Elderly Man With Shoulder Pain Following Fall

An 82-year-old man presents with shoulder pain resulting from a fall the day before. He has had intermittent episodes of light-headedness, chest pain, and "flutterings in the chest" over the past week--including one this morning. Episodes last about 2 hours and resolve spontaneously. He denies any loss of consciousness, weakness, or worsening of symptoms with exertion. He also denies headache, abdominal pain, and other injuries. His medical history includes coronary artery disease (treated with bypass grafting 10 years earlier); prostate cancer; and chronic lymphocytic leukemia, for which he is receiving chemotherapy.

This well-nourished elderly man is in mild distress. Temperature is 37.1°C (98.8°F); heart rate, 133 beats per minute and regular; respiration rate, 16 breaths per minute; and blood pressure, 108/67 mm Hg. Head, eyes, ears, nose, and throat are normal; neck is supple with no jugular venous distention. A totally implantable venous access system line is visible in his chest, but breath sounds are clear and no murmurs, rubs, or gallops are audible. The abdomen is normal. Trace edema is present in the lower extremities symmetrically.

The 12-lead ECG is as shown. The computerized interpretation is "sinus tachycardia with first-degree atrioventricular (AV) block."

Which of the following do you think best explains the ECG findings?

A. Sinus tachycardia with first-degree AV block.

B. Atrial fibrillation.

C. Atrial flutter.

D. AV nodal reentry tachycardia.

E. AV tachycardia with antidromic conduction.

Correct answer: D

The computer's "diagnosis" is first-degree AV block (A). However, it appears that the computer has misinterpreted ventricular repolarization activity (T waves) as atrial activity (P waves) with a prolonged PR segment preceding the QRS complex (Figure 1, small arrow). Instead, the narrow QRS-complex tachycardia (rate, 126 beats per minute) shown in this 12-lead ECG is consistent with a supraventricular tachycardia.

The term "supraventricular tachycardia" (SVT) refers to paroxysmal tachydysrhythmias that require atrial or AV nodal tissue for their initiation and maintenance.¹ SVTs are broadly categorized as:

•Atrial tachydysrhythmias (ie, atrial tachycardia, atrial flutter, atrial fibrillation).

•AV tachydysrhythmias (ie, AV nodal reentry tachycardia, AV reentry tachycardia, and junctional tachycardia).

This man's tachycardia occurs at a regular rate, which makes atrial fibrillation (B) less likely. In addition, there appears to be no regular atrial activity occurring at a rapid rate, such as would be seen in atrial flutter (C).

PATHOPHYSIOLOGY OF REENTRANT TACHYCARDIAS

Most SVTs involve a reentry mechanism. AV nodal reentry tachycardia (AVNRT) and AV reentry tachycardia (AVRT) are both forms of tachycardia produced by reentry circuits. The reentry loop causes repeated activation of the atria and ventricles.

AVRT. In AVRT that results from Wolff-Parkinson-White syndrome, the reentry loop involves the normal AV nodal pathway and an accessory AV bypass tract. In AVRT with antidromic conduction (E), ventricular activation occurs down the bypass tract, with retrograde conduction through the AV node reactivating the atria. Thus, antidromic conduction results in aberrant depolarization of the ventricles and a wide QRS-complex tachycardia. Because this patient has a regular narrow QRS-complex tachycardia, AVRT with antidromic conduction is not likely. This leaves AVNRT (D) as the most probable diagnosis.

AVNRT. This is the most common SVT involving a reentry mechanism; it accounts for about 60% of cases.¹ Because the reentry circuit that produces AVNRT is localized to the AV node, ventricular depolarization occurs along the normal pathways from the AV node, through the bundle of His and the bundle branches. Thus, the QRS complex is narrow and has normal morphology. The atria are depolarized in a retrograde fashion from the nodal reentry circuit.

What the ECG shows. Because atrial activation often occurs simultaneously with or immediately following ventricular depolarization through the reentry loop, atrial activity often is not apparent on the 12-lead ECG--or it appears as an abnormal deflection within or just after the QRS complex. This retrograde activation of the atria can produce a pseudo r9 in lead V₁ or a pseudo s in the inferior leads.² On this patient's ECG, a small deflection is seen toward the end of the QRS complex (see Figure 1, large arrow), strongly suggesting abnormal atrial activation simultaneous with or just after ventricular activation.

CLINICAL PRESENTATION AND TREATMENT OF AVNRT

AVNRT is usually induced by premature atrial or ventricular ectopic beats in combination with various precipitants, such as excessive caffeine or alcohol intake, illicit drug use, or hyperthyroidism. Most often, AVNRT is not associated with significant structural heart disease. In AVNRT, the heart rate ranges from 120 to 250 beats per minute and QRS complexes are narrow and regular.³ Although most patients complain of palpitations, the clinical presentation can vary from asymptomatic to cardiac failure and frank shock.

Treatment focuses on interruption of the reentry circuit. Because this circuit involves the AV node, pharmacologic agents and maneuvers that slow conduction through the AV node can be used to terminate AVNRT. Potential therapies include vagal maneuvers (such as carotid sinus massage), adenosine, b-blockers (eg, esmolol), and calcium channel blockers (eg, diltiazem). If the dysrhythmia results in cardiovascular collapse, electrical cardioversion is warranted. Long-term therapy for recurrent episodes includes prophylactic AV blocking agents used either on an ongoing basis or episodically (the "pill-in-the-pocket" approach) and catheter ablation of the reentry circuit.

OUTCOME OF THIS CASE

The patient was admitted to the cardiology service; normal levels of cardiac enzymes ruled out acute myocardial infarction. AVNRT was diagnosed, and the patient underwent radiofrequency catheter ablation of the reentry circuit on hospital day 3. After the ablation, the patient's recurrent symptoms and episodic tachycardia resolved. A follow-up ECG was obtained 1 week later (Figure 2). This 12-lead ECG shows sinus rhythm at a rate of 58 beats per minute, with P wave activity distinct from the T wave and no abnormal deflection at the end of the QRS complex. Note that the patient does demonstrate a prolonged PR interval consistent with first- degree AV block! *

References:

REFERENCES:

1.

Delacretaz E. Clinical practice. Supraventricular tachycardia.

N Engl J Med

. 2006;354:1039-1051.

2.

Kalbfleisch SJ, el-Atassi R, Calkins H, et al. Differentiation of paroxysmal narrow QRS complex tachycardias using the 12-lead electrocardiogram.

J Am Coll Cardiol

. 1993;21:85-89.

3.

Kazzi AA, Wong H. Other supraventricular tachydysrhythmias. In: Chan TC, Brady WJ, Harrigan RA, et al, eds.

ECG in Emergency Medicine and Acute Care

. Philadelphia: Elsevier-Mosby; 2005:105-111.