A 63-year-old man presents to the emergency department (ED) for an evaluation of new-onset renal failure. The patient’s primary care physician referred him to the ED after routine laboratory tests demonstrated a blood urea nitrogen (BUN) level of 83 mg/dL (30 mmol/L) and a creatinine level of 4.4 mg/dL (389 µmol/L).
The patient reports feeling well, without any current symptoms. He denies having any chest discomfort, difficulty breathing, or palpitations. He has a history of urinary hesitancy secondary to benign prostatic hypertrophy, but he is voiding as usual. His medical history is also significant for diabetes mellitus, hypertension, and a remote history of syncope.
{mosimage}On physical examination, the patient is afebrile, with a heart rate of 71 bpm, a respiratory rate of 16 breaths/min, and a blood pressure of 160/85 mm Hg. The patient appears well and is in no acute distress. His heart rhythm is regular, with a normal S1 and S2 and a III/VI systolic crescendo-decrescendo murmur that is loudest at the left sternal border. No rubs or gallops are appreciated, and the patient has no jugular venous distention. His lungs are clear bilaterally, and his abdomen is soft, without any tenderness or masses. He has 1+ peripheral edema of both legs.
A repeat chemistry panel is significant for a normal potassium level of 3.8 mEq/L (3.8 mmol/L), a BUN level of 96 mg/dL (34 mmol/L), and a creatinine level of 4.7 mg/dL (415 µmol/L). After a nephrologist is consulted, the patient is admitted to the hospital for further workup of renal failure and possible dialysis.
Before the patient is transferred and after a few hours in the ED, the nurse observes that he is markedly bradycardic. On repeat physical examination, the patient is resting comfortably and alert, with a regular pulse of 36 bpm and a blood pressure of 156/79 mm Hg. Otherwise, his physical findings are unchanged. An ECG (see Image) is obtained while the nurse places external cardiac pacer pads on the patient and brings resuscitation equipment to the bedside.
What diagnosis does the ECG suggest, and what is the emergency treatment for this condition?
HINT
Observe the relationship between the P waves and the QRS complexes.
Authors:
Adam Landman, MD, MS, MIS, Department of Emergency Medicine, UCLA, Los Angeles, CA
Rick G. Kulkarni, MD, FACEP, 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, CT
eMedicine Editors:
Erik D. Schraga, MD, Department of Emergency Medicine, Kaiser Permanente, Santa Clara Medical Center, CA
John Vozenilek, MD, FACEP, Clinical Assistant Professor of Emergency Medicine, Assistant Professor of Medical Education, Feinberg School of Medicine, Northwestern University, Chicago, IL
ANSWER
Third-degree, or complete, heart block: This patient has a third-degree, or complete, heart block, which is a dysfunction of the cardiac conduction system in which atrial impulses are not conducted to the ventricles through the atrioventricular (AV) node. As the ECG demonstrates, the P waves occur at a regular rate of approximately 85-90 bpm; however, the QRS complexes occur independently of the P waves, at a rate of approximately 30 bpm. Although impulses are generated regularly by the sinoatrial (SA) node, a block somewhere in the conduction system prevents the atrial impulses from being conducted to the ventricles through the His bundle–Purkinje system. A ventricular escape mechanism occurs in the absence of an atrial impulse at a markedly slower rate.
In complete heart block, the site of conduction dysfunction can be in the AV node (21%), the His bundle (14-18%), or the Purkinje system below the His bundle (60%). The width of the QRS complex can provide insight into the origin of the block. A narrow QRS width (
Patients with complete heart block may be asymptomatic, or they may have symptoms of hypoperfusion, such as syncope, light-headedness, or angina. Those with underlying heart disease may have worsening of heart-failure symptoms, such as orthopnea, dyspnea on exertion, peripheral edema, or fatigue. Patients with slow escape rhythms are more likely to have symptoms than patients with faster rhythms because the low cardiac output limits perfusion.
Complete heart block may be acquired or congenital. Children with congenital complete heart block are most often asymptomatic and occasionally require an implanted pacemaker. Acquired complete heart block can result from a variety of causes. Acquired blocks at the AV node result from intense vagal tone, inferior myocardial infarction, or a variety of medications (eg, beta-blockers, calcium channel blockers, digitalis), whereas blocks distal to the AV node are most commonly caused by acute anterior myocardial infarction. Other etiologies include electrolyte disturbances, cardiac surgery, cardiac tumors, Chagas disease, myoendocarditis, myxedema, Lyme disease, and infiltrative processes (eg, sarcoid amyloid). AV block in the setting of calcific aortic stenosis is common because the AV node is located near the aortic outflow tract.
The initial focus of treatment should be on reversing etiologies such as electrolyte imbalances, ischemia, and the adverse effects of drugs that block the AV node. The initial diagnostic workup should include a thorough history-taking and physical examination, determination of digoxin and electrolyte levels, and serial electrocardiography with tests of cardiac enzymes. Patients with complete heart block should be given oxygen with continuous cardiac monitoring. Two large-bore intravenous lines and transcutaneous pacing pads should also be placed.
Treatment of third-degree heart block follows the American Heart Association’s Advanced Cardiac Life Support algorithm for bradycardia.1 Treatment options vary according to the extent of the patient’s symptoms. If the patient has any evidence of hypoperfusion, transcutaneous pacing should be administered until transvenous pacing is initiated. Patients can be given narcotics and sedatives to help them tolerate the discomfort of transcutaneous pacing. Atropine may be used, but it is often of minimal utility if the block is distal to the AV node. Furthermore, atropine may extend ischemia in patients with heart block secondary to myocardial infarction. The American College of Cardiology and the American Heart Association recommend placing a permanent pacemaker when patients with third-degree heart block have symptoms or escape rates 2 If transcutaneous pacing fails and if the patient continues to be symptomatic while awaiting transvenous pacing, catecholamines can be considered.
This patient likely had a block below the His bundle, given the wide QRS complex with a rate of 29 bpm. Despite severe bradycardia, the patient remained asymptomatic. A cardiologist was consulted, and the patient remained in stable condition while a temporary transvenous pacer wire was placed. He was admitted to the cardiac care unit for further diagnostic workup and implantation of a permanent pacemaker. The patient’s renal failure and heart block were likely separate and unrelated problems. Although case reports describe hyperkalemia to be a cause of complete heart block, a MEDLINE/PubMed literature search did not reveal any studies in which renal failure in the absence of hyperkalemia or digitalis intoxication was linked to complete heart block.3,4
References:
Cummins RO, ed. ACLS Provider Manual. 4th ed. Dallas, TX: American Heart Association; 2004: 145-56.
Gregoratos G, Abrams J, Epstein AE, et al. ACC/AHA/NASPE 2002 guideline update for implantation of cardiac pacemakers and antiarrhythmia devices: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Committee on Pacemaker Implantation). Last updated: 2002. Available at: http://www.guideline.gov/summary/summary.aspx?ss=15&doc_id=3439&nbr=2665.
Przybojewski JZ, Knott-Craig CJ. Hyperkalaemic complete heart block. a report of 2 unique cases and a review of the literature. S Afr Med J 1983 Mar 12;63(11):413-20. [MEDLINE: 6828949]
Tiberti G, Bana G, Bossi M. Complete atrioventricular block with unwidened QRS complex during hyperkalemia. Pacing Clin Electrophysiol 1998 Jul;21(7):1480-82. [MEDLINE: 9670195]
