Unlock the mysteries of arrhythmias with our comprehensive guide! From altered pacemaker cell function to re-entry mechanisms, explore the intricate factors contributing to abnormal heart rhythms. Discover practical interventions for tachycardia and bradycardia, and unravel the clinical implication...
The mechanisms of arrhythmias
Altered function of the pacemaker cells (SAN) may determine pathological bradycardia (slow heart rate)
or tachycardia (heightened rate). Tachycardia may occur in spells (paroxysmal sinus tachycardia)
that often are perceived by the patient as panic attacks. It sometimes responds well to the activation
of the vagus through a carotid massage (interpreted by the body as an increased pressure at the
carotid baroceptors) or Valsalva manoeuvre; however, one must keep in mind that the vagus, by
increasing K conductances, might make the duration of the action potentials in atrial muscle more
heterogeneous (cells with higher expression of K channels have shorter durations and will experience a
greater shortening), so vagal activation may favour the onset of atrial fibrillation.
Ectopic beats may also be generated, in principle, by any cell in the heart that depolarizes anomalously
to threshold, due to any kind of problems, from electrolyte imbalance to hypoxia and lack of energy, or
calcium overload. Such anomalous ectopic beats are called afterdepolarizations (AD) and may occur
during the repolarization of the cell (Early AD, EAD) or later (premature beats or Delayed AD,
DAD). The former are usually due to a repolarization defect (e.g. impaired K currents), while the latter
are usually due to excessive depolarizing power (anomalous Na currents, excessive LCR from Ca2+
overload...)
Healthy cardiac tissue should not suffer, in principle, because of an AD:
• the anomalous action potential should propagate to all the tissue of the myocardium and then
get extinguished
• if there is a block of conduction, some areas of the myocardium might not be reached, but once
the impulse has invaded all the tissue that could be activated it gets extinguished
Still, in some cases an ectopic beat may generate a sustained arrhythmia.
In principle, the genesis of a sustained arrhythmia requires the simultaneous occurrence of one (or
a repetitive) anomalous impulse and a (stable or momentary) defect of conduction.
The main mechanism is the onset of a re-entrant process, through which an anomalous impulse,
after travelling across the myocardium, invades back its own point of origin.
In principle, this should be impossible in most cases, because the time needed to travel even a long path
in the myocardium is generally shorter than the duration of the refractory period, so when an impulse
reaches back to its origin point it should find it unexcitable.
Furthermore, since impulses travel in all directions in an excitable tissue, there is no reason why an
anomalous impulse should propagate unidirectionally so to circle back to the origin.
However, if
• a unidirectional block (structural, stable, or functional, momentary) is encountered
• impulse conduction speed is reduced enough for it to circle, coming back to the origin when the
tissue has regained its excitability
the impulse may get extinguished at the site of block but be able to overcome it when it faces it from the
other side, having invaded the rest of the myocardium, “re-enter” the region of origin, which has in the
meantime become excitable again, and go on recycling.
77 Body At Work II
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