Robert Robichaux

Periods of Highly Synchronous, Non-Reentrant Endocardial Activation Cycles Occur During Long-Duration Ventricular Fibrillation

Periods of Highly Organized Activation During VF Background: Little is known about long‐duration ventricular fibrillation (LDVF), lasting 1–10 minutes when resuscitation is still possible.

Cardiovascular implantable electronic device implantation with uninterrupted dabigatran: comparison to uninterrupted warfarin.

While continuation of oral anticoagulation (OAC) with warfarin may be preferable to interruption and bridging with heparin for patients undergoing cardiovascular implantable electronic device (CIED) implantation, it is uncertain whether the same strategy can be safely used with dabigatran.

In a swine model, chest compressions cause ventricular capture and, by means of a long-short sequence, ventricular fibrillation.

Background—During resuscitation, fibrillation often recurs. In swine, we studied refibrillation after long-duration ventricular fibrillation, investigating an association with chest compressions (CCs). Methods and Results—In protocol A, 47 episodes of long-duration ventricular fibrillation lasting at least 2.5 minutes were induced in 8 animals. After defibrillation, CCs were required for 35 episodes and delivered with a pneumatic device (Lucas cardiopulmonary resuscitation). In 9 episodes, refibrillation occurred within 2 seconds of CC initiation (group 1) and in 26 episodes, CCs were delivered without refibrillation (group 2). From the ECG and intracardiac electrodes, the RR interval preceding CCs, the shortest cycle length during the first 2 CCs (short), and the preceding cycle length (long) were measured. A similar study was conducted in 3 more animals without intracardiac catheters (protocol B). In protocol A, the mean RR before CC was 665±292 ms in group 1 and 769±316 in group 2. CCs stimulated ventricular beats in all 35 episodes. The short and long intervals were shorter in group 1 (215±31 and 552±210 ms) than in group 2 (402±153 and 699±147 ms) (P=0.009 and P=0.04, respectively). The prematurity index (short/RR) was lower in group 1 than in group 2 (0.35±0.09 vs 0.58±0.21; P<0.01). A short interval <231 ms predicted refibrillation with 88% sensitivity and 91% specificity. In protocol B, CCs were required in 11 episodes, causing ventricular stimulation in all of them and ventricular fibrillation within the first 2 CCs in 3. Conclusions—Under some conditions, CC during resuscitation can stimulate the ventricles and initiate ventricular fibrillation by a long-short sequence.

Purkinje activation precedes myocardial activation following defibrillation after long-duration ventricular fibrillation

BACKGROUND While reentry within the ventricular myocardium (VM) is responsible for the maintenance of short-duration ventricular fibrillation (SDVF; VF duration <1 minute), Purkinje fibers (PFs) are important in the maintenance of long-duration ventricular fibrillation (LDVF; VF duration >1 minute). OBJECTIVE The purpose of this study was to test the hypothesis that the mechanisms of defibrillation may also be different for SDVF and LDVF. METHODS A multielectrode basket catheter was deployed in the left ventricle of eight beagles. External defibrillation shocks were delivered with a ramp-up protocol after SDVF (20 seconds) and LDVF (150 seconds). Earliest VM and PF activations were identified after the highest energy shock that failed to terminate VF and the successful shock. RESULTS Defibrillation was successful after 36 +/- 12 and 181 +/- 14 seconds for SDVF and LDVF, respectively. The time after shock delivery until earliest activation was detected for failed shocks and was significantly longer after LDVF (138.7 +/- 24.1 ms) than after SDVF (75.6 +/- 8.7 ms). Earliest postshock activation after SDVF typically initiated in the VM (14 of 16 episodes), while it always initiated in the PF (16 of 16 episodes) after LDVF. Sites of earliest activity during sinus rhythm correlated with sites of earliest postshock activation for PF-led cycles but not for VM-led cycles. CONCLUSION Earliest recorded postshock activation is in the Purkinje system after LDVF but not after SDVF. This difference raises the possibility that the optimal defibrillation strategy is different for SDVF and LDVF.

Effect of Chest Compressions on Ventricular Activation

External mechanical forces can cause ventricular capture and fibrillation (i.e., commotio cordis). In animals, we showed that chest compressions (CCs) can also cause the phenomenon. The aim of the present study was to determine whether ventricular capture by CCs occurs in humans. Electronic rhythm strips were analyzed in 31 cases of out-of-hospital cardiac arrest. The timing of the CCs was identified from the changes in thoracic impedance between the defibrillator pads. Ventricular capture was defined as QRS complexes of similar morphology occurring intermittently but synchronized with the CC artifact and impedance waveform. Only intermittent ventricular capture was identified to avoid misclassifying constant motion artifacts or intrinsic rhythm as ventricular capture. Of the 29 patients who received CCs for ≥1 minute, minimal or stable motion artifact was present in 24. Intermittent ventricular capture was found in 7 of the 24 patients. In the patients with ventricular capture, the number of ventricular activations (from ventricular capture and native beats) was greater during the CCs than when the CCs was not being performed (18 ± 8.9 vs 9.7 ± 4.0 activations in 15 seconds, p = 0.01). However, in patients without ventricular capture, they were similar (6.8 ± 8.2 vs 7.2 ± 8.8 activations in 15 seconds, p = 0.47). Refibrillation occurred in 22 patients; it began during the CCs in 16 and closely following their initiation in 3. In conclusion, CCs during cardiopulmonary resuscitation can electrically stimulate the heart. Additional studies evaluating the effect of ventricular capture on cardiopulmonary resuscitation outcomes, its relation to refibrillation, and methods to prevent or time ventricular capture by CCs are warranted.