BACKGROUND
A 66-year-old man presents to the Emergency Department (ED) with chest pain and shortness of breath that started several hours ago as he was cleaning his porch. His chest pain is dull in quality and radiates to his neck and arms, and when asked to rate the severity of the pain, he indicates a 5 in a range from 1 to 10 (with 10 being the worst). The chest pain is not associated with diaphoresis, nausea, or vomiting. The patient also had exertional weakness for 4 days. He denies having dizziness, lightheadedness, or loss of consciousness.
The patient underwent a 3-vessel coronary artery bypass 8 years ago. Since then, he has had stable angina that occurs approximately once a month. His medical history is also clinically significant for hyperlipidemia, hypertension, and poorly controlled insulin-dependent diabetes mellitus. His medication regimen includes hydrochlorothiazide, insulin, isosorbide dinitrate, simvastatin, aspirin, and sublingual nitroglycerin as needed. The patient smokes 2 packs of cigarettes per day. The review of systems yields unremarkable findings.
The patient is afebrile but appears uncomfortable. The cardiovascular examination reveals bradycardia. His heart rate is 39 bpm and regular, his blood pressure is 130/53 mm Hg, and his respiratory rate is 18 breaths per minute. His first and second heart sounds are normal. No murmur or gallop is present. Except for evidence of his previous surgery, his other physical findings are normal.
The patient’s laboratory results are normal except for mildly elevated troponin I levels. An ECG is obtained (see Image 1).
What is the diagnosis?
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HINT
Identify the P waves.
Authors:
Salyka Sengsayadeth,
Resident,
Internal Medicine,
Vanderbilt University
Ehab S. Kasasbeh, MD,
Resident,
Department of Internal Medicine,
James H. Quillen College of Medicine,
East Tennessee State University
Ryland P. Byrd, Jr, MD,
Chief of Pulmonary Medicine,
Medical Director of Respiratory Therapy,
Quillen Mountain Home Veterans Affairs Medical Center,
Professor,
Department of Internal Medicine,
Division of Pulmonary Diseases and Critical Care Medicine,
James H. Quillen College of Medicine,
East Tennessee State University
eMedicine Editors:
Erik D. Schraga, MD,
Department of Emergency Medicine,
Kaiser Permanente,
Santa Clara Medical Center, Calif
Rick G. Kulkarni, MD,
Assistant Professor,
Yale School of Medicine,
Section of Emergency Medicine,
Department of Surgery,
Attending Physician,
Medical Director,
Department of Emergency Services,
Yale-New Haven Hospital, Conn
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ANSWER
Complete atrioventricular (AV) heart block: In the normal heart, conduction of action potentials from the atria to the ventricles occurs through the AV node. The His-Purkinje conduction system subsequently transmits these impulses to the ventricular myocardium. Delays or interruptions in conducting these depolarizations result in AV blocks. The 3 types of AV block are first degree (slowed conduction with no missed beats), second degree (missed beats, often in a regular ratio of 2:1, 3:2, or higher), and third degree (complete). AV block may be caused by anatomic or functional impairment of the conduction system and it can be transient or permanent.
The characteristic ECG findings of third-degree AV block are atrial impulses that consistently fail to reach the ventricles, atrial and ventricular rhythms that are independent of each other, variable P-R intervals, consistent P-P and R-R intervals, and atrial rates faster than ventricular rates. In addition, maintenance of the ventricular rhythm depends on spontaneous depolarization of ventricular tissue. Complete heart block occurring at the AV node is typically associated with slow but stable junctional escape rhythms and normal QRS complexes. If the AV block is below the bundle of His, subjunctional escape rhythms further slow heart rates and widen QRS complexes.
Patients with third-degree AV block may present with weakness, dyspnea, dizziness, presyncope, and/or syncope. In some patients, the transition from a partial to a complete AV block may result in ventricular asystole lasting several seconds to several minutes. In addition, a patient’s heart rate may be insufficient to maintain cardiac output, and hypotension and worsening of any symptoms of heart failure or angina pectoris may result. Findings from physical examination include a slow but regular heart rate, widened pulse pressure, variable intensity in the first heart sound, and cannon venous pulsations.
The most common causes of third-degree (complete) AV heart block are fibrosis and sclerosis of the conducting system and myocardial ischemia or myocardial infarction (MI). Other etiologies of AV heart block include infiltrative diseases of the myocardium (including sarcoidosis and amyloidosis), aortic valve disease, congenital heart disease, acute rheumatic fever, myocarditis, endocarditis, advanced hyperkalemia, infiltrating malignancies, thyroid dysfunction, Lyme disease, and neuromuscular diseases. Drug-induced AV heart block should be considered in patients who have taken drugs that impair the ability of the conduction system to transmit depolarizations. These drugs include digoxin, calcium channel blockers, beta blockers, and amiodarone.
Complete heart block occurs in 5-15% of acute MIs. In an inferior MI, first- or second-degree heart block usually precedes complete heart block. Complete heart block in the setting of an inferior MI typically lasts less than a week, and it is usually associated with a stable junctional escape rhythm with a narrow QRS complex. With an inferior MI, the AV block is presumed to reflect ischemia in the AV node, which receives its blood supply from the right coronary artery in 90% of individuals. This conduction defect generally resolves in 1-2 weeks because collateral vessels from the left coronary artery system increasingly supply the AV node and prevent complete infarction.
In the setting of an anterior MI, complete heart block results from extensive damage to the left ventricle, including the conducting system distal to the AV node. For this reason, the QRS complex is typically widened. A second-degree AV block or a bifascicular block often precedes a complete heart block. The mortality rate of patients with an anterior MI and a complete heart block can be as high as 70%. Death is typically caused by heart failure rather than the heart block per se.
The therapy for complete heart block begins with correction of the reversible causes of the dysrhythmia, such as treating myocardial ischemia and discontinuing drugs that suppress the conduction of cardiac action potential. In urgent situations, intravenous atropine may be used to reverse decreases in AV nodal conduction. If the patient’s condition responds to atropine, the conduction dysfunction is at the level of the AV node. The conduction system distal to the AV node is relatively unresponsive to atropine.
In patients with a wide-complex escape rhythm and suspected acute MI, atropine should be withheld or used only with extreme caution, as it may result in unopposed sympathetic stimulation. The subsequent risk of increased ventricular irritability and potential arrhythmia is likely to be greater than the improbable benefit on the conducting system distal to the AV node. When this occurs, or when the complete heart block is unresponsive to atropine, temporary and/or permanent placement of a pacemaker may be necessary. With a few exceptions, electrophysiologic studies are not typically indicated in patients with complete AV block.
References
Aplin M, Engstrom T, Vejlstrup N, et al: Prognostic importance of complete atrioventricular block complicating myocardial infarction. Am J Cardiol 2003 Oct 1; 92(7): 853-6. MEDLINE: 14516893
Josephson ME: Clinical Cardiac Electrophysiology: Techniques and Interpretations. 2nd ed. Philadelphia, Pa.: Lea and Febiger; 1993: 726-821.
Massie B, Granger C: Bradycardias and conduction disturbances. In: Tierney LM, McPhee SJ, Papadakis MA, eds. Current Medical Diagnosis and Treatment. 44th ed. New York, NY: McGraw-Hill/Appleton & Lange; 2005: Chapter 10.
