Abstract 13487: AMSA Partly Reflects Changes in Myocardial Oxygen Consumption during Resuscitation from Ventricular Fibrillation
Background: Previous studies have shown that VF amplitude and frequency contain information predictive of electrical shock success or failure. One useful method - which simultaneously incorporates amplitude and frequency - is AMSA (AMplitude Spectral Area). AMSA has been useful in predicting shock success; yet, the underlying mechanisms driving AMSA and the responsiveness to electrical shocks remain incompletely understood. We examined the relationship between AMSA and myocardial metabolism while investigating the effects of erythropoietin (EPO) on resuscitation from VF.
Methods: An open-chest swine model of VF and extracorporeal circulation (ECC) was used; measuring coronary blood flow and sampling blood from the aorta (Ao) and great cardiac vein (gcv). VF was induced and left untreated for 8 min after which ECC was started and maintained for 10 min adjusting the flow to generate a coronary perfusion pressure of 10 mmHg. Pigs were randomized 1:1 to receive EPO (5,000 U/kg) or 0.9% NaCl before starting ECC.
Results: During untreated VF, AMSA (mV·Hz) declined from 13.5±4.3 at min 1 to 7.1±2.1 at min 8 (p<0.001). During ECC, AMSA returned to initial levels corresponding to 12.9±4.5 at min 2 of ECC and to 13.8±3.9 at min 8 of ECC. Of various metabolic measurements, AMSA correlated with myocardial O2 consumption (Figure) but not with myocardial lactate production or P(gcv-Ao)CO2 gradient. A statistically insignificant trend favored higher AMSA levels in the EPO group at ECC 2 min (14.3±5.2 vs 11.3±3.4; p=0.193) and ECC 8 min (15.7±4.4 vs 12.0±2.4; p=0.053) and correspondingly higher myocardial O2 consumption (µl/min·unit of tissue-1) at ECC 2 min (50±27 vs 37±20; p=0.31) and ECC 8 min (43±20 vs 31±10; p=0.15).
Conclusion: In a swine model of VF in which coronary perfusion pressure was precisely controlled by ECC, AMSA was partly correlated with MVO2 suggesting that AMSA could be useful to assess interventions expected to alter myocardial metabolism during resuscitation.
- © 2012 by American Heart Association, Inc.