INTRODUCTION: Pulmonary Embolism (PE) can present with a variety of cardiac arrhythmias and conduction abnormalities. We describe a case of complete heart block secondary to a large saddle PE.
CASE PRESENTATION: A 77 year-old man presented to the emergency department with the complaint of acute onset dyspnea 2 days prior to arrival. In the emergency department, an electrocardiogram (ECG) revealed complete heart block (CHB) with an idioventricular rhythm (Right bundle branch morphology) of 55 beats per minute and an underlying sinus rhythm. He had no known previous cardiac problems, and had not experienced any dizziness or syncope. His past medical history was remarkable for hypertension, gastroesophageal reflux and dyslipidemia. A computed-tomography (CT) scan of his chest showed large saddle pulmonary embolism. Heparin infusion was initiated after an initial bolus dose. Within a few hours he began to have increasing dyspnea, respiratory distress, and worsening hypoxia. He was then given thrombolytic therapy after placement of an IVC filter. Repeat chest CT revealed lysis of the saddle PE but smaller thrombi present in more distal pulmonary vessels. The next morning, an ECG revealed CHB with an idioventricular rhythm, now of left bundle branch morphology. Two days after his presentation, ECG showed a sinus rhythm with 1st degree AV block, right bundle branch block (RBBB) and a left anterior fascicular block. Echocardiogram was performed and showed normal left ventricular size with ejection fraction of 68%, dilated right ventricle with a right ventricular systolic pressure was 53 mmHg. His symptoms improved and he was discharged in good condition. At a follow-up visit, he was noted to have continued tri-fascicular block, and underwent uncomplicated implantation of a dual-chamber pacing system.
DISCUSSIONS: Although electrocardiographic changes associated with pulmonary embolism are common, the presence of complete atrioventricular block is rare. It is well known that patients with acute pulmonary embolism may have findings of cor pulmonale including sinus tachycardia, new S1Q3 QRS pattern in lead I, and negatively directed T wave in lead III, and incomplete or complete RBBB. The mechanism by which RBBB occurs is thought to be related to right ventricular dilatation. Since the right bundle branch is relatively superficial in its path along the right ventricular side of the septum, it may be particularly sensitive to acute distension of the right ventricular cavity. In this case the mechanism by which the patient developed complete heart block is not clear. We believe he had pre-existing conduction system disease involving his AV node, His-Purkinje system, right bundle branch and left anterior fascicle, although no previous electrocardiograms had been performed. It is possible that the embolism triggered a hyperadrenergic state resulting in stimulation of the Bezold-Jarish reflex leading to an increase in the efferent vagal response, decrease in sympathetic tone, and subsequent complete atrioventricular block in the setting of an already diseased conduction system. Another plausible, though less likely, scenario is that the massive embolism triggered transient myocardial ischemia to the AV node resulting in transient complete heart block.
CONCLUSION: Our case suggests that complete heart block can be produced by pulmonary embolism and subsequent treatment for the PE may result in restoration of a more stable rhythm.
DISCLOSURE: Rita Mukerji, No Financial Disclosure Information; No Product/Research Disclosure Information