Sinus Node

The normal heartbeat arises from the SA node that serves as the pacemaker of the heart under normal conditions. Bradycardia resulting form SA node dysfunction originates from either failure of impulse generation or failure of impulse conduction. In the past, the term “sick sinus syndrome” has been used to describe a variety of sinus bradyarrhythmias with many etiologies. More appropriate classification of SA node dysfunction includes inappropriate sinus bradycardia, sinus pause or arrest, sinus exit block, and bradycardia-tachycardia syndrome.

Sinus bradycardia (heart rate <60) does not necessarily imply SA node dysfunction, and even a heart rate less than 40 at rest can be asymptomatic in well-trained athletes. Sinus bradycardia is considered pathologic when patients are symptomatic or when there is failure to appropriately increase heart rate during activity or exercise. Sinus pause or arrest occurs when the SA node transiently fails to exhibit automaticity and does not fire. Sinus exit block similarly results in a pause but the SA node does fire. The impulse is either delayed or fails to propagate beyond the SA node, resulting in failure of atrial depolarization. Bradycardia-tachycardia syndrome refers to sinus node dysfunction with both bradycardia and tachycardia. Typically bradycardia episodes follow the termination of tachycardia events and can be associated with clinical symptoms of presyncope or syncope. Management can be challenging, as pharmacotherapy to treat fast rhythms predisposes to slow ones and vice versa. Commonly, insertion of a pacemaker for the symptomatic bradycardia, in conjunction with pharmacological treatment for the tachycardia, is required.

Treatment for SA node dysfunction depends on the clinical status of the patient and presumed etiology. If the bradycardia is transient and not associated with hemodynamic compromise, no therapy is necessary. Correction of any metabolic abnormalities, minimizing vagal-inducing maneuvers, and removal or dose reduction of medications such as beta-blockers, calcium channel antagonists, and lithium may be necessary. If the bradycardia is sustained or severe enough to cause hemodynamic instability, therapy with anti-muscarinic agents (atropine) or beta-agonist (isoproterenol) may be initiated. Percutaneous or transvenous pacing may be necessary in some patients in the acute setting and can be a bridge to permanent pacemaker placement. Patients that are relatively stable but are symptomatic from sinus node dysfunction virtually always require permanent pacing.

Atrioventricular Node

Disturbances in conduction through the AV node or His-Purkinje system are classified as atrioventricular blocks. These may be temporary or permanent, depending on the etiology of the delayed conduction. In adults, the most common causes are drug toxicity, coronary artery disease, and degenerative disease of the conduction system. Many other conditions, such as electrolyte disturbances, myocarditis, sarcoidosis, scleroderma, and hypervagal responses, can cause AV block. The P-R interval is a measure of the conduction time through the AV node and bundle of His. When the P-R interval is prolonged (>210 milliseconds), a patient has first-degree AV block. Second-degree AV block is when intermittent failure of the conduction of the impulse to the ventricles occurs. In Mobitz type I, second-degree AV block (Wenckebach block), there is progressive prolongation of the P-R interval until failure of conduction to the ventricle occurs (Figure 1). The P-R interval then shortens following the dropped beat. This failure in conduction originates from the AV node itself and the QRS complex remains narrow. In Mobitz type II, second-degree AV block, there is intermittent failure of conduction reaching the ventricles that is not associated with progressive prolongation of the P-R interval. There is not a shortened P-R interval following the dropped beat. This failure in conduction is considered “infranodal” and originates from the His-Purkinje system. The QRS complex may be prolonged, and this type of AV block is more concerning. There is a significant likelihood of progression to complete heart block associated with inadequate ventricular response with this rhythm. Third-degree or complete heart block results from failure of all impulses through the AV node and His-Purkinje system, resulting in atrioventricular disassociation. The ventricles rely on their innate automaticity which produces a typical wide QRS escape rhythm between 40 and 50 beats per minute. The atrial rate is commonly faster, producing multiple P waves with no relationship to the ventricular QRS complexes (Figure 2).

Figure 1 Rhythm strip shows progressive P-R prolongation and a subsequent “dropped” QRS complex, followed by shortening of the P-R interval which is diagnostic of Mobitz type I, second-degree AV block.

Figure 2 Rhythm strip shows atrial P waves and ventricular QRS complexes occurring at different rates and with no relationship between them, which is characteristic of third-degree AV block.

Management of AV block depends on the hemodynamic stability of the patient, the transient nature of the dysrhythmia, and where the focus originates from within the conduction system. Acute pharmacotherapy relies upon atropine and isoproterenol. Isoproterenol use should be avoided in patients with ischemia heart disease because of the associated increase in myocardial oxygen demand. There is no long-term pharmacotherapy for AV block, and removal of any of the common offending agents, such as digitalis or beta-blockers, should first be attempted. Temporary pacing is used for those with ongoing instability, and permanent pacing is typically required for Mobitz type II second-degree AV block and third-degree AV block.

Sinus Tachycardia

Sinus tachycardia should be considered a physiological reflex rather than a true dysrhythmia, but it is an important sign for which the etiology must be sought. Fever, hypovolemia, and anemia all appropriately increase heart rate to at least maintain or increase cardiac output. Blunting this reflex with pharmacotherapy without knowledge of the etiology can be dangerous. Thyrotoxicosis, pheochromocytomas, or side effects of sympathomimetic drugs also cause sinus tachycardia without regard for reflex mechanisms. The primary goal for management of sinus tachycardia is to find and appropriately treat the confounding condition. Sinus tachycardia will resolve with resolution of this inciting process.

Paroxysmal Supraventricular Tachycardia

The term “paroxysmal supraventricular tachycardia” actually describes a diverse group of tachyarrhythmias, the two most common being atrioventricular nodal re-entry tachycardia (AVNRT) and atrioventricular re-entry tachycardia (AVRT). They both have in common dual conduction pathways, each with different rates of conduction. As described previously, this allows for the possibility of re-entry and the potential for a self-propagating tachyarrhythmia focus. In AVNRT, the two pathways reside in or around the AV node itself. Antegrade conduction typically occurs through the slower pathway, while the retrograde conduction occurs through the faster pathway. Rates of 140–220 beats/min are typical, and P waves are not seen on ECG since retrograde atrial activation and antegrade ventricular activation occur simultaneously. The QRS complex is typically narrow because the antegrade conduction to the ventricles uses the normal AV node and His-Purkinje system. In comparison, AVRT also has two conduction pathways, but the additional pathway is remote from the AV node and resides in the atrioventricular groove, where it is commonly referred to as an “accessory pathway.” Similar to AVNRT, antegrade conduction occurs through the AV node and His-Purkinje system, while retrograde conduction occurs via the accessory pathway. The QRS complex for AVRT is also narrow, and since the accessory pathway only conducts retrograde, it is not seen on ECG and is considered “concealed.”

Acute management depends on the stability of the patients with paroxysmal supraventricular tachycardia. Urgent direct-current cardioversion is indicated when myocardial ischemia, acute heart failure, or hypotension result. In hemodynamically stable patients, pharmacological intervention with the intent to slow or break AV nodal conduction is the mainstay of treatment. Intravenous adenosine is the first-line drug of choice due to its potent yet short-lived depressant effects on AV nodal conduction. Adenosine will successfully terminate greater than 90% of tachyarrhythmias due to AVNRT and AVRT. Calcium channel blockers or beta-blockers (verapamil/diltiazem or metoprolol) are also useful, particularly when adenosine is not successful, although they should be used with caution due to possible hypotensive and bradycardic effects.

When the accessory pathway has the potential for antegrade conduction, the QRS complex will be wide, since conduction occurs between the ventricular myocytes themselves rather than the His-Purkinje system. Wolfe-Parkinson-White syndrome occurs when the accessory pathway allows both antegrade and retrograde conduction, and commonly a delta wave or pre-excitation can be seen in the early QRS complex (Figure 4). This syndrome can present in early adulthood, and the initial presentation can be ventricular fibrillation. Management in these patients where conduction occurs antegrade through the accessory pathway varies from narrow complex AVRT as described previously. Adenosine will only be effective if the antegrade conduction occurs through the AV node. Otherwise it can precipitate atrial fibrillation, which can result in degeneration to ventricular fibrillation when an antegrade accessory pathway exists in these patients. Calcium channel blockers and digoxin are contraindicated, because they will slow conduction in the AV node and enhance conduction through the accessory pathway. Class I and class III antiarrhythmics, which include flecainide, procainamide, and ibutilide, are able to depress the conduction across the accessory pathway, decrease the ventricular rate, and likely terminate the wide QRS tachyarrythmia. Direct-current cardioversion is used with hemodynamic instability or if failure of antiarrhythmic therapy occurs.

Figure 4 Lead II in this ECG shows a prominent delta wave consistent with the diagnosis of Wolfe-Parkinson-White syndrome.