Approach

The goals of treatment are to ameliorate symptoms caused by AV block (regardless of degree) and to prevent syncope and sudden cardiac death (in advanced AV block).

Asymptomatic: first-degree AV block or type I second-degree heart block

No specific treatment is required. Patients are at low risk for progression to higher-degree AV block. ECGs may be rechecked if symptoms develop, but do not need to be rechecked on a routine basis.

Symptomatic: first-degree AV block or type I second-degree heart block

Occasionally, patients with profound first-degree AV block (>300 milliseconds) or those with type I second-degree heart block will develop associated symptoms and should be treated. The first line of treatment is to stop all AV-nodal blocking medications. The most common medications include beta-blockers, nondihydropyridine calcium-channel blockers, and digitalis. While discontinuing these medicines may improve AV conduction, they are not likely to completely reverse a clinically significant AV block.

If symptoms are severe enough, permanent pacemaker implantation should be considered. For AV block, usually a dual-chamber (1 right atrial and 1 right ventricular lead) pacemaker is placed. The entire procedure usually takes a few hours and requires an overnight hospital stay. Biventricular pacemaker with or without an implantable cardioverter-defibrillator (ICD) placement may be considered when the left ventricular ejection fraction (LVEF) is ≤35%.[38][39][40]

Asymptomatic or mildly to moderately symptomatic: type II second-degree AV block or third-degree AV block

Medications blocking the AV node should be stopped first. Also, condition-specific management should ensue, which should help treat any potentially reversible conditions causing AV-nodal blockade. This includes treating acute coronary syndrome (i.e., antiplatelet medications, urgent revascularization) and medication toxicity (e.g., glucagon for beta-blocker toxicity, calcium for calcium-channel toxicity, or digoxin antibody for digitalis toxicity). When present, electrolyte or pH disturbances and hypoxemia should be treated appropriately.

These patients are at risk for progression to slower ventricular rates and development or worsening of symptoms.[41] In the absence of a reversible cause, these patients should undergo permanent pacemaker implantation. ICD placement may be considered when the LVEF is ≤35%. In patients with high-degree or complete heart block and LVEF of 36% to 50%, cardiac resynchronization therapy (CRT) may reduce total mortality and hospitalizations, and improve symptoms and quality of life (QOL).[42]

Severely symptomatic: type II second-degree AV block or third-degree AV block

As with asymptomatic or mildly to moderately symptomatic patients, those with severely symptomatic type II second-degree AV block or third-degree AV block (of irreversible cause) should receive aggressive supportive therapy, condition-specific management, and discontinuation of all AV-nodal blocking medications. Temporary pacing is used specifically with these types of AV block. Severe symptoms include syncope or persistent, severe lightheadedness indicating profound decreases in the ventricular rate. Transvenous pacing is much more reliable than transcutaneous pacing and should be performed by a cardiologist when the heart block leads to hemodynamic instability. If the condition does not improve, permanent pacemaker or ICD placement should be performed. In patients with high-degree or complete heart block and LVEF of 36% to 50%, CRT may reduce total mortality and hospitalizations, and improve symptoms and QOL.[42]

Considerations for causative medications

While discontinuing AV-nodal blocking medications (i.e., beta-blockers, nondihydropyridine calcium-channel blockers, and digitalis) may improve AV conduction, complete reversal of clinically significant AV block is an unlikely result. This modest effect should be weighed in the long term against the potential medication benefit, such as the mortality benefit of beta-blockers in patients with CAD or salutary effects on blood pressure and heart rate.

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