Duration Of Untreated Ventricular Fibrillation Research Articles

Pralidoxime-Induced Potentiation of the Pressor Effect of Adrenaline and Hastened Successful Resuscitation by Pralidoxime in a Porcine Cardiac Arrest Model.

Pralidoxime potentiated the pressor effect of adrenaline and facilitated restoration of spontaneous circulation (ROSC) after prolonged cardiac arrest. In this study, we hypothesised that pralidoxime would hasten ROSC in a model with a short duration of untreated ventricular fibrillation (VF). We also hypothesised that potentiation of the pressor effect of adrenaline by pralidoxime would not be accompanied by worsening of the adverse effects of adrenaline. After 5min of VF, 20 pigs randomly received either pralidoxime (40mg/kg) or saline, in combination with adrenaline, during cardiopulmonary resuscitation (CPR). Coronary perfusion pressure (CPP) during CPR, and ease of resuscitation were compared between the groups. Additionally, haemodynamic data, severity of ventricular arrhythmias, and cerebral microcirculation were measured during the 1-h post-resuscitation period. Cerebral microcirculatory blood flow and brain tissue oxygen tension (PbtO2) were measured on parietal cortices exposed through burr holes. All animals achieved ROSC. The pralidoxime group had higher CPP during CPR (P = 0.014) and required a shorter duration of CPR (P = 0.024) and smaller number of adrenaline doses (P = 0.024). During the post-resuscitation period, heart rate increased over time in the control group, and decreased steadily in the pralidoxime group. No inter-group differences were observed in the incidences of ventricular arrhythmias, cerebral microcirculatory blood flow, and PbtO2. Pralidoxime improved CPP and hastened ROSC in a model with a short duration of untreated VF. The potentiation of the pressor effect of adrenaline was not accompanied by the worsening of the adverse effects of adrenaline.

Real-Time Ventricular Fibrillation Amplitude-Spectral Area Analysis to Guide Timing of Shock Delivery Improves Defibrillation Efficacy During Cardiopulmonary Resuscitation in Swine.

BackgroundThe ventricular fibrillation amplitude spectral area (AMSA) predicts whether an electrical shock could terminate ventricular fibrillation and prompt return of spontaneous circulation. We hypothesized that AMSA can guide more precise timing for effective shock delivery during cardiopulmonary resuscitation.Methods and ResultsThree shock delivery protocols were compared in 12 pigs each after electrically induced ventricular fibrillation, with the duration of untreated ventricular fibrillation evenly stratified into 6, 9, and 12 minutes: AMSA‐Driven (AD), guided by an AMSA algorithm; Guidelines‐Driven (GD), according to cardiopulmonary resuscitation guidelines; and Guidelines‐Driven/AMSA‐Enabled (GDAE), as per GD but allowing earlier shocks upon exceeding an AMSA threshold. Shocks delivered using the AD, GD, and GDAE protocols were 21, 40, and 62, with GDAE delivering only 2 AMSA‐enabled shocks. The corresponding 240‐minute survival was 8/12, 6/12, and 2/12 (log‐rank test, P=0.035) with AD exceeding GDAE (P=0.026). The time to first shock (seconds) was (median [Q1–Q3]) 272 (161–356), 124 (124–125), and 125 (124–125) (P<0.001) with AD exceeding GD and GDAE (P<0.05); the average coronary perfusion pressure before first shock (mm Hg) was 16 (9–30), 10 (6–12), and 3 (−1 to 9) (P=0.002) with AD exceeding GDAE (P<0.05); and AMSA preceding the first shock (mV·Hz, mean±SD) was 13.3±2.2, 9.0±1.6, and 8.6±2.0 (P<0.001) with AD exceeding GD and GDAE (P<0.001). The AD protocol delivered fewer unsuccessful shocks (ie, less shock burden) yielding less postresuscitation myocardial dysfunction and higher 240‐minute survival.ConclusionsThe AD protocol improved the time precision for shock delivery, resulting in less shock burden and less postresuscitation myocardial dysfunction, potentially improving survival compared with time‐fixed, guidelines‐driven, shock delivery protocols.

Abstract 127: Severity of Postresuscitation Myocardial Dysfunction Is Dependent on the Duration of Untreated Cardiac Arrest

Introduction: The duration of untreated ventricular fibrillation (VF) is one of the major determinant for outcome of cardiac arrest (CA). We investigated the relationship between different durations of untreated VF and post-resuscitation myocardial dysfunction and survival in a pig model. Methods: An established model of myocardial infarction followed by CA and CPR was used. Twenty pigs(35-43 Kg) were subjected to 3 different untreated VF intervals, prior to mechanical CPR and defibrillation: 8-10 min; 12-13 min; or 14-15 min. Arterial and central venous pressures were invasively monitored. Ejection fraction (EF) was echocardiographically assessed together with termodilution cardiac output (CO) and high sensitivity cardiac troponin T (hs-cTnT) assay. Ninety six hr survival was evaluated. Results: All the animals were resuscitated, except for 2 in the 14-15 min VF duration (Table). More than 80% of animals survived when the duration of VF was below 13 min, compared to only 17% after 14-15 min (Fig A). The duration of untreated VF correlated with the number of defibrillations required prior to resuscitation (r=0.60, p=0.01, Table). Longer durations of VF were characterized by higher post-resuscitation heart rate and right atrium pressure and by lower post-resuscitation CO and EF (p&lt;0.01, Table). Ninety six hr EF recovered in all animals except in the pig that survived after 14-15 min VF. EF correlated with the number of defibrillation delivered (Fig B) and with hs-cTnT release (r=-0.84, p&lt;0.0001). Conclusions: In this model, post-resuscitation myocardial dysfunction and survival were affected by the duration of untreated VF in a time-dependent manner.

Variable effects of high-dose adrenaline relative to standard-dose adrenaline on resuscitation outcomes according to cardiac arrest duration

Aim of the studyAdjustment of adrenaline (epinephrine) dosage according to cardiac arrest (CA) duration, rather than administering the same dose, may theoretically improve resuscitation outcomes. We evaluated variable effects of high-dose adrenaline (HDA) relative to standard-dose adrenaline (SDA) on resuscitation outcomes according to CA duration. MethodsTwenty-eight male domestic pigs were randomised to the following 4 groups according to the dosage of adrenaline (SDA 0.02mg/kg vs. HDA 0.2mg/kg) and duration of CA before beginning cardiopulmonary resuscitation (CPR): 6min SDA, 6min HDA, 13min SDA, or 13min HDA. After the predetermined duration of untreated ventricular fibrillation, CPR was provided. ResultsAll animals in the 6min SDA, 6min HDA, and 13min HDA groups were successfully resuscitated, while only 4 of 7 pigs in the 13min SDA group were successfully resuscitated (p=0.043). HDA groups showed higher right atrial pressure, more frequent ventricular ectopic beats, higher blood glucose, higher troponin-I, and more severe metabolic acidosis than SDA groups. Animals of 13min groups showed more severe metabolic acidosis and higher troponin-I than animals of 6min groups. All successfully resuscitated animals, except two animals in the 13min HDA group, survived for 7 days (p=0.121). Neurologic deficit score was not affected by the dose of adrenaline. ConclusionHDA showed benefit in achieving restoration of spontaneous circulation in 13min CA, when compared with 6min CA. However, this benefit did not translate into improved long-term survival or neurologic outcome.

Estimation of the duration of ventricular fibrillation using ECG single feature analysis

The duration of untreated ventricular fibrillation (VF) is of paramount importance for CPR success. Moreover, therapeutic interventions taking into account the interval between cardiac arrest onset and initiation of CPR improve outcome. This study was performed to investigate whether VF feature analysis could be used to estimate the duration of VF in patients with out-of-hospital cardiac arrest. Demographic data recorded according to the Utstein guidelines and ECG recordings of 376 cardiac arrest patients from three European areas were analysed. Ten features in the time and frequency domain derived from different sub-bands of the initial VF ECG (n=127) were evaluated. The correlation between VF ECG features and cardiac arrest times was investigated using Pearson's correlation coefficient in a subset of 40 patients with reliably estimated downtimes and artefact-free initial VF tracings. No significant correlation (p<.05) between any of the VF ECG features and downtime could be found. The duration of cardiac arrest could not be estimated reliably from human VF ECG single feature analysis.

Evolution of the Stone Heart After Prolonged Cardiac Arrest

We hypothesized that progressive impairment in diastolic function during cardiopulmonary resuscitation (CPR) precedes evolution of the "stone heart" after failure of CPR. We therefore measured sequential changes in left ventricular (LV) volumes and free-wall thickness of the heart during CPR in an experimental model. Prospective, observational animal study. Medical research laboratory in an university-affiliated research and educational institute. Domestic pigs. Ventricular fibrillation (VF) was induced in 40 anesthetized male domestic pigs weighing between 38 kg and 43 kg. After 4 min, 7 min, or 10 min of untreated VF, electrical defibrillation was attempted. Failing to reverse VF in each instance, precordial compression at a rate of 80/min was begun coincident with mechanical ventilation. Coronary perfusion pressures (CPPs) were computed from the differences in time-coincident diastolic aortic and right atrial pressures. Left ventricular (LV) systolic and diastolic ventricular volumes and thickness of the LV free wall were estimated with transesophageal echocardiography. The stroke volumes (SVs) were computed from the differences in decompression diastolic and compression systolic volumes. Free-wall thickness was measured on the hearts at autopsy. Significantly greater CPPs were generated with the 4 min of untreated cardiac arrest. Progressive reductions in LV diastolic and SV and increases in LV free-wall thickness were documented with increasing duration of untreated VF. A stone heart was confirmed at autopsy in each animal that failed resuscitative efforts. Correlations with indicator dilution method and physical measurements at autopsy corresponded closely with the echocardiographic measurements. Progressive impairment in diastolic function terminates in a stone heart after prolonged intervals of cardiac arrest.

A Comparison of Biphasic and Monophasic Waveform Defibrillation After Prolonged Ventricular Fibrillation

Study objectiveTo compare the effects of biphasic defibrillation waveforms and conventional monophasic defibrillation waveforms on the success of initial defibrillation, postresuscitation myocardial function, and duration of survival after prolonged duration of untreated ventricular fibrillation (VF), including the effects of epinephrine. DesignProspective, randomized, animal study. SettingAnimal laboratory and university-affiliated research and educational institute. ParticipantsDomestic pigs. InterventionsVF was induced in 20 anesthetized domestic pigs receiving mechanical ventilation. After 10 min of untreated VF, the animals were randomized. Defibrillation was attempted with up to three 150-J biphasic waveform shocks or a conventional sequence of 200-J, 300-J, and 360-J monophasic waveform shocks. When reversal of VF was unsuccessful, precordial compression was performed for 1 min, with or without administration of epinephrine. The protocol was repeated until spontaneous circulation was restored or for a maximum of 15 min. Measurements and resultsNo significant differences in the success of initial resuscitation or in the duration of survival were observed. However, significantly less impairment of myocardial function followed biphasic shocks. Administration of epinephrine reduced the total electrical energy required for successful resuscitation with both biphasic and monophasic waveform shocks. ConclusionsLower-energy biphasic waveform shocks were as effective as conventional higher-energy monophasic waveform shocks for restoration of spontaneous circulation after 10 min of untreated VF. Significantly better postresuscitation myocardial function was observed after biphasic waveform defibrillation. Administration of epinephrine after prolonged cardiac arrest decreased the total energy required for successful resuscitation.

Effect of ventilation on resuscitation in an animal model of cardiac arrest.

The need for ventilation during the initial management of cardiac arrest is an important public health problem that is being debated. The present study was designed to determine whether ventilation affects return of spontaneous circulation from cardiac arrest in a swine model with an interval of untreated ventricular fibrillation of 6 minutes, as reported in witnessed out-of-hospital human cardiac arrest. Twenty-four animals were randomly assigned to two groups: one that received ventilation during the first 10 minutes of chest compression and one that did not. Coronary perfusion pressure and minute ventilation were continuously recorded. Arterial and mixed venous blood gases were measured at intervals. Return of spontaneous circulation was defined prospectively as an aortic systolic blood pressure of > 80 mm Hg for > 5 minutes and was the primary outcome variable. All animals were anesthetized, paralyzed, and intubated. Ventricular fibrillation was induced and persisted for 6 minutes without chest compression, followed by mechanical chest compression for 10 minutes and then attempted defibrillation. Animals without return of spontaneous circulation were given epinephrine, ventilation, and chest compression for an additional 3 minutes. Defibrillation was again attempted, and animals were assessed for return of spontaneous circulation. There were no significant differences between the two groups in baseline prearrest mean cardiac index, coronary perfusion pressure, or arterial and mixed venous blood gases. However, after 9 minutes of chest compression, significant differences were noted between the ventilated and nonventilated groups. The nonventilated group had significantly (P < .05) lower mean arterial PO2 (38 +/- 17 mm Hg compared with 216 +/- 104 mm Hg) and higher PCO2 (62 +/- 16 mm Hg compared with 35 +/- 8 mm Hg), lower mixed venous PO2 (15 +/- 7 mm Hg compared with 60 +/- 7 mm Hg). Nine of 12 (75%) of the ventilated animals, and only 1 of 12 (8%) of the nonventilated animals had return of spontaneous circulation after cardiac arrest (P < .002). In this animal model of cardiac arrest, ventilation was important for resuscitation. The importance of ventilation could be related to the prolonged duration of untreated ventricular fibrillation and the significantly greater hypoxia and hypercarbic acidosis found in the nonventilated animals.