Monday, February 23, 2015

Wide Complex Tachycardia in a Young Adult

Wide Complex Tachycardia in a Young Adult
Case presentation: 
A 24 - year - old female patient with no medical history of significance, transported to the emergency department via paramedics, had been complaining of sudden weakness and palpitations. All her symptoms had resolved prior to the paramedics ’ arrival at the scene. In the emergency department, the patient noted a recurrence of her symptoms; examination at that time demonstrated an alert patient with minimal distress.



The vital signs were: blood pressure 100/70 mmHg, pulse 240 beats/minute, and respiration 38 per minute. The monitor revealed a rapid, wide complex rhythm (pictured).  was undertaken with a return of a normal mental status and the second ECG noted here.


The remainder of the examination normalized as well.
Question: Of the listed interventions, the most appropriate initial intervention is:

A. Intravenous diltiazem
B. Oral metoprolol
C. Intravenous procainamide
D. Oral amiodarone
E. Intravenous potassium

Answer: C
Diagnosis: Antidromic tachycardia in Wolff – Parkinson –White syndrome

Discussion: The case rhythm strip demonstrates a wide complex tachycardia (WCT). The electrocardiogram reveals the classic electrocardiographic triad of Wolff – Parkinson – White (WPW) syndrome, including a shortened PR interval, widened QRS complex, and delta wave.
WPW syndrome is a form of ventricular pre - excitation involving an accessory conduction pathway. This accessory conduction pathway bypasses the atrioventricular (AV) node, creating a direct electrical connection between the atria and ventricles – in essence, removing the protective,
rate - limiting effect of the AV node and subjecting the ventricles to excessive rates when the patient experiences a dysrhythmia. The ventricles are “ pre - excited ” with atrial impulse conduction over the accessory pathway (AP), which arrives at the ventricular myocardium sooner than the same impulse conducted through the AV node. The electrocardiographic defi nition of WPW (Figure) relies on the following electrocardiographic features: (1) a PR interval less than 0.12 seconds; (2) slurring of the initial segment of the QRS complex (delta wave); (3) a widened QRS complex; and (4) secondary repolarization changes refl ected in ST segment and T wave changes. The
PR interval is shortened because the impulse progressing down the AP is not subjected to the physiologic slowing that occurs in the AV node. Thus, the ventricular myocardium is activated by two separate pathways (the AP and the AV node), resulting in a fused – or widened – QRS complex. The initial part of the complex, the delta wave, represents aberrant activation of the ventricular myocardium through the AP, while the terminal portion of the QRS represents normal activation through the His – Purkinje system from impulses that have traveled through both the AV node and the AP. This classic triad of electrocardiographic fi ndings, when encountered in the setting
of a symptomatic dysrhythmia, represents WPW  syndrome. These dysrhythmias include paroxysmal
supraventricular tachycardia (also known as atrioventricular reciprocating tachycardia [AVRT]),
A. Normal sinus rhythm with PR interval shortening, a delta wave (arrow), and a widened QRS complex. B. Normal sinus rhythm with PR interval shortening, a delta wave (arrow), and a widened QRS complex. Note that the delta wave has a negative polarity. C. Antidromic tachycardia with wide QRS complexes. Note the initial slurring of the QRS complex, which is termed the delta wave (arrow).

figure :A. Normal sinus rhythm with PR interval shortening, a delta wave (arrow), and a widened QRS complex. B. Normal sinus rhythm with PR interval shortening, a delta wave (arrow), and a widened QRS complex. Note that the delta wave has a negative polarity. C. Antidromic tachycardia with wide QRS complexes. Note the initial slurring of the QRS complex, which is termed the delta
wave (arrow). 

 atrial fibrillation, and ventricular fibrillation (Figure ). The most frequently encountered rhythm disturbance is AVRT, with two subtypes described; these two subtypes are classified based upon the direction of conduction through the AP (antegrade versus retrograde) and the resultant QRS complex width. Activation of the ventricular myocardium and impulse propagation occurs through either the AV node or the AP. With antegrade conduction through the AV node with impulse return to the atria via the AP, the AVRT is referred to as orthodromic. Orthodromic AVRT, the most common form of AVRT, presents electrocardiographically with a narrow QRS complex – and is indistinguishable from typical AV nodal  reciprocating tachycardia, i.e., persistent supraventricular tachycardia (PSVT).

The least common form of AVRT is antidromic tachycardia, which is seen in approximately 10% of WPW PSVT patients. In this rhythm presentation, the AP conducts the impulse from the atria to the ventricles in antegrade fashion. The impulse returns to the atria via the bundle branches, His – Purkinje fi bers, and the AV node.



In this form of AVRT, the QRS complex is wide due to inefficient conduction of the impulse through the ventricular myocardium – i.e., the His–Purkinje system is not used. The QRS complexes appear wide (essentially, an exaggeration of the delta wave), and the ECG displays a very rapid, wide complex tachycardia that is indistinguishable from that of ventricular tachycardia. The ventricular
rates are rapid, with a range of 180–240 beats per minute. This form of AVRT places the patient at risk for arrhythmic decompensation due to the loss of AV node protection of the ventricle from rapid rates. The initial treatment of the antidromic AVRT, i.e., the wide complex tachycardia, focuses on interrupting the re-entrant circuit. Electrical cardioversion should be applied to all patients with hemodynamic instability. Additionally, tachycardias with ventricular rates approaching 300 per minute are at an increased risk for ventricular fibrillation, resulting from myocardial ischemia due to reduced perfusion of the heart as well as subsequent depolarizations falling on the electrically vulnerable repolarization phase. In the hemodynamically stable patient, the agent of first choice would be either procainamide or amiodarone. Agents such as calcium channel antagonists, beta-adrenergic blocking agents, or digoxin, which act primarily on the AV node, are contraindicated
since they will facilitate conduction down the AP and could potentially lead to an increased ventricular rate with ventricular fibrillation.

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