Heart Rhythm Disorders
Heart Rhythm Disorders - Related Videos
01:29
Disturbances in Heart Rhythm
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2025
Arrhythmia or dysrhythmia refers to an abnormal heart rhythm caused by a defect in the heart's conduction system. It can cause the heart to beat irregularly, too quickly, or too slowly, leading to symptoms like chest pain, shortness of breath, and fainting. Factors such as stress, caffeine, alcohol, nicotine, cocaine, certain drugs, congenital defects, diseases, and electrolyte abnormalities can trigger arrhythmias. Arrhythmias are categorized by their speed, rhythm, and origin. A slow heart...
11:50
EEG Mu Rhythm in Typical and Atypical Development
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Cited by 3 •
2014
Assessment of the EEG mu rhythm provides a unique methodology for examining brain activity and when combined with behaviorally based assays, can be a powerful tool for elucidating aspects of social cognition, such as imitation, in clinical populations.
05:46
Recording and Analysis of Circadian Rhythms in Running-wheel Activity in Rodents
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Cited by 35 •
2013
Circadian rhythms in voluntary wheel-running activity in mammals are tightly coupled to the molecular oscillations of a master clock in the brain. As such, these daily rhythms in behavior can be used to study the influence of genetic, pharmacological, and environmental factors on the functioning of this circadian clock.
12:09
Patient-specific Modeling of the Heart: Estimation of Ventricular Fiber Orientations
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Cited by 14 •
2013
A methodology to estimate ventricular fiber orientations from in vivo images of patient heart geometries for personalized modeling is described. Validation of the methodology performed using normal and failing canine hearts demonstrate that that there are no significant differences between estimated and acquired fiber orientations at a clinically observable level.
09:48
Heterotopic Cervical Heart Transplantation in Mice
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Cited by 24 •
2015
The cuff technique shortens and facilitates the model of heterotopic cervical heart transplantation in mice by avoiding technically challenging suture anastomoses of small vessels. The technical details shown in this video paper should allow researches to establish this model in their laboratories.
FAQs
Ion channel activity helps determine how cardiac cells depolarize, recover, and respond to incoming impulses. Pharmacological changes in these channels can modify excitability, conduction, and the refractory period, which is the interval when tissue is less responsive to another impulse. These effects help explain how antiarrhythmic drugs can alter abnormal electrical activity and restore more coordinated cardiac signaling.
The refractory period limits how soon cardiac tissue can respond to a subsequent electrical impulse. Altering this interval changes the tissue’s ability to sustain or interrupt abnormal rhythm patterns. Pharmacological evaluation therefore considers refractory-period effects alongside conduction and excitability, because a treatment may provide rhythm control while also producing unwanted electrical consequences, including proarrhythmic risk.
Autonomic signaling is one pathway through which drugs can modify cardiac electrical behavior. Changing this signaling can influence impulse formation and the responsiveness of cardiac tissue, complementing direct effects on ion channels. Considering both mechanisms helps pharmacologists explain why a treatment changes rhythm behavior and supports evaluation of therapeutic benefit, adverse effects, and dosing requirements.
Assessment compares the intended change in rhythm-related electrical behavior with unwanted effects produced by the treatment. Researchers examine effects on depolarization, refractory periods, conduction, and excitability, then consider adverse effects and proarrhythmic risk. This balanced evaluation helps determine whether an antiarrhythmic drug’s potential therapeutic benefit justifies its electrical and pharmacological liabilities.
Pharmacological approaches are studied when researchers need to select or evaluate treatments for disorders such as atrial fibrillation and ventricular arrhythmias. Investigations examine how candidate drugs modify cardiac electrical mechanisms and whether those changes correspond to therapeutic benefit. The same studies also address adverse effects, proarrhythmic risk, and dosing, linking mechanism-focused findings to treatment assessment.
These studies can characterize how an antiarrhythmic drug changes impulse formation and conduction-related properties, including depolarization, refractory periods, and excitability. They can also support judgments about therapeutic benefit, adverse effects, proarrhythmic risk, and appropriate dosing. Applying these measures to atrial fibrillation and ventricular arrhythmias connects cellular electrical mechanisms with clinically relevant treatment evaluation.