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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]

Objectives: Nitric oxide (NO) is a critical regulator of vascular tone and signal transduction in the cardiovascular system. NO is synthesized by three unique enzymes (nitric oxide synthases [NOS]): endothelial and neuronal NOS, both constitutively expressed, and inducible NOS (iNOS), which is induced by proinflammatory stimuli and subsequently produces a burst of NO. NO has been implicated as both an injurious and a beneficial mediator after cardiac arrest and resuscitation. A previous study in swine found that iNOS expression is absent in the myocardium prior to cardiac arrest and that it increases after 10 minutes of untreated ventricular fibrillation (VF), decreases somewhat during the early postresuscitation period, and then steadily increases up to 6 hours postresuscitation. Because this time course of iNOS expression mirrors that of postresuscitation myocardial dysfunction, this study was designed to test the hypothesis that selective inhibition of iNOS improves postresuscitation outcomes in swine., Methods: Thirty-two domestic swine of either sex were randomly assigned to receive one of the following treatments 15 minutes after return of spontaneous circulation (ROSC): (1) N(G) -nitro-l-arginine methyl ester (l-NAME), a global NO inhibitor; (2) aminoguanidine (AG), a selective iNOS inhibitor; or (3) saline as control. After 10 minutes of untreated VF, swine received a standard resuscitation protocol. Twenty-four-hour survival, neurological status, left ventricular (LV) function, and hemodynamic measurements were obtained., Results: Return of spontaneous circulation occurred in 28 of 32 animals (88%). Only successfully resuscitated animals were assigned to treatment groups and completed the study. There were no differences in survival or neurological outcomes between groups. There were also no differences in LV function or hemodynamic variables found between the control group and the AG group. Global inhibition of NOS with l-NAME post-ROSC increased aortic pressure and transiently decreased pulse pressure. Treatment with l-NAME also increased LV end diastolic pressure and decreased cardiac output within 30 minutes post-ROSC, which was sustained throughout the 4-hour measurements, compared to both the control and the AG groups. In addition, LV ejection fraction recovered to baseline measurements in both the control and AG groups, but failed to recover in the l-NAME group., Conclusions: Global inhibition of NOS after cardiac arrest and resuscitation markedly worsens hemodynamic variables. Selective inhibition of iNOS after cardiac arrest and resuscitation does not prevent postresuscitation myocardial stunning. There were no significant differences in neurological outcome or survival between treatment groups., (© 2015 by the Society for Academic Emergency Medicine.)

Glucagon-like peptide-1 (GLP-1) has protective effects in the heart. We hypothesized that GLP-1 would mitigate coronary microvascular and left ventricular (LV) dysfunction if administered after cardiac arrest and resuscitation (CAR). Eighteen swine were subjected to ventricular fibrillation followed by resuscitation. Swine surviving to return of spontaneous circulation (ROSC) were randomized to receive an intravenous infusion of either human rGLP-1 (10 pmol·kg(-1)·min(-1); n = 8) or 0.9% saline (n = 8) for 4 h, beginning 1 min after ROSC. CAR caused a decline in coronary flow reserve (CFR) in control animals (pre-arrest, 1.86 ± 0.20; 1 h post-ROSC, 1.3 ± 0.05; 4 h post-ROSC, 1.25 ± 0.06; P < 0.05). GLP-1 preserved CFR for up to 4 h after ROSC (pre-arrest, 1.31 ± 0.17; 1 h post-ROSC, 1.5 ± 0.01; 4 h post-ROSC, 1.55 ± 0.22). Although there was a trend toward improvement in LV relaxation in the GLP-1-treated animals, overall LV function was not consistently different between groups. 8-iso-PGF(2α), a measure of reactive oxygen species load, was decreased in post-ROSC GLP-1-treated animals [placebo, control (NS): 38.1 ± 1.54 pg/ml; GLP-1: 26.59 ± 1.56 pg/ml; P < 0.05]. Infusion of GLP-1 after CAR preserved coronary microvascular and LV diastolic function. These effects may be mediated through a reduction in oxidative stress.

Background: In cardiac arrest, the ventricular fibrillation (VF) waveform, particularly amplitude spectral area (AMSA) and slope, predicts the return of spontaneous circulation (ROSC), but it is unknown whether the predictive utility differs in an acute myocardial infarction (MI), prior MI, or normal myocardium and if the waveform can distinguish the underlying myocardial state. We hypothesized that in a swine model of VF cardiac arrest, AMSA and slope predict ROSC after a shock independent of substrate and distinguish an acute from nonacute MI state., Methods and Results: MI was induced by occlusion of the left anterior descending artery. Post MI swine recovered for a 2-week period before induction of VF. VF was untreated for 8 minutes in 10 acute MI, 10 post MI, and 10 control swine. AMSA and slope predicted ROSC after a shock independent of myocardial state. For AMSA >31 mV-Hz, the odds ratio was 62 (P≤0.001) compared with AMSA <19 mV-Hz. For slope >3.1 mV/s, odds ratio was 52 (P≤0.001) compared with slope <1.8 mV/s. With chest compressions, AMSA and slope were significantly lower for acute MI swine compared with control swine, whereas in post MI swine the waveform characteristics were similar to control swine. In particular, for an AMSA >33.5 mV-Hz, the sensitivity to identify an acute from nonacute (control or post MI) state was 83%., Conclusions: In a swine model of VF cardiac arrest, AMSA and slope predict ROSC independent of myocardial substrate. Furthermore, with chest compressions, the VF waveform evolves differently and may offer a means to distinguish an acute MI.

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.)

Background: The post-cardiac arrest syndrome includes a decline in myocardial microcirculation function. Inhibition of the platelet IIb/IIIa glycoprotein receptor has improved myocardial microvascular function post-percutaneous coronary intervention. Therefore, we evaluated such inhibition with eptifibatide for its effect on myocardial microcirculation function post-cardiac arrest and resuscitation., Methods: Four groups of swine were studied in a prospective, randomized, blinded, placebo-controlled protocol including; eptifibatide administered during CPR (Group 1, n=5), after resuscitation (Group 2, n=4), during and after resuscitation (Group 3, n=5), or placebo (Group 4, n=10). CPR was initiated following 12min of untreated VF. Those successfully resuscitated were studied during a 4-h post-resuscitation period. Coronary flow reserve, a measure of microcirculation function (in the absence of coronary obstruction), as well as parameters of left ventricular systolic and diastolic function, were measured pre-arrest and serially post-resuscitation., Results: Coronary flow reserve was preserved during the post-resuscitation period, indicating normal microcirculatory function in the eptifibatide-treated animals, but not in the placebo-treated group. However, LV function declined equally in both groups during the first 4h after cardiac arrest., Conclusion: Inhibition of platelet IIb/IIIa glycoprotein receptors with eptifibatide post-resuscitation prevented myocardial microcirculation dysfunction. Left ventricular dysfunction post-resuscitation was not improved with eptifibatide, and perhaps transiently worse at 30min post-resuscitation. Post-cardiac arrest ventricular dysfunction may require a multi-modality treatment strategy for successful prevention or amelioration., (Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.)

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: This study was designed to compare 24-h survival rates and neurological function of swine in cardiac arrest treated with one of three forms of simulated basic life support CPR., Methods: Thirty swine were randomized equally among three experimental groups to receive either 30:2 CPR with an unobstructed endotracheal tube (ET) or continuous chest compression (CCC) CPR with an unobstructed ET or CCC CPR with a collapsable rubber sleeve on the ET allowing air outflow but completely restricting air inflow. The swine were anesthetized but not paralyzed. Two min of untreated VF was followed by 9 min of simulated single rescuer bystander CPR. In the 30:2 CPR group, each set of 30 chest compressions was followed by a 15-s pause to simulate the realistic duration of interrupted chest compressions required for a single rescuer to deliver 2 mouth-to-mouth ventilations. The other two groups were provided continuous chest compressions (CCC) without assisted ventilations. At 11 min post-arrest a biphasic defibrillation shock (150 J) was administered followed by a period of advanced cardiac life support., Results: In the 30:2 group, 8 of 10 animals had good neurological function at 24-h post-resuscitation. In the CCC open airway group, 10 of 10, and in the CCC inspiratory obstructed group, 9 of 10. The number of shocks (P<0.05) and epinephrine doses (P<0.05) required for ROSC was greater in the 30:2 CPR group than in the other two groups., Conclusions: There were no differences in 24-h survival with good neurological function among these three different CPR protocols., (Copyright 2010 Elsevier Ireland Ltd. All rights reserved.)

Objective: Complete recoil of the chest wall between chest compressions during cardiopulmonary resuscitation is recommended, because incomplete chest wall recoil from leaning may decrease venous return and thereby decrease blood flow. We evaluated the hemodynamic effect of 10% or 20% lean during piglet cardiopulmonary resuscitation., Design: Prospective, sequential, controlled experimental animal investigation., Setting: University research laboratory., Subjects: Domestic piglets., Interventions: After induction of ventricular fibrillation, cardiopulmonary resuscitation was provided to ten piglets (10.7 +/- 1.2 kg) for 18 mins as six 3-min epochs with no lean, 10% lean, or 20% lean to maintain aortic systolic pressure of 80-90 mm Hg. Because the mean force to attain 80-90 mm Hg was 18 kg in preliminary studies, the equivalent of 10% and 20% lean was provided by use of 1.8- and 3.6-kg weights on the chest., Measurements and Main Results: Using a linear mixed-effect regression model to control for changes in cardiopulmonary resuscitation hemodynamics over time, mean right atrial diastolic pressure was 9 +/- 0.6 mm Hg with no lean, 10 +/- 0.3 mm Hg with 10% lean (p < .01), and 13 +/- 0.3 mm Hg with 20% lean (p < .01), resulting in decreased coronary perfusion pressure with leaning. Microsphere-determined cardiac index and left ventricular myocardial blood flow were lower with 10% and 20% leaning throughout the 18 mins of cardiopulmonary resuscitation. Mean cardiac index decreased from 1.9 +/- 0.2 L . M . min with no leaning to 1.6 +/- 0.1 L . M . min with 10% leaning, and 1.4 +/- 0.2 L . M . min with 20% leaning (p < .05). The myocardial blood flow decreased from 39 +/- 7 mL . min . 100 g with no lean to 30 +/- 6 mL . min . 100 g with 10% leaning and 26 +/- 6 mL . min . 100 g with 20% leaning (p < .05)., Conclusions: Leaning of 10% to 20% (i.e., 1.8-3.6 kg) during cardiopulmonary resuscitation substantially decreased coronary perfusion pressure, cardiac index, and myocardial blood flow.

Objective. To analyze the effect of basic resuscitation efforts on gasping and of gasping on survival. Methods. This is secondary analysis of a previously reported study comparing continuous chest compressions (CCC CPR) versus chest compressions plus ventilation (30:2 CPR) on survival. 64 swine were randomized to 1 of these 2 basic CPR approaches after either short (3 or 4 minutes) or long (5 or 6 minutes) durations of untreated VF. At 12 minutes of VF, all received the same Guidelines 2005 Advanced Cardiac Life Support. Neurologically status was evaluated at 24 hours. A score of 1 is normal, 2 is abnormal, such as not eating or drinking normally, unsteady gait, or slight resistance to restraint, 3 severely abnormal, where the animal is recumbent and unable to stand, 4 is comatose, and 5 is dead. For this analysis a neurological outcome score of 1 or 2 was classified as "good", and a score of 3, 4, or 5 was classified as "poor." Results. Gasping was more likely to continue or if absent, to resume in the animals with short durations of untreated VF before basic resuscitation efforts. With long durations of untreated VF, the frequency of gasping and survival was better in swine receiving CCC CPR. In the absence of frequent gasping, intact survival was rare in the long duration of untreated VF group. Conclusions. Gasping is an important phenomenon during basic resuscitation efforts for VF arrest and in this model was more frequent with CCC-CPR.

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.

Study Objective: Assisted ventilation may adversely affect out-of-hospital cardiac arrest outcomes. Passive ventilation offers an alternate method of oxygen delivery for these patients. We compare the adjusted neurologically intact survival of out-of-hospital cardiac arrest patients receiving initial passive ventilation with those receiving initial bag-valve-mask ventilation., Methods: The authors performed a retrospective analysis of statewide out-of-hospital cardiac arrests between January 1, 2005, and September 28, 2008. The analysis included consecutive adult out-of-hospital cardiac arrest patients receiving resuscitation with minimally interrupted cardiopulmonary resuscitation (CPR) consisting of uninterrupted preshock and postshock chest compressions, initial noninvasive airway maneuvers, and early epinephrine. Paramedics selected the method of initial noninvasive ventilation, consisting of either passive ventilation (oropharyngeal airway insertion and high-flow oxygen by nonrebreather facemask, without assisted ventilation) or bag-valve-mask ventilation (by paramedics at 8 breaths/min). The authors determined adjusted neurologically intact survival from hospital and public records and by telephone interview and mail questionnaire. The authors compared adjusted neurologically intact survival between ventilation techniques by using generalized estimating equations., Results: Among the 1,019 adult out-of-hospital cardiac arrest patients in the analysis, 459 received passive ventilation and 560 received bag-valve-mask ventilation. Adjusted neurologically intact survival after witnessed ventricular fibrillation/ventricular tachycardia out-of-hospital cardiac arrest was higher for passive ventilation (39/102; 38.2%) than bag-valve-mask ventilation (31/120; 25.8%) (adjusted odds ratio [OR] 2.5; 95% confidence interval [CI] 1.3 to 4.6). Survival between passive ventilation and bag-valve-mask ventilation was similar after unwitnessed ventricular fibrillation/ventricular tachycardia (7.3% versus 13.8%; adjusted OR 0.5; 95% CI 0.2 to 1.6) and nonshockable rhythms (1.3% versus 3.7%; adjusted OR 0.3; 95% CI 0.1 to 1.0)., Conclusion: Among adult, witnessed, ventricular fibrillation/ventricular tachycardia, out-of-hospital cardiac arrest resuscitated with minimally interrupted cardiac resuscitation, adjusted neurologically intact survival to hospital discharge was higher for individuals receiving initial passive ventilation than those receiving initial bag-valve-mask ventilation.

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: 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.

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.

Background: The Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care recommend that for adult cardiac arrest the single rescuer performs "two quick breaths followed by 15 chest compressions." This cycle is continued until additional help arrives. Previous studies have shown that lay persons and medical students take 16 +/- 1 and 14 +/- 1 s, respectively, to perform these "two quick breaths." The purpose of this study was to determine the time required for trained professional paramedic firefighters to deliver these two breaths and the effects that any increase in the time it takes to perform rescue breathing would have on the number of chest compressions delivered during single rescuer BLS CPR. We hypothesized that trained professional rescuers would also take substantially longer then the Guidelines recommendation for delivering the two rescue breaths before every 15 compressions during simulated single rescuer BLS CPR., Methods: Twenty-four paramedic firefighters currently certified to perform BLS CPR were evaluated for their ability to deliver the two recommended breaths within 4 s according to the AHA 2000 CPR Guidelines. Alternatively, a simplified technique of continuous chest compression BLS CPR (CCC) was also taught and compared with standard BLS CPR (STD). Without revealing the purpose of the study the paramedics were asked to perform single rescuer BLS CPR on a recording Resusci Anne while being videotaped., Results: The mean length of time needed to provide the "two quick breaths" during STD-CPR was 10 +/- 1 s. The mean number of chest compressions/min delivered with AHA BLS CPR was only 44 +/- 2. Continuous chest compression CPR resulted in 88 +/- 5 compressions delivered per minute (STD versus CCC; p < 0.0001)., Conclusions: Trained professional emergency rescue workers perform rescue breathing somewhat faster than lay rescuers or medical students, but still require two and one half times longer than recommended. The time required to perform these breaths significantly decreases the number of chest compressions delivered per minute. This may affect outcome as experimental studies have shown that more than 80 compressions delivered per minute are necessary for survival from prolonged cardiac arrest.

Survival rates from out-of-hospital cardiac arrest continue to be low despite periodic updates in the Guidelines for Emergency Medical Services and periodic improvements such as the addition of automatic external defibrillators (AEDs). The low incidence of bystander cardiopulmonary resuscitation (CPR), substantial time without chest compressions throughout the resuscitation effort, and a lack of response to initial defibrillation after prolonged ventricular fibrillation contribute to these unacceptably poor results. Resuscitation guidelines are only revised every 5 to 7 years and can be difficult to change because of the lack of randomized controlled trials in humans. Such trials are rare because of a number of logistical difficulties, including the problem of obtaining informed consent. An alternative approach to advancing resuscitation science is for evidence-based demonstration projects in areas that have adequate records, so that one may determine whether the new approach improves survival. This is reasonable because the current guidelines make provisions for deviations under certain local circumstances or as directed by the emergency medical services medical director. A wealth of experimental evidence indicates that interruption of chest compressions for any reason in patients with cardiac arrest is deleterious. Accordingly, a new approach to out-of-hospital cardiac arrest called cardiocerebral resuscitation (CCR) was developed that places more emphasis on chest compressions for witnessed cardiac arrest in adults and de-emphasizes ventilation. There is also emphasis on chest compressions before defibrillation in circulatory phase of cardiac arrest. CCR was initiated in Tucson, Arizona, in November 2003, and in two rural Wisconsin counties in early 2004.

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.

Stagnant survival rates in out-of-hospital cardiac arrest remain a great impetus for advancing resuscitation science. International resuscitation guidelines, with all their advantages for standardizing resuscitation therapeutic protocols, can be difficult to change. A formalized evidence-based process has been adopted by the International Liason Committee on Resuscitation (ILCOR) in formulating such guidelines. Currently, randomized clinical trials are considered optimal evidence, and very few major changes in the Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care are made without such. An alternative approach is to allow externally controlled clinical trials more weight in Guideline formulation and resuscitation protocol adoption. In Tucson, Arizona (USA), the Fire Department cardiac arrest database has revealed a number of resuscitation issues. These include a poor bystander CPR rate, a lack of response to initial defibrillation after prolonged ventricular fibrillation, and substantial time without chest compressions during the resuscitation effort. A local change in our previous resuscitation protocols had been instituted based upon this historical database information.

Although arginine vasopressin (AVP) has been shown to be a promising drug during cardiopulmonary resuscitation (CPR), concern has been raised about the potential for AVP-mediated vasoconstriction of the coronary arteries. In a prospective, randomized laboratory investigation employing an established porcine model, the effects of AVP on haemodynamic variables, left anterior descending (LAD) coronary artery cross sectional area employing intravascular ultrasound (IVUS), and return of spontaneous circulation were studied. During sinus rhythm, the LAD coronary artery cross sectional area was measured by IVUS at baseline, and 90 s and 5 min after AVP (0.4 U/kg IV). Following a 60 min recovery, ventricular fibrillation was induced. At 4 min, chest compressions were initiated; AVP (0.4 U/kg IV) was injected at 5.5 min, and defibrillation performed at 8 min. LAD coronary artery cross sectional area was measured by IVUS at the pre-arrest baseline, 90 s after drug injection during CPR, and 5 min after return of spontaneous circulation. Compared with baseline, the mid-LAD coronary artery cross sectional area increased significantly (P<.05) 90 s and 5 min after AVP administration (9.2+/-.5mm2 versus 10.7+/-.6mm2 versus 11.7+/-.6mm2, respectively) during normal sinus rhythm. Similarly during ventricular fibrillation and CPR plus AVP, the mid-LAD coronary artery cross sectional area increased at 90 s after AVP compared with baseline (9.5+/-.6mm2 versus 11.0+/-.7mm2; P<.05). Moreover, the cross sectional area increased further 5 min after return of spontaneous circulation (9.5+/-.6mm2 versus 14.0+/-.8mm2, P<.05). In conclusion, in this experimental model with normal coronary arteries, AVP resulted in significantly increased LAD coronary artery cross sectional area during normal sinus rhythm, during ventricular fibrillation with CPR, and after return of spontaneous circulation.

Objective: To compare the effect on postresuscitation left ventricular function of vasopressin vs. epinephrine used during cardiopulmonary resuscitation in a swine model of prolonged prehospital ventricular fibrillation., Design: Prospective, randomized experimental study., Setting: University large animal resuscitation research laboratory., Subjects: Forty-eight swine (29 +/- 1 kg)., Interventions: Resuscitation after 12.5 mins of untreated ventricular fibrillation, randomizing animals during cardiopulmonary resuscitation to treatment with epinephrine, vasopressin, or vasopressin followed by a vasopressin antagonist administered in the postresuscitation period., Measurements and Main Results: Serial measurements of left ventricular systolic and diastolic function (prearrest, postresuscitation at 30 mins and 6 hrs) and 24-hr survival. Animals receiving vasopressin had more postresuscitation left ventricular dysfunction than those receiving epinephrine (p < .05). The vasopressin antagonist produced vasodilation and improved early postresuscitation left ventricular systolic and diastolic function but did not have a lasting effect on such postresuscitation ventricular function and decreased 24-hr survival compared with the use of vasopressin alone (3/16 vs. 10/16 survivors; p < .05)., Conclusions: Vasopressin use during cardiopulmonary resuscitation results in worse postresuscitation left ventricular function early but did not compromise 24-hr outcome. Reversal of vasopressin's effect with a specific V-1 antagonist in the postresuscitation period did not improve survival.

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.

Study Objective: After prolonged ventricular fibrillation (VF), precountershock cardiopulmonary resuscitation (CPR) will improve myocardial "readiness" for defibrillation compared with immediate defibrillation., Methods: After 10 minutes of untreated VF, 32 swine (27+/-1 kg) were randomly assigned to receive immediate countershocks (DEFIB), CPR for 3 minutes followed by countershocks (CPR), or CPR for 3 minutes plus intravenous epinephrine followed by countershocks (CPR+EPI). VF waveform was evaluated by fast Fourier transformation., Results: VF amplitude and median frequency by fast Fourier transformation decreased during the untreated VF interval in all groups, and the median frequency subsequently increased during each minute of precountershock CPR. Although the VF median frequency in the 3 groups did not differ after 10 minutes of untreated VF (8.9+/-0.8 Hz versus 8.4+/-0.5 Hz versus 7.3+/-0.5 Hz, respectively), immediately before the first shock the VF median frequency was much lower in the DEFIB group than in either the CPR or CPR+EPI groups (8.9+/-0.8 Hz versus 13.1+/-0.8 Hz versus 13.8+/-0.9 Hz, respectively; P <.01). None of the 10 animals in the DEFIB group attained return of spontaneous circulation after the first set of shocks versus 5 of 10 animals in the CPR group and 6 of 12 animals in the CPR+EPI group (DEFIB versus each CPR group; P <.05). Cardiac output 1 hour after resuscitation was substantially worse in the DEFIB group than in the CPR or CPR+EPI groups (74+/-7 mL/kg per minute versus 119+/-7 mL/kg per minute versus 104+/-15 mL/kg per minute; P <.05)., Conclusion: Precountershock CPR can result in substantial physiologic benefits compared with immediate defibrillation in the setting of prolonged VF. Moreover, these benefits can be attained with or without the addition of intravenous epinephrine.

Study Objective: The optimal ratio of chest compressions to ventilations during cardiopulmonary resuscitation (CPR) is unknown. We determine 24-hour survival and neurologic outcome, comparing 4 different chest compression-ventilation CPR ratios in a porcine model of prolonged cardiac arrest and bystander CPR., Methods: Forty swine were instrumented and subjected to 3 minutes of ventricular fibrillation followed by 12 minutes of CPR by using 1 of 4 models of chest compression-ventilation ratios as follows: (1) standard CPR with a ratio of 15:2; (2) CC-CPR, chest compressions only with no ventilations for 12 minutes; (3) 50:5-CPR, CPR with a ratio of 50:5 compressions to ventilations, as advocated by authorities in Great Britain; and (4) 100:2-CPR, 4 minutes of chest compressions only followed by CPR with a ratio of 100:2 compressions to ventilations. CPR was followed by standard advanced cardiac life support, 1 hour of critical care, and 24 hours of observation, followed by a neurologic evaluation., Results: There were no statistically significant differences in 24-hour survival among the 4 groups (standard CPR, 7/10; CC-CPR, 7/10; 50:5-CPR, 8/10; 100:2-CPR, 9/10). There were significant differences in 24-hour neurologic function, as evaluated by using the swine cerebral performance category scale. The animals receiving 100:2-CPR had significantly better neurologic function at 24 hours than the standard CPR group with a 15:2 ratio (1.5 versus 2.5; P =.007). The 100:2-CPR group also had better neurologic function than the CC-CPR group, which received chest compressions with no ventilations (1.5 versus 2.3; P =.027). Coronary perfusion pressures, aortic pressures, and myocardial and kidney blood flows were not significantly different among the groups. Coronary perfusion pressure as an integrated area under the curve was significantly better in the CC-CPR group than in the standard CPR group (P =.04). Minute ventilation and PaO (2) were significantly lower in the CC-CPR group., Conclusion: In this experimental model of bystander CPR, the group receiving compressions only for 4 minutes followed by a compression-ventilation ratio of 100:2 achieved better neurologic outcome than the group receiving standard CPR and CC-CPR. Consideration of alternative chest compression-ventilation ratios might be appropriate.

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 2002 Elsevier Science Ireland Ltd.)

Background: Post resuscitation myocardial stunning is well described and recognized as a significant contributor to poor long-term outcome following cardiac arrest. Optimal strategies for treatment have not been determined., Methods: Ten domestic swine (49+/-3 kg) underwent 15 min of untreated ventricular fibrillation before being successfully resuscitated. Left ventricular systolic and diastolic function was measured at pre-arrest baseline, at 30 min and at 6 h post resuscitation. Five animals were treated immediately after resuscitation with intra-aortic balloon counterpulsation (IABP) and five were given dobutamine (5 mcg/kg per min)., Results: No baseline differences were found. At 30 min post resuscitation pulmonary capillary wedge pressure and LVEDP were significantly higher (16+/-3 vs. 7+/-1 and 20+/-2 vs. 11+/-1 mmHg) while LV isovolumic relaxation ('Tau') was significantly longer (34+/-2 vs. 20+/-2 ms) in the IABP treated versus the dobutamine treated animals. Likewise, at 6 h post resuscitation LV ejection fraction was significantly less (21+/-6 vs. 39+/-4%), and LVEDP significantly higher (18 vs. 10 mmHg) in the IABP group. Heart rate was not different between the groups at any time post resuscitation., Conclusion: Dobutamine was superior to IABP for treatment of post resuscitation left ventricular systolic and diastolic dysfunction. The hypothesized advantage of IABP for treatment of post resuscitation myocardial stunning without excessively raising the heart rate like dobutamine was not realized.

The best method for employment of phased chest and abdominal compression-decompression (Lifestick) cardiopulmonary resuscitation (CPR) has yet to be determined. Of particular concern with using this technique is the combining of ventilation with the phased compressions and decompressions. Twenty domestic swine (50+/-1 kg) were equally divided into four groups. Following 10 min of untreated VF, CPR was begun. Group 1 received Lifestick (LS) CPR with only passive ventilation ('passive'); Group 2 received LS-CPR with synchronized positive pressure ventilations (ppv) at a chest compression ratio of 15:2 (15:2 S); Group 3 had LS-CPR with synchronized ppv at 5:1 (5:1 S); and Group 4 received LS-CPR with asynchronous ppv at 5:1 (5:1 A). Endpoints included hemodynamics, blood gases, minute ventilation, and 24 h outcome. Asynchronous ventilation (5:1 A) had significantly worse hemodynamics including aortic and right atrial systolic, aortic diastolic, and coronary perfusion pressures than the other groups (P<0.05). Passive ventilation had the poorest arterial and mixed venous blood gases (P<0.05), but did not differ from 15:2 S in minute ventilation produced (8 vs 10 l/min). No differences in outcome were seen. The ventilation technique combined with LS-CPR can make a significant difference in hemodynamics as well as ventilation. Optimizing other forms of basic and advanced cardiac life support through different ventilation methods deserves new consideration, including a re-examination of the current single rescuer recommendation of a 15:2 ratio. Optimal ventilation strategy when using the LS device at 60 compressions per min appears to be 5:1 S. Such data is important for conducting clinical trials with this new CPR adjunct.

Open chest cardiac massage has been shown to be superior to closed-chest cardiopulmonary resuscitation for both hemodynamics produced during resuscitation and ultimate resuscitation success. The inexperience of many rescuers with emergency thoracotomy, along with the associated morbidity contributes to the continued reluctance in the use of invasive cardiopulmonary resuscitation techniques. A device has been developed for performing 'minimally invasive' direct cardiac massage. This technique was compared to standard closed-chest CPR for resuscitation results in 20 swine during prolonged ventricular fibrillation cardiac arrest. Minimally invasive direct cardiac massage was superior to closed-chest CPR for return of spontaneous circulation (7/10 vs. 2/10; P<0.02) and coronary perfusion pressure at 30 min of CPR (17+/-9 vs. 6+/-6 mmHg; P<0.05). No significant injuries altering outcome were found with the invasive device. Throughout most of the time course of the study no significant differences in end-tidal expired carbon dioxide levels were noted. Nor were there any differences in 24-h survival. Improvements in assuring proper placement of the device on the epicardium should make this technique a potent advanced cardiac life support adjunct.

Background: Vasoconstriction during cardiopulmonary resuscitation (CPR) improves coronary perfusion pressure (CPP) and thereby outcome. The combination of endothelin-1 (ET-1) plus epinephrine improved CPP during CPR compared with epinephrine alone in a canine cardiac arrest model. The effect of the combination on outcome variables, such as successful resuscitation and survival, has not been investigated., Methods and Results: Twenty-seven swine were randomly provided with 1 mg epinephrine (Epi group) or 1 mg epinephrine plus 0.1 mg ET-1 (ET-1 group) during a prolonged ventricular fibrillatory cardiac arrest. ET-1 resulted in substantially superior aortic relaxation pressure and CPP during CPR. These hemodynamic improvements tended to increase initial rates of restoration of spontaneous circulation (8 of 10 versus 8 of 17, P=0.12). However, continued intense vasoconstriction from ET-1 led to higher aortic diastolic pressure and very narrow pulse pressure after resuscitation. The mean pulse pressure 1 hour after resuscitation was 7+/-8 mm Hg with ET-1 versus 24+/-1 mm Hg with Epi, P<0.01. Most importantly, the postresuscitation mortality was dramatically higher in the ET-1 group (6 of 8 versus 0 of 8 in the Epi group, P<0.01)., Conclusions: These data establish that administration of ET-1 during CPR can result in worse postresuscitation outcome. The intense vasoconstriction from ET-1 improved CPP during CPR but had detrimental effects in the postresuscitation period.