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Research in the late 2000s has linked this finding to ventricular fibrillation, particularly in those who have fainted or have a family history of sudden cardiac death. [5] [6] [7] Although there is a significant relationship between ventricular fibrillation and some early repolarization's patterns, the overall lifetime occurrence of idiopathic ventricular fibrillation is exceptionally rare. [8]
In the heart, contractions must be spaced to maintain a rhythm. Unlike in muscle, repolarization occurs at a slow rate (100 ms). This prevents the heart from undergoing sustained contractions because it forces the refractory period and cardiac action potential firing to be of the same length of time.
In a normal heart, the heart rate is the rate at which the sinoatrial node depolarizes since it is the source of depolarization of the heart. Heart rate, like other vital signs such as blood pressure and respiratory rate, change with age. In adults, a normal heart rate is between 60 and 100 bpm (normocardic), whereas it is higher in children. [56]
Recent studies have shown a connection between early repolarization and sudden cardiac death, which is identified as early repolarization syndrome. The condition is shown in both ventricular fibrillation without other structural heart defects as well as an early depolarization pattern, which can be seen on ECG. [21]
The action potential passes along the cell membrane causing the cell to contract, therefore the activity of the sinoatrial node results in a resting heart rate of roughly 60–100 beats per minute. All cardiac muscle cells are electrically linked to one another, by intercalated discs which allow the action potential to pass from one cell to the ...
The cardiac action potential has five phases. I to1 is active during phase 1, causing a fast repolarization of the action potential. The cardiac transient outward potassium current (referred to as I to1 or I to [1]) is one of the ion currents across the cell membrane of heart muscle cells.
Long QT syndrome (LQTS) is a condition affecting repolarization (relaxing) of the heart after a heartbeat, giving rise to an abnormally lengthy QT interval. [7] It results in an increased risk of an irregular heartbeat which can result in fainting, drowning, seizures, or sudden death. [1]
J waves or Osborn waves, which represent an early repolarization and delayed depolarization of the heart ventricles, are thought to be caused by the high catecholamines surge released in patients with subarachnoid hemorrhage or brain damage, the issue that might lead to ventricular fibrillation and cardiac arrest in unmanaged patients. [39] [40]
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