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| ==Causes== | | ==Causes== |
| ===Abnormal automaticity===
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| Automaticity is a measure of the propensity of a fiber to initiate an impulse spontaneously. The product of a [[Hypoxia (medical)|hypoxic]] myocardium can be hyperirritable myocardial cells. These may then act as pacemakers. The ventricles are then being stimulated by more than one [[pacemaker]]. Scar and dying tissue is inexcitable, but around these areas usually lies a penumbra of hypoxic tissue that is excitable. Ventricular excitability may generate re-entry arrhythmias.
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| It is interesting to note that most cardiac myocardial cells with an associated increased propensity to arrhythmia development have an associated loss of [[membrane potential]]. That is, the maximum diastolic potential is less negative and therefore exists closer to the [[threshold potential]]. Cellular depolarisation can be due to a raised external concentration of [[potassium]] ions K<sup>+</sup>, a decreased intracellular concentration of [[sodium]] ions Na<sup>+</sup>, increased permeability to Na<sup>+</sup>, or a decreased permeability to K<sup>+</sup>. The ionic basic automaticity is the net gain of an intracellular positive charge during diastole in the presence of a voltage-dependent channel activated by potentials negative to –50 to –60 mV.
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| Myocardial cells are exposed to different environments. Normal cells may be exposed to hyperkalaemia; abnormal cells may be perfused by normal environment. For example, with a healed myocardial infarction, abnormal cells can be exposed to an abnormal environment such as with a myocardial infarction with myocardial ischaemia. In conditions such as myocardial ischaemia, possible mechanism of arrhythmia generation include the resulting decreased internal K<sup>+</sup> concentration, the increased external K<sup>+</sup> concentration, norepinephrine release and acidosis.<ref>Ho K 1993</ref> When myocardial cell are exposed to hyperkaliemia, the maximum diastolic potential is depolarized as a result of the alteration of Ik1 potassium current, whose intensity and direction is strictly dependant on intracellular and extracellular potassium concentrations. With Ik1 suppressed, an hyperpolarizing effect is lost and therefore there can be activation of [[funny current]] even in myocardial cells (which is normally suppressed by the hyperpolarizing effect of coexisting potassium currents). This can lead to the instauration of automaticity in ischemic tissue.
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| ===Re-entry===<!-- This section is linked from [[Ventricular fibrillation]] -->
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| The role of re-entry or '''circus motion''' was demonstrated separately by Mines and Garrey.<ref>Mines GR 1913, Garrey WE 1914</ref> Mines created a ring of excitable tissue by cutting the atria out of the [[ray fish]]. Garrey cut out a similar ring from the [[turtle]] ventricle. They were both able to show that, if a ring of excitable tissue was stimulated at a single point, the subsequent waves of depolarisation would pass around the ring. The waves eventually meet and cancel each other out, but, if an area of transient block occurred with a [[refractory period (physiology)|refractory period]] that blocked one wavefront and subsequently allowed the other to proceed retrogradely over the other path, then a self-sustaining circus movement phenomenon would result. For this to happen, however, it is necessary that there be some form of non-uniformity. In practice, this may be an area of [[ischaemic]] or [[infarct]]ed myocardium, or underlying [[Myocardial scarring|scar tissue]].
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| It is possible to think of the advancing wave of depolarisation as a dipole with a head and a tail. The length of the refractory period and the time taken for the dipole to travel a certain distance—the propagation velocity—will determine whether such a circumstance will arise for re-entry to occur. Factors that promote re-entry would include a slow-propagation velocity, a short refractory period with a sufficient size of ring of conduction tissue. These would enable a dipole to reach an area that had been refractory and is now able to be depolarised with continuation of the [[wavefront]].
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| In clinical practice, therefore, factors that would lead to the right conditions to favour such re-entry mechanisms include increased heart size through [[hypertrophy]] or dilatation, drugs which alter the length of the refractory period and areas of cardiac disease. Therefore, the substrate of ventricular fibrillation is transient or permanent conduction block. Block due either to areas of damaged or refractory tissue leads to areas of myocardium for initiation and perpetuation of fibrillation through the phenomenon of re-entry.
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| ===Causes in Alphabetical Order=== | | ===Causes in Alphabetical Order=== |