Diagnosis and management of cardiac dysrhythmias

Sinus node

The normal heartbeat arises from the SA node, which serves as the pacemaker of the heart under normal conditions. Bradycardia arising from SA nodal dysfunction originates from either failure of impulse generation or failure of the conduction of that impulse. In the past, the term “sick sinus syndrome” was used to describe a range of conditions that reflect such dysfunctions. Currently, bradyarrhythmias arising from the SA node are described as one of the following: inappropriate sinus bradycardia, sinus pause or arrest, sinus exit block, and tachycardia-bradycardia (aka tachy-brady) syndrome.

Sinus bradycardia is defined as a heart rate below 60 beats per minute (bpm). This alone does not signify SA nodal dysfunction, as heart rates below even 40 bpm can be asymptomatic and considered normal in well-trained athletes or active individuals. Sinus bradycardia is considered pathologic, then, when patients are symptomatic (e.g., syncope, chest pain, shortness of breath) or when there is a failure to appropriately increase the heart rate during activity. 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 still depolarizes normally. The impulse is either delayed or fails to propagate beyond the SA node, resulting in failure of atrial depolarization. Tachycardia-bradycardia syndrome refers to sinus node dysfunction with both tachycardia and bradycardia. Typically, bradycardic episodes follow the termination of tachycardia events and can be associated with the clinical symptoms of presyncope or syncope. Management can be challenging, as pharmacotherapy to treat fast rhythms often predisposes patients to slow ones, and vice versa. Commonly, insertion of a pacemaker in situations of tachycardia-bradycardia syndrome may be necessary to treat the symptomatic bradycardia, in conjunction with pharmacologic treatment for the tachycardia.

Treatment for SA node dysfunction depends on the clinical status of the patient and the presumed cause. If the bradycardia is transient and not associated with hemodynamic compromise, no therapy is necessary. Investigation into the cause of bradycardia should include correction of metabolic and electrolyte abnormalities, minimizing maneuvers that could increase vagal tone, and the cessation or reduction in dosage of potentially offending medications, such as beta blockers, calcium channel antagonists, and lithium. If the bradycardia is sustained, or severe enough to lead to hemodynamic instability, therapy with antimuscarinic agents such as atropine or beta-agonists should be considered. Percutaneous or transvenous pacing may be necessary in some patients in the acute setting and can act as a bridge for those patients until a permanent pacemaker is placed. Transcutaneous pacing can be used effectively in greater than 90% of patients, but should not be used long-term due to pain and loss of capture due to muscle impedance. Therefore, patients who require over 30 minutes of pacing would need conversion to transvenous pacing or permanent device. Patients who are hemodynamically stable but symptomatic from sinus node dysfunction almost always require permanent pacing.

Atrioventricular node

Disturbances in conduction through the AV node or His-Purkinje system are classified as AV blocks. These blocks may be temporary or permanent, depending on the cause of 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 PR interval is a measure of the conduction time through the AV node and bundle of His. When the PR interval is prolonged (more than 210 ms), a patient has first-degree AV block. Second-degree AV block occurs with intermittent failure of the conduction of the impulse to the ventricles. In Mobitz type I, second-degree AV block (Wenckebach block), there is progressive prolongation of the PR interval until failure of conduction to the ventricle occurs ( Fig. 1 ). The PR 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 PR interval. There is not a shortened PR 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 AV disassociation. The ventricles rely on their innate automaticity, which produces a typical wide QRS escape rhythm between 40 and 50 bpm. The atrial rate is commonly faster, producing multiple P waves with no relationship to the ventricular QRS complexes ( Fig. 2 ).

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 ischemic 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. It should be noted that the 2018 guidelines from the American Heart Association still recommend chronotropic pharmacotherapy, such as with dopamine or epinephrine, as an alternative bridge to a permanent pacing device or transvenous pacing, as it has been shown to be as effective as external pacing when atropine is ineffective.