![]() ![]() This means that a PAC may cause a "compensatory pause" as the SA node restarts its pacemaker depolarization. The premature complex may also upset the timing of the SA node, placing it back into a refractory period when it should be depolarizing for its next scheduled beat. The aberrant P-wave also has a different morphology from a sinus P-wave because of its different anatomical origin. This produces an extra P-wave, and consequently a shortening from previous P-P intervals is seen. P-waves have different morphology (at least three)Ī premature atrial contraction (PAC) is generated by a depolarization instigated outside of the SA node. This rhythm is benign, and once the underlying lung disease is treated, it should resolve. MAT frequently occurs in the setting of severe lung disease and, more specifically, during an exacerbation of lung disease. ![]() By definition, MAT must have at least three distinctly different P-wave morphologies (figure 1.4) and a ventricular rate of greater than 100 bpm.įigure 1.4: Three distinct P-wave morphologies in a case of MAT. Thus, each QRS complex will be preceded by a P-wave however, each P-wave will have a different morphology because they originate from different areas. The multiple foci within the atrium generate consecutive action potentials that are all conducted to the ventricles. ![]() The multiple foci result in P-waves with multiple morphologies and irregular intervals (see figure 1.4). The pathophysiology of MAT is not clear, although several theories exists (e.g., triggered activity, reentry, or abnormal automaticity). Multifocal atrial tachycardia (MAT) is caused by the presence of multiple ectopic foci. Parasympathetic stimulation or changes in AV node refractoriness can modify how many P-waves pass into the ventricle, but the the resultant rhythm is “regularly irregular." When the heart rate is elevated, then distinguishing flutter from fibrillation becomes challenging and slowing ventricular rate pharmaceutically (adenosine) helps the flutter waves reemerge for a definitive diagnosis to be made.įigure 1.3: Atrial flutter - "sawtooth" P-waves with lower frequency than the fibrillation waves of atrial fibrillation. As with atrial fibrillation, the AV node's refractory period prevents most of the P-waves from progressing to the ventricle, but commonly the AV conduction will be 2-to-1, so with an atrial rate of 300 bpm the ventricular rate will be 150 bpm. The cavotricuspid isthmus (CTI) usually provides the circuit for the slower reentrant current to become established (typical atrial flutter), but other sites of reentry and slow conducting circuits are possible (atypical atrial flutter) and are usually associated with structural heart disease or sites of previous surgical or ablations procedures. The slower reentry current produces an atrial rate of 250–350 bpm (compared to the 400–600 of atrial flutter), and P-waves are present but have a characteristic “sawtooth” pattern (figure 1.3 and middle panel figure 1.2). When this occurs, the ventricular rate rises to 100–200 bpm, and QRS complexes can be “irregularly irregular” with a varying R-R interval (left panel, figure 1.2).įigure 1.1: An ECG of atrial fibrillation showing lack of P-waves and low-amplitude fibrillation waves between QRS complexes.įigure 1.2: Comparison of atrial arrhythmias, including atrial fibrillation (left), atrial flutter (middle), and multifocal atrial tachycardia (MAT) (right).Ītrial flutter is caused by a macroreentrant current, rather than the multiple sites of aberrant depolarization seen in fibrillation. This means the ventricular rate does not rise to 400–600 bpm (which would be catastrophic), but some of the atrial fibrillation activity can be "lucky" and reach the AV node when it is not in a refractory period. The rapid atrial depolarizations are transmitted to the atrioventricular (AV) node, but far from all are conducted through to the ventricle because of the node's long refractory period. Because the atrial rate is so fast, the ECG shows “coarse fibrillatory waves” (figure 1.1) the action potentials produced are low amplitude, and P-waves will not be seen. Causes include hypertension, valvular and ischemic heart disease, and genetics (e.g., mutation of 10q22–q24 on chromosome 10). The rapid depolarizations result in a very fast atrial rate from 400 to 600 bpm. These aberrant depolarizations are often the result of myocardial remodeling and frequently originate within the muscular sleeves that extend into the pulmonary veins from the atria. \)Ītrial fibrillation is the most common cardiac arrhythmia and is caused by rapidly firing potentials in the atrial myocardium. ![]()
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