35-year-old woman presents to the emergency department with palpitations and chest pain. She is aware of her heart beating fast but not irregularly. She notes associated discomfort in the center of her chest.
A 35-year-old woman presents to the emergency department with palpitations and chest pain. She is aware of her heart beating fast but not irregularly. She notes associated discomfort in the center of her chest. She denies dyspnea, light-headedness, diaphoresis, and nausea. Her medical history is remarkable only for noncompliance with metoprolol therapy; she does not know why this agent was prescribed for her. She admits to recent alcohol and cocaine use.
Her vital signs are normal, except for a heart rate of 140 beats per minute. No jugular venous distention is noted; the lungs are clear; and the heart rate is regular, without murmurs, gallops, or rubs. The chest wall is nontender. The initial ECG is shown here.
Which of the following best explains the ECG findings?
WHAT THE ECG SHOWs
The ECG (Figure 1) shows a narrow-complex regular rhythm (Table) at 134 beats per minute. Based on this tracing, 2 possibilities can be excluded:
•Atrial fibrillation, which--although a common tachydysrhythmia--is uniformly irregular.
•Ventricular tachycardia, which characteristically features a widened QRS complex (greater than 0.12 second).
Junctional tachycardias. These regular, narrow-complex dysrhythmias range from 70 to 130 beats per minute, although they may be faster at times. (The rate of a normal junctional rhythm ranges from 40 to 60 beats per minute.) A PR interval of less than 0.12 second suggests a junctional origin. Retrograde activation of the atria may occur with this rhythm, and the P9 wave (which may be inverted) can occur before, during, or after the QRS complex. In this tracing, however, the PR interval appears to be normal (slightly more than 0.16 second). Thus, this tachycardia does not seem to be of junctional origin. The P-wave morphology does appear atypical in some leads; the cause of this abnormality is discussed below.
Atrial flutter. This is a common supraventricular tachydysrhythmia. Because it is often regular, it is a consideration here. The atria generally flutter at a rate of 250 to 350 beats per minute (300 beats per minute on average). However, one-to-one conduction of atrial activity through the atrioventricular (AV) node to the ventricles is rare, given the constraints of intrinsic nodal conduction capacity. Thus, atrial flutter is usually associated with a degree of conduction block; this results most typically in a rate ratio of 2:1 (2 atrial flutter waves for every ventricular QRS complex). This translates to a narrow-complex tachycardia with a rate of approximately 150 beats per minute.
The ventricular rate in the tracing shown here approaches 150 but is closer to 130 beats per minute. Moreover, flutter waves (tiny atrial deflections) separated by about 5 small boxes on the ECG (ie, occurring at a rate of 300 beats per minute) are apparent on the tracing of a patient with atrial flutter; these appear to march through the QRS complexes. In this woman's ECG, however, there appears to be a real P wave (with a fixed PR interval) in front of every QRS complex. Thus, atrial flutter is unlikely.
Sinus tachycardia. This dysrhythmia is extremely common; in most patients, it results from physiologic stress (eg, catecholamine surge, fever, dehydration, anemia, toxins, hyperthyroidism, hypoxia). It typically begins and ends gradually, does not hover at a fixed rate (since the physical stress varies), and thus is not paroxysmal. An exception is sinus node reentrant tachycardia, a reentry dysrhythmia with a microcircuit localized to the sinus node that begins and ends suddenly.1
Sinus tachycardia characteristically features an upright P wave in lead II (as well as lead I and probably lead aVF), and the morphology of this P wave matches that of P waves in the same person while in normal sinus rhythm.2,3 A closer look at the P wave in lead II (Figure 2, circle) is the key to deciphering this tracing. First, it is not upright. Second, it differs from the patient's P wave in lead II in a baseline tracing (Figure 3). These findings rule out sinus tachycardia.
Significance of left P-wave axis deviation. The change in the P wave in lead II suggests an abnormal P-wave axis. Like the QRS axis, the P-wave axis is determined by examining the deflections of the P waves in the limb leads and calculating the major P-wave vector. The P wave in Figures 1 and 2 is deflected upward in lead I, downward in lead aVF, and downward in lead II. Thus, we can conclude that the P-wave axis is deviated to the left, to between 230 and 290 degrees. This is distinctly abnormal for a P-wave vector, which normally lies between 0 degrees and +75 degrees; usually, it falls between about +45 and +60 degrees.3
The patient's baseline ECG (see Figure 3) shows a normal upright P wave in lead II; this finding indicates that atrial activity originated at the sinus node. An abnormal P-wave vector, such as that seen in Figures 1 and 2, suggests that an ectopic atrial focus is serving as the "pacemaker"--ie, that the dysrhythmia originates somewhere other than the sinus node. Thus, the rhythm in this case is atrial tachycardia.
Features of atrial tachycardia. This somewhat rare dysrhythmia may stem from reentry, triggered activity, or enhanced automaticity. The atrial rate is usually 150 to 250 beats per minute (slower than atrial flutter). There may be a degree of block; most commonly, it is second-degree AV block with 2:1 conduction. When such a dysrhythmia occurs in paroxysms, suspect digitalis intoxication, the classic "PAT (paroxysmal atrial tachycardia) with block."1
Atrial tachycardia--a true dysrhythmia--must be differentiated from the physiologic response represented by sinus tachycardia. In the latter, appropriate management consists of identifying the underlying cause and addressing it. Sinus tachycardia should not be "slowed down" with b-adrenergic blockers; remember to "treat the patient, not the dysrhythmia." In contrast, some patients with atrial tachycardia respond only to pharmacotherapy that directly targets the dysrhythmia.
Outcome of this case. The patient had stopped taking metoprolol that had been prescribed for treatment of atrial tachycardia. Once the drug was reinstituted, normal sinus rhythm was restored (see Figure 3).