Outcomes by rescue shock number during the metabolic phase of porcine ventricular fibrillation resuscitation.

BACKGROUND: Optimal resuscitation duration before the first rescue shock (RS) to maximize the probability of success after prolonged ventricular fibrillation (VF) cardiac arrest remains unknown. The purpose of this study was to determine the occurrence of return of spontaneous circulation (ROSC) and survival by RS attempt after 12 minutes of untreated VF. METHODS: This was a secondary analysis of prospectively collected data from an institutional animal care and use committee-approved protocol. Fifty-three swine (30-35 kg) were instrumented under anesthesia. Ventricular fibrillation was electrically induced. After 12 minutes of untreated VF, cardiopulmonary resuscitation (CPR) was initiated (and continued as necessary (prn)) and a standard dose of epinephrine (0.01 mg/kg) was given (and repeated every 3 (q3) minutes prn). The first RS was delivered after 3 minutes of CPR (and q3 minutes thereafter prn). Each failed RS was followed (in series) by vasopressin (0.57 mg/kg), amiodarone (4.3 mg/kg), and sodium bicarbonate (1 mEq/kg) prn. Resuscitation continued until ROSC or 20-minute elapsed time. The primary outcomes were ROSC and 20-minute survival. Data were analyzed using descriptive statistics. RESULTS: After 3 minutes of resuscitation, 1 animal (1.9% [95% confidence interval {CI, 0.3-10.0]) achieved ROSC on RS1 and survived. After 6 minutes of resuscitation, 17 animals (32.1% [95% CI, 21.1-45.5]) achieved ROSC on RS2 and 15 (28.3% [95% CI, 18.0-41.6]) survived. Twelve additional animals had ROSC and survival with continued resuscitation. In 23 animals, ROSC was never achieved and efforts were terminated per protocol. CONCLUSION: Our data suggest that during the metabolic phase of VF, 3 minutes of CPR and 1 standard dose of epinephrine may be insufficient to achieve ROSC on the first RS attempt. A longer duration of CPR and/or additional vasopressors may increase the likelihood of successful defibrillation.

Towards the automated analysis and database development of defibrillator data from cardiac arrest.

BACKGROUND: During resuscitation of cardiac arrest victims a variety of information in electronic format is recorded as part of the documentation of the patient care contact and in order to be provided for case review for quality improvement. Such review requires considerable effort and resources. There is also the problem of interobserver effects. OBJECTIVE: We show that it is possible to efficiently analyze resuscitation episodes automatically using a minimal set of the available information. METHODS AND RESULTS: A minimal set of variables is defined which describe therapeutic events (compression sequences and defibrillations) and corresponding patient response events (annotated rhythm transitions). From this a state sequence representation of the resuscitation episode is constructed and an algorithm is developed for reasoning with this representation and extract review variables automatically. As a case study, the method is applied to the data abstraction process used in the King County EMS. The automatically generated variables are compared to the original ones with accuracies ≥ 90% for 18 variables and ≥ 85% for the remaining four variables. CONCLUSIONS: It is possible to use the information present in the CPR process data recorded by the AED along with rhythm and chest compression annotations to automate the episode review.

Quantitative waveform measures of the electrocardiogram as continuous physiologic feedback during resuscitation with cardiopulmonary bypass.

BACKGROUND: There are few if any real-time physiologic measures that currently provide feedback during resuscitation from cardiac arrest. Such measures could be used to guide therapy not simply based on process guidelines but on the physiologic response of the patient from moment to moment. To this end, we applied an existing technology - quantitative waveform measures (QWMs) of the ventricular fibrillation (VF) electrocardiogram (ECG) - as a continuous measure of myocardial response to reperfusion with cardiopulmonary bypass (CPB) after prolonged cardiac arrest. METHODS: Sixteen domestic, mixed-breed swine were sedated, anesthetized and paralyzed. Mechanical ventilation with room air was provided. Large diameter bypass catheters were placed in the right external jugular vein and right femoral artery for cardiopulmonary bypass (CPB). VF was induced with a 3-s 100mA transthoracic shock and left untreated for 15, 20, 25, or 30min, followed by 10min of centrifugal pump CPB (Bard CPS). Continuous Lead II ECG was recorded with an electronic data acquisition system (Power Lab, ADInstruments). Four QWMs representing 4 signal characteristics of the VF ECG were calculated in 5-s windows throughout the course of untreated VF and resuscitation with CPB. RESULTS: Four animals were assigned to each VF duration group. QWM recovery was inversely correlated with untreated VF duration, and was drastically reduced above 20min of untreated VF. Return of spontaneous circulation (ROSC) was highly unlikely after 20min of untreated VF. CONCLUSION: QWMs of the VF ECG provided a real-time metric of myocardial electrophysiologic response to reperfusion with CPB. Resuscitation from greater than 20min of untreated cardiac arrest was unlikely. QWMs may be useful for titrating CPB duration before defibrillation and assessing CPR quality independently of process guidelines.

A randomized comparison of cardiocerebral and cardiopulmonary resuscitation using a swine model of prolonged ventricular fibrillation.

BACKGROUND: Cardiocerebral resuscitation (CCR) is reportedly superior to cardiopulmonary resuscitation (CPR) for primary cardiac arrest in the prehospital setting. This study was done using a swine model of prolonged ventricular fibrillation (VF) to quantify the effect of the emergency medical services component of CCR with intraosseous access (CCR-IO) compared with standard CPR with intravenous access (CPR-IV) as it is typically performed during out-of-hospital cardiac arrest (OHCA) resuscitation in a prospective randomized fashion. METHODS: Fifty-three animals were instrumented under anesthesia and VF was electrically induced. After 10 min of untreated VF, baseline characteristics were recorded, and animals were block randomized to one of two resuscitation schemes. The controls had mechanical chest compressions at 100/min with ventilations at a ratio of 30:2. Consistent with clinical practice, two 30-s pauses in chest compressions occurred to simulate attempts to accomplish endotracheal intubation at minutes 1 and 3 of CPR and successful IV access was simulated to occur three additional minutes after endotracheal intubation. The CCR group had continuous uninterrupted mechanical chest compressions at 100/min. No active ventilations were provided. A tibial IO needle was placed in real time for vascular access. Both groups received epinephrine (0.1 mg/kg) as soon as access became available followed by 2.5 min of chest compressions before the first 120 J rescue shock attempt. After successful rescue shock, standardized post-resuscitative care was provided to a 20-min endpoint. Failed rescue shock was followed by continued chest compressions with positive pressure ventilation in both groups, repeat doses of epinephrine (0.01 mg/kg) every 3 min, and rescue shock every minute as long as a shockable rhythm persisted. Group comparisons were assessed using descriptive statistics. Proportions with 95% confidence intervals were calculated for VF termination, ROSC, and survival. RESULTS: Baseline characteristics and chemistries between the two groups at VF induction and after 10 min of non-treatment were mathematically the same. The proportions of VF termination (0.50 vs. 0.82), ROSC (0.30 vs. 0.59), and 20-min survival (0.19 vs. 0.40) all strongly favored the CCR-IO group. CONCLUSION: In this swine model of witnessed VF arrest with no bystander-initiated resuscitation, CCR-IO resulted in substantial improvement in all three outcomes relative to typical emergency medical services provided CPR-IV.

Association of intramyocardial high energy phosphate concentrations with quantitative measures of the ventricular fibrillation electrocardiogram waveform.

BACKGROUND: Quantitative measures of the ventricular fibrillation (VF) electrocardiogram (ECG) have been correlated with the success of rescue shocks, making them ideal measures for guiding resuscitative interventions. Correlation of intramyocardial energy stores with the change in quantitative VF ECG measures would provide mechanistic insight into their utility. We sought to investigate the relationship between intramyocardial energy stores and four quantitative ECG measures. METHODS: Eighteen mixed-breed, domestic swine were sedated, anaesthetized and paralyzed. Swine were block randomized into three groups receiving 5, 10, or 15 min of untreated VF. Thoracotomy was performed and the heart was delivered. VF was induced by a 100 mA transthoracic shock while ECG was recorded. Biopsies of myocardial tissue were taken from the left and right ventricles after the prescribed duration of VF. Adenosine triphosphate (ATP) and adenosine diphosphate (ADP) concentrations in the tissue samples were measured. ECG data immediately prior to each biopsy were analyzed by each of four quantitative ECG methods: Scaling Exponent (ScE), Median Slope (MS), Amplitude Spectrum Area (AMSA), and logarithm of the Absolute Correlation (LAC). ATP and ADP concentrations of VF duration groups were compared. ATP and ADP concentrations were regressed against each quantitative ECG measure. RESULTS: ATP concentrations differed between VF duration groups, but ADP concentrations differed only between 5 and 10 min groups. A significant association existed between ATP and three quantitative measures--ScE, MS, and AMSA--but no significant relationship was found for ADP. CONCLUSION: Intramyocardial ATP levels correlate with quantitative measures of the ECG during ventricular fibrillation.

Effects of pre-arrest and intra-arrest hypothermia on ventricular fibrillation and resuscitation.

BACKGROUND: Hypothermia has been shown to improve survival and neurological outcomes for ventricular fibrillation (VF) cardiac arrest. The electrophysiological mechanisms of hypothermia are not well-understood, nor are the effects of beginning cooling during the resuscitation. METHODS AND RESULTS: We hypothesized that inducing hypothermia prior to the onset of VF would slow the deleterious changes seen in the ECG during VF and that inducing hypothermia at the start of resuscitation would increase the rates of ROSC and short-term survival in a porcine model of prolonged VF. We randomly assigned 42 domestic swine (27.2+/-2.3 kg) to either pretreatment with hypothermia before induction of VF (PRE), normothermic resuscitation (NORM) or intra-resuscitation hypothermia (IRH). During anesthesia, animals were instrumented via femoral cutdown. Lead II ECG was recorded continuously. PRE animals were cooled before the induction of VF, with a rapid infusion of 4 degrees normal saline (30mL/kg). VF was induced electrically, left untreated for 8min, then mechanical CPR began. During CPR the NORM animals got 30mL/kg body-temperature saline and the IRH animals got 30mL/kg 4 degrees saline. In all groups first rescue shocks were delivered after 13min of VF. We calculated the VF scaling exponent (ScE) for the entire 8min period (compared using GEE). ROSC and survival were compared with Fisher's exact test. Mean temperature in degrees C at the onset of VF was PRE=34.7 degrees (+/-0.8), NORM=37.8 (+/-0.9), and IRH=37.9 (+/-0.9). The ScE values over time were significantly lower after 8min in the PRE group (p=0.02). ROSC: PRE=10/14 (71%), NORM=6/14 (43%) and IRH=12/14 (86%); p for IRH vs. NORM=0.02. Survival: PRE=9/14 (64%), NORM=5/14 (36%), IRH 8/14 (57%). CONCLUSION: Hypothermia slowed the decay of the ECG waveform during prolonged VF. IRH improved ROSC but not short-term survival compared to NORM. It is possible to rapidly induce mild hypothermia during CPR using an IV infusion of ice-cold saline.

Logarithm of the absolute correlations of the ECG waveform estimates duration of ventricular fibrillation and predicts successful defibrillation.

BACKGROUND: Measures of the ventricular fibrillation (VF) waveform may enable better allocation of cardiac arrest treatment by discriminating which patients should receive immediate defibrillation versus alternate therapies such as CPR. We derive a new measure based on the 'roughness' of the VF waveform, the Logarithm of the Absolute Correlations (LAC), and assess and contrast how well the LAC and the previously published scaling exponent (ScE) predict the duration of VF and the likelihood of return of spontaneous circulation (ROSC) under both optimal experimental and commercial-defibrillator sampling conditions. METHODS AND RESULTS: We derived the LAC and ScE from two different populations--an animal study of 44 swine and a retrospective human sample of 158 out-of-hospital VF arrests treated with a commercial defibrillator. In the animal study, the LAC and ScE were calculated on 5s epochs of VF recorded at 1000 samples/s and then down sampled to 125 samples/s. In the human study, the LAC and ScE were calculated using 6s epochs recorded at 200 samples/s that occurred immediately prior to the initial shock. We compared the LAC and ScE measures using the Spearman correlation coefficients (CC) and areas under the receiver operating characteristic curve (AUC). RESULTS: In the animal study, the LAC and ScE were highly correlated at 1000 sample/s (CC=0.93) but not at 125 samples/s (CC=-0.06). These correlations were reflected in how well the measures discriminated VF of < or =5 versus >5 min: AUC at 1000 samples/s was similar for LAC compared to ScE (0.71 versus 0.76). However AUC at 125 samples was greater for LAC compared to ScE (0.75 versus 0.62). In the human study, the LAC measure was a better predictor of ROSC following initial defibrillation as reflected by an AUC of 0.77 for LAC compared to 0.57 for ScE. CONCLUSIONS: The LAC is an improvement over the ScE because the LAC retains its prognostic characteristics at lower ECG sampling rates typical of current clinical defibrillators. Hence, the LAC may have a role in better allocating treatment in resuscitation of VF cardiac arrest.

The effect of adenosine A1 receptor antagonism on return of spontaneous circulation and short-term survival in prolonged ventricular fibrillation.

BACKGROUND: Endogenous adenosine (ADO) is cardioprotective during ischemia and its myocardial concentration increases during untreated ventricular fibrillation (VF). We have previously shown that ADO A1 receptor (ADOA1R) antagonism hastens the time-dependent decay in VF waveform morphology during the circulatory phase of cardiac arrest. OBJECTIVE: To determine the effect of ADOA1R antagonism on ROSC and short-term survival in prolonged VF. METHODS: Thirty-six swine were assigned by block randomization to one of three groups: a group that received only vehicle (CONTROL), an ADOA1R antagonist pretreatment group (PRE), and a group that was given ADOA1R antagonist during resuscitation (DURING). The animals were instrumented under anesthesia, and ADOA1R antagonist or vehicle, per group assignment, was infused 5 minutes prior to VF induction. At minute 8 of untreated VF, chest compression with ventilation was initiated and a standard drug cocktail, with ADOA1R antagonist or vehicle, was given. The first rescue shock (150 J biphasic) was delivered after 11 minutes of VF. Proportions with 95% confidence intervals (CIs) were calculated for the two outcome measures. RESULTS: The baseline characteristics and chemistry values for the three groups were mathematically the same. The DURING group had a greater proportion of female animals (seven of 12) in comparison with the CONTROL group (two of 12) (p=0.03). ADOA1R antagonism hastened the decay of VF as previously demonstrated, but the rate of ROSC was the same for all groups: CONTROL=seven of 12, PRE=six of 12, and DURING=seven of 12. There were also no differences in short-term survival: CONTROL=four of 12, PRE=five of 12, and DURING=seven of 12. CONCLUSIONS: In this study, ADOA1R antagonism had no effect on outcome whether given before induction of VF or upon resuscitation after 8 minutes of untreated VF. The role of endogenous ADO in prolonged VF remains unclear.

A blinded, randomized controlled evaluation of an impedance threshold device during cardiopulmonary resuscitation in swine.

BACKGROUND: An impedance threshold device (ITD) has been designed to enhance circulation during CPR. A recent study suggests that the ITD does not improve hemodynamics and that it may actually worsen outcomes. We sought to independently assess the effect of the ITD on coronary perfusion pressure (CPP) and passive ventilation (PaCO(2) and PaO(2)) during standard CPR (S-CPR), and its impact on the return of spontaneous circulation (ROSC) and short-term survival in a blinded fashion. METHODS: Thirty male swine were instrumented under anesthesia. Ventricular fibrillation (VF) was electrically induced. CPP was continuously recorded. After 8 min of untreated VF, baseline characteristics were documented and S-CPR initiated. After 3 cycles of S-CPR, an ABG was drawn and drugs were given. Following 6 additional cycles of S-CPR, an ABG was drawn and the first rescue shock was delivered. Group comparisons were assessed using descriptive statistics. Proportions with 95% confidence intervals were calculated for outcomes. RESULTS: Baseline characteristics between the two groups were the same. The mean CPP in the ITD group was 51.2 mmHg [95% CI: 37.7, 64.7] compared to 50.2 mmHg [95% CI: 37.0, 63.4] in the sham group. The PaCO(2) and PaO(2) were 68 Torr [95% CI: 55.7, 79.5] and 103 Torr [95% CI: 76, 129] in the ITD group and 59 Torr [95% CI: 49.1, 68.5] and 137 Torr [95% CI: 83, 191] in the sham group. The rate of ROSC was 14/15 in both groups and 13 animals in each groups survived. CONCLUSIONS: In this independent blinded study, use of the active ITD had no significant impact on CPP, passive ventilation, or outcomes compared to the sham device.

The effect of ischemia on ventricular fibrillation as measured by fractal dimension and frequency measures.

INTRODUCTION: Most animal studies of ventricular fibrillation (VF) waveform characteristics involve healthy animals with VF initiated by electric shock. However, clinical VF is usually the result of ischemia. The waveform characteristics in these two types of VF may differ. The angular velocity (AV), frequency ratio (FR) and median frequency (MF) are three frequency-based measures of VF. The scaling exponent (ScE), the logarithm of the absolute correlations (LAC) and the Hurst exponent (HE) are three measures of the fractal dimension of VF. HYPOTHESIS: We hypothesized that these quantitative measures would differ between ischemic and electrically initiated VF. METHODS: VF was induced in 14 swine by electric shock and in 12 swine by ischemia. For ischemia induced VF animals, an angioplasty catheter was positioned in the mid-LAD and the balloon inflated. A mean of 891+/-608 (S.D.)s later, VF occurred. For electrically induced animals, an AC current was passed through a catheter in the RV. Following initiation by either method, VF was recorded for 7min. Sequential 5s epochs were analyzed for AV, FR, MF and fractal dimension measures. RESULTS: Ischemic VF demonstrated a significantly higher fractal dimension as estimated by the ScE for the first 0-90s (p=0.021) and for 90-180s (p=0.016). The Hurst exponent was significantly higher for ischemic VF for both 0-90s (p<0.0001) and 90-180s (p<0.0001). The fractal dimension as estimated by the LAC method was not significantly different for 0-90s (p=0.056) but was highly significant for 90-180s (p=0.001). During the initial 90s the groups did differ in all measures of frequency as follows: AV (p<0.001), FR (p<0.001), MF (p<0.001). These differences did not persist beyond 90s except for a mild elevation of the FR after 270s (p<0.02). CONCLUSION: Fractal based measures indicate an increase in the fractal dimension of ischemia induced VF for the first 180s when compared to electrically induced VF. Frequency-based measures uniformly demonstrate a pattern of higher frequencies for electrically induced VF for the first 90s. The increased fractal dimension and decreased frequencies associated with ischemia induced VF may reflect changes in the underlying myocardial physiology that can be used to guide therapies.

Adenosine A1 receptor antagonism hastens the decay in ventricular fibrillation waveform morphology during porcine cardiac arrest.

BACKGROUND: Endogenous adenosine (ADO) is known to be cardioprotective during acute myocardial ischemia. Coronary sinus ADO concentration has recently been shown to increase nearly 13-fold over baseline levels after 5 min of untreated ventricular fibrillation (VF). The role of ADO in VF has never been previously examined. The objective of this study was to determine the effect of ADO receptor antagonism, as measured by the scaling exponent (ScE), on the degeneration of VF over time during the circulatory phase of cardiac arrest. METHODS AND RESULTS: A well-established swine model of prolonged VF arrest was used for this experiment. Eighteen domestic mixed-breed swine were assigned by block randomization to receive either DTI-0017 (5mg/kg), a potent ADO A(1) receptor antagonist or placebo in a double-blind fashion. The animals were instrumented under general anesthesia and acclimatized. The assigned solution was infused over 5 min. One minute after the infusion was completed, VF was induced with a 3s, 60 Hz, 100 mA transthoracic shock and left untreated. Lead II ECG was monitored continuously and recorded at 1000 samples/s. It was determined a priori that evaluation of the plots would be limited to a previously observed plateau phase historically occurring between 5 and 8 min corresponding to the circulatory phase of cardiac arrest. The scaling exponent values over this period were calculated for each of the 18 recordings using custom MATLAB routines. Using the Wald statistic to produce the Chi square distributions the null hypothesis, that there was no difference between the two groups, was tested. The Wald statistic calculation based on eight epochs from 300 to 475 s in placebo and DTI groups was significant to reject the null hypothesis of no difference in the groupxtime interaction at the 0.015 level (Chi square distribution for Wald=17.49, d.f.=7). CONCLUSIONS: In this swine model, adenosine A(1) receptor antagonism accelerated the natural decay in the ECG VF waveform during the circulatory phase of cardiac arrest. Our findings would suggest that endogenous adenosine has cardioprotective effects during sudden cardiac arrest by slowing the time-dependent degeneration of VF.

The frequency ratio: an improved method to estimate ventricular fibrillation duration based on Fourier analysis of the waveform.

BACKGROUND: CPR prior to defibrillation improves survival from prolonged ventricular fibrillation (VF) by over 10%, based on recent studies. Waveform analysis could identify those patients with VF of over 5 to 7-min duration who should receive CPR first. A method based on the changes in the Fourier-derived frequency spectrum over time could improve the ability to identify prolonged VF. METHODS AND RESULTS: The Fourier frequency spectra were calculated on 5-s epochs of VF from 45 swine for 12.5 min. The average power at each frequency shows a marked loss of frequencies above 8 Hz occurring at 5 min accompanied by an increase in the power in frequency spectra from 3 to 5 Hz. A measure termed the frequency ratio is defined as the ratio of the power in the high frequency band from 8 to 24 Hz compared to the power in the low frequency band from 3 to 5 Hz. The frequency ratio is shown to detect 90% of epochs with VF less than 5 min while allowing selection of 74% of those epochs over 5 min. When the frequency ratio is set to detect 90% of episodes of VF under 7 min, it is able to select 88% of those traces with VF over 7 min. The receiver operating curve (ROC) for the frequency ratio has an area under the curve of 0.91 at 5 min and 0.95 at 7 min of VF duration. CONCLUSIONS: The frequency ratio is an improved frequency-based measure of VF duration. Waveform analysis techniques could determine which patients should receive shock first and which should receive a period of CPR prior to shock, thereby increasing probability of survival.

Angular velocity: a new method to improve prediction of ventricular fibrillation duration.

Ventricular fibrillation (VF) is a leading cause of sudden death. Electrical defibrillation is the primary modality of treatment, but evidence is accumulating that its use in the late stage of VF prior to providing ventilation, chest compressions and the administration of appropriate medication is detrimental. In VF of <5 min duration a 'shock first' strategy is effective. In VF of 5> min duration a 'perfuse first' approach is more effective. Because of the difficulty in determining the duration of VF in the clinical setting we have sought to develop method which analyze 5 s intervals of VF waveform and quickly provide an estimate of duration. Such methods would be useful in directing clinical interventions. Using methods of nonlinear dynamics and fractal geometry we have previously derived a quantitative measure of VF duration, namely the scaling exponent (ScE). In this study we report on a novel method also based on nonlinear dynamics, the angular velocity (AV). By constructing a flat, circular disk-shaped structure in a three-dimensional phase space and measuring the velocity of rotation of the position vector over time, a statistic is developed which rises from 58 rad/s at 1 min to 79 rad/s at 4 min and then decreases in a linear manner to 32 rad/s at 12.5 min. Using ScE and AV probability density estimated, VF of <5 min duration can be identified with 90% sensitivity on the basis of a single 5 s recording of the waveform. The combination of ScE and AV can be used in developing strategies for the treatment of VF during the different clinical phases of VF.

Ventricular fibrillation scaling exponent can guide timing of defibrillation and other therapies.

BACKGROUND: The scaling exponent (ScE) of the ventricular fibrillation (VF) waveform correlates with duration of VF and predicts defibrillation outcome. We compared 4 therapeutic approaches to the treatment of VF of various durations. METHODS AND RESULTS: Seventy-two swine (19.5 to 25.7 kg) were randomly assigned to 1 of 9 groups (n=8 each). VF was induced and left untreated until the ScE reached 1.10, 1.20, 1.30, or 1.40. Animals were treated with either immediate countershock (IC); 3 minutes of CPR before the first countershock (CPR); CPR for 2 minutes, then drugs given with 3 more minutes of CPR before the first shock (CPR-D); or drugs given at the start of CPR with 3 minutes of CPR before the first shock (Drugs+CPR). Return of spontaneous circulation (ROSC) and 1-hour survival were analyzed with chi2 and Kaplan-Meier survival curves. IC was effective when the ScE was low but had decreasing success as the ScE increased. No animals in the 1.30 or 1.40 groups had ROSC from IC (0 of 16). CPR did not improve first shock outcome in the 1.20 CPR group (3 of 8 ROSC). Kaplan-Meier survival analyses indicated that IC significantly delayed time to ROSC in both the 1.3 (P=0.0006) and the 1.4 (P=0.005) groups. CONCLUSIONS: VF of brief to moderate duration is effectively treated by IC. When VF is prolonged, as indicated by an ScE of 1.3 or greater, IC was not effective and delayed time to ROSC. The ScE can help in choosing the first intervention in the treatment of VF.

Immediate defibrillation versus interventions first in a swine model of prolonged ventricular fibrillation.

OBJECTIVES: we compared time-dependent rescue shock success when delivered immediately, to defibrillation preceded by 3 min of CPR, with and without high dose epinephrine (HDE) in a swine model of prolonged ventricular fibrillation (VF). Our hypotheses were that pretreatment with CPR and HDE would produce higher rates of successful first-shock defibrillation and would prevent decay of the VF waveform, as measured by the scaling exponent (ScE), when compared to immediate defibrillation. We also sought to determine the predictive value of the ScE in determining post-shock outcomes. METHODS: we anesthetized and instrumented 60 domestic swine (19.6-26.4 kg). VF was induced electrically and was untreated for 8, 11 or 14 min. ECG was recorded digitally at a rate of 1000 samples/s with 5-s epochs used to calculate the ScE. We assigned randomly swine to seven groups (number denotes timing of first rescue shock). Three groups had rescue shocks as the first intervention (RSF) after 8 min of VF (RSF-8), 11 min of VF (RSF-11), or 14 min of VF (RSF-14): two groups had CPR for 3 min (then rescue shock) beginning at 8 min (CPR-11) or 11 min of VF (CPR-14); and two groups got CPR for 3 min with 0.1 mg/kg epinephrine (adrenaline) (then rescue shock) beginning at 8 min of VF (HDE-11) or 11 min of VF (HDE-14). Fixed-dose 70 J BDW rescue shocks were used for all shocks. Defibrillation outcome was classified immediately and 30 s post-shock as successful (either restoration of spontaneous circulation [ROSC] or restoration of organized electrical activity [ROEA]), or failed (remained in VF, or asystole). Data were analyzed with RMANOVA, multiple logistic regression, Fisher's exact tests, and ROC curves. RESULTS: successful first-shock defibrillation occurred in 3/8 (38%) RSF-8; 1/9 (11%) RSF-11; 2/9 (22%) CPR-11; 7/9 (77%) HDE-11; 0/9 (0%) RSF-14; 0/7 (0%) CPR-14; and 1/8 (13%) HDE-14, (p=0.059 IRS-8 vs. HDE-11). First-shock ROSC occurred in 5/9 (56%) HDE-11 animals, 1/8 (13%) HDE-14 and zero in all other groups (p=0.03). Mean ScE values at 11 min VF for the RSF-11 (1.46) was higher than both CPR-11 (1.26), and HDE-11 (1.27); and RSF-14 (1.60) was higher than CPR-14 (1.47) and HDE-14 (1.46); group by time p=0.002. ROC areas under the curves using the ScE as a predictor of shock outcome were 0.84 for immediate success, 0.85 for sustained success, and 0.81 for ROSC. CONCLUSIONS: HDE-11 showed a tendency for producing a higher rate of first-shock success and ROSC. Interventions prior to rescue shock prevented deterioration of the VF waveform and improved rescue shock outcomes. The ScE accurately predicted 81-85% of post-rescue shock outcomes.

Dynamic nature of electrocardiographic waveform predicts rescue shock outcome in porcine ventricular fibrillation.

STUDY OBJECTIVE: Survival decreases with duration of ventricular fibrillation, and it is possible that failed rescue shocks increase myocardial damage. Structure in the ECG signal during ventricular fibrillation can be quantified by using the scaling exponent, a dimensionless measure that correlates with ventricular fibrillation duration. This study examined whether the scaling exponent could predict rescue shock success and whether unsuccessful rescue shocks altered the structure of the ventricular fibrillation waveform and the responsiveness to subsequent rescue shocks. METHODS: Ventricular fibrillation was electrically induced in 44 anesthetized swine, which were randomly assigned to receive 70-J biphasic rescue shocks at 2, 4, 6, 8, or 10 minutes. If rescue shocks failed, up to 2 subsequent rescue shocks were performed at 2-minute intervals. The scaling exponent was calculated at 1-second intervals from ECG to quantify the organization of the ventricular fibrillation waveform. RESULTS: A total of 92 rescue shocks were delivered, of which 23 successfully converted ventricular fibrillation to an organized rhythm (immediate success). After these 23 rescue shocks, 14 swine sustained organized rhythms for more than 30 seconds (sustained success). Lower scaling exponent values were associated with increased probability of successful rescue shocks. Receiver operating characteristic curves had an area under the curve of 0.86 for immediate rescue shock success and 0.93 for sustained rescue shock success. Failed rescue shocks increased the rate of scaling exponent increase over time but did not appear to affect subsequent rescue shock success when the scaling exponent was taken into account. CONCLUSION: Highly deterministic ventricular fibrillation, reflected by a low scaling exponent, predicted rescue shock success regardless of antecedent failed rescue shocks. In addition, unsuccessful rescue shocks might decrease post-rescue shock ventricular fibrillation waveform organization.