A case report reappraising the usefulness of Valsalva manoeuvre in drug-refractory ventricular tachycardia

Abstract

Background: Ventricular tachycardia (VT) is often misdiagnosed as supraventricular tachycardia with aberrancy. Twelve-lead electrocardiogram remains a key diagnostic tool to differentiate them while providing insights to aid localization of VT. The use of Valsalva manoeuvre (VM) in terminating VT is not conventionally recommended due to lack of robust evidence of its effectiveness and poor understanding of its mechanism in terminating VT.

Case summary: A 74-year-old man with history of ischaemic heart disease was admitted with broad complex tachycardia. VT-1 was diagnosed following failed tachycardia termination by adenosine. Haemodynamic compromise necessitated synchronized cardioversion with successful reversion. However, a different VT-2 occurred after cardioversion. VM led to successful termination of VT-2. Subsequently, recurrent episodes of VT-2 occurred with consistent termination by VM. Transthoracic echocardiogram, cardiac magnetic resonance imaging, and a coronary angiogram were performed. Findings suggested that these are likely scar-related VT. VT-1 originated from an anteroseptal scar, whilst VT-2, responsive to VM, likely originated from the Purkinje fibres. Patient remained eurhythmic after Day 1 following amiodarone and beta-blocker initiation. An implantable cardioverter-defibrillator was implanted prior to discharge.

Discussion: VM is one of the vagal manoeuvres which are commonly used as initial management of supraventricular tachycardia. Its role in management of VT is obscure. Anecdotal case series recorded its successful use for managing particular VT. Exact mechanism remains elusive although postulated to involve change in cardiac size during strain and release of acetylcholine.

Keywords: Case report; Vagal manoeuvre; Valsalva manoeuvre; Ventricular tachycardia.

Figure 1

Atrioventricular dissociation (blue circles), dominant S in V1, notching and slurring of S wave (Josephson’s sign) in V2, qR pattern in V6, and fusion beats (red circles) in Lead II favours ventricular tachycardia rather than supraventricular tachycardia with aberrancy. Left bundle branch block morphology, inferior axis with QS in V1 and V2 suggest a ventricular tachycardia with an anteroseptal exit (ventricular tachycardia-1).

Figure 2

The significant difference from Figure 1 can be appreciated in positive QRS amplitude in V1 and V2, i.e. right bundle branch block pattern (ventricular tachycardia-2). Inferior axis deviation remained the same. There is capture beat in lead II (red circle) together with positive concordance in chest leads V1 to V6 suggesting a more basal origin. Involvement of Purkinje system is suggested by the right bundle branch block morphology with sharp initial QRS deflection.

Figure 3

Telemetry tracing showing episodes of ventricular tachycardia (ventricular tachycardia-2) repeatedly terminated with vagal manoeuvre.

Figure 4

Baseline electrocardiogram of the patient demonstrated sinus rhythm with left ventricular hypertrophy voltage criteria, left ventricular strain pattern, and Q waves in V1–V3.

Figure 5

Crude electrocardiogram localization for site of origin for ventricular tachycardia. Q waves usually indicates the myocardial region where ventricular tachycardia is originating. Hence an inferior axis implies an origin opposite the inferior wall, i.e. the anterior wall. LBBB, left bundle branch block; LV, left ventricle; RBBB, right bundle branch block; RV, right ventricle.