Little-studied waves in the heart may be cause of defibrillation failure
Vanderbilt University researchers believe a slow electrochemical wave, known as a damped wave, may be one of the reasons that low-voltage defibrillation shocks fail to halt fibrillation in cardiac patients.
The findings by Vanderbilt University researchers John Wikswo, Veniamin Sidorov, Rubin Aliev, Marcella Woods, Franz Baudenbacher and Petra Baudenbacher were published in the Nov. 14 issue of Physical Review Letters.
Fibrillation is a series of rapid, disorganized contractions in the heart caused by multiple uncoordinated, self-generated electrochemical waves that prevent the heart from pumping blood, quickly causing death.
“In normal conditions, an electrochemical wave moves smoothly across the heart, like expanding ripples in a lake when you toss in a stone. This wave then triggers a smooth and orderly contraction of the muscle,” Wikswo, the Gordon A. Cain University Professor and Director of the Vanderbilt Institute for Integrative Biosystems Research and Education, said. “In fibrillation, it is as if someone continually throws in lots of rocks at different spots in the lake. In the resulting confusion, no blood gets pumped.”
The application of a strong electrical shock, either with paddles on the chest or with an implantable defibrillator, is the best way to stop fibrillation. Ideally, a defibrillation shock would stop all waves in the heart and prevent new waves from arising spontaneously.
“You want to use as low a voltage shock as possible to minimize tissue damage and, for implantable defibrillators, to save your batteries,” Wikswo continued. “However, if the voltage is too low, fibrillation returns immediately and you have to try again. The puzzle is why.”
Wikswos study explores the possibility that some waves might not be fully extinguished by a low voltage defibrillation shock, or new waves might be created by the shock, causing defibrillation to fail. If these remaining or new waves were the difficult-to-detect damped propagating waves, they could propagate slowly within the heart wall, rather than slowly dying out as previously expected. This might cause the heart to return to fibrillation or another cardiac arrhythmia.
“Damped propagating waves are not generally well understood, largely because they are difficult to view and to study,” Wikswo said. “It turns out cardiac tissue provides a beautiful example of these waves.”
Although cardiac graded responses have been considered for some time, recent advances in high-speed imaging, data processing and numerical modeling are just now allowing their quantitative analysis as damped, propagating waves.
To study the damped waves, Wikswos team initiated a wave with a strong stimulus that moved smoothly across the heart. They then created a damped wave with a weaker stimulus and sent it in the wake of the first.
“If you timed it just right you could find that the second wave would hesitate and then split in two,” Wikswo continued. “One half would get smaller and slowly die, while the other half would sharply increase and eventually become a self-continuing wave on its own.”
This second, self-continuing wave could be a cause of defibrillation failure.
“What surprised us is the ease with which we could create damped waves that hung around for 50 milliseconds, which is a long time when you are defibrillating the heart,” Wikswo said.
The research, conducted by studying the rabbit heart, lays the foundation for future studies to determine if the waves created under experimental conditions also occur spontaneously following defibrillation.
Future studies based on this research will be conducted to better understand how to manage these waves, the effect of anti-arrhythmic drugs on them, and whether these findings could be used to improve the efficiency of cardiac defibrillators.
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