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 (AV) nodal tissue (Medi 2009). It encompasses such arrhythmias as atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (Wolff‐Parkinson‐White syndrome) (AVRT), atrial flutter, atrial fibrillation, and the sinus tachycardias. More specificity can be applied when SVT is used to describe those tachycardias that involve a nodal dependent re‐entrant circuit, such as that found in AVNRT or AVRT (Medi 2009). The incidence of SVT in the United States is approximately 35 cases per 100,000 population annually, with a prevalence of approximately 2.25 cases per 1000 population (Medi 2009). We identified no data to indicate incidence and prevalence in other regions.

These arrhythmias result from the establishment of a re‐entry circuit within (or inclusive of) the atrioventricular 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 2005; Wellens 2003). It is these symptoms that 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) (Akhtar 1993; Delacretaz 2006; McGuire 2007; Scheinman 2005; Wellens 2003), it is believed that this atrial ectopic complex stimulates a re‐entry circuit.

The mechanism of AVRT differs in the existence of accessory pathways (bundles of Kent). These conductive accessory pathways pass through the atrioventricular septum and thus provide for a larger re‐entry circuit, albeit one that passes through the AV node and is similarly affected by increased vagal tone (McGuire 2007; Scheinman 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 reversion of the arrhythmia. The use of pharmacologic agents such as adenosine and calcium channel blockers (verapamil and diltiazem) is well known and has been the subject of systematic review and meta‐analysis to determine their levels of effectiveness in this setting (Delaney 2011; Holdgate 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 within medical circles globally. Vagal manoeuvres have 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 1998; Mehta 1988; Taylor 1999; Wen 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 blockers or radio frequency ablation in order to improve patient quality of life. Recent studies have also identified increased troponin I enzyme levels (0.02 ng/dL to 1.05 ng/dL, mean 0.20 ng/dL) in people suffering episodic SVT in 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 2011; Redfearn 2005; Zellweger 2003). These studies also suggest that enzyme levels rise with increasing age of the patient, although the consequences are again at this time unquantified (Carlberg 2011; Redfearn 2005; Zellweger 2003).

Description of the intervention

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

• posture of the patient (supine)

• pressure generation within the intrathoracic cavity (40 mmHg)

• duration of strain (15 seconds)

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

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

• Phase 1 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 2 is defined by the end of this transient period, resulting in decreasing aortic pressure and increasing heart rate.

• Phase 3 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 4 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.

We have selected the VM for review as it provides a simple, quantifiable (method), and non‐invasive means of inducing increased vagal tone. Other 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 VM is a simple, quantifiable, and non‐invasive method of increasing vagal tone, 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 baroreceptor activity and increased vagal tone. However, this also has potentially deleterious side effects such as increased intraocular pressure and profound hypotension as a consequence of unfettered vagal stimulation (Junqueira 2007; Looga 2004; Taylor 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, which occurs in phase 4 of the VM, and it is at this point that reversion of the arrhythmia is most likely to occur (Looga 2004; Waxman 1980). Recently, efforts have been made to provide a standard of instruction of the VM for use in the haemodynamically stable patient suffering AVNRT, including the use of a 10 ml syringe to generate the 40 mmHg pressure required (Smith 2009a; Taylor 2004).

Why it is important to do this review

There is currently 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 2009b). The effectiveness of the VM is challenged by the lack of available interventional and observational non‐randomised clinical studies (7.3% to 54% of study sample) (Taylor 1999; Taylor 2004; Waxman 1980) and the many definitions of method (specifically variations in the three elements of posture, pressure, and duration) (Smith 2009b). We hoped with this review to ascertain the nature of evidence available to demonstrate VM effectiveness, and the need for further study to define the effectiveness of the VM for the development of future therapy regimens in the treatment of SVT.