The introduction of specialist cardiac care centres within the hospital network in England in 2015 has led to increased conveyance times for acutely unwell patients accessing the ambulance service (Association of Ambulance Chief Executives (AACE), 2015). This problem is even more significant in rural areas (AACE, 2014) and has created a need for additional treatment for potentially life-threatening arrhythmias by appropriately trained paramedics, prior to arrival at hospital.
To treat each cardiac condition most appropriately, paramedics need to be able to accurately recognise many arrhythmias and target them with specific drugs. Prehospital practice relies upon doing the ‘best for the most’ with the least risk, and England (2016) espouses that drugs are often selected on their ability to perform more than one function. This approach is already reflected in the current paramedic guidelines (Brown et al, 2019), using hydrocortisone succinate to treat an adrenal crisis, anaphylaxis and life-threatening asthma.
Narrow-complex tachycardias, more commonly known as supraventricular tachycardias (SVTs), affect approximately 35 per 100 000 people per year (Sohinki and Obel, 2014; Brugada et al, 2019), with UK figures around 200 000 per year (NHS England, 2013). While each arrhythmia is treated with a specific drug in hospital, the Resuscitation Council (UK) (2015) advises that all will positively respond to intravenous (IV) amiodarone in some way.
Supraventricular tachyarrhythmias and current paramedic treatment
Transient SVTs are known as paroxysmal SVTs (PSVTs). Table 1 outlines the commonly encountered regular and irregular narrow complex tachyarrhythmias. Atrial flutter can be either regular or irregular, depending on the rate of conduction (Colucci et al, 2010).
Atrioventricular nodal re-entry tachycardia (AVNRT) is the most commonly occurring regular tachyarrhythmia among adults and accounts for 50–60% of all narrow complex tachyarrhythmias (Colucci at al, 2010).
Current paramedic treatment for patients presenting with PSVT involves vagal manoeuvres and carotid sinus massage (CSM) (Brown et al, 2019). Vagal manoeuvres include any technique designed to stimulate cranial nerve 10 (the vagus nerve) (Wang and Estes, 2002). The most used (modified Valsalva) manoeuvre involves the patient blowing into a 10 ml syringe while semi-recumbent followed by a passive leg raise while supine. It is designed to stimulate sympathetic nervous function by lowering intra-aortic pressure (Hayes, 2018).
In a review of the Cochrane database, Smith et al (2015a) showed mixed success rates of the Valsalva manoeuvre of just 19–54%. Appelboam et al's (2015) REVERT trial showed success rates at conversion to normal sinus rhythm (NSR) to be just 43% with a modified Valsalva. This leaves over 50% of patients in unresolved PSVT. The Valsalva manoeuvre has also been shown to be less effective in terminating AVNRT, the most common tachyarrhythmia (Corbacioglu et al, 2017).
The Joint Royal Colleges Ambulance Liaison Committee (JRCALC) clinical practice guidelines (Brown et al, 2019) recommended CSM to correct PSVT. CSM stimulates baroreceptors within the internal carotid arteries, which results in transient atrioventricular (AV) block. This can slow a narrow-complex tachyarrhythmia and help the paramedic differentiate between SVT, atrial flutter and atrial fibrillation (AF) (Hutchins, 2013). However, it carries a high risk of dislodging clots from carotid plaques (Adlington and Cumberbatch, 2009). In older patients, there is an increased risk of CSM being performed over the site of an atheromatous plaque as a result of their increasing frequency with age. Several studies have shown incidence of adverse neurological events (cerebrovascular accidents (CVAs), expressive dysphasia and confusion), although risk rates are relatively low at around 1% (Walsh et al, 2006; Lafuente et al, 2017).
Prehospital recognition of PSVT
If left untreated, or it treatment is unsuccessful, PSVTs can increase in rate, resulting in profound hypotension (Ashok et al, 2008). Pharmacological or electrical conversion of PSVT requires accurate identification of the arrhythmia (Hutchins, 2013) to avoid potentially fatal outcomes. The need for accuracy would be even greater in the prehospital environment as there is no specialist cardiac care to hand if the incorrect treatment is administered. With narrow-complex tachyarrhythmias, an increased rate can make it difficult to distinguish between regular and irregular rhythms (Resuscitation Council (UK), 2015). Several level-two studies have taken place among American, Canadian and Australian emergency medical services (EMS) personnel, with successful rhythm recognition at between 70–97% (Table 2). However, American and Canadian ambulance services also benefit from regular physician input via telemetry, enhancing rhythm recognition, which is not routinely available to the more autonomous UK ambulance services.
| Study | Study size | Study type | Paramedic SVT recognition | Country |
|---|---|---|---|---|
| McCabe et al, 1992 | 37 | Prospective study Level 2 | 26/27 (70.3%) | USA |
| Gausche et al, 1994 | 106 | Prospective study Level 2 | 84/106 (79%) | USA |
| Furlong et al, 1995 | 41 | Prospective study Level 2 | 31/41 (75.6%) | USA |
| Lozano et al, 1995 | 244 | Prospective study Level 2 | 221/244 (91%) | USA |
| Wittwer and Muhr, 1997 | 102 | Prospective study Level 2 | 74/102 (72.5) | USA |
| Morrison et al, 2001 | 201 | Non-randomised controlled study Level 2 | 180/201 (90%) | Canada |
| Goebel et al, 2004 | 224 | Retrospective analysis Level 3 | 188/224 (83.9%) | USA |
| Smith et al, 2015b | 123 | Retrospective analysis Level 3 | 119/123 (96.7%) | Australia |
| Honarbakhsh et al, 2017 | 44 | Randomised controlled trial Level 1 | 43/44 (98%) | UK |
To date, there has only been one randomised controlled trial (RCT) involving UK paramedics correctly identifying PSVT (Honarbakhsh et al, 2017), and this was in the context of adenosine administration. While the study demonstrated a 98% success rate at recognising PSVT, it had a low statistical power owing to the small sample of 44 patients. The study also involved paramedics with specialist skill sets only and is not reflective of the general paramedic population. A prospective audit of senior house officers (SHOs) in a UK hospital demonstrated that, without an adequate checklist and additional training, even emergency department (ED) physicians only recognise PSVT correctly in 63% of cases (O'Rourke, 2010). Such additional training is not routinely available to many paramedics and could incur a huge cost to nationalise and implement.
Current treatments for PSVT
The in-hospital adult advanced life support (ALS) treatment for narrow complex tachycardia depends upon the presence of adverse features (Figure 1). For haemodynamically-compromised patients with PSVT, synchronised direct-current (DC) cardioversion is the initial recommended treatment (Resuscitation Council (UK), 2015). If three synchronised shocks fail to revert the rhythm, diluted IV amiodarone 300 mg is used. Adenosine or verapamil are the suggested first-line treatments for stable patients with PSVT.
There is a paucity of literature surrounding the use of prehospital cardioversion by non-physician-led services. A single case study involving Australian Mobile Intensive Care (MICA) paramedics (Smith et al, 2013) discusses the safety of paramedic cardioversion. Morphine is used for analgesia and midazolam for sedation, both of which are available to UK paramedics in a specialist setting (England, 2016). While the study concluded that prehospital cardioversion is safe with specialist input, it is isolated practice among senior Australian paramedics and, to date, no controlled trials have taken place. However, there is little evidence supporting the use of cardioversion in an autonomous paramedic-led system.
Cardioversion in a patient, who is later found to be in AF and is subsequently not anticoagulated prior to the procedure, can easily result in the dislodging of a clot, potentially causing a CVA or myocardial infarction (MI) (Lip et al, 2015). Noted complications include those secondary to the analgesia and sedation (hypotension and respiratory depression), which would further increase the risk to an already haemodynamically compromised patient. Cardioversion should take place in a specialist hospital environment as it carries the risk of ‘R on T’ (where the R wave ‘interrupts’ the T wave), converting PSVT to ventricular fibrillation (VF) or asystole (Fitzmaurice, 2008).
Adenosine and verapamil have been successfully used to terminate PSVT in Australian and American paramedic systems (Brywczynski, 2012; Smith et al, 2014) for the last decade. Adenosine is a potent anti-arrhythmic that rapidly terminates stable PSVT in 92% of cases (Delaney et al, 2011), with only transient side effects, usually shorter in duration than 30 seconds. However, it only works on nodal-dependent PSVTs (AVNRT and AVRT) as it works specifically to slow AV conduction through the activation of potassium channels or inhibition of the inward calcium channels at the AV node (Bohm, 1987). The risk with adenosine comes when it is administered to patients in other narrow-complex tachycardias where PSVT has been incorrectly identified.
When administered to a patient in atrial flutter, adenosine can convert a stable 2:1 conduction at 150 beats per minute (bpm) to a haemodynamically unstable 1:1 conduction at 300 bpm (Mallet, 2004). If left untreated, this can result in the patient going into VF (Borke, 2017). When administered to patients in AF, adenosine can increase the heart rate to above 250 bpm, especially in those with aberrant pathways such as those seen with Wolff-Parkinson-White (WPW) syndrome (Ellis, 2017). WPW, concurrent with AVRT, occurs in 0.1–0.3% of the population (Hutchins, 2013) and occurs when a re-entrant pathway establishes between the atria and ventricles. All AV-nodal blockers will increase conduction down the aberrant pathway, causing further haemodynamic compromise (Fox et al, 2008). Incorrect rhythm identification in the prehospital environment can lead to adenosine being administered with fatal consequences.
Amiodarone
Amiodarone was first identified as a treatment for narrow-complex tachyarrhythmias in 1983 (Forrogos et al, 1983) and has been consistently used as a treatment for PSVT since. It currently forms part of the UK paramedic formulary for use in shock-resistant VF (Brown et al, 2019). It is presented in an undiluted form (300 mg/10 ml), which can be added to 100 ml bags of 5% dextrose to create the appropriate format for pharmacological conversion of PSVT, similar to the way tranexamic acid (TXA) is drawn up by paramedics (Resuscitation Council (UK), 2015). The major metabolite of amiodarone, desethylamiodarone (DEA), has multiple anti-arrhythmic properties, making it ideal for use on a variety of tachyarrhythmias (Siddoway, 2003; Resuscitation Council (UK), 2015).
Although amiodarone is considered a class III antiarrhythmic (Table 3) under the older Vaughan Williams classification; as it prolongs the QT interval (Siddoway, 2013), it exhibits properties of four antiarrhythmic classes. It has beta blockade, calcium channel blockade and potassium/sodium pump blockade properties. Beta blockade is more strongly seen in the IV preparations and oral amiodarone has better potassium channel-blocking abilities, causing QT prolongation (Tsu, 2013).
| Class | Action | Examples |
|---|---|---|
| 1a | Na+ Channel blocker |
Quinidine |
| 1b | Na+ Channel blocker |
Lidocaine |
| 1c | Na+ Channel blocker |
Flecainide |
| 2 | Beta blocker |
Propanolol |
| 3 | K+ Channel blocker | Amiodarone |
| 4 | Ca2+ Channel blocker | Verapamil |
| 5 | Direct Nodal inhibition |
Digoxin |
A prospective study conducted in 1983 on 121 patients (Graboys et al, 1983) demonstrated that amiodarone is safe for use in multiple narrow-complex tachyarrhythmias, including SVT, AF and atrial flutter. It showed a 92% success rate in terminating SVT when all other drug therapies had failed. As amiodarone can be used regardless of the arrhythmia, it increases the safety profile for its use in life-threatening situations where judgement is easily compromised and rhythm recognition is often poor (Aacharya et al, 2011). The study was limited to those patients taking oral amiodarone for long-term arrhythmia suppression, limiting its value for comparison in IV use. However, amiodarone has a long half-life, even in a single dose, so the analysis of the side effects is useful. While 75% of the patients enrolled experienced side effects, most of them felt that these were sufficiently minor and they continued with treatment.
In 1989, Kadish and Morady first identified the potential for IV use of amiodarone to terminate PSVT (Kadish and Morady, 1989). Several studies involving amiodarone being infused mid-arrhythmia have shown high levels of success in terminating PSVT, with more limited success in terminating other tachyarrhythmias (Table 4). Levine et al (1996) conducted a multi-centre double-blinded RCT involving 273 patients with ventricular tachyarrhythmias and profound hypotension. IV amiodarone was administered over a 24-hour period. The study focused primarily upon pulsed ventricular tachycardia (VT) rather than PSVT; however, it showed that fewer than 6% of patients experienced adverse effects. The study's findings are not completely transferable as it included patients with multiple confounding factors who have had their cardiac medications withdrawn as part of enrolment. Despite its shortcomings, this study demonstrated success in the suppression of tachyarrhythmias, and most patients experienced a longer interval between episodes of arrhythmia. There have been few more recent studies regarding the efficacy of amiodarone in terminating PSVT as newer drugs are targeted at specific arrhythmias.
| Author | Arrhythmias | Number treated | Number successful |
|---|---|---|---|
| Wellens et al (1984) | AVRT (WPW) | 9 | 3 |
| Maggioni et al (1986) | Uncommon AVNRT | 1 | 1 |
| Holt et al (1985) | AF | 7 | 1 |
| Storelli et al (1985) | PSVT |
33 |
33 |
| Bucknall et al (1986) | Atrial flutter |
1 |
1 |
| Leak (1986) | AF | 4 | 4 |
| Gornes et al (1984) | AVNRT |
7 |
7 |
| Waleffe et al (1978) | Concealed bypass tract | 2 | 2 |
| Alboni et al (1984) | Concealed bypass tract |
14 |
8 |
| Installe et al (1981) | AF |
18 |
6 |
Oral amiodarone takes between 9 and 16 days to reach maximal efficiency but IV amiodarone has a far quicker onset of action (Kadish and Morady, 1989). In their case report, Farhan and Yaseen (2015) documented two cases of amiodarone-induced extreme hypotension, one of which resulted in death. However, both of these cases involved bolus administration distal to the ante-cubital fossa (ACF). Amiodarone would therefore need to be diluted and administered slowly. However, should hypotension occur, this is rectifiable with fluids, reducing the cardiovascular risk to the patient (AACE, 2016).
Administration
Although recent literature (Richard et al, 2013; Rees et al, 2015) recommends that amiodarone be delivered via a central venous catheter, insertion of the devices is neither safe nor appropriate in the prehospital environment. Best practice recommends placement under sterile conditions using ultrasound guidance and confirming correct location with a chest x-ray (Bodenham et al, 2016). More distal IV access is considered at greater risk of phlebitis from amiodarone administration (Rees et al, 2015). Ensuring that amiodarone is delivered via a more proximal cannula would help to mitigate this risk. Dilution with dextrose 5% (D5W) 100 ml is recommended to prevent hypotension, which is currently accepted practice (Resuscitation Council (UK), 2015). Paramedics are used to delivering drugs in this manner as it forms part of a patient group directive (PGD) for TXA (Brown et al, 2019).
While not recommended in a bolus for patients with left ventricular dysfunction or heart failure (National Institute for Health and Care Excellence (NICE), 2017), a study involving patients with heart failure and left ventricular impairment, as well as an analysis of two RCTs, demonstrated that amiodarone is safe for use in cardiovascularly compromised patients (Cadrin-Tourigney et al, 2014). As more than 7 million patients encountered in the prehospital environment have cardiac comorbidities (British Heart Foundation, 2018), having a treatment safe in these circumstances is preferable.
Amiodarone has been found to cause lung pathology in some patients but the evidence shows this to be limited to those taking long-term oral amiodarone for rhythm suppression (Voruganti and Cadaret, 2017). Case reports discuss patients presenting with shortness of breath while on oral amiodarone to suppress PSVT. Amiodarone-induced interstitial pneumonitis was found to be the underlying cause once a chest x-ray was performed (Sweidan et al, 2009; Voruganti and Cadaret, 2017). Once the amiodarone had been withdrawn, the pneumonitis decreased. There is no evidence of interstitial disease emanating from a single IV dose of amiodarone. Patients who had been administered IV amiodarone would be hospitalised post treatment for monitoring and would easily be able to undergo a chest x-ray to exclude any lung disease.
Conclusion
The use of synchronised DC cardioversion carries the need for additional analgesia and sedation, which in turn carries risk. Adenosine—while a proven treatment for PSVT—can be fatal to the patient if the underlying tachyarrhythmia is incorrectly identified. Amiodarone is not the first-line treatment for many narrow complex tachyarrhythmias but it is a proven appropriate alternative that is safe across a wide range of underlying rhythms. Its safety profile has been consistently demonstrated across a range of arrhythmias and it would not require a change to current drug regulations for paramedics, without independent prescribing, to carry it. With a risk-benefit analysis, amiodarone is the most effective, safe and therefore appropriate treatment for use in PSVT in the prehospital environment.
Further research, possibly in the form of a multi-trust RCT, would be necessary to determine whether the use of amiodarone by paramedics is both effective and necessary in the prehospital setting. Additional training on ECG rhythm recognition would be required, alongside a newly developed PGD to facilitate the change in practice. Investigating the number of patients who are pre-alerted to hospitals with unstable PSVT would initially demonstrate the place for a change in practice in the prehospital environment.