Abstract 2413: Mild Hypothermia Slows the Decay of Quantitative Ventricular Fibrillation Waveform Morphology during Prolonged Cardiac Arrest
Introduction: The benefits of hypothermia in treating ventricular fibrillation (VF) are myriad, but poorly understood. Patients who are cold are often resuscitated after prolonged cardiac arrest. One contributory mechanism may be the slowing of metabolic processes during VF.
Hypothesis: We hypothesized that the time-dependent deterioration of the electrocardiographic (ECG) waveform during VF would be slowed by mild hypothermia, when compared to normothermic VF.
Methods: We randomly assigned 42 domestic swine (weighing 27.2 ±2.3 kgs) to either pretreatment with hypothermia before induction of VF (n=14) or normothermic VF (n=28). After induction of anesthesia, animals were instrumented via femoral cutdown. Lead II ECG was recorded continuously. The hypothermia animals were cooled, starting at 5 minutes before induction of VF, with a rapid infusion of ice-cold normal saline (30 mL/kg). Normothermic animals received no additional fluid prior to induction of VF. VF was induced with a 3s, 60 Hz transthoracic shock and was untreated for 8 minutes. We calculated the VF scaling exponent (ScE), a non-linear dynamical measure, q 5s for the entire 8 minute period. Temperatures are reported in degrees C. ScE data were compared using splined GEE.
Results: The mean temperature at the onset of VF was 34.6° (±0.8) for the hypothermia group and 37.8° (±0.8) for the normothermia group. The ScE values over time were significantly lower after 3 minutes in the hypothermia group, as shown in the figure⇓ (p=0.08 for 0 to3 min and p=0.004 for 3 to 8 min).
Conclusion: Mild hypothermia slowed the decay of the ECG waveform during prolonged VF and has a beneficial electrophysiological effect during VF.