HistoryThird-degree atrioventricular (AV) block (complete heart block) has a wide range of clinical presentations. Occasionally, patients are asymptomatic or have only minimal symptoms related to hypoperfusion. In these situations, symptoms include the following: Show
Patients with narrow complex escape rhythms (eg, those whose escape rhythm occurs above the His bundle) are more likely to have minimal symptoms. More commonly, however, patients are profoundly symptomatic, especially if a wide-complex escape rhythm is present, indicating that the origin of the pacemaker is below the His bundle. In such cases, symptoms can include the following:
Because an acute myocardial infarction (MI) can cause complete heart block, patients who concurrently experience an MI can have associated symptoms from the MI, including chest pain, dyspnea, nausea or vomiting, and diaphoresis. Third-degree AV block may be an underlying condition in patients who present with sudden cardiac death. Patients who have a history of cardiac disease may be on medications that affect the conduction system through the AV node (AVN), including the following:
The patient’s history of cardiac interventions should be carefully investigated; aortic valve surgery, septal alcohol ablation, proximal anterior descending artery stenting (complicated by compromised flow in the first septal perforator branch), and ablation of the slow or fast pathway of the AVN all may result in third-degree AV block.  Physical ExaminationInitial triage of patients with third-degree atrioventricular (AV) block (complete heart block) consists of determining symptoms, assessing vital signs, and looking for evidence of compromised peripheral perfusion. In particular, the physical examination findings of patients with third-degree AV block will be notable for bradycardia, which can be severe. Careful examination of the neck veins can often show evidence of cannon ‘a’ waves. A variable intensity S1 may be heard on auscultation. In addition, the pulse rate may be slow. If the slow rate or loss of atrial contraction prior to ventricular contraction has caused heart failure, then venous pressures will be elevated, including the jugular venous pressure. Any new murmurs or gallops should be noted, because strong associations exist between cardiomyopathies, mitral calcification, aortic calcification, or endocarditis and complete AV block. If heart failure is present as evidenced by rales, an S3 gallop, peripheral edema, or hepatomegaly, then a more compelling need for immediate pacing exists. Because endocarditis, rheumatic fever, and Lyme disease cause heart block, pay attention to any signs of infection or skin rashes during the general examination. This is particularly true in endemic areas for Lyme disease. Neurologic examination may provide clues to the etiology of AV block because neuromuscular disease, especially myotonic dystrophy and Duchenne muscular dystrophy, can cause AV block. Signs of congestive heart failure as a result of decreased cardiac output may be present and may include the following:
Patients may have signs of hypoperfusion, including the following:
In patients with concomitant myocardial ischemia or myocardial infarction (MI), corresponding signs such as the following may be evident on examination:
Regularized atrial fibrillation is the classic sign of complete heart block due to digitalis toxicity. This rhythm occurs because of the junctional escape rhythm.
Author Coauthor(s) Daniel Brito Guzman, MD Assistant Professor of Non-Invasive Cardiology, Department of Cardiovascular and Thoracic Surgery, WVU Heart and Vascular Institute Daniel Brito Guzman, MD is a member of the following medical societies: American College of Physicians, American Thoracic Society Disclosure: Nothing to disclose. Specialty Editor Board Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Received salary from Medscape for employment. for: Medscape. Brian Olshansky, MD, FESC, FAHA, FACC, FHRS Professor Emeritus of Medicine, Department of Internal Medicine, University of Iowa College of Medicine Brian Olshansky, MD, FESC, FAHA, FACC, FHRS is a member of the following medical societies: American College of Cardiology, American Heart Association, Cardiac Electrophysiology Society, European Society of Cardiology, Heart Rhythm Society Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Astra Zeneca, Artivion<br/>DSMB. Chief Editor Jeffrey N Rottman, MD Professor of Medicine, Department of Medicine, Division of Cardiovascular Medicine, University of Maryland School of Medicine; Cardiologist/Electrophysiologist, University of Maryland Medical System and VA Maryland Health Care System Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association, Heart Rhythm Society Disclosure: Nothing to disclose. Additional Contributors Eddy S Lang, MDCM, CCFP(EM), CSPQ Associate Professor, Senior Researcher, Division of Emergency Medicine, Department of Family Medicine, University of Calgary Faculty of Medicine; Assistant Professor, Department of Family Medicine, McGill University Faculty of Medicine, Canada Eddy S Lang, MDCM, CCFP(EM), CSPQ is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, Canadian Association of Emergency Physicians Disclosure: Nothing to disclose. Theodore J Gaeta, DO, MPH, FACEP Clinical Associate Professor, Department of Emergency Medicine, Weill Cornell Medical College; Vice Chairman and Program Director of Emergency Medicine Residency Program, Department of Emergency Medicine, New York Methodist Hospital; Academic Chair, Adjunct Professor, Department of Emergency Medicine, St George's University School of Medicine Theodore J Gaeta, DO, MPH, FACEP is a member of the following medical societies: American College of Emergency Physicians, New York Academy of Medicine, Society for Academic Emergency Medicine, Council of Residency Directors in Emergency Medicine, Clerkship Directors in Emergency Medicine, Alliance for Clinical Education Disclosure: Nothing to disclose. James P Daubert, MD Professor of Medicine, Cardiology Division, Duke University School of Medicine James P Daubert, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American Heart Association, Heart Rhythm Society Disclosure: Partner received equity interest from Medtronic for none; Received honoraria from Boston Scientific for speaking and teaching; Received consulting fee from CV Therapeutics for consulting; Received consulting fee from Cryocor for consulting. Andrew C Corsello, MD Consulting Staff, Department of Internal Medicine, Division of Cardiology, Cardiovascular Consultants of Maine, PA Disclosure: Nothing to disclose. Adam S Budzikowski, MD, PhD, FHRS Assistant Professor of Medicine, Division of Cardiovascular Medicine, Electrophysiology Section, State University of New York Downstate Medical Center, University Hospital of Brooklyn Adam S Budzikowski, MD, PhD, FHRS is a member of the following medical societies: European Society of Cardiology, Heart Rhythm Society Disclosure: Received consulting fee from Boston Scientific for speaking and teaching; Received honoraria from St. Jude Medical for speaking and teaching; Received honoraria from Zoll for speaking and teaching. Michael D Levine, MD Assistant Professor, Department of Emergency Medicine, Section of Medical Toxicology, Keck School of Medicine of the University of Southern California Michael D Levine, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, American College of Medical Toxicology, American Medical Association, Phi Beta Kappa, Society for Academic Emergency Medicine, Emergency Medicine Residents' Association Disclosure: Nothing to disclose. Abrar H Shah, MD Clinical Assistant Professor, Department of Medicine, University of Rochester Medical Center; Consulting Staff, Department of Medicine (Cardiology), Strong Memorial Hospital, Geneva General Hospital; Consulting Staff, Department of Cardiology, Highland Hospital; Consulting Staff, Department of Cardiology and Electrophysiology, Park Ridge Hospital Disclosure: Nothing to disclose. How would you describe a complete heart block?Complete heart block occurs when the electrical signal can't pass normally from the atria, the heart's upper chambers, to the ventricles, or lower chambers. If the atrioventricular (AV) node is damaged during surgery, complete heart block may result. Sometimes complete heart block occurs spontaneously without surgery.
What treatment may help a patient with a complete AV block?Transcutaneous pacing is the treatment of choice for any symptomatic patient. All patients who have third-degree atrioventricular (AV) block (complete heart block) associated with repeated pauses, an inadequate escape rhythm, or a block below the AV node (AVN) should be stabilized with temporary pacing.
What causes a complete heart block?Coronary artery disease with and without a heart attack is one of the most common causes of heart block. Cardiomyopathies which are diseases that weaken the heart muscle can also result in wire damage.
Which coronary artery is affected in complete heart block?CHB is most commonly associated with an occlusion of the right coronary artery (RCA) [3]. The mortality rate of MI is higher if complete heart block is present [1-3]. Thus, prompt recognition of CHB in myocardial infarctions is essential to prevent further deterioration.
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The adaptations of a client with complete heart block would most likely include:
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