrest., Conclusion: In our swine model of VF cardiac arrest, we documented that normal breathing continued for the first minute following cardiac arrest.

Objective: To determine the relationship of electrocardiographic rhythm during cardiac arrest with survival outcomes., Design: Prospective, observational study., Setting: Total of 411 hospitals in the National Registry of Cardiopulmonary Resuscitation., Patients: Total of 51,919 adult patients with pulseless cardiac arrests from April 1999 to July 2005., Measurements and Main Results: Registry data collected included first documented rhythm, patient demographics, pre-event data, event data, and survival and neurologic outcome data. Of 51,919 indexed cardiac arrests, first documented pulseless rhythm was ventricular tachycardia (VT) in 3810 (7%), ventricular fibrillation (VF) in 8718 (17%), pulseless electrical activity (PEA) in 19,262 (37%) and asystole 20,129 (39%). Subsequent VT/VF (that is, VT or VF occurring during resuscitation for PEA or asystole) occurred in 5154 (27%), with first documented rhythm of PEA and 4988 (25%) with asystole. Survival to hospital discharge rate was not different between those with first documented VF and VT (37% each, adjusted odds ratio [OR]) 1.08; 95% confidence interval [CI] 0.95-1.23). Survival to hospital discharge was slightly more likely after PEA than asystole (12% vs. 11%, adjusted OR 1.1; 95% CI 1.00-1.18), Survival to discharge was substantially more likely after first documented VT/VF than PEA/asystole (adjusted OR 1.68; 95% CI 1.55-1.82). Survival to discharge was also more likely after PEA/asystole without subsequent VT/VF compared with PEA/asystole with subsequent VT/VF (14% vs. 7% for PEA without vs. with subsequent VT/VF; 12% vs. 8% for asystole without vs. with subsequent VT/VF; adjusted OR 1.60; 95% CI, 1.44-1.80)., Conclusions: Survival to hospital discharge was substantially more likely when the first documented rhythm was shockable rather than nonshockable, and slightly more likely after PEA than asystole. Survival to hospital discharge was less likely following PEA/asystole with subsequent VT/VF compared to PEA/asystole without subsequent VT/VF.

Introduction: Factors that affect resuscitation to a perfusing rhythm (ROSC) following ventricular fibrillation (VF) include untreated VF duration, acute myocardial infarction (AMI), and possibly factors reflected in the VF waveform. We hypothesized that resuscitation of VF to ROSC within 3min is predicted by the VF waveform, independent of untreated VF duration or presence of acute MI., Methods: AMI was induced by the occlusion of the left anterior descending coronary artery. VF was induced in normal (N=30) and AMI swine (N=30). Animals were resuscitated after untreated VF of brief (2min) or prolonged (8min) duration. VF waveform was analyzed before the first shock to compute the amplitude-spectral area (AMSA) and slope., Results: Unadjusted predictors of ROSC within 3min included untreated VF duration (8min vs 2min; OR 0.11, 95%CI 0.02-0.54), AMI (AMI vs normal; OR 0.11, 95%CI 0.02-0.54), AMSA (highest to lowest tertile; OR 15.5, 95%CI 1.7-140), and slope (highest to lowest tertile; OR 12.7, 95%CI 1.4-114). On multivariate regression, untreated VF duration (P=0.011) and AMI (P=0.003) predicted ROSC within 3min. Among secondary outcome variables, favorable neurological status at 24h was only predicted by VF duration (OR 0.22, 95% CI 0.05-0.92)., Conclusions: In this swine model of VF, untreated VF duration and AMI were independent predictors of ROSC following VF cardiac arrest. AMSA and slope predicted ROSC when VF duration or the presence of AMI were unknown. Importantly, the initial treatment of choice for short duration VF is defibrillation regardless of VF waveform.

Background: Some clinical studies have suggested that chest compressions before defibrillation improve survival in cardiac arrest because of prolonged ventricular fibrillation (VF; ie, within the circulatory phase). Animal data have also supported this conclusion, and we have previously demonstrated that preshock chest compressions increase the VF median frequency and improve the likelihood of a return of spontaneous circulation in normal swine. We hypothesized that chest compressions before defibrillation in a swine model of acute myocardial ischemia would also increase VF median frequency and improve resuscitation outcome., Methods and Results: Twenty-six swine were subjected to balloon occlusion of the left anterior descending coronary artery for 2 hours. The balloon was removed and VF was induced and untreated for 8 minutes. Swine were then treated with up to 3 stacked defibrillation shocks (n=13, shock-first group) or 3 minutes of chest compressions before shock (n=13, preshock cardiopulmonary resuscitation group). In the preshock cardiopulmonary resuscitation group, median frequency was increased from 7.0+/-0.8 to 13.9+/-1.6 Hz after chest compressions (P=0.002). Despite the improved median frequency in the preshock cardiopulmonary resuscitation group, 24-hour survival with favorable neurological status was significantly worse in the preshock cardiopulmonary resuscitation group (1/13) compared with the shock-first group (8/13, P=0.01)., Conclusions: In a swine model of prolonged VF in acute myocardial ischemia, 24-hour survival with favorable neurological status was more likely when defibrillation was performed first without preceding chest compressions. Myocardial substrate is an important factor in determining the optimal resuscitation strategy.

Objective: The etiology of postresuscitation myocardial stunning is unknown but is thought to be related to either ischemia occurring during cardiac arrest and resuscitation efforts and/or reperfusion injury after restoration of circulation. A potential common pathway for postischemia/reperfusion end-organ dysfunction is microvascular injury. We hypothesized that myocardial microcirculatory function is markedly abnormal in the postresuscitation period., Design: In vivo study of myocardial microvascular function., Setting: University animal laboratory., Subjects: Five swine (25 +/- 2 kg)., Interventions: Measurements before and after cardiac arrest and resuscitation., Measurements and Main Results: Baseline data were not different among the five subjects. Left ventricular ejection fraction was significantly lower at all postresuscitation time periods (p < .05), reaching a nadir of 19% at 1 hr postresuscitation. Cardiac output declined following fibrillation and resuscitation and was significantly lower than baseline at 1 and 4 hrs postresuscitation (p < .05). Prearrest coronary flow reserve, a ratio of normal to maximal intracoronary flow velocity, was 3.4 ("normal" ratio is 2:4), but was below normal (<2) throughout the 4-hr post resuscitation period (p < .05)., Conclusion: This in vivo study showed that normal myocardial microcirculatory function is quickly lost after prolonged ventricular fibrillation and resuscitation. As early as 30 min postresuscitation the myocardial microcirculatory function is less than 50% of its prearrest baseline level. This dysfunction persists for at least 4 hrs. During the postresuscitation period, both left ventricular ejection fraction and cardiac output decline from their prearrest levels. No cause and effect relationship was proven, but a parallel decline in left ventricular function and coronary flow reserve is evident.

Objective: The optimal biphasic defibrillation dose for children is unknown. Postresuscitation myocardial dysfunction is common and may be worsened by higher defibrillation doses. Adult-dose automated external defibrillators are commonly available; pediatric doses can be delivered by attenuating the adult defibrillation dose through a pediatric pads/cable system. The objective was to investigate whether unattenuated (adult) dose biphasic defibrillation results in greater postresuscitation myocardial dysfunction and damage than attenuated (pediatric) defibrillation., Design: Laboratory animal experiment., Setting: University animal laboratory., Subjects: Domestic swine weighing 19 +/- 3.6 kg., Interventions: Fifty-two piglets were randomized to receive biphasic defibrillation using either adult-dose shocks of 200, 300, and 360 J or pediatric-dose shocks of approximately 50, 75, and 85 J after 7 mins of untreated ventricular fibrillation. Contrast left ventriculograms were obtained at baseline and then at 1, 2, 3, and 4 hrs postresuscitation. Postresuscitation left ventricular ejection fraction and cardiac troponins were evaluated., Measurements and Main Results: By design, piglets in the adult-dose group received shocks with more energy (261 +/- 65 J vs. 72 +/- 12 J, p < .001) and higher peak current (37 +/- 8 A vs. 13 +/- 2 A, p < .001) at the largest defibrillation dose needed. In both groups, left ventricular ejection fraction was reduced significantly at 1, 2, and 4 hrs from baseline and improved during the 4 hrs postresuscitation. The decrease in left ventricular ejection fraction from baseline was greater after adult-dose defibrillation. Plasma cardiac troponin levels were elevated 4 hrs postresuscitation in 11 of 19 adult-dose piglets vs. four of 20 pediatric-dose piglets (p = .02)., Conclusions: Unattenuated adult-dose defibrillation results in a greater frequency of myocardial damage and worse postresuscitation myocardial function than pediatric doses in a swine model of prolonged out-of-hospital pediatric ventricular fibrillation cardiac arrest. These data support the use of pediatric attenuating electrodes with adult biphasic automated external defibrillators to defibrillate children.

Introduction: In cardiac arrest due to prolonged ventricular fibrillation (VF), defibrillation is more likely to result in a perfusing rhythm if chest compressions are performed first. Furthermore, the VF waveform can predict the shockability of VF and thus automated external defibrillators (AEDs) are being designed to analyze the VF waveform to direct therapies. However, it is unknown whether the VF waveform is dependent on recording direction, which could be altered by incorrect placement of AED patches., Materials and Methods: VF was induced in 26 patients with ischemic cardiomyopathy and 19 patients with dilated cardiomyopathy and recorded in six limb leads. Frequency characteristics (mean, median, dominant frequency, and bandwidth) were computed as well as amplitude-based measures: amplitude spectral area (AMSA), slope, signal amplitude, and slope divide by signal amplitude (slope-amp)., Results: Frequency characteristics were similar in all leads. However, AMSA, slope, and signal amplitude were significantly affected (P<0.001) by lead. In particular, for ischemic cardiomyopathy patients, between leads I and II, AMSA varied from 29.4+/-3.2 to 49.3+/-4.6 mV Hz (mean+/-SEM, P<0.001) and slope varied from 1.5+/-0.2 to 2.4+/-0.3 mV/s (P<0.001). Slope-amp was similar in all leads. There were no significant differences between ischemic and dilated cardiomyopathy patients., Conclusions: Amplitude measures of VF are significantly affected by limb lead ECG recording direction. This work suggests that AED patches must be correctly and consistently placed if amplitude-based measures are used to decide whether to deliver a defibrillatory shock.

Objective: In cardiac arrest resulting from ventricular fibrillation, the ventricular fibrillation waveform may be a clue to its duration and predict the likelihood of shock success. However, ventricular fibrillation occurs in different myocardial substrates such as ischemia, heart failure, and structurally normal hearts. We hypothesized that ventricular fibrillation is altered by myocardial infarction and varies from the acute to postmyocardial infarction periods., Design: An animal intervention study was conducted with comparison to a control group., Setting: This study took place in a university animal laboratory., Subjects: Study subjects included 37 swine., Interventions: Myocardial infarction was induced by occlusion of the midleft anterior descending artery. Ventricular fibrillation was induced in control swine, acute myocardial infarction swine, and in postmyocardial infarction swine after a 2-wk recovery period., Measurements and Main Results: Ventricular fibrillation was recorded in 11 swine with acute myocardial infarction, ten postmyocardial infarction, and 16 controls. Frequency (mean, median, dominant, and bandwidth) and amplitude-related content (slope, slope-amp [slope divided by amplitude], and amplitude-spectrum area) were analyzed. Frequencies at 5 mins of ventricular fibrillation were altered in both acute myocardial infarction (p < .001 for all frequency characteristics) and postmyocardial infarction swine (p = .015 for mean, .002 for median, .002 for dominant frequency, and <.001 for bandwidth). At 5 mins, median frequency was highest in controls, 10.9 +/- .4 Hz; lowest in acute myocardial infarction, 8.4 +/- .5 Hz; and intermediate in postmyocardial infarction, 9.7 +/- .5 Hz (p < .001 for acute myocardial infarction and p = .002 for postmyocardial infarction compared with control). Slope and amplitude-spectrum area were similar among the three groups with a shallow decline after minute 2, whereas slope-amp remained significantly altered for acute myocardial infarction swine at 5 mins (p = .003)., Conclusions: Ventricular fibrillation frequencies depend on myocardial substrate and evolve from the acute through healing phases of myocardial infarction. Amplitude related measures, however, are similar among these groups. It is unknown how defibrillation may be affected by relying on the ventricular fibrillation waveform without considering myocardial substrate.

Aim: This study was designed to test the hypothesis that immediate post-shock chest compressions improve outcome from prolonged ventricular fibrillation (VF) compared with typical "hands off" period (i.e., delayed post-shock compressions) associated with AED use., Materials and Methods: After 7.5 min of untreated VF, 36 domestic swine (26+/-1 kg) were treated with 200 J biphasic shocks and randomly assigned to: (1) 1 min of immediate post-shock chest compressions or (2) simulated pre-hospital automated external defibrillator (AED) care with delays in post-shock chest compressions. Return of spontaneous circulation (ROSC) occurred in 7/18 immediate chest compressions animals within 2 min of the first shock versus 0/18 AED animals (P<0.01). Ten of 18 immediate chest compressions animals attained ROSC compared with 3/18 AED animals (P<0.05). Nine of 18 immediate chest compressions swine were alive at 24 and 48 h compared with 3/18 AED swine (P<0.05). All 48-h survivors had good neurologic outcomes. Among the 21 animals that defibrillated with the first shock, ROSC was attained in 7/10 immediate chest compressions animals within 2 min of the first shock compared with 0/11 AED animals (P=0.001), and 48-h survival was attained in 8/10 versus 3/11, respectively (P<0.05)., Conclusions: Immediate post-shock chest compressions can substantially improve outcome from prolonged VF compared with simulated pre-hospital AED care.

Aim: Increases in serum cytokines have been reported after successful resuscitation from prolonged ventricular fibrillation (VF). Pro-inflammatory cytokines can stimulate inducible nitric oxide synthase (iNOS) to produce excessive levels of nitric oxide (NO). High levels of both myocardial inflammatory cytokines and nitric oxide levels can depress myocardial contractile function. We hypothesized that myocardial pro-inflammatory cytokines and iNOS activity would increase following successful resuscitation from prolonged ventricular fibrillation cardiac arrest, and that such increases would parallel the development of post-resuscitation myocardial dysfunction., Methods: Ventricular fibrillation cardiac arrest was induced in seven domestic swine (25+/-5 kg). After 10 min of untreated VF, the animals were defibrillated and resuscitated. Left ventricular (LV) systolic and diastolic function measurements, serum samples (arterial and coronary sinus) for IL-8 cytokine quantification, and LV myocardial biopsies were collected before, during, and after resuscitation. Quantification of myocardial endothelial (eNOS) and inducible (iNOS) nitric oxide synthase protein levels were determined using immunoblot analyses and protein localization was examined using immunohistochemistry., Results: Post-resuscitation LV systolic and diastolic functions were depressed while increases in both coronary sinus IL-8 levels and myocardial iNOS activity were found. Compared to pre-arrest baseline, levels of iNOS protein increased during VF (p < or = 0.05) and continued to increase throughout the post-resuscitation study period of 6 h (p < or = 0.05)., Conclusions: Myocardial inflammatory cytokines and iNOS activity increase during and after prolonged cardiac arrest and successful resuscitation. These increases correspond to the well described decrease in LV function post-resuscitation.

Purpose of Review: To summarize current opinion and advances in pediatric cardiopulmonary resuscitation, including etiology, pathophysiology, rationale for interventions, and postresuscitation management., Recent Findings: Cardiac arrest and ventricular fibrillation in children are not as uncommon as previously reported. Out-of-hospital cardiac arrests occur in 8-20 children/100,000/year, and in-hospital arrests occur in 2-6% admitted to a pediatric intensive care unit. Most pediatric arrests are precipitated by asphyxia or circulatory shock, but approximately 10% are precipitated by ventricular tachycardia or fibrillation. In addition, greater than 1/4 of children with in-hospital cardiac arrests have ventricular tachycardia or fibrillation at some time during the event. After out-of-hospital arrests, approximately 10% survive to hospital discharge, whereas greater than 25% survive to discharge after in-hospital arrests. Appropriate interventions differ during the four phases of cardiac arrest: prearrest, no-flow, low-flow, and postresuscitation. Close monitoring and prompt cardiopulmonary resuscitation can minimize the no-flow phase, good quality cardiopulmonary resuscitation is important during the low-flow phase, defibrillation is necessary for ventricular fibrillation, and aggressive supportive care is important during the postresuscitation phase., Summary: Recent advances in our understanding of the etiology, pathophysiology, and therapies tied to the timing, phase, and duration of cardiac arrest can improve outcomes for children. New epidemiological data and multicenter studies are ushering in the era of evidence-based pediatric resuscitation therapeutics.

Background: The deleterious effects of positive pressure ventilation may be prevented by substituting passive oxygen insufflation during advanced cardiac life support (ACLS) cardiopulmonary resuscitation (CPR)., Methods: We compared 24-h neurologically normal survival among three different ventilation scenarios for ACLS in a realistic swine model of out-of-hospital prolonged ventricular fibrillation (VF) cardiac arrest. No bystander CPR was provided during the first 8 min of untreated VF before the simulated arrival of an emergency medical system (EMS). Thirty-six swine were randomly assigned to one of three experimental groups. Group I (standard ventilation) was mechanically ventilated at 10 respirations per minute (RPM) at a tidal volume (TV) of 10 ml/kg with 100% oxygen. Group II (hyperventilation) was ventilated at 35 RPM at a TV of 20 ml/kg with 100% oxygen. In Group III (insufflation) animals, a nasal cannula was placed in the oropharynx to administer oxygen continuously at 10 l/min., Results: There was no significant difference in the 24h neurologically normal survival among groups (standard: 2/12, hyperventilation: 2/12, insufflation: 4/12; p=.53)., Conclusions: Passive insufflation may be an acceptable alternative to the currently recommended positive pressure ventilation during resuscitation efforts for out-of-hospital VF cardiac arrest. Potential advantages of this technique include: (1) easier to teach, (2) easier to administer, (3) prevention of the adverse effects of positive pressure ventilation and (4) allows EMS personnel to concentrate upon other critically important duties.

Objectives: We sought to develop a method to evaluate the rapidly changing cardiac dimensions during sustained ventricular fibrillation (VF). We also present details of our CPR research imaging program to facilitate this avenue of clinically important research., Background: The changes in cardiac dimensions occurring during the initial critical electrical phase of sustained VF are not entirely known. Conventional cardiac magnetic resonance imaging (CMR) functional imaging lacks the temporal resolution necessary to capture the dynamic changes within this early time period of sustained VF. We hypothesized that changes in the middle short axis slice of the ventricles will reflect changes in ventricular volumes accurately., Methods: Ventricular dimensions were determined from CMR for 30 min of untreated VF in a closed chest, closed pericardium model in seven swine. Ungated steady-state free precession images (SSFP) from the cardiac base to the apex were acquired, taking care to align the anatomical short axis (SAX) imaging planes maximally. The middle slice of the ventricles was determined as the mathematical center of the stack of SAX slices. We then compared the relative changes of right ventricle (RV) and left ventricle (LV) volumes to relative changes in mid-ventricular single slice area., Results: During 30 min of sustained VF, there was an excellent correlation between the changes in exact mid-slice area and the quantitative changes in ventricular volumes (r(2)>0.95)., Conclusions: Mid-slice area data can be used as a surrogate marker of prompt ventricular volume changes during VF. By imaging the heart 10 times faster, the rapid anatomical changes occurring during the initial few minutes of sustained VF can be understood better.

Objective: Future automated external defibrillators are being designed to direct rescue efforts (chest compressions first vs. defibrillation) by inferring the duration of ventricular fibrillation based on its waveform characteristics such as frequency content. This approach assumes that the ventricular fibrillation waveform is an appropriate surrogate for ventricular fibrillation duration and is not affected by structural heart disease. We hypothesized that an acute myocardial infarction may alter the frequency content of ventricular fibrillation., Design: Animal intervention study with comparison to control group., Setting: University animal laboratory., Subjects: Twenty-seven swine., Interventions: Acute myocardial infarction was induced by occlusion of the mid-left anterior descending artery. Ventricular fibrillation was induced in swine with acute myocardial infarction and control swine., Measurements and Main Results: Ventricular fibrillation was induced in 11 swine with an acute myocardial infarction and in 16 control swine. Ventricular fibrillation waveforms were analyzed for mean, median, and dominant frequency, as well as bandwidth and amplitude. All frequency characteristics were significantly (p < .001) altered in swine with acute myocardial infarction compared with controls. Specifically, these characteristics were significantly depressed and varied little over time in swine with acute myocardial infarction compared with controls., Conclusions: These data establish that ventricular fibrillation during an acute myocardial infarction has an altered frequency content and time evolution compared with ventricular fibrillation without coronary obstruction. Frequency characteristics such as mean, median, dominant, and bandwidth show little variation in time after an acute myocardial infarction and are not suitable surrogates for ventricular fibrillation duration. These findings have important implications for the development of "smart" automated external defibrillators designed to determine duration of ventricular fibrillation from the waveform characteristics.

Background: For prolonged VF, perfusion of the myocardium by pre-shock chest compressions can improve myocardial readiness for successful defibrillation. Characteristics of the VF waveform correlate with the duration of VF when there is no structural heart disease. A "smart" automated external defibrillator (AED) could therefore analyze the VF waveform, determine if VF has been prolonged, and then direct rescuers to either deliver a shock first or chest compressions first. We hypothesized that ischemic heart failure might alter the waveform content of ventricular fibrillation compared with normal hearts, complicating the determination of VF duration., Methods: Myocardial infarction was induced by ligating the proximal left coronary artery. Six weeks later, VF was then induced in 10 rats with myocardial infarction and heart failure (MI-CHF) and 9 control rats. Waveforms were analyzed for total signal amplitude, median frequency, dominant frequency and bandwidth (the frequency interval containing 50% of the total amplitude about the median frequency)., Results: All of these VF waveform characteristics were altered substantially in MI-CHF rats compared to normal controls. In particular, MI-CHF rats had decreased signal amplitude early in VF (p=0.02), a broader bandwidth (p=0.001) and different frequency characteristics over time (p<0.001)., Conclusions: VF waveforms vary over time in a typical manner among rats with and without ischemic heart failure. However, the time-course and waveform characteristics of ventricular fibrillation are altered in rats with myocardial infarctions and ischemic heart failure compared to normal controls. These findings have important implications regarding the use of waveform analyses to determine the duration of VF.

Background: Ventricular fibrillation and ventricular tachycardia are less common causes of cardiac arrest in children than in adults. These tachyarrhythmias can also begin during cardiopulmonary resuscitation (CPR), presumably as reperfusion arrhythmias. We determined whether the outcome is better for initial than for subsequent ventricular fibrillation or tachycardia., Methods: All cardiac arrests in persons under 18 years of age were identified from a large, multicenter, in-hospital cardiac-arrest registry. The results from children with initial ventricular fibrillation or tachycardia, children in whom ventricular fibrillation or tachycardia developed during CPR, and children with no ventricular fibrillation or tachycardia were compared by chi-square and multivariable logistic-regression analysis., Results: Of 1005 index patients with in-hospital cardiac arrest, 272 (27 percent) had documented ventricular fibrillation or tachycardia during the arrest. In 104 patients (10 percent), ventricular fibrillation or tachycardia was the initial pulseless rhythm; in 149 patients (15 percent), it developed during the arrest. The time of initiation of ventricular fibrillation or tachycardia was not documented in 19 patients. Thirty-five percent of patients with initial ventricular fibrillation or tachycardia survived to hospital discharge, as compared with 11 percent of patients with subsequent ventricular fibrillation or tachycardia (odds ratio, 2.6; 95 percent confidence interval, 1.2 to 5.8). Twenty-seven percent of patients with no ventricular fibrillation or tachycardia survived to hospital discharge, as compared with 11 percent of patients with subsequent ventricular fibrillation or tachycardia (odds ratio, 3.8; 95 percent confidence interval, 1.8 to 7.6)., Conclusions: In pediatric patients with in-hospital cardiac arrests, survival outcomes were highest among patients in whom ventricular fibrillation or tachycardia was present initially than among those in whom it developed subsequently. The outcomes for patients with subsequent ventricular fibrillation or tachycardia were substantially worse than those for patients with asystole or pulseless electrical activity., (Copyright 2006 Massachusetts Medical Society.)

Background: The recommended dose for pediatric defibrillation is 2 J/kg, based on animal studies of brief duration ventricular fibrillation (VF) and a single pediatric study of short duration in-hospital VF. In a piglet model of out-of-hospital (prolonged) cardiac arrest, this recommended dose was usually ineffective at terminating VF. We, therefore, hypothesized that pediatric dose defibrillation may be less effective for prolonged out-of-hospital pediatric VF., Methods: We evaluated retrospectively all cardiac arrests in children less than 13 years old in Tucson from November 1998 to April 2003, with special attention to all children in ventricular fibrillation. We determined the rate of ventricular fibrillation termination after pediatric dose shocks in this cohort, and compared this rate with a published historical pediatric in-hospital defibrillation control group. A pediatric dose shock was defined as 2 J/kg (+/-10 J). All shocks in both groups were provided as monophasic damped sinusoidal waveforms., Results: Thirteen of 151 (9%) children with out-of-hospital cardiac arrest had documented VF. Eleven children received a total of 14 pediatric dose shocks. The median minimum untreated dispatch-to-shock time in unwitnessed arrest or collapse-to-shock in witnessed arrest for those 11 children was 11 min (interquartile range 25-75%; 9-15.5 min). Seven of the 14 pediatric dose shocks terminated the VF (six to asystole, one to pulseless electrical activity). Nine children (68%) died in the emergency department and four (31%) in the pediatric intensive care unit; none survived to hospital discharge. Failure to terminate VF after a pediatric dose shock in this study group with prolonged out-of-hospital ventricular fibrillation was substantially more common than the previously reported in-hospital data (7/14 versus 5/57; OR 10.4; 95% CI 2.6-42; P=0.001)., Conclusions: Termination of VF after a pediatric defibrillation dose is substantially worse for prolonged pediatric out-of-hospital VF cardiac arrest compared with in-hospital (short duration) ventricular fibrillation. The optimal pediatric defibrillation dose for prolonged VF is not known.

Background: Most out-of-hospital ventricular fibrillation (VF) is prolonged (>5 minutes), and defibrillation from prolonged VF typically results in asystole or pulseless electrical activity. Recent visual epicardial observations in an open-chest, open-pericardium model of swine VF indicate that blood flows from the high-pressure arterial system to the lower-pressure venous system during untreated VF, thereby overdistending the right ventricle and apparently decreasing left ventricular size. Therefore, inadequate left ventricular stroke volume after defibrillation from prolonged VF has been postulated as a major contributor to the development of pulseless rhythms., Methods and Results: Ventricular dimensions were determined by MRI for 30 minutes of untreated VF in a closed-chest, closed-pericardium model in 6 swine. Within 1 minute of untreated VF, mean right ventricular volume increased by 29% but did not increase thereafter. During the first 5 minutes of untreated VF, mean left ventricular volume increased by 34%. Between 20 and 30 minutes of VF, stone heart occurred as manifested by dramatic thickening of the myocardium and concomitant substantial decreases in left ventricular volume., Conclusions: In this closed-chest swine model of VF, substantial right ventricular volume changes occurred early and did not result in smaller left ventricular volumes. The changes in ventricular volumes before the late development of stone heart do not explain why defibrillation from brief duration VF (<5 minutes) typically results in a pulsatile rhythm with return of spontaneous circulation, whereas defibrillation from prolonged VF (5 to 15 minutes) does not.

Objectives: This study was designed to compare outcome after adult defibrillation dosing versus pediatric dosing in a piglet model of prolonged prehospital ventricular fibrillation (VF)., Background: Weight-based 2 to 4 J/kg monophasic defibrillation dosing is recommended for children in VF, but impractical for automated external defibrillator (AED) use. Present AEDs can only provide adult shock doses or newly developed attenuated adult doses intended for children. A single escalating energy sequence (50/75/86 J) of attenuated adult-dose biphasic shocks (pediatric dosing) is at least as effective as escalating monophasic weight-based dosing for prolonged VF in piglets, but this approach has not been compared to standard adult biphasic dosing., Methods: Following 7 min of untreated VF, piglets weighing 13 to 26 kg (19 +/- 1 kg) received either biphasic 50/75/86 J (pediatric dose) or biphasic 200/300/360 J (adult dose) therapies during simulated prehospital life support., Results: Return of spontaneous circulation was attained in 15 of 16 pediatric-dose piglets and 14 of 16 adult-dose piglets. Four hours postresuscitation, pediatric dosing resulted in fewer elevations of cardiac troponin T (0 of 12 piglets vs. 6 of 11 piglets, p = 0.005) and less depression of left ventricular ejection fraction (p < 0.05). Most importantly, more piglets survived to 24 h with good neurologic scores after pediatric shocks than adult shocks (13 of 16 piglets vs. 4 of 16 piglets, p = 0.004)., Conclusions: In this model, pediatric shocks resulted in superior outcome compared with adult shocks. These data suggest that adult defibrillation dosing may be harmful to pediatric patients with VF and support the use of attenuating electrodes with adult biphasic AEDs to defibrillate children.

Primary Objective: In a swine model of out-of-hospital ventricular fibrillation (VF) cardiac arrest, we established that automated external defibrillator (AED) defibrillation could worsen outcome from prolonged VF compared with manual defibrillation. Worse outcomes were due to substantial interruptions and delays in chest compressions for AED rhythm analyses and shock advice. In particular, the mean interval from first AED shock to first post-shock compressions was 46+/-6s. We hypothesized that the delay from shock to provision of chest compressions is similar in the out-of-hospital setting., Materials and Methods: We conducted a retrospective observational review of AED-treated adult VF cardiac arrest victims over a 26-month period to determine the interval from the first AED defibrillation attempt to the initial provision of post-shock chest compressions for out-of-hospital VF cardiac arrests. A two-tiered, single emergency medical service (EMS) system with AED-equipped first responders serves our area of 400 km2 with a population of 487,000 people. The defibrillators record a detailed sequence of events during the resuscitation effort that includes the electrocardiogram with real clock times and a recording of surrounding audible actions., Results: A median of 38 s (IQR 15, 61 s) elapsed between the first shock and the initiation of chest compressions. Approximately half of the delay was due to mechanical/electronic factors and the remainder due to human factors. Of 64 adults in VF, 45 (70%) died before hospital admission, 19 (30%) survived to admission and 10 (16%) survived to hospital discharge., Conclusion: Substantial delays in the provision of post-shock chest compressions are typical in this EMS system with AED-equipped first responders.

Background: Derived variables of ventricular fibrillation, such as the frequency distribution by fast Fourier transformation and its evolution over time, have been used to determine the optimum timing for defibrillation. We hypothesized that these frequency variables would differ among neonatal, young child and older child populations due to cardiac developmental and size differences. Such differences may have important implications for developing defibrillation algorithms for pediatric patients and for extrapolating adult defibrillation algorithms to children in VF., Methods: Ventricular fibrillation was induced and recorded for 6 min in 4 kg (n = 11), 14 kg (n = 10), and 24 kg (n = 16) piglets, corresponding to neonatal, young child and older children. Mean, median, and dominant frequencies were computed in 30 s intervals and compared among weight classes., Results: All frequency variables in all weight groups showed first a decline at 1.25-1.75 min, followed by a gradual rise and plateau. There were significant differences for mean, median and dominant frequencies among weight classes. Specifically, 14 kg piglets showed higher frequency variables overall with a time evolution that was different from that of 4 and 24 kg piglets. Mean frequency showed the most stable time evolution with the least moment-to-moment variability., Conclusion: The frequency waveform characteristics and time course are somewhat different in 14 kg piglets compared with 4 and 24 kg piglets. If similar differences are demonstrable among children of different weights and ages, AEDs designed to determine optimal timing of defibrillation shocks in adults by frequency waveform characteristics may require modification for use in children with VF.

Objective: To evaluate published data regarding the treatment of prolonged pediatric defibrillation, with special emphasis on the use of attenuated adult biphasic shocks for pediatric defibrillation., Design: Review relevant human and animal literature., Results: Rhythm analysis algorithms from two manufacturers of automated external defibrillators can accurately distinguish shockable from nonshockable rhythms in children. Theoretical considerations and transthoracic impedance data from animals and children suggest that pediatric defibrillation doses should not necessarily vary in a simple weight-based manner. Two piglet studies have established that an attenuated adult biphasic dosage can be successfully used for 3.5- to 24-kg animals in ventricular fibrillation. One study established that the attenuated adult biphasic dosage was at least as safe and effective as the standard monophasic weight-based dosing., Conclusion: This review supports the American Heart Association's new guidelines for pediatric automated external defibrillator usage: "Automated external defibrillators may be used for children 1 to 8 yrs of age who have no signs of circulation. Ideally the device should deliver a pediatric dose. The arrhythmia detection system used in the device should demonstrate high specificity for pediatric shockable rhythms, i.e., it will not recommend delivery of a shock for nonshockable rhythms."

Objectives: To compare immediate countershocks (defibrillation 1st) with precountershock cardiopulmonary resuscitation (CPR 1st) for prolonged ventricular fibrillation (VF)., Design: Randomized, controlled trial., Setting: University animal laboratory., Subjects: Thirty swine (27 +/- 1 kg)., Interventions: After 8 mins of untreated ventricular fibrillation, swine were randomly assigned to receive either immediate countershocks or CPR for 90 secs followed by countershocks., Measurements and Main Results: After the first set of shocks, nine of 15 CPR 1st animals attained return of spontaneous circulation vs. 0 of 15 defibrillation 1st animals (p <.001), and pulseless electrical activity occurred in only one of 15 CPR 1st animals vs. ten of 15 defibrillation 1st animals (p <.01). The ultimate outcomes in the two groups were not different: Return of spontaneous circulation and 24-hr survival occurred in 15 of 15 CPR 1st and 13 of 15 defibrillation 1st animals. Good neurologic outcome at 24 hrs occurred in 12 of 15 CPR 1st and nine of 15 defibrillation 1st animals. None of the animals was successfully resuscitated with defibrillation alone; all successfully resuscitated animals were provided with chest compressions during the resuscitation. The ventricular fibrillation median frequency by fast Fourier transformation decreased during the untreated ventricular fibrillation interval in both groups (9.7 +/- 0.3 Hz and 10.1 +/- 0.2 Hz after 1 min vs. 8.8 +/- 0.3 Hz and 8.9 +/- 0.5 Hz at 8 mins, respectively). Because the ventricular fibrillation median frequency substantially increased after CPR 1st, it was much higher in the CPR 1st group before the first shock (15.1 +/- 0.9 Hz vs. 8.9 +/- 0.5 Hz, p <.001). The ventricular fibrillation median frequency before the first countershock was much higher in the animals that attained return of spontaneous circulation after the first set of shocks vs. those that did not (16.1 +/- 1.3 Hz vs. 10.0 +/- 0.6 Hz, p <.0001), Conclusions: Precountershock CPR can result in substantial physiologic benefits and superior response to initial defibrillation attempts compared with immediate defibrillation in the setting of prolonged ventricular fibrillation.

Aim: To compare the safety and efficacy of attenuated adult biphasic shocks with standard monophasic weight-based shocks in a piglet model of prolonged prehospital ventricular fibrillation (VF)., Background: If attenuated adult shocks are safe and effective for prehospital pediatric VF, automated external defibrillators (AEDs) can be easily adapted for pediatric use., Methods: After 7 min of untreated VF, piglets were randomized to treatment with attenuated adult biphasic shocks or weight-based monophasic shocks. The attenuated adult biphasic group received 200/300/360 J shocks, attenuated by specialized pediatric electrodes to 51/78/81 J and the monophasic weight-based control group received 2/4/4 J/kg shocks. Forty-eight female piglets were studied, 16 in each of three weight categories: 4 kg (neonatal), 14 kg (younger child) and 24 kg (older child). The primary outcome measures of efficacy and safety were 24h survival with good neurological outcome and post-resuscitation left ventricular ejection fraction (LVEF), respectively., Results: For the 24 kg piglets, attenuated adult biphasic shocks resulted in superior 24 h survival with good neurological outcome (6/8 versus 0/8, P < 0.001) and greater LVEF 4 h post-resuscitation (34 +/- 4% versus 18 +/- 5%, P < 0.05). For the 14 and 4 kg piglets, 24 h survival with good neurological outcome occurred in 7/8 versus 5/8 and 7/8 versus 3/8, respectively, and LVEF 4 h post-resuscitation was 30 +/- 3% versus 36 +/- 6% and 30 +/- 3% versus 22 +/- 4%, respectively., Conclusions: The escalating attenuated adult biphasic dosage strategy was at least as safe and effective as the standard weight-based monophasic dose over a wide range of weights in this piglet model of prehospital VF. This work supports the concept of using an attenuated adult biphasic dosage in children.

Objectives: This study was designed to determine the optimal dose of dobutamine in the treatment of post-resuscitation left ventricular dysfunction., Background: Global left ventricular dysfunction following successful resuscitation from prolonged, ventricular fibrillation cardiac arrest, negatively impacts long-term survival. Dobutamine can overcome this global myocardial stunning. Previous data indicate a dose of 10 mcg/kgmin improves systolic and diastolic function, but markedly increases the heart rate., Methods: Twenty swine (24 +/- 0.4 kg) were randomized to one of four doses (0, 2, 5, and 7.5 mcg/kgmin) of dobutamine for the treatment of post-resuscitation myocardial dysfunction following 12.5 min of untreated ventricular fibrillation cardiac arrest. Cardiac function was measured at pre-arrest baseline and serially for 6 h post-resuscitation. Left ventricular function was evaluated by contrast ventriculograms, left ventricular pressures, +dP/dt, Tau, -dP/dt, and cardiac output. Myocardial oxygen consumption and myocardial blood flow were measured to assess the functional significance of any dobutamine-mediated heart rate responses., Results: Left ventricular dysfunction was evident at 25 min and peaked 4 h post-resuscitation. Significant (P < 0.05) improvements in ventricular systolic (EF, CO) and diastolic (LVEDP, Tau) function were evident within minutes of dobutamine initiation and persisted at 6h for the 5 and 7.5 mcg/kgmin groups. Tachycardia manifested with all dobutamine doses, but only affected myocardial oxygen consumption significantly (P < 0.05) at the highest dose (7.5 mcg/kgmin)., Conclusions: Dobutamine at 5 mcg/kgmin appears optimal for restoring systolic and diastolic function post-resuscitation without adversely affecting myocardial oxygen consumption.

Interposed abdominal compression cardiopulmonary resuscitation (IAC-CPR) is an innovative basic life support technique requiring no mechanical adjuncts. Optimizing its performance remains a challenge. Hand-position technique over the abdomen during interposed abdominal compression (IAC) may be important. The purpose of this study was to determine if there is a difference in efficacy depending on the type of abdominal hand-position used. Two different hand positions were studied: open hands, placed side by side, resulting in diffuse abdominal compression and stacked hands, with one on top of the other, producing a more focal compression of the abdomen. Thirty swine were cannulated with micromanometer-tipped pressure transducers in the ascending aorta (Ao) and right atrium (RA), and Millar Doppler-tipped catheters in the descending aorta and inferior vena cava (IVC) to determine flow patterns during cardiopulmonary resuscitation (CPR), During CPR there were no differences in aortic systolic or right atrial systolic pressures. Both forms of IAC-CPR produced greater aortic diastolic and right atrial diastolic pressures then standard CPR (STD-CPR) (P<0.05). Coronary perfusion pressures (CPP), however, were not different. Blood flow directions and velocity patterns showed that STD-CPR chest compressions produce caudally directed blood flow in both the descending aorta and the IVC, and that such flows reverse (becoming cranially directed) during the relaxation phase of chest compression. IAC-CPR produced similar blood flow patterns in the aorta and IVC, as seen with STD-CPR. There were no differences in blood flow patterns between the different forms of IAC-CPR. No CPR-produced trauma difference was found. Abdominal hand position (diffuse or stacked) did not affect blood flow in either the aorta or IVC or resuscitation success in this experimental model. There was a trend towards better outcomes with stacked hands IAC-CPR with 90 versus 70% survival with STD-CPR.

Study Objective: We sought to determine whether the delays in chest compressions and defibrillation associated with an automated external defibrillator would adversely affect outcome compared with manual defibrillation in a swine model of out-of-hospital prolonged ventricular fibrillation., Methods: After 8 minutes of untreated ventricular fibrillation, 16 swine (33+/-4 kg) were randomly assigned to automated external defibrillator defibrillation or manual defibrillation with the same biphasic truncated exponential waveform 150-J shock through the same type of pads. Defibrillation with the automated external defibrillator was performed as recommended by the manufacturer, and manual defibrillation was provided per American Heart Association Guidelines. The primary outcome measure was 24-hour survival with good neurologic outcome. Data are described as means+/-SD., Results: None of 8 animals in the automated external defibrillator group survived for 24 hours, whereas 5 of 8 animals in the manual defibrillation group survived 24 hours, all with good neurologic outcome (P=.027). The time interval from simulated defibrillator arrival to first compressions was 98+/-18 seconds in the automated external defibrillator group versus 68+/-15 seconds in the manual defibrillation group. In particular, the interval from first shock to first chest compressions was 46+/-18 seconds versus 22+/-16 seconds, respectively. The mean percentage of time that chest compressions were performed in the first minute after the first countershock was 15%+/-13% versus 40%+/-15%, respectively. As a result, return of spontaneous circulation within 5 minutes of simulated defibrillator arrival occurred in only 1 of 8 animals in the automated external defibrillator group versus 6 of 8 animals in the manual defibrillation group., Conclusion: The longer delays in chest compressions with automated external defibrillator defibrillation versus manual defibrillation can worsen the outcome from prolonged ventricular fibrillation.

Objective: Amiodarone has been shown to be superior to both placebo and lidocaine in improving survival to hospital admission for victims of out-of-hospital refractory ventricular fibrillation. Concern had been expressed about the known vasodilatatory effects of amiodarone if given without precedent vasoconstrictive medications. The haemodynamic effects of intravenous amiodarone administered during ongoing CPR have not been systemically investigated. Our intention was to verify if amiodarone alone produced significantly lower resuscitation haemodynamics than did either adrenaline (epinephrine) alone or the combination of amiodarone and adrenaline., Design: Prospective, randomized, comparative study., Setting: Research laboratory of a medical school., Subjects: Thirty mongrel dogs., Interventions: After 8 min of untreated VF, defibrillation was attempted once at 3 J/kg and external chest compressions and ventilation started. Those animals resistant to the defibrillation attempt were randomized, ten to an adrenaline (0.02 mg/kg) group, ten to an amiodarone (5 mg/kg) group, and ten to a group receiving a combination of both drugs., Measurements and Main Results: Aortic systolic and diastolic, and coronary perfusion pressures were all significantly lower in the group receiving amiodarone alone than in the other two groups. Amiodarone combined with adrenaline produced pressures during CPR similar to adrenaline alone., Conclusion: Amiodarone can be safely administered simultaneously in combination with adrenaline and such a combination results in similar haemodynamic support as adrenaline alone. Amiodarone administered alone produces significantly lower coronary perfusion pressure than when combined with adrenaline.

Background: Interruptions to chest compression-generated blood flow during cardiopulmonary resuscitation (CPR) are detrimental. Data show that such interruptions for mouth-to-mouth ventilation require a period of "rebuilding" of coronary perfusion pressure to obtain the level achieved before the interruption. Whether such hemodynamic compromise from pausing to ventilate is enough to affect outcome is unknown., Methods and Results: Thirty swine (weight 35 +/- 2 kg) underwent 3 minutes of untreated ventricular fibrillation before 12 minutes of basic life support CPR. Animals were randomized to receive either standard airway (A), breathing (B), and compression (C) CPR with expired-gas ventilation in a 15:2 compression-to-ventilation ratio or continuous chest compression CPR. Those randomized to the standard 15:2 group had no chest compressions for a period of 16 seconds each time the 2 ventilations were delivered. Defibrillation was attempted at 15 minutes of cardiac arrest. All resuscitated animals were supported in an intensive care environment for 1 hour, then in a maintenance facility for 24 hours. The primary end point of neurologically normal 24-hour survival was significantly better in the experimental group receiving continuous chest compression CPR (12 of 15 versus 2 of 15; P<0.0001)., Conclusions: Mouth-to-mouth ventilation performed by single layperson rescuers produces substantial interruptions in chest compression-supported circulation. Continuous chest compression CPR produces greater neurologically normal 24-hour survival than standard ABC CPR when performed in a clinically realistic fashion. Any technique that minimizes lengthy interruptions of chest compressions during the first 10 to 15 minutes of basic life support should be given serious consideration in future efforts to improve outcome results from cardiac arrest.

Abstract: Aim: The aim of this investigation was to estimate and contrast the global incidence and outcome of out-of-hospital cardiac arrest (OHCA) to provide a better understanding of the variability in risk and survival of OHCA. Methods: We conducted a review of published English-language articles about incidence of OHCA, available through MEDLINE and EmBase. For studies including adult patients and both adult and paediatric patients, we used Utstein data reporting guidelines to calculate, summarize and compare incidences per 100,000 person-years of attended OHCAs, treated OHCAs, treated OHCAs with a cardiac cause, treated OHCA with ventricular fibrillation (VF), and survival-to-hospital discharge rates following OHCA. Results: Sixty-seven studies from Europe, North America, Asia or Australia met inclusion criteria. The weighted incidence estimate was significantly higher in studies including adults than in those including adults and paediatrics for treated OHCAs (62.3 vs 34.7; P <0.001); and for treated OHCAs with a cardiac cause (54.6 vs 40.8; P =0.004). Neither survival to discharge rates nor VF survival to discharge rates differed statistically significant among studies. The incidence of treated OHCAs was higher in North America (54.6) than in Europe (35.0), Asia (28.3), and Australia (44.0) (P <0.001). In Asia, the percentage of VF and survival to discharge rates were lower (11% and 2%, respectively) than those in Europe (35% and 9%, respectively), North America (28% and 6%, respectively), or Australia (40% and 11%, respectively) (P <0.001, P <0.001). Conclusions: OHCA incidence and outcome varies greatly around the globe. A better understanding of the variability is fundamental to improving OHCA prevention and resuscitation. [Copyright &y& Elsevier]

Background: Continued breathing following ventricular fibrillation has here-to-fore not been described. Methods: We analyzed the spontaneous ventilatory activity during the first several minutes of ventricular fibrillation (VF) in our isoflurane anesthesized swine model of out-of-hospital cardiac arrest. The frequency and type of ventilatory activity was monitored by pneumotachometer and main stream infrared capnometer and analyzed in 61 swine during the first 3 to 6 minutes of untreated VF. Results: During the first minute of VF, the air flow pattern in all 61 swine was similar to those recorded during regular spontaneous breathing during anesthesia and was clearly different from the patterns of gasping. The average rate of continued breathing during the first minute of untreated VF was 10 breaths per minute. During the second minute of untreated VF, spontaneous breathing activity either stopped or became typical of gasping. During minutes 2 to 5 of untreated VF, most animals exhibited very slow spontaneous ventilatory activity with a pattern typical of gasping; and the pattern of gasping was crescendo-decrescendo, as has been previously reported. In the absence of therapy, all ventilatory activity stopped 6 minutes after VF cardiac arrest. Conclusion: In our swine model of VF cardiac arrest, we documented that normal breathing continued for the first minute following cardiac arrest. [ABSTRACT FROM AUTHOR]

Context: Cardiac arrests in adults are often due to ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT), which are associated with better outcomes than asystole or pulseless electrical activity (PEA). Cardiac arrests in children are typically asystole or PEA. Objective: To test the hypothesis that children have relatively fewer in-hospital cardiac arrests associated with VF or pulseless VT compared with adults and, therefore, worse survival outcomes. Design, Setting, and Patients: A prospective observational study from a multicenter registry (National Registry of Cardiopulmonary Resuscitation) of cardiac arrests in 253 US and Canadian hospitals between January 1, 2000, and March 30, 2004. A total of 36 902 adults ( 18 years) and 880 children (<18 years) with pulseless cardiac arrests requiring chest compressions, defibrillation, or both were assessed. Cardiac arrests occurring in the delivery department, neonatal intensive care unit, and in the out-of-hospital setting were excluded. Main Outcome Measure: Survival to hospital discharge. Results: The rate of survival to hospital discharge following pulseless cardiac arrest was higher in children than adults (27% [236/880] vs 18% [6485/36 902]; adjusted odds ratio [OR], 2.29; 95% confidence interval [CI], 1.95-2.68). Of these survivors, 65% (154/236) of children and 73% (4737/6485) of adults had good neurological outcome. The prevalence of VF or pulseless VT as the first documented pulseless rhythm was 14% (120/880) in children and 23% (8361/36 902) in adults (OR, 0.54; 95% CI, 0.44-0.65; P<.001). The prevalence of asystole was 40% (350) in children and 35% (13 024) in adults (OR, 1.20; 95% CI, 1.10-1.40; P = .006), whereas the prevalence of PEA was 24% (213) in children and 32% (11 963) in adults (OR, 0.67; 95% CI, 0.57-0.78; P<.001). After adjustment for differences in preexisting conditions, interventions in place at time of arrest, witnessed and/or monitored status, time to defibrillation of VF or pulseless VT, intensive care unit location of arrest, and duration of cardiopulmonary resuscitation, only first documented pulseless arrest rhythm remained significantly associated with differential survival to discharge (24% [135/563] in children vs 11% [2719/24 987] in adults with asystole and PEA; adjusted OR, 2.73; 95% CI, 2.23-3.32). Conclusions: In this multicenter registry of in-hospital cardiac arrest, the first documented pulseless arrest rhythm was typically asystole or PEA in both children and adults. Because of better survival after asystole and PEA, children had better outcomes than adults despite fewer cardiac arrests due to VF or pulseless VT. [ABSTRACT FROM AUTHOR]

The article reviews a study by S. Wang and colleagues on the effect of continuous compressions and 30:2 cardiopulmonary (CPR) resuscitation on global ventilation/perfusion values during resuscitation. Their study provides evidence that continuous chest compression is as effective as chest compression plus rescue breathing for 12 minutes of CPR for ventricular fibrillation cardiac arrest. It explains how oxygenation and ventilation was maintained in 12 minutes of CPR without rescue breaths. The limitations of the study are discussed.

The article comments on the paper "Prearrest administration of low-molecular weight heparin in porcine cardiac arrest: Hemodynamic effects and resuscibility," by M. Pyette and colleagues. According to the authors, the porcine ventricular fibrillation cardiac arrest model used in the study is well described and used in many resuscitation laboratories. The authors claims there are potential shortcomings in the model, but do not believe that the swine cardiac arrest model itself is the major issue.

The article presents a study which examines practice patterns of amiodarone use during in-hospital cardiac arrest. The study included all patients with an in-hospital ventricular fibrillation (VF) or pulseless ventricular tachycardia (pVT) event from January 1, 2000 to July 31, 2005. It was found that there has been an increase in amiodarone use for VF/pVT events over the past 5 years.

Background: Left ventricular dysfunction after resuscitation from cardiac arrest has been well described. Treatment with dobutamine improves post-resuscitation left ventricular function. Right ventricular function following resuscitation has not been investigated. The purposes of this study were to examine right ventricular function following resuscitation and determine whether dobutamine would improve post-resuscitation right ventricular function. Methods and results: Right ventricular function was measured in 28 swine (29±1 kg) before and after resuscitation from 15 min of untreated ventricular fibrillation. Twelve animals received dobutamine at 10 mcg/kg/min while 16 animals served as untreated controls. Among controls, right ventricular dysfunction post-resuscitation was demonstrated by a decrease in right ventricular ejection fraction and an increase in right ventricular end-diastolic pressure. Among animals treated with dobutamine, there was a significant improvement in right ventricular function post-resuscitation compared to untreated controls. Conclusions: This study establishes that right ventricular systolic and diastolic dysfunction does occur after prolonged cardiac arrest from ventricular fibrillation. Dobutamine can ameliorate post-resuscitation right ventricular dysfunction. [Copyright &y& Elsevier]

Aim: Inhaled nitric oxide (iNO) during cardiopulmonary resuscitation (CPR) improved systemic hemodynamics and outcomes in a preclinical model of adult in-hospital cardiac arrest (IHCA) and may also have a neuroprotective role following cardiac arrest. The primary objectives of this study were to determine if iNO during CPR would improve cerebral hemodynamics and mitochondrial function in a pediatric model of lipopolysaccharide-induced shock-associated IHCA.Methods: After lipopolysaccharide infusion and ventricular fibrillation induction, 20 1-month-old piglets received hemodynamic-directed CPR and were randomized to blinded treatment with or without iNO (80 ppm) during and after CPR. Defibrillation attempts began at 10 min with a 20-min maximum CPR duration. Cerebral tissue from animals surviving 1-h post-arrest underwent high-resolution respirometry to evaluate the mitochondrial electron transport system and immunohistochemical analyses to assess neuropathology.Results: During CPR, the iNO group had higher mean aortic pressure (41.6 ± 2.0 vs. 36.0 ± 1.4 mmHg; p = 0.005); diastolic BP (32.4 ± 2.4 vs. 27.1 ± 1.7 mmHg; p = 0.03); cerebral perfusion pressure (25.0 ± 2.6 vs. 19.1 ± 1.8 mmHg; p = 0.02); and cerebral blood flow relative to baseline (rCBF: 243.2 ± 54.1 vs. 115.5 ± 37.2%; p = 0.02). Among the 8/10 survivors in each group, the iNO group had higher mitochondrial Complex I oxidative phosphorylation in the cerebral cortex (3.60 [3.56, 3.99] vs. 3.23 [2.44, 3.46] pmol O2/s mg; p = 0.01) and hippocampus (4.79 [4.35, 5.18] vs. 3.17 [2.75, 4.58] pmol O2/s mg; p = 0.02). There were no other differences in mitochondrial respiration or brain injury between groups.Conclusions: Treatment with iNO during CPR resulted in superior systemic hemodynamics, rCBF, and cerebral mitochondrial Complex I respiration in this pediatric cardiac arrest model. [ABSTRACT FROM AUTHOR]

Presents a case of a fire ignited by a defibrillation attempt in a 10-day-old infant. Sources of fire during a defibrillation attempt; Recommendations from the Emergency Care Research Institute to prevent fires during defibrillation attempts; Implications of the development of a fire during patient care.