The rate at which the sinus node discharges usually is faster than other latent or subsidiary automatic cardiac pacemakers. Subsidiary pacemakers can become dominant in the settings of acidosis, ischemia, sympathetic stimulation, and use of certain drugs. Normal automaticity can be suppressed by pacing but generally resumes after pacing stops.
Abnormal automaticity can be due to cell damage and abnormal depolarization. The partial depolarization and failure to reach or maintain the normal maximum diastolic potential may induce automatic discharge. Examples include accelerated junctional rhythm (i.e., nonparoxysmal junctional tachycardia), accelerated ventricular rhythms, certain atrial tachycardias, some ventricular tachycardias (VTs) in patients without structural heart disease, exercise-induced VT, and VT during the first several hours of acute myocardial infarction (MI).
Triggered activity is initiated by afterdepolarizations. If they occur before full repolarization, they are called early afterdepolarizations (EADs); if they occur after completion of repolarization, they are called delayed afterdepolarizations (DADs).
Occurring during phase 2 or 3 of the action potential, EADs are thought to be responsible for VTs associated with prolonged repolarization, such as long QT syndromes (acquired or congenital) and torsades de pointes (TdP) VT. Slower rates, including pauses after extrasystoles, augment EADs.
Occurring during phase 4, DADs have been recorded in Purkinje fibers and atrial and ventricular muscle. Faster rates may augment DADs. This type of triggered activity may underlie rhythms, such as those due to digitalis toxicity or catecholamine excess, acidosis, MI, and certain VTs (e.g., catecholaminergic polymorphic VT).
Conduction delay or block can facilitate the development of reentry, the most common mechanism responsible for tachycardias.
Reentry requires the following:
Alternate or separate pathways of conduction defined by anatomic barriers (e.g., myocardial scar, atrioventricular [AV] node, or an accessory pathway) or functional properties—contiguous fibers with different electrophysiologic properties (e.g., local differences in refractoriness, excitability, or anisotropic intercellular resistances)
An area of unidirectional block in one pathway
An area of conduction in the alternate pathway that is slow enough for the propagating and returning impulse to meet and excite tissue proximal to the block that has since recovered
Reentry is thought to be the mechanism underlying most pathologic tachycardias, including atrial flutter, AV nodal reentry, AV reentry involving accessory pathways (including Wolff-Parkinson-White [WPW] syndrome), and most VTs associated with ischemic heart disease and previous MI. Disordered reentry may cause atrial fibrillation or be passive due to triggered activity from the pulmonary veins.
Narrow QRS complex tachycardia
A narrow QRS complex tachycardia (QRS duration < 120 ms and rate > 100 bpm) indicates a supraventricular origin with ventricular activation occurring via the fast-conducting His-Purkinje system. The acute management of a regular narrow QRS complex tachycardia will depend on the hemodynamic state of the patient. In most but certainly not all instances the patient remains hemodynamically stable even if the rhythm is rapid; this is especially the case if the patient is younger and otherwise healthy; however, AV nodal and AV reentry tachycardias ( Fig. 4.1 ) can cause severe symptoms of presyncope and frank syncope at any rate because of the retrograde atrial depolarization and atrial contraction against closed AV valves; this in turn produces not only loss of stroke volume but also, via atrial stretch receptor activation, reflex systemic hypotension, which can be refractory.
If the patient is stable, the first thing to try is a Valsalva maneuver (bearing down with closed mouth) or carotid sinus massage (if there is no carotid bruit or known vascular disease). If this is ineffective, it should be repeated with the patient in the Trendelenburg position or in combination. If this is ineffective, then adenosine between 6 mg or escalating doses of 12 mg or 18 mg given as an intravenous (IV) bolus followed by a saline “chaser” should be used; this will be expected to either terminate the tachycardia if it is dependent on the AV node for its maintenance or be diagnostic for what the atrial rhythm is during tachycardia, if the tachycardia is AV node independent. For example, sometimes a narrow QRS complex tachycardia, thought to be AV node or AV reentry, in fact turns out to be atrial flutter; adenosine, by producing AV block, thus allowing the atrial rhythm to be visible, will be diagnostic.
In some instances, adenosine is ineffective (sometimes due to the presence of theophylline or high levels of caffeine). If this is the case, a second option would be to give IV verapamil 5 to 15 mg; it is important to know that verapamil should not be given to the patient with a wide QRS complex tachycardia. If neither of these therapies is effective, a DC shock given with anesthesia may be effective; however, it should be recognized that adenosine and verapamil are indeed highly effective in terminating almost all supraventricular tachycardias (SVTs) and that if they do not work it is entirely possible that that the tachycardia is not an SVT but might be sinus tachycardia. IV digoxin is rarely given to terminate narrow QRS complex tachycardias because its action is not that of a direct AV nodal blocker but produces AV block through vagal mechanisms. Adenosine should not be given to heart transplant patients because prolonged asystole may follow; the effects of adenosine can be longer lasting in these patients than would be expected. The normal duration of action of adenosine is 10 to 20 seconds. Whereas theophylline and caffeine diminish the effects of adenosine, dipyridamole accentuates them. Adenosine can cause bronchospasm and atrial fibrillation; if the latter occurs in a patient with WPW syndrome, the atrial fibrillation can be potentially lethal.