Increased cycle length during long-duration ventricular fibrillation is caused by decreased upstroke velocity as well as prolonged refractoriness.
BACKGROUND
Cycle length (CL) increases as ventricular fibrillation (VF) progresses.


OBJECTIVE
The purpose of this study was to test the hypotheses that increased CL is due to increased diastolic interval (DI), not increased action potential duration (APD), and that the DI increase is not solely due to increased postrepolarization refractoriness.


METHODS
In 10 swine, VF was recorded for 20 minutes using a floating microelectrode through a hole in a 504-electrode epicardial plaque. Mean APD, DI, action potential amplitude (APA), maximum change in voltage during the AP upstroke (V(max)), and CL were calculated from the floating microelectrode recordings each minute of VF. The refractory period was estimated from the minimum DI (DI(min)). In two animals, rapid pacing was performed to gauge refractoriness.


RESULTS
As VF progressed, CL, DI, and DI(min) increased (P <.05), whereas APD, V(max), and APA decreased (P <.05). At 20 minutes, DI(min) was not different from mean DI at VF onset. Pacing captured, but 53% of paced wavefronts blocked within the plaque.


CONCLUSIONS
Increasing CL in VF is due to increased DI and not APD, which shortens. The increase in DI(min) over time is much less than the increase in mean DI, indicating that the myocardium is excitable during much of the DI. This finding, along with the ability to pace at a CL shorter than the native VF CL and the poor paced wavefront propagation, suggests that the increase in DI is due not only to increased postrepolarization refractoriness but also to poor wavefront propagation because of decreased APA and V(max) secondary to global ischemia caused by VF.
Robertson
Peter G
PG
Department of Medicine, Division of Cardiovascular Disease, University of Alabama at Birmingham, Birmingham, Alabama 35294-0007, USA.
Huang
Jian
J
Chen
Kang A
KA
Chen
Xiaozhong
X
Dosdall
Derek J
DJ
Tabereaux
Paul B
PB
Smith
William M
WM
Ideker
Raymond E
RE
D000200:Action Potentials; D000818:Animals; D002304:Cardiac Pacing, Artificial; D003971:Diastole; D004562:Electrocardiography; D022062:Electrophysiologic Techniques, Cardiac; D006329:Heart Conduction System / Q000503:physiopathology; D008839:Microelectrodes; D009200:Myocardial Contraction; D034421:Sus scrofa; D014693:Ventricular Fibrillation / Q000503:physiopathology*