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In a typical heartbeat, a tiny cluster of cells at the sinus node sends out an electrical signal. The signal then travels through the atria to the atrioventricular (AV) node and into the ventricles, causing them to contract and pump blood.

A heart arrhythmia (uh-RITH-me-uh) is an irregular heartbeat. A heart arrhythmia occurs when the electrical signals that tell the heart to beat don't work properly. The heart may beat too fast or too slow. Or the pattern of the heartbeat may be inconsistent.

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Heart arrhythmia treatment may include medicines, devices such as pacemakers, or a procedure or surgery. The goals of treatment are to control or get rid of fast, slow or otherwise irregular heartbeats. A heart-healthy lifestyle can help prevent heart damage that can trigger some heart arrhythmias.

A heart rate below 60 beats a minute is considered bradycardia. But a low resting heart rate doesn't always mean there's a problem. If you're physically fit, your heart may be able to pump enough blood to the body with less than 60 beats a minute.

Premature heartbeats are extra beats that occur one at a time, sometimes in patterns that alternate with a regular heartbeat. If the extra beats come from the top chamber of the heart, they are called premature atrial contractions (PACs). If they come from the bottom chamber, they are called premature ventricular contractions (PVCs).

A premature heartbeat may feel like your heart skipped a beat. These extra beats are generally not a concern. They rarely mean you have a more serious condition. Still, a premature beat can trigger a longer lasting arrhythmia, especially in people with heart disease. Occasionally, having very frequent premature ventricular beats may lead to a weak heart.

If you feel like your heart is beating too fast or too slow, or it's skipping a beat, make an appointment for a health checkup. You may be told to see a doctor trained in heart diseases, called a cardiologist.

A type of arrhythmia called ventricular fibrillation can cause a dramatic drop in blood pressure. This can cause the person to fall to the ground within seconds, also called collapse. Soon the person's breathing and pulse will stop. Ventricular fibrillation is an emergency that needs immediate medical help. It's the most frequent cause of sudden cardiac death.

The heart's electrical system controls the heartbeat. The heart's electrical signals start in a group of cells at the top of the heart called the sinus node. They pass through a pathway between the upper and lower heart chambers called the atrioventricular (AV) node. The movement of the signals causes the heart to squeeze and pump blood.

Blood-thinning medicines can lower the risk of stroke related to atrial fibrillation and other heart arrhythmias. If you have a heart arrhythmia, ask a healthcare professional if you need to take a blood thinner.

Entrainment of cortical rhythms to acoustic rhythms has been hypothesized to be the neural correlate of pulse and meter perception in music. Dynamic attending theory first proposed synchronization of endogenous perceptual rhythms nearly 40 years ago, but only recently has the pivotal role of neural synchrony been demonstrated. Significant progress has since been made in understanding the role of neural oscillations and the neural structures that support synchronized responses to musical rhythm. Synchronized neural activity has been observed in auditory and motor networks, and has been linked with attentional allocation and movement coordination. Here we describe a neurodynamic model that shows how self-organization of oscillations in interacting sensory and motor networks could be responsible for the formation of the pulse percept in complex rhythms. In a pulse synchronization study, we test the model's key prediction that pulse can be perceived at a frequency for which no spectral energy is present in the amplitude envelope of the acoustic rhythm. The result shows that participants perceive the pulse at the theoretically predicted frequency. This model is one of the few consistent with neurophysiological evidence on the role of neural oscillation, and it explains a phenomenon that other computational models fail to explain. Because it is based on a canonical model, the predictions hold for an entire family of dynamical systems, not only a specific one. Thus, this model provides a theoretical link between oscillatory neurodynamics and the induction of pulse and meter in musical rhythm.

Figure 2. (A) EEG revealed synchronized fluctuations in induced beta- and gamma-band power that anticipated tone onsets, were sensitive to intensity accents, and persisted when expected tones were omitted. Evoked activity occurred after tone onsets and were strongly diminished after tone omissions (Snyder and Large, 2005; reprinted with permission). (B) A periodic rhythm elicited a steady-state evoked potential (SS-EP) at the stimulus repetition frequency, and meter imagery elicited subharmonic resonances corresponding to the metric interpretation of this periodic rhythm (Nozaradan et al., 2011; reprinted with permission). (C) fMRI showed that listening to musical rhythms recruits both auditory and motor areas of the brain even in perception tasks without a motor component (Chen et al., 2008a; reprinted with permission). (D) Functional connectivity analysis revealed a cortico-subcortical network including the putamen, SMA, and PMC under conditions that may require internal generation of the pulse (Grahn and Rowe, 2009; reprinted with permission). (E) MEG revealed oscillatory interactions in a striato-thalamo-cortical network (Fujioka et al., 2012; reprinted with permission).

Figure 3. Interaction of excitatory and inhibitory neuronal populations gives rise to population rhythms in sensory and motor networks. When sensory stimuli are presented in a periodic pattern, auditory cortical oscillations entrain to the structure of the stimulus stream. The perception of pulse and meter in music also involves broadly distributed motor systems. Auditory-motor coupling is reciprocal, as vestibular stimulation can influence auditory rhythm perception. Connections within and between sensory and motor systems are assumed to be plastic.

Figure 4. (A) Intrinsic oscillatory dynamics can take the form of a Hopf bifurcation, where a value = 0 is the critical point, between damped (left) and spontaneous (right) oscillation. (B) Mode locking in the canonical model. Within each resonance region (shaded), the canonical model mode-locks to input at the ratio shown in figure (c: coupling strength, f: oscillator's intrinsic frequency, f0: input frequency). Insets show the inputs and traces produced by a canonical model. (C) Architecture of a model that captures interacting oscillatory dynamics in sensory and motor networks. A rhythm is input to a sensory network; sensory and motor networks are reciprocally connected, providing input to one another.

Figure 6. Each stimulus pattern contained eight events distributed over eight pulse cycles. Complexity was varied by manipulating the number of events that fell in phase versus anti-phase with the intended pulse. At complexity level 0, all eight events were in-phase, at complexity level 1, one event was anti-phase, at complexity level 2, two events were anti-phase, and so on. Level 4 was the most complex, with four events in-phase and four events anti-phase. One isochronous control (level 0), two level 1 patterns, two level 2 patterns, two level 3 patterns, and four level 4 patterns were used, for a total of 11 rhythms.

Figure 7. (A) Tapping frequencies were normalized to a 2 Hz (120 bpm) tempo to allow comparison between trials at different tempos. Tapping frequency distributions (red histograms) were computed by binning normalized instantaneous tapping frequencies from 0 to 5.00 Hz in bin widths of 0.05 Hz. Distributions were computed for each rhythm separately, including every tap interval across trials. Black lines show amplitude spectrum of the stimulus envelope for comparison. (B) Circular means of tap phases for each trial (blue circles) and grand mean for each complexity level (red line).

(A) EEG revealed synchronized fluctuations in induced beta- and gamma-band power that anticipated tone onsets, were sensitive to intensity accents, and persisted when expected tones were omitted. Evoked activity occurred after tone onsets and were strongly diminished after tone omissions (Snyder and Large, 2005; reprinted with permission). (B) A periodic rhythm elicited a steady-state evoked potential (SS-EP) at the stimulus repetition frequency, and meter imagery elicited subharmonic resonances corresponding to the metric interpretation of this periodic rhythm (Nozaradan et al., 2011; reprinted with permission). (C) fMRI showed that listening to musical rhythms recruits both auditory and motor areas of the brain even in perception tasks without a motor component (Chen et al., 2008a; reprinted with permission). (D) Functional connectivity analysis revealed a cortico-subcortical network including the putamen, SMA, and PMC under conditions that may require internal generation of the pulse (Grahn and Rowe, 2009; reprinted with permission). (E) MEG revealed oscillatory interactions in a striato-thalamo-cortical network (Fujioka et al., 2012; reprinted with permission).

Interaction of excitatory and inhibitory neuronal populations gives rise to population rhythms in sensory and motor networks. When sensory stimuli are presented in a periodic pattern, auditory cortical oscillations entrain to the structure of the stimulus stream. The perception of pulse and meter in music also involves broadly distributed motor systems. Auditory-motor coupling is reciprocal, as vestibular stimulation can influence auditory rhythm perception. Connections within and between sensory and motor systems are assumed to be plastic. ff782bc1db