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

Author:

Lwin Tin Sanda1ORCID,Mitrakrishnan Rayno Navinan1ORCID,Alama Mohamed1ORCID,Chin Shui Hao2ORCID

Affiliation:

1. Department of Cardiology, Kettering General Hospital, NHS, Rothwell Road, Kettering, NN16 8UZ, UK

2. Department of Cardiology, Glenfield Hospital, University of Leicester NHS Trust, Groby Road, Leicester, LE3 9QP, UK

Abstract

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.

Publisher

Oxford University Press (OUP)

Subject

Cardiology and Cardiovascular Medicine

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