All ETDs from UAB

Advisory Committee Chair

Vladimir G Fast

Advisory Committee Members

Steven M Pogwizd

Jack Rogers

Document Type


Date of Award


Degree Name by School

Master of Science in Biomedical Engineering (MSBME) School of Engineering


Background: Defibrillation shocks are commonly used to interrupt life-threatening cardiac arrhythmias, but these strong electrical shocks may cause post-shock arrhythmias, the ionic mechanism of which is not well known. Strong shocks cause electroporation and diastolic Cai2+ increase, which may possibly lead to focal arrhythmias via spontaneous Cai2+ rise (SCR), activation of inward Na+-Ca2+ exchange current (INCX), and rise in membrane potential (Vm). The objective of this study was to examine the role of intracellular calcium and the Cai2+-dependent ionic mechanism in post-shock arrhythmias. Methods: Experiments were performed in patterned cultures of neonatal rat myocytes. Fluorescent dyes and two 16x16 photodiode arrays were utilized to perform simultaneous optical mapping of Vm and Cai2+ to assess the occurrence of SCRs. To elucidate the ionic mechanism of post-shock arrhythmias, drugs were applied including a Cai2+ chelator BAPTA, an INCX inhibitor KB-R7943, and an inhibitor of the inward rectifier current (IK1) BaCl2. Results: Optical mapping at the arrhythmia source demonstrated that Vm upstrokes always preceded Cai2+ transients, and the Vm-Cai2+ delay during arrhythmic beats did not differ from the delay during paced beats. Analysis of the diastolic Cai2+ changes revealed a slow gradual rise of diastolic Cai2+ consistent with membrane electroporation, but no significant Cai2+ rises preceding Vm upstrokes were observed. Application of BAPTA-AM decreased the duration of post-shock arrhythmias whereas application of KB-R7943 increased the arrhythmia duration. These findings indicate that, despite the absence of SCRs, changes in Cai2+ did affect post-shock arrhythmias. This effect could potentially be mediated by Cai2+ inhibition of the outward component of the IK1 current and destabilization of resting Vm. This hypothesis was supported by results of BaCl2 application, which increased the arrhythmia duration. Conclusions. Post-shock arrhythmias are not caused by spontaneous Cai2+ rises and the inward NCX current. However, these arrhythmias are dependent on Cai2+ changes, probably via Cai2+-dependent modulation of the outward IK1 current.

Included in

Engineering Commons



To view the content in your browser, please download Adobe Reader or, alternately,
you may Download the file to your hard drive.

NOTE: The latest versions of Adobe Reader do not support viewing PDF files within Firefox on Mac OS and if you are using a modern (Intel) Mac, there is no official plugin for viewing PDF files within the browser window.