Variation of cycle length in epicardial electrograms: a quantification of chaos of ventricular fibrillation using a sock electrode array

2002 ◽  
Author(s):  
P.-W.E. Hsia ◽  
K.W. Hellmann ◽  
R. Mahmud
Keyword(s):  
Ventricular Fibrillation ◽  
Cycle Length ◽  
Electrode Array

scholarly journals Intramural optical mapping of Vm and Cai2+ during long-duration ventricular fibrillation in canine hearts

2012 ◽  
Vol 302 (6) ◽  
pp. H1294-H1305 ◽  
Author(s):  
Wei Kong ◽  
Raymond E. Ideker ◽  
Vladimir G. Fast
Keyword(s):  
Ventricular Fibrillation ◽  
Action Potential ◽  
Short Duration ◽  
Action Potential Duration ◽  
Cycle Length ◽  
The Other ◽  
Membrane Voltage ◽  
Long Duration ◽  
Intracellular Ca ◽  
Rapid Pacing

Intramural gradients of intracellular Ca2+ (Cai2+) Cai2+ handling, Cai2+ oscillations, and Cai2+ transient (CaT) alternans may be important in long-duration ventricular fibrillation (LDVF). However, previous studies of Cai2+ handling have been limited to recordings from the heart surface during short-duration ventricular fibrillation. To examine whether abnormalities of intramural Cai2+ handling contribute to LDVF, we measured membrane voltage ( Vm) and Cai2+ during pacing and LDVF in six perfused canine hearts using five eight-fiber optrodes. Measurements were grouped into epicardial, midwall, and endocardial layers. We found that during pacing at 350-ms cycle length, CaT duration was slightly longer (by ≃10%) in endocardial layers than in epicardial layers, whereas action potential duration (APD) exhibited no difference. Rapid pacing at 150-ms cycle length caused alternans in both APD (APD-ALT) and CaT amplitude (CaA-ALT) without significant transmural differences. For 93% of optrode recordings, CaA-ALT was transmurally concordant, whereas APD-ALT was either concordant (36%) or discordant (54%), suggesting that APD-ALT was not caused by CaA-ALT. During LDVF, Vm and Cai2+ progressively desynchronized when not every action potential was followed by a CaT. Such desynchronization developed faster in the epicardium than in the other layers. In addition, CaT duration strongly increased (by ∼240% at 5 min of LDVF), whereas APD shortened (by ∼17%). CaT rises always followed Vm upstrokes during pacing and LDVF. In conclusion, the fact that Vm upstrokes always preceded CaTs indicates that spontaneous Cai2+ oscillations in the working myocardium were not likely the reason for LDVF maintenance. Strong Vm-Cai2+ desynchronization and the occurrence of long CaTs during LDVF indicate severely impaired Cai2+ handling and may potentially contribute to LDVF maintenance.

High-dose lidocaine does not affect defibrillation efficacy: implications for defibrillation mechanisms

1998 ◽  
Vol 274 (4) ◽  
pp. H1113-H1120 ◽  
Author(s):  
Michael R. Ujhelyi ◽  
J. Jason Sims ◽  
Allison Winecoff Miller
Keyword(s):  
Ventricular Fibrillation ◽  
Cycle Length ◽  
Low Dose ◽  
High Dose ◽  
Channel Blockade ◽  
Group 3 ◽  
Baseline Values ◽  
Group 2 ◽  
Very High ◽  
Group 1

This study assessed the effect of low (10 mg ⋅ kg−1 ⋅ h−1) and very high (18 mg ⋅ kg−1 ⋅ h−1) doses of lidocaine on defibrillation energy requirements (DER) to relate changes in indexes of sodium-channel blockade with changes in DER values using a dose-response study design. In group 1 (control; n = 6 pigs), DER values were determined at baseline and during treatment with 5% dextrose in water (D5W) and with D5W added to D5W. In group 2 ( n = 7), DER values were determined at baseline and during treatment with low-dose lidocaine followed by high-dose lidocaine. In group 3 ( n = 3), DER values were determined at baseline and high-dose lidocaine. Group 3 controlled for the order of lidocaine treatment with the addition of high-dose lidocaine after baseline. DER values in group 1 did not change during D5W. In group 2, low-dose lidocaine increased DER values by 51% ( P = 0.01), whereas high-dose lidocaine added to low-dose lidocaine reduced DER values back to within 6% of baseline values ( P = 0.02, low dose vs. high dose). DER values during high-dose lidocaine in group 3 also remained near baseline values (16.2 ± 2.7 to 12.9 ± 2.7 J), demonstrating that treatment order had no impact on group 2. Progressive sodium-channel blockade was evident as incremental reduction in ventricular conduction velocity as the lidocaine dose increased. Lidocaine also significantly increased ventricular fibrillation cycle length as the lidocaine dose increased. However, the greatest increase in DER occurred when ventricular fibrillation cycle length was minimally affected, demonstrating a negative correlation ( P = 0.04). In summary, lidocaine has an inverted U-shaped DER dose-response curve. At very high lidocaine doses, DER values are similar to baseline and tend to decrease rather than increase. Increased refractoriness during ventricular fibrillation may be the electrophysiological mechanism by which high-dose lidocaine limits the adverse effects that low-dose lidocaine has on DER values. However, there is a possibility that an unidentified action of lidocaine is responsible for these effects.

scholarly journals Do changes in local cardiac electrophysiology influence ventricular fibrillation cycle length?

2002 ◽  
Vol 39 ◽  
pp. 92
Author(s):  
Taresh Tanela ◽  
George Horvath ◽  
Darlene Racker ◽  
Jeffrey Goldberger ◽  
Alan Kadish
Keyword(s):  
Ventricular Fibrillation ◽  
Cardiac Electrophysiology ◽  
Cycle Length

Is there a correlation between ventricular fibrillation cycle length and electrophysiological and anatomic properties of the canine left ventricle?

2004 ◽  
Vol 287 (2) ◽  
pp. H823-H832
Author(s):  
Taresh Taneja ◽  
George Horvath ◽  
Darlene K. Racker ◽  
David Johnson ◽  
Jeffrey Goldberger ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Left Ventricle ◽  
Cycle Length

Regional and Temporal Variation of Ventricular and Conduction Tissue Activity During Ventricular Fibrillation in Canines

2021 ◽  
Author(s):  
Nicholas Tan ◽  
Georgios Christopoulos ◽  
Thomas P. Ladas ◽  
Zhi Jiang ◽  
Alan M. Sugrue ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Left Ventricle ◽  
Electrical Activity ◽  
Cycle Length ◽  
Time Interval ◽  
Apical Region ◽  
Free Wall ◽  
Purkinje System ◽  
Regularity Index ◽  
Rigorous Study

Background: Rigorous study of ventricular fibrillation (VF) is not feasible in humans. The spatiotemporal characteristics of prolonged VF remain undefined, limiting our understanding of this lethal rhythm. Methods: VF was mapped in 4 canines. The endocardial and epicardial left ventricle (LV) and right ventricle (RV) were sequentially mapped at 0 to 15, 15 to 30, 30 to 45, and 45 to 60 minutes post-induction. Ten consecutive beats were used to determine average cycle length and regularity index of ventricular and His-Purkinje system signals in discrete regions during each time interval. Results: Average VF time was 58±12 minutes. The shortest ventricular cycle length was present in the RV apical region (70±10 msec) at 0 to 15 minutes and at 15 to 30 minutes (89±31 msec) and LV apical region at 45 to 60 minutes (242±163 msec). The His-Purkinje system cycle length was the shortest at the RV outflow tract (75±3 msec) at 0 to 15 minutes, RV inflow and free wall (89±12 msec) at 15 to 30 minutes, LV apical region (83±14 msec) at 30 to 45 minutes, and inferior and inferolateral LV (145±23 msec) at 45 to 60 minutes. Regularity index was the highest in the RV inflow and free wall (78%) at 0 to 15 minutes, RV apical region (86%) at 15 to 30 minutes, LV septum and epicardial anterior RV (80%) at 30 to 45 minutes, and anterior and anterolateral LV (75%) at 45 to 60 minutes. Conclusions: These data suggest significant regional changes in electrical activity throughout VF in canines. A transition of fastest electrical activity from RV to LV apical regions across VF was observed. Further studies are warranted to confirm the above findings.

Effects of heart isolation, voltage-sensitive dye, and electromechanical uncoupling agents on ventricular fibrillation

2003 ◽  
Vol 284 (5) ◽  
pp. H1818-H1826 ◽  
Author(s):  
Hao Qin ◽  
Matthew W. Kay ◽  
Nipon Chattipakorn ◽  
David T. Redden ◽  
Raymond E. Ideker ◽  
...  
Keyword(s):  
Ventricular Fibrillation ◽  
Pattern Analysis ◽  
Electrode Array ◽  
Left Ventricular ◽  
Control Data ◽  
Voltage Sensitive Dye ◽  
Activation Patterns ◽  
Langendorff Perfusion ◽  
Perfusion Apparatus ◽  
Diacetyl Monoxime

We tested whether the interventions typically required for optical mapping affect activation patterns during ventricular fibrillation (VF). A 21 × 24 unipolar electrode array (1.5 mm spacing) was sutured to the left ventricular epicardium of 16 anesthetized pigs, and four episodes of electrically induced VF (30-s duration) were recorded. The hearts were then rapidly excised and connected to a Langendorff perfusion apparatus. Four of the hearts were controls, in which 24 additional VF episodes were then mapped. In the remaining 12 hearts, four VF episodes were mapped after isolation, four more episodes were mapped after exposure to the voltage-sensitive dye di-4-ANEPPS, and six more episodes were mapped after exposure to the electromechanical uncoupling agents diacetyl monoxime (DAM; 20 mmol/l, n = 6) or cytochalasin D (CytoD; 10 μmol/l, n = 6). VF episodes were separated by 4 min. VF activation patterns were quantified using custom pattern analysis algorithms. From comparisons with time-corrected control data, all interventions significantly changed VF patterns. Most changes were broadly consistent with slowing and regularization due to loss of excitability. Heart isolation had the largest effect on VF patterns, followed by CytoD, DAM, and dye.

Purkinje involvement in arrhythmias after coronary artery reperfusion

2002 ◽  
Vol 282 (4) ◽  
pp. H1189-H1196 ◽  
Author(s):  
David O. Arnar ◽  
James B. Martins
Keyword(s):  
Ventricular Tachycardia ◽  
Coronary Artery ◽  
Ventricular Fibrillation ◽  
Cycle Length ◽  
Ischemic Myocardium ◽  
Risk Zone ◽  
Purkinje System ◽  
Mean Cycle

Previous studies have indicated that the endocardium may be responsible for a large portion of ventricular tachycardia (VT) seen with reperfusion of ischemic myocardium. To evaluate the role of the Purkinje system in nonreentrant VT arising from the endocardium after reperfusion, the anterior descending coronary artery was occluded for 20 min and then reperfused in 23 dogs after instrumentation of the risk zone with 21 multipolar plunge needles. VT with focal Purkinje origin was defined as a focal endocardial VT with Purkinje potentials recorded before the earliest endocardial myopotential. A total of 19 VTs (mean cycle length 214 ± 2 ms) were observed with 11 (58%) having focal Purkinje origin. Fifty-eight percent of the VTs degenerated to ventricular fibrillation, with occurrences of two or more independent foci per complex (seen in 7 of 11 compared with 1 of 8 nonsustained VTs). In conclusion, these data show that Purkinje tissue may be important in the genesis of reperfusion VT.

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