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Cardiac Arrhythmias: Difference between revisions
→Mechanisms of Arrhythmia
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[[File:Mechanisms.svg|right|thumb|400px|'''Figure 3.''' The different mechanisms of arrhythmia.]] | [[File:Mechanisms.svg|right|thumb|400px|'''Figure 3.''' The different mechanisms of arrhythmia.]] | ||
Structural abnormalities or electric changes in the cardiomyocytes can impede impulse formation or change cardiac propagation facilitating arrhythmias. We briefly discuss the main causes of | Structural abnormalities or electric changes in the cardiomyocytes can impede impulse formation or change cardiac propagation, therefore facilitating arrhythmias. We briefly discuss the pathofysiological mechanisms of the main causes of arrhythmia. | ||
== Abnormal Impulse Formation== | == Abnormal Impulse Formation== | ||
The mechanism of abnormal automaticity is similar to the normal automaticity of sinus node cells. Abnormal automaticity can be caused by changes in the cell ion channel characteristics due to drugs or changes in the electrotonic environment. Abnormal automaticity can result from an increase of normal automaticity in non-sinus node cells or a truly abnormal automaticity in cells that don't exhibit a phase 4 diastolic depolarization. | The mechanism of abnormal automaticity (in contrast to normal automaticity) is similar to the normal automaticity of sinus node cells. Abnormal automaticity can be caused by changes in the cell ion channel characteristics due to drugs or changes in the electrotonic environment. Abnormal automaticity can result from an increase of normal automaticity in non-sinus node cells or a truly abnormal automaticity in cells that don't exhibit a phase 4 diastolic depolarization. | ||
===Abnormal Automaticity=== | ===Abnormal Automaticity=== | ||
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===Triggered Activity=== | ===Triggered Activity=== | ||
Triggered activity is activity of a cell triggered by a preceding activation. Due to early or delayed afterdepolarizations the | Triggered activity is activity of a cell triggered by a preceding activation. Due to early or delayed afterdepolarizations the membrane potential depolarizes and, when reaching a threshold potential, activates the cell. These afterdepolarizations are depolarizations of the membrane potential initiated by the preceding action potential. Depending on the phase of the action potential in which they arise, they are defined as early or late afterdepolarizations (figure 3). | ||
* In early afterdepolarizations depolarization occurs during the action potential (phase 2 and 3) by a diversity of causes. Early afterdepolarizations can increase duration of the repolarization phase of the action potential. This increase can create heterogeneity in refractoriness and thereby creating the substrate for a re-entry circuit (see below). | * In early afterdepolarizations depolarization occurs during the action potential (phase 2 and 3) by a diversity of causes. Early afterdepolarizations can increase duration of the repolarization phase of the action potential. This increase can create heterogeneity in refractoriness and thereby creating the substrate for a re-entry circuit (see below). | ||
* Delayed afterdepolarizations occur after the cell has recovered after completion of repolarization. In delayed afterdepolarization an abnormal Ca2+ handling of the cell is probably responsible for the afterdepolarizations due to release of Ca<sup>2+</sup> from the storage of Ca2<sup>+</sup> in the sarcoplasmatic reticulum. The accumulation of Ca<sup>2+</sup> increases membrane potential and thus depolarizes the cell when it reaches a certain threshold. | * Delayed afterdepolarizations occur after the cell has recovered after completion of repolarization. In delayed afterdepolarization an abnormal Ca2+ handling of the cell is probably responsible for the afterdepolarizations due to release of Ca<sup>2+</sup> from the storage of Ca2<sup>+</sup> in the sarcoplasmatic reticulum. The accumulation of Ca<sup>2+</sup> increases membrane potential and thus depolarizes the cell when it reaches a certain threshold. | ||