Research Explains How Low Sodium Weakens The Heart’s Electrical Signals

New investigation explains really debased levels of nan electrolyte sodium successful nan humor tin disrupt nan timing of nan heartbeat successful patients taking wide utilized rhythm-control medications specified arsenic flecainide, which is commonly prescribed for atrial fibrillation and different accelerated aliases irregular bosom rhythms.

The study, by Virginia Tech researchers astatine nan Fralin Biomedical Research Institute successful nan journal Heart Rhythm, was conducted utilizing guinea pig hearts and showed that blocking cardiac sodium channels pinch commonly prescribed medicine specified arsenic flecainide tin make nan heart's electrical conduction unusually delicate to moreover humble reductions successful humor sodium levels.

Although sodium is often associated pinch dietary salt, erstwhile measured successful aesculapian settings it refers to nan attraction of sodium ions successful nan humor - a facet for nervus and musculus function. When those levels driblet beneath a captious level, a information known as hyponatremia, electrical signaling successful nan bosom tin go unstable, particularly successful patients connected sodium transmission blockers.

Doctors person agelong known that sodium transmission blockers tin slow cardiac conduction, and that debased sodium levels are risky. But what wasn't clear is why nan operation of nan 2 is truthful problematic. This study helps explicate nan mechanism."

Steven Poelzing, study's elder writer and nan James and Deborah Petrine Professor pinch nan Fralin Biomedical Research Institute astatine VTC

The researchers recovered that erstwhile sodium channels are impaired, nan bosom relies much heavy connected backup pathways to support electrical signals moving. One of those pathways involves electrical interactions betwixt neighboring bosom cells successful very constrictive spaces - a process known as ephaptic coupling. 

Another pathway involves nan travel of potassium ions done channels that helps reset nan heart's electrical state. When sodium levels fall, these mechanisms don't compensate arsenic they usually would, causing conduction to slow much than expected.

"If you person nan correct magnitude of sodium successful your blood, electrical activity will still move done nan bosom astatine nan correct velocity - moreover erstwhile sodium channels are blocked," Poelzing said. "But if you driblet excessively debased - because of vomiting, diarrhea, definite medications, aliases a aesculapian information - nan supplier whitethorn abruptly go detrimental."

Importantly, nan study shows that interfering pinch either ephaptic coupling aliases nan nett outward travel of potassium ions reduces nan heart's sensitivity to debased sodium erstwhile sodium channels are blocked. That penetration opens nan doorway to much targeted strategies for managing conduction risks successful patients who trust connected sodium transmission blockers.

"This doesn't mean each diligent needs to interest but it is straight applicable to nan objective guidance of arrhythmias," said Poelzing, who is pinch nan Fralin Biomedical Research Institute's Center for Vascular and Heart Research. "For immoderate patients connected narcotics for illustration flecainide, observant monitoring of sodium levels whitethorn beryllium conscionable arsenic important arsenic managing nan arrhythmia itself."

The findings besides underscore nan request for physicians to beryllium alert of hidden interactions betwixt supplier therapy and electrolyte imbalances - peculiarly debased sodium levels - particularly successful older adults aliases hospitalized patients, who whitethorn beryllium much prone to hyponatremia.

"The study indicates that mean sodium levels shouldn't beryllium an afterthought - particularly for those connected bosom hit medications," Poelzing said. "A speedy speech pinch your expert mightiness thief forestall a much superior problem down nan line."

Poelzing is besides a professor of Biomedical Engineering and Mechanics in nan Virginia Tech College of Engineering.

The study was led by Poelzing and William Adams, who was a student successful nan Translational Biology, Medicine, and Health postgraduate programme moving successful Poelzing's laboratory erstwhile nan investigation took place. Research Assistant Professor Hoeker was among nan co-authors. The investigation was supported by nan National Heart, Lung, and Blood Institute of nan National Institutes of Health.