Third Degree Atrioventricular Block

The third degree atrioventricular block may rarely be asymptomatic, more often having hypoperfusion- related symptoms, such as fatigability, chest pain, dyspnea, dizziness, irritability, apathy, inability to concentrate, forgetfulness, confusion. In severe cases, syncope and sudden death occur.

Facing a patient with associated symptoms like severe chest pain, nausea, dyspnea and diaphoresis, the clinician should consider an acute myocardial infarction as the cause of the complete heart block [1]. On the other hand, chronic cardiac patients undergo different kinds of treatment that have a potential to induce heart block: digitalis, calcium channel blockers, beta blockers and medication that can induce hyperkalemia, like angiotensin-converting enzyme inhibitors and angiotensin receptor blockers.

In addition to symptoms caused by the heart block, patients may have complaints linked to the cause of the block, like ischemia, myocarditis, hypothyroidism, cardiomyopathy, hypothermia and electrolyte disturbances [1]. Children with congenital third degree atrioventricular block may be symptomatic from birth [2].

In a patient with very low heart rate, the stimulus probably originates in the ventricles and is not due to a junctional pacemaker thus having a poor prognosis [3].

The physical examination of third degree atrioventricular block patients will often show signs of decreased perfusion and those of underlying disease.

Inspection may show turgescent jugular veins and cannon " a" waves caused by the contraction of the right atrium against the closed tricuspid valve, peripheral edema or skin rashes if the cause of the block is Lyme disease, endocarditis, or rheumatic fever.

Palpation may reveal hepatomegaly in heart failure patients, while auscultation reveals pulmonary rales, variable first heart sound, murmurs caused by mitral or aortic calcification or cardiomyopathies and a low heart rate. Arterial pressure may be low.

Blood workup should include a complete blood cell count (in order to diagnose infection and anemia), renal function, electrolytes (especially potassium, given that hyperpotassemia is a cause of third degree atrioventricular block by itself), prothrombin time, activated partial thromboplastin time (having in mind that emergency cardiostimulation may be necessary) and digoxin level. If myocarditis is suspected, every effort should be put into determining its cause: human immunodeficiency virus infection, Lyme disease, adenovirus or enterovirus infection.

A chest radiograph may offer clues about the cardiac silhouette and possible associated pneumonia. Transthoracic echocardiography may find aortic and mitral calcification or abscesses, hypertrophic cardiomyopathy and left ventricle systolic function.

The diagnosis is established using a 12 lead electrocardiogram, showing complete atrioventricular dissociation [4], with constant R-R intervals and either narrow (<120 msec) or wide ventricular complexes, depending on the site of the stimulus: atrioventricular junction, His bundle or ventricular myocardium. The atrial rate is faster than the ventricular one, which is usually 30-40 beats per minute. The electrocardiogram may also show ischemia, in which case cardiac enzymes should be measured and coronarography should be performed. Anterior myocardial infarctions complicated with complete atrioventricular block have higher instability risk [2]. A complete atrioventricular block is the most frequent bradyarrhythmia in myocardial infarctions [5].

If symptoms are intermittent and the electrocardiogram shows no abnormalities when the patient presents, an ambulatory monitoring or loop recorder is indicated [6] [7]. Furthermore, an electrophysiological study may be useful in cases where the origin of the stimulus is uncertain or in cases where symptoms seldom occur [8].

Other tests, like tilt table testing and carotid sinus massage, are to be performed in cases where the more plausible diagnosis is reflex syncope, not intermittent third degree atrioventricular block. If a patient only has symptoms after performing an effort, exercise testing is called for.

1. Barra S, Providencia R, Paiva L, et al. A review on advanced atrioventricular block in young or middle aged adults. Pacing Clin Electrophysiol. 2012;35(11):1395–1405.
2. Hayden GE, Brady WJ, Pollack M, et al. Electrocardiographic manifestations: Diagnosis of atrioventricular block in the emergency department. J Emerg Med. 2004;26(1):95–106.
3. Ufberg JW, Clark JS. Bradydysrhythmias and atrioventricular conduction blocks. Emerg Med Clin N Am. 2006;24(1):1–9.
4. Swart G, Brady WJ, DeBehnke DJ, Ma OJ, Aufderheide TP. Acute myocardial infarction complicated by hemodynamically unstable bradyarrhythmia: prehospital and ED treatment with atropine. Am J Emerg Med. 1999;17(7):647–652.
5. Deal N. Evaluation and management of bradydysrhythmias in the emergency department. Emerg Med Pract. 2013;15(9):1–15.
6. Bergfeldt L, Edvardsson N, Rosenqvist M, et al. Atrioventricular block progression in patients with bifascicular block assessed by repeated electrocardiography and a bradycardia-detecting pacemaker, Am J Cardiol. 1994;74:1129-1132.
7. Brignole M, Sutton R, Menozzi C, et al. Early application of an implantable loop recorder allows effective specific therapy in patients with recurrent suspected neurally mediated syncope, Eur Heart J. 2006;27:1085-1092.
8. Moya A, Garcia-Civera R, Croci F, et al. Diagnosis, management, and outcomes of patients with syncope and bundle branch block, Eur Heart J. 2011;32:1535-1541.