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.

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.