Mechanisms of Tachydysrhythmias

There are three accepted mechanisms for dysrhythmias: (1) increased automaticity in a normal or ectopic site, (2) reentry in a normal or accessory pathway, and (3) afterdepolarizations causing triggered rhythms. While treatment is best directed by an understanding of the underlying process, uncertainty still exists over the precise mechanism of many dysrhythmias, and therapy is still often empiric.

An ectopic focus is an area of the heart, away from the normal sinus node pacemaker, that acquires independent pacemaker activity and usurps the pacemaking role. The result can be a single extrasystole or multiple extra depolarizations. These ectopic pacemakers can be the result of (1) enhanced automaticity of subsidiary pacemaker cells (i.e., in the AV node or infranodal conduting system) or (2) abnormal automaticity of myocardial cells, which seldom possess pacemaking activity (i.e., Purkinje cells). Dysrhythmias due to an ectopic focus usually have a gradual onset ("warmup period"). The termination is also gradual, as opposed to the abrupt onset and termination seen with reentry or triggered mechanisms.

Reentry was initially described when researchers took myocardial tissue and increased the K + concentration in a part of the tissue. They found that when stimulated, a rhythm was sustained without further stimulation at certain K+ concentrations. Reentry requires a temporary or permanent unidirectional block in one limb of a circuit and slower-than-normal conduction around the entire circuit. These conditions are secondary to disease, drugs, accessory pathways, or when tissue is stimulated during the partial refractory period (before full repolarization), as with premature depolarizations.

As indicated in Fig.;...24-.3, the inciting impulse traveling in the normal downward direction encounters the two limbs, finds limb a blocked, and travels down limb b. Upon reaching the bottom portion of the circuit where the two limbs rejoin, the impulse can then travel retrograde up limb a and reach the upper connection of the circuit. Normally, conduction is so rapid that the impulse would encounter limb b still refractory to stimulation, and no further propagation would occur. However, if conduction around the circuit were slow enough, limb b would be able to conduct the impulse again in the antegrade direction. With the right size circuit and conduction velocity, an electric impulse can be maintained traveling around the circuit in a cyclic manner. Each time the impulse passes the upper and lower limb connections, a depolarization occurs.

FIG. 24-3. Reentry circuit.

Reentry can occur around anatomically defined circuits, resulting in a regular rapid rhythm such as paroxysmal supraventricular tachycardia. Conversely, reentry can also occur in a disorganized and chaotic fashion through a syncytium of myocardial tissue—as seen, for example, in atrial or ventricular fibrillation.

Triggered dysrhythmias are due to the oscillations of the transmembrane potential during or after repolarization (afterpotentials). Under ideal conditions of rate, afterpotentials reach threshold and trigger a complete depolarization (afterdepolarization). Once triggered, this process may be self-sustaining. Triggered dysrhythmias associated with early afterpotentials are enhanced by slow heart rates and usually treated by accelerating the ventricular rate with positive chronotropic drugs or electrical pacing. Triggered dysrhythmias associated with delayed afterpotentials are enhanced by fast heart rates. Treatment with agents that have a negative chronotropic action is usually effective.

The urgency with which tachydysrhythmias require treatment is guided by two considerations: (1) evidence of hypoperfusion (shock, altered mental status, anginal chest pain, or pulmonary edema) and (2) the potential to degenerate into a more serious dysrhythmia or cardiac arrest. The two treatment methods most commonly used are intravenous drugs for the clinically stable patient and synchronized cardioversion or defibrillation for the unstable patient. Some tachydysrhythmias are amenable to overdrive electrical pacing but frequently require rates over 200 in order to capture the ventricle.

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