Description of the condition

Supraventricular tachycardia (SVT) is a generic term applied in reference to any tachycardia originating above the ventricles, and which involves atrial tissue or atrioventricular nodal tissue (Medi et al 2009). It encompasses such arrhythmias as atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia (Wolff Parkinson White Syndrome), atrial flutter, atrial fibrillation, and the sinus tachycardias. More specificity can be applied when SVT is used to describe those tachycardias which involve a nodal dependent reentrant circuit , such as that found in atrioventricular nodal reentrant tachycardia (AVNRT) or atrio‐ventricular reentrant tachycardia (AVRT) (Medi et al 2009). The incidence of SVT is approximately 35 cases per 100,000 population annually, with a prevalence of approximately 2.25 cases per 1000 population (Medi et al 2009).

These arrhythmias result from the establishment of a re‐entry circuit within (or inclusive of) the atrio‐ventricular node. They are usually episodic in nature, and may result in the patient exhibiting signs and symptoms ranging from tachycardia or palpitations, shortness of breath, chest pain, anxiety, nausea and dizziness to presyncope/syncope as a consequence of reduced cardiac output (McGuire 2007; Scheinman and Yang 2005; Wellens 2003). It is these symptoms which usually precipitate an ambulance request or attendance at hospital. The establishment of AVNRT is believed to occur as a result of a premature atrial complex delivered across the AV node during the relative refractory period. As a consequence of the identification of dual nodal tract pathways for conduction of atrial impulses (fast depolarisation with slow repolarisation and slow depolarisation with fast repolarisation) (McGuire 2007; Scheinman and Yang 2005; Wellens 2003) it is believed that this atrial ectopic complex stimulates a re‐entry circuit.

The mechanism of AVRT differs, in that the existence of accessory pathways (Bundles of Kent) between the atria and ventricles provide for a larger re‐entry circuit, albeit one which passes through the AV node and is thus similarly affected by increased vagal tone (McGuire 2007; Scheinman and Yang 2005; Wellens 2003).

A range of therapies (vagal manoeuvres, pharmacological therapy or synchronised direct current countershock therapy) are employed within emergency medicine and prehospital emergency care practice in order to extend the refractoriness of AV nodal tissue, which will result in termination of the arrhythmia. The use of pharmacologic agents such as Adenosine and Calcium Channel Blockers (Verapamil and Diltiazem) are well known and have been the subject of systematic review and meta‐analysis to determine their levels of effectiveness in this setting (Delaney et al 2011; Holdgate and Foo 2009). Synchronised Direct Current Countershock therapy is generally reserved for those patients who are rapidly decompensating as a consequence of the arrhythmia, and although the evidence is somewhat limited within the literature there is support for this practice globally within medical circles. The use of vagal manoeuvres also been employed for some time, with demonstrated effectiveness in reverting AVNRT and AVRT of between 12% and 54% (with a median of 25%) across the range of studies conducted (Lim et al 1998; Mehta et al 1988; Taylor et al 1999; Wen et al 1998).

The arrhythmia is usually transient, and may be precipitated by such factors as cardiac disease, stimulant use, electrolyte imbalance and stress. In certain circumstances the frequency of episodes or consequences of episodic poor perfusion associated with SVT may require more significant therapies such as beta blocker or Radio Frequency ablation in order to improve patient quality of life (Akhtar et al 1993; Delacretaz 2006). Recent studies have also identified increased Troponin I enzyme levels (0.02 ng/dL to 1.05 ng/dL, mean 0.20ng/dL) in patients suffering episodic SVTin the absence of infarction, and although no studies have quantified the potential for patient harm at this time, it is suggested that these elevated Troponin I levels may be linked with myocardial damage (Carlberg et al 2011; Redfearn et al 2005; Zellweger et al 2003). These studies also suggest that enzyme levels rise with increasing age of the patient, although the consequences are again at this time not quantified (Carlberg et al 2011; Redfearn et al 2005; Zellweger et al 2003).

Description of the intervention

The Valsalva Manoeuvre was first published by Antonio Maria Valsalva in 1704, in his seminal work De Aura Humane Tractatus, as a means of expelling pus from the middle ear of a patient afflicted with this infection (Jellinek 2006; Junqueira 2007; Waxman et al 1980; Yale 2005). It has continued to retain relevance in modern medicine across a range of medical and scientific disciplines, and although it is unclear exactly when the manoeuvre was first applied to terminating haemodynamically stable supraventricular tachycardia (in the form of AVNRT or AVRT) it is likely to have coincided with the advent of the ECG (Einthoven 1906).The Valsalva Manoeuvre constitutes three specific elements in order to provide a maximum effect as follows (Taylor and Wong 2004).

• Posture of the patient (supine)

• Pressure generation within the intrathoracic cavity (40mmHg)

• Duration of strain (15 seconds)

These elements provide a set of values which, when adhered to, should maximise vagal response and terminate the arrhythmia (in the absence of any compliance or other patient issues which may affect performance or the nature of effect).

The Valsalva manoeuvre is defined by four phases of activity, first described by Hamilton et al in 1936 as follows (Junqueira 2007)

• Phase one can be defined by a transient increase in pressure within the thoracic aorta, coupled with a compensatory decrease in heart rate triggered by the baroreceptors within the aortic arch. This pressure increase results from the compressive effect of the generated intrathoracic pressure on the thoracic aorta.

• Phase two is defined by the end of this transient period, resulting in decreasing aortic pressure and increasing heart rate.

• Phase three occurs at the end of the strain phase of the VM (and includes a resulting decrease in intrathoracic pressure exerted on the aorta), leading to a brief pressure drop within the aorta and a compensatory rise in heart rate.

• Phase four occurs as a result of increased venous return (and a subsequent increase in preload) resulting in increased aortic pressure as cardiac output is elevated, and a compensatory decrease in heart rate.

The Valsalva manoeuvre has been selected for review in the prehospital and emergency medical setting as it provides a simple, quantifiable (method) and cost effective means of inducing increased vagal tone. Other vagal manoeuvres such as Carotid Sinus Massage and Dive Reflex therapy have limitations within the prehospital setting regarding patient safety, standardisation and reproducibility, and the logistics of application (for example, the acquisition and use of ice).

How the intervention might work

The Valsalva Manoeuvre is a simple, non‐invasive and cost effective method of increasing vagal tone and thereby increasing the refractory period of myocardial cells in order to terminate the established nodal re‐entry circuit . The manoeuvre was traditionally performed by expiring against a closed glottis to increase intrathoracic pressure, thereby triggering baro‐receptor activity and increased vagal tone, however this also potentiality deleterious side effects such as increased intra‐occular pressure and profound hypotension as a consequence of unfettered vagal stimulation (Junqueira 2007; Looga 2004; Taylor and Wong 2004; Vaisrub 1974). Since Rushmer introduced the measurement of intraoral pressure in 1947 (Junqueira 2007), the manoeuvre is now more commonly described and instructed as an exhalation against a defined pressure (measurable) in order to avoid significant side effects and to improve performance and patient safety. Maximum vagal response occurs on release of the sustained intrathoracic pressure (phase four of the manoeuvre), and it is at this point that reversion of the arrhythmia is most likely to occur (Looga 2004; Waxman et al 1980). Recently, efforts have been made to provide a standard of instruction of the manoeuvre for use in the haemodynamically stable patient suffering AVNRT, including the use of a 10ml syringe to generate the 40mmHg pressure required (Taylor and Wong 2004; Smith and Boyle 2009).

Why it is important to do this review

Currently there are a plethora of definitions of Valsalva performance, and it is used across a variety of medical and scientific disciplines to promote different effects (cardiac or non‐cardiac) (Smith et al 2009). The effectiveness of the Valsalva manoeuvre is challenged by the range of reported clinical studies (6.1% to 54% of study sample), and the plethora of definitions of method (specifically variations in the three elements of posture, pressure and duration) (Smith et al 2009). This review will ascertain the nature and level of evidence available to provide support for a standardised approach to performance, and will indicate the nature of study required to define the effectiveness of the Valsava Manouvre for the development of future therapy regimens in the treatment of SVT.