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Cardiac Arrhythmias: Difference between revisions
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The cardiac action potential is a result of ions flowing through different ion channels. Ion channels are passages for ions (mainly Na<sup>+</sup>, K<sup>+</sup>, Ca<sup>2+</sup> and Cl<sup>-</sup>) that facilitate movement through the cell membrane. Changes in structure of these channels can open, inactivate or close and control current inside and outside the myocytes. Due to different activity and expression of ion channels, the various parts of the cardiac conduction channel have slightly different action potential characteristics. Ion channels are mostly a passive passage, where movement of ions are caused by the electrochemical activity gradient. In addition to these passive ion channels a few ATP-dependent channels exist to fine-tune the action potential. These changes of membrane potential produce and action potential lasting a few hundreds of milliseconds. Disorders is single channels can lead to arrhythmias, as seen in the section [[Primary_Arrhythmias]]. The action potential is conducted throughout the heart by the depolarization of the immediate environment of the cells and through intracellular coupling with gap-junctions. The communication pores are located in cell to cell adhesion structures, the intercalated disks. | The cardiac action potential is a result of ions flowing through different ion channels. Ion channels are passages for ions (mainly Na<sup>+</sup>, K<sup>+</sup>, Ca<sup>2+</sup> and Cl<sup>-</sup>) that facilitate movement through the cell membrane. Changes in structure of these channels can open, inactivate or close and control current inside and outside the myocytes. Due to different activity and expression of ion channels, the various parts of the cardiac conduction channel have slightly different action potential characteristics. Ion channels are mostly a passive passage, where movement of ions are caused by the electrochemical activity gradient. In addition to these passive ion channels a few ATP-dependent channels exist to fine-tune the action potential. These changes of membrane potential produce and action potential lasting a few hundreds of milliseconds. Disorders is single channels can lead to arrhythmias, as seen in the section [[Primary_Arrhythmias]]. The action potential is conducted throughout the heart by the depolarization of the immediate environment of the cells and through intracellular coupling with gap-junctions. The communication pores are located in cell to cell adhesion structures, the intercalated disks. | ||
In summary during the depolarization, sodium ions stream into the cell followed by a influx of Ca<sup>2+</sup> ions (both from the inside (sarcoplasmatic reticulum) and outside of the cell). These Ca<sup>2+</sup> ions cause the actual muscular contraction. Shortly thereafter K+ ions stream out of the cell. During repolarization the ion concentration returns to its precontraction state. The action potential can be divided in five phases: | In summary during the depolarization, sodium ions stream into the cell followed by a influx of Ca<sup>2+</sup> ions (both from the inside (sarcoplasmatic reticulum) and outside of the cell). These Ca<sup>2+</sup> ions cause the actual muscular contraction. Shortly thereafter K+ ions stream out of the cell. During repolarization the ion concentration returns to its precontraction state. The action potential can be divided in five phases: \ | ||
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[[File:Example.jpg]] | |||
===Phase 0: Rapid Depolarization=== | ===Phase 0: Rapid Depolarization=== | ||
Rapid depolarization is started once the membrane potential reaches a certain threshold (about -70 to -60 mV), independent of the size of the depolarizing stimulus. This produces a rapid influx of Na<sup>+</sup> and a rapid upstroke of the action potential. At higher potentials (-40 to -30) Ca<sup>2+</sup> influx participates in the upstroke. In sinus node and AV node a slower upstroke can be observed (Figure 1). This caused because the upstroke in these cells are mainly mediated by the slower acting Ca<sup>2+</sup> ion channels. The slow activation and inactivation produce a slower upstroke. | Rapid depolarization is started once the membrane potential reaches a certain threshold (about -70 to -60 mV), independent of the size of the depolarizing stimulus. This produces a rapid influx of Na<sup>+</sup> and a rapid upstroke of the action potential. At higher potentials (-40 to -30) Ca<sup>2+</sup> influx participates in the upstroke. In sinus node and AV node a slower upstroke can be observed (Figure 1). This caused because the upstroke in these cells are mainly mediated by the slower acting Ca<sup>2+</sup> ion channels. The slow activation and inactivation produce a slower upstroke. | ||