Tachyarrhythmias

A tachyarrhythmia is an abnormally fast rhythm, with a rate > 100 bpm.

As there are many different tachyarrhythmias, to aid in diagnosis and management, clinicians categorize them based on the origin of the rhythm:

1. supraventricular tachyarrhythmias: the rhythm originates or involves the structures above the level of the ventricles, namely the atria and AV junction

2. ventricular tachyarrhythmias: the rhythm originates in the ventricles

More info about where this info is obtained from can be found here.

Mechanisms of Arrhythmogenesis

Every arrhythmia needs two things: 

1. a trigger - something to initiate the arrhythmia. This is typically a premature beat (a.k.a. an extrasystole), which is discussed later.

2. a substrate - something to keep the arrhythmia going so it doesn't falter out.

There are a few different mechanisms by which arrhythmias can be triggered or maintained. These can be organized into disordered impulse generation or disordered impulse conduction.

Abnormal impulse generation refers to one of two mechanisms: increased automaticity or triggered afterdepolarizations. Abnormal impulse conduction, as a mechanism of arrhythmogenesis, usually refers to re-entry.

Usually, arrhythmias result from multiple mechanisms interacting. For example, an arrhythmia can be triggered by an afterdepolarization but subsist through re-entry.

This module will discuss these mechanisms further below.

When the sinus node fires faster because of sympathetic stimulation (i.e. exercise, fear, pain, hypovolemia, and so on), increased automaticity occurs physiologically and is called enhanced normal automaticity.

When the sinus node fires faster aberrantly, outside of normal physiologic responses, it is known as abnormal automaticity. Potential causes of this include:

• Parasympathetic inhibition: with medications or disruptions of the vagus nerve.

• Pathologic states: outside of adrenergic stimulation, sinus automaticity can be enhanced by hypokalemia, digoxin toxicity, and hypoxia/ischemia. These pathologies reduce Na/K pump activity, thereby reducing the hyperpolarizing current, and leading to sinus nodal hyperexcitability.

You may also get abnormal automaticity in non-pacemaker cells. Various factors (i.e. hypokalemia, digoxin, hypoxemia, mechanical stretch) can provoke automaticity in cells other than the dominant pacemaker, leading to something known as a ectopic focus (also known as a driver). With enough automaticity, these ectopic foci can cause overdrive suppression of the sinus node and take over as the dominant pacemaker, leading to a tachyarrhythmia.

Afterdepolarizations occur under conditions involving an excess of intracellular calcium, which can be seen in conditions involving excess catecholamines, digitalis, hypokalemia, hypercalcemia, hypertrophy, and heart failure. The intracellular calcium overload increases the activity of the sodium-calcium exchanger (NCX). The depolarizing current generated by the NCX (which displaces 1 intracellular calcium ion for 3 extracellular sodium ions) causes afterdepolarization.