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.

Treatment-Resistant Wide-Complex Tachycardia in a Three-Year-Old Girl

“…If stable, the next steps are to determine whether it is a wide-or narrow-complex tachycardia, and whether there is a monomorphic or polymorphic QRS. Wide-and monomorphic-complex tachycardias are often due to VT, but may also be caused by hyperkalemia, toxins [11] or underlying SVTa [1]. Differentiating VT and SVTa can be challenging.…”

“…Differentiating VT and SVTa can be challenging. In the absence of electrolyte abnormalities or drug/poison exposures, the presence of capture beats, fusion beats and atrioventricular dissociation on ECG with a monomorphic WCT are more suggestive of VT rather than SVTa [1] and there are ECG algorithms to help make this distinction [2]. Furthermore, in adult populations, adenosine may be both therapeutic and diagnostic at differentiating VT from SVTa, as one study showed that 90% of SVTa was terminated by adenosine, whereas only 2% of VT was terminated by adenosine [12].…”

“…In the pediatric population, specifically, treatment of monomorphic WCT consists of synchronized cardioversion if unstable [9] and initial trial of VMs if stable, followed by medical management [1,8]. VMs such as carotid sinus massage, putting an ice-cold towel on the face, or the Valsalva maneuver ostensibly increase parasympathetic tone, hypothesized to cause acetylcholine release via the vagus nerve, reducing beta-adrenergic and cyclic adenosine monophosphate stimulation of the ventricular myocardium, thereby terminating sympathetic-triggered arrhythmias, such as SVT or certain types of VT [1,7,16]. In the case we present here, VMs were attempted with transient efficacy but were not successful at terminating the tachyarrhythmia.…”

“…WCT may be monomorphic or polymorphic. Generally, monomorphic WCT represents either ventricular tachycardia (VT) or supraventricular tachycardia with aberrancy (SVTa), and effectively discerning VT from SVTa can be difficult [1]. There are electrocardiogram (ECG) algorithms to help make this distinction [2], yet VT is often misdiagnosed as SVTa [3].…”

“…On the contrary, VT in children is most commonly idiopathic and benign, but can be related to cardiomyopathy, structural heart disease, channelopathies or electrolyte imbalances, all of which carry increased mortality rates [4]. Monomorphic WCT in a hemodynamically stable patient, regardless of the patient's age, may respond to a trial of vagal maneuvers [1,7,8], but rapid IV administration of adenosine [9], with the possible addition of a beta-blocker or calcium channel blocker infusion [10], and/or amiodarone/procainamide loading [9], may also be necessary. We present a case of monomorphic WCT due to VT in a previously healthy three-year-old girl that was significantly refractory to initial treatments, which illustrates that not all monomorphic WCT is equally responsive to routine treatment and medication adverse events, such as shock, must be monitored.…”