Dataset Information

Endocardial Activation Drives Activation Patterns During Long-Duration Ventricular Fibrillation and Defibrillation.

ABSTRACT:

Background

Understanding the mechanisms that drive ventricular fibrillation is essential for developing improved defibrillation techniques to terminate ventricular fibrillation (VF). Distinct organization patterns of chaotic, regular, and synchronized activity were previously demonstrated in VF that persisted over 1 to 2 minutes (long-duration VF [LDVF]). We hypothesized that activity on the endocardium may be driving these activation patterns in LDVF and that unsuccessful defibrillation shocks may alter activation patterns.

Methods and results

The study was performed using a 64-electrode basket catheter on the left ventricle endocardium and 54 6-electrode plunge needles inserted into the left ventricles of 6 dogs. VF was induced electrically, and after short-duration VF (10 seconds) and LDVF (7 minutes), shocks of increasing strengths were delivered every 10 seconds until VF was terminated. Endocardial activation patterns were classified as chaotic (varying cycle lengths and nonsynchronous activations), regular (highly repeatable cycle lengths), and synchronized (activation that spreads rapidly over the endocardium with diastolic periods between activations).

Conclusions

The results showed that the chaotic pattern was predominant in early VF, but the regular pattern emerges as VF progressed. The synchronized pattern only emerged occasionally during late VF. Failed defibrillation shocks changed chaotic and regular activation patterns to synchronized patterns in LDVF but not in short-duration VF. The regular and synchronized patterns of activation were driven by rapid activations on the endocardial surface that blocked and broke up transmurally, leading to an endocardial to epicardial activation rate gradient as LDVF progressed.

SUBMITTER: Panitchob N

PROVIDER: S-EPMC5737741 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundMeasures 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 resultsWe 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).ResultsIn 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.ConclusionsThe 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.