The normal electrical conduction system of the heart allows electrical impulses generated by the heart's own pacemaker (the sinoatrial node) to spread to and stimulate the muscular layer of the heart (myocardium) in both the<unk> and the ventricles. When the myocardium is stimulated it contracts, and if this occurs in an orderly manner allows blood to be pumped to the body. In<unk> , the normal regular electrical impulses generated by the sinoatrial node are overwhelmed by disorganized electrical waves, usually originating from the roots of the pulmonary veins. These disorganized waves conduct intermittently through the atrioventricular node, leading to irregular activation of the ventricles that generate the heartbeat. Pathology The primary pathologic change seen in<unk>  is the progressive fibrosis of the<unk>  This fibrosis is due primarily to<unk>  dilation; however, genetic causes and inflammation may be<unk> ctors in some individuals. Dilation of the<unk> can be due to almost any structural abnormality of the heart that can cause a rise in the pressure within the heart. This includes valvular heart disease (such as mitral stenosis, mitral regurgitation, and tricuspid regurgitation), hypertension, and congestive heart<unk> ilure. Any inflammatory state that<unk> fects the heart can cause fibrosis of the<unk>  This is typically due to sarcoidosis but may also be due to autoimmune disorders that create autoantibodies against myosin heavy chains. Mutation of the lamin AC gene is also associated with fibrosis of the<unk> that can lead to<unk> . Once dilation of the<unk> has occurred, this begins a chain of events that leads to the activation of the renin–angiotensin–aldosterone system (RAAS) and subsequent increase in the matrix metalloproteinases and disintegrin, which leads to<unk>  remodeling and fibrosis, with loss of<unk>  muscle mass. This process occurs gradually, and experimental studies have revealed patchy<unk>  fibrosis may precede the occurrence of<unk>  and may progress with prolonged durations of<unk> . Fibrosis is not limited to the muscle mass of the<unk> and may occur in the sinus node (SA node) and atrioventricular node (AV node), correlating with sick sinus syndrome. Prolonged episodes of<unk>  have been shown to correlate with prolongation of the sinus node recovery time; this suggests that dysfunction of the SA node is progressive with prolonged episodes of<unk> . Along with fibrosis, alterations in the<unk> that predispose to<unk> <unk> fect their electrical properties, as well as their responsiveness to the autonomic nervous system. The<unk>  remodeling that includes the pathologic changes described above has been referred to as<unk>  myopathy. Electrophysiology Conduction Sinus rhythm 230px<unk>  230px There are multiple theories about the cause of<unk> . An important theory is that the regular impulses produced by the sinus node for a normal heartbeat are overwhelmed by rapid electrical discharges produced in the<unk> and adjacent parts of the pulmonary veins. Sources of these disturbances are either automatic foci, often localized at one of the pulmonary veins, or a small number of localized sources in the form of either a re-entrant leading circle or electrical spiral waves (rotors); these localized sources may be in the left atrium near the pulmonary veins or in a variety of other locations through both the left or right atrium. Three fundamental components<unk> vor the establishment of a leading circle or a rotor: slow conduction velocity of the cardiac action potential, a short refractory period, and a small wavelength. Meanwhile, the wavelength is the product of velocity and refractory period. If the action potential has<unk> st conduction, with a long refractory period and/or conduction pathway shorter than the wavelength, an<unk>  focus would not be established. In multiple wavelet theory, a wavefront will break into smaller daughter wavelets when encountering an obstacle, through a process called vortex shedding. But, under the proper conditions, such wavelets can reform and spin around a center, forming an<unk>  focus. In a heart with<unk> , the increased calcium release from the sarcoplasmic reticulum and increased calcium sensitivity can lead to an accumulation of intracellular calcium and causes downregulation of L-type calcium channels. This reduces the duration of action potential and the refractory period, thus<unk> voring the conduction of re-entrant waves. Increased expression of inward-rectifier potassium ion channels can cause a reduced<unk>  refractory period and wavelength. The abnormal distribution of gap junction proteins such as GJA1 (also known as Connexin 43), and GJA5 (Connexin 40) causes non-uniformity of electrical conduction, thus causing the arrhythmia.<unk>  can be distinguished from<unk>  flutter <unk> L), which appears as an organized electrical circuit usually in the right atrium.<unk> L produces characteristic saw-toothed F-waves of constant amplitude and frequency on an ECG, whereas<unk>  does not. In<unk> L, the discharges circulate rapidly at a rate of 300 beats per minute (bpm) around the atrium. In<unk> , there is no such regularity, except at the sources where the local activation rate can exceed 500 bpm. Although<unk>  and<unk>  flutter are distinct arrhythmias,<unk>  flutter may degenerate into<unk> , and an individual may experience both arrhythmias at different times. Although the electrical impulses of<unk>  occur at a high rate, most of them do not result in a heartbeat. A heartbeat results when an electrical impulse from the<unk> passes through the atrioventricular (AV) node to the ventricles and causes them to contract. During<unk> , if all of the impulses from the<unk> passed through the AV node, there would be severe ventricular tachycardia, resulting in a severe reduction of cardiac output. This dangerous situation is prevented by the AV node since its limited conduction velocity reduces the rate at which impulses reach the ventricles during<unk> .
Atrial fibrillation
Arrhythmia
Atrial flutter
Sinus arrhythmia
Ventricular flutter
Supraventricular tachycardia
Torsades de pointes
Atrial tachycardia