Supraventricular tachycardias (SVTs) are fast heart rhythms originating from the sinus node, atrial tissue or atrioventricular junctional tissue. They include physiological sinus tachycardia but are often taken to refer to pathological SVTs. They can cause clinical signs such as weakness, and if sustained, can lead to tachycardia-induced cardiomyopathy and congestive heart failure (Shinbane et al, 1997). One particular type of SVT is caused by the presence of an accessory pathway of conducting tissue between the atria and ventricles, bypassing the atrioventricular node, allowing a rapid re-entrant conducting circuit to occur. This case report describes a case of a pathological SVT in a young Labrador Retriever, with differential diagnoses of an accessory pathway-mediated tachycardia or a focal atrial tachycardia.
Case report
A 3-year-old male Labrador Retriever was referred following the detection of a sustained tachycardia while undergoing investigations following a two-day history of lethargy and vomiting. Physical examination revealed a laterally recumbent, normothermic (38.3°C) dog in good body condition (37 kg). The dog had congested mucous membranes and an elevated respiratory rate (48 breaths per minute) with no adventitious lung sounds. The dog's heart rate was approximately 300 beats per minute (bpm), with a regular rhythm and no audible murmur. The femoral pulses were very hypokinetic, making possible deficits difficult to appreciate.
An electrocardiogram (ECG) (Figure 1) revealed a narrow QRS complex tachycardia (QRS duration of 60 milliseconds) at a rate of 300 bpm with regular R-R intervals (200 milliseconds), and alternating R wave height (electrical alternans). P waves were not clearly visible, and there was a slurred upstroke to the R wave. The differential diagnoses for this ECG pattern would be an accessory pathway-mediated tachycardia (orthodromic atrioventricular reciprocating tachycardia) with aberrant conduction, focal atrial tachycardia with aberrant conduction, focal atrial tachycardia with incidental accessory pathway and ventricular pre-excitation, or more rarely, antidromic atrioventricular reciprocating tachycardia with an accessory pathway located very near the atrioventricular node.
A focused echocardiogram (Figure 2a) revealed a moderately dilated left atrium (left atrium: aorta 1.99 (normal <1.60), Hansson method (Hansson et al, 2002) and right atrium, a mildly dilated right ventricle and a scant pleural effusion. The left ventricle was not dilated, but systolic function appeared reduced (although the tachycardia complicated the assessment of this because of the reduced diastolic left ventricular filling). A brief abdominal ultrasound showed a very small amount of free abdominal fluid adjacent to the liver. This was considered likely to be secondary to the sustained tachycardia, although a pre-existing cardiomyopathy (such as dilated cardiomyopathy) could not be excluded.
Serum biochemistry analysis on admission showed elevated alkaline phosphatase – 168 U/l (0–160), alanine aminotransaminase – 445 U/l (0–100), bilirubin - 42umol/l (0–15) and bile acids - 77umol/l (0–5). These liver biochemical abnormalities could have been caused by primary or reactive liver disease, liver congestion from right-sided congestive heart failure, hypoxia from reduced cardiac output or a combination of these. Further liver investigations were not pursued as the biochemical abnormalities, and lethargy and vomiting resolved with treatment of the tachycardia.
An initial vagal manoeuvre (pressure applied to the eye to stimulate the oculocardiac reflex) was attempted to terminate the rhythm, but was unsuccessful. Subsequently, three intravenous (IV) boluses of diltiazem (Diltiazam Hydrochloride, Akorn Inc., Lake Forest, IL 60045) (0.1mg/kg) were given slowly at 10-minute intervals. After the third bolus, the supraventricular tachycardia terminated and was initially replaced by a multiform ventricular tachycardia (Figure 3). This was treated with lidocaine (Lidocaine hydrochloride, Hameln pharmaceuticals Ltd, Gloucester, UK) as a single IV bolus (2mg/kg) followed by a constant rate infusion (50micrograms/kg/min). The rhythm then became predominantly a uniform wide complex tachycardia of approximately 150 bpm (an accelerated idioventricular rhythm), with intermittent narrow QRS complexes and varying P wave morphology. The ventricular arrhythmia was likely caused by transient myocardial damage following the sustained tachycardia (for example, myocardial hypoxia as a result of reduced diastolic time for coronary perfusion). A single bolus each of pimobendan (Vetmedin, Boehringer Ingelheim, Bracknell, UK) (0.15mg/kg IV) and furosemide (Dimazon, MSD Animal Health, Milton Keynes, UK) (1mg/kg IV) were given to treat the congestive heart failure, and a single bolus of maropitant (Cerenia, Zoeitis, Belgium) (1mg/kg IV) as an anti-emetic owing to the history of vomiting on presentation.
The dog was hospitalised and treatment was continued with a lidocaine constant rate infusion (50ug/kg/min IV), furosemide (1mg/kg IV) every 12 hours, pimobendan (0.27mg/kg per os) every 12 hours and diltiazem (Diltstar Modified Release, Sanofi-Winthrop Industrie, France) (1.6mg/kg per os) every 8 hours. Overnight, the ECG showed paroxysmal accelerated idioventricular rhythm alternating with sinus rhythm, and supraventricular ectopic beats with negative ectopic P’ waves at a rate of up to 150 bpm (ECG trace not shown). The supraventricular ectopic beats may also have been secondary to myocardial damage caused by the sustained tachycardia, or an underlying primary rhythm abnormality, but these were at a much slower rate and were therefore differentiated from the initial presenting supraventricular tachycardia. Ptyalism was noted and suspected to indicate nausea caused by the lidocaine constant rate infusion (rather than related to vomiting before presentation), which was therefore reduced (25micrograms/kg/min).
A full echocardiogram performed 12 hours after admission (Figure 2b) showed resolution of the left atrial dilation (left atrial:aortic ration of 1.58) and right ventricular dilation, and only equivocal mild right atrial dilation. Left ventricular systolic function was normal. No structural abnormalities were detected.
After 36 hours, sinus rhythm was fully restored with a heart rate of 100 bpm. The dog's demeanour was bright, and respiratory rate (28 breaths per minute) and rhythm appeared normal. Tertiary referral for an electrophysiological study and radiofrequency catheter ablation, if an accessory pathway was identified, was recommended but declined. The owners elected to continue medical therapy. The dog was discharged with diltiazem (1.6mg/kg per os) modified release tablets every 8 hours, and a short course of pimobendan (0.13mg/kg per os) every 12 hours for 3 days.
Two weeks after discharge the dog was reassessed. He was reported to be very bright and active at home. Physical examination was unremarkable. A 24-hour ambulatory ECG (Holter monitor, Lifecard, Spacelabs, Hertford) was fitted. Analysis revealed a mean heart rate of 91 bpm (normal range 60–90 bpm) with occasional supraventricular premature beats with no visible P’ waves (rate 198–220 bpm), but no supraventricular tachycardia was recorded. Ventricular preexcitation was not seen during the recording. Repeat serum biochemistry analysis was performed and the previously raised liver parameters had normalised. Long-term treatment with diltiazem (1.6mg/kg per os) every 8 hours was continued and to date, 6 months later, the dog has not relapsed.
Discussion
This case report describes the medical treatment of an SVT, which may present as incidentally detected arrhythmias or cause clinical signs such as weakness, lethargy, vomiting, vacant mentation, syncope (usually as a result of abrupt termination and overdrive suppression of the sinoatrial node) or congestive heart failure (right and/or left sided) (Finster et al, 2008). Any tachycardia arising from cardiac tissue above the ventricles is termed an SVT. This includes physiological sinus tachycardia, but the term SVT is most commonly used to describe pathological supraventricular tachyarrhythmias. These include focal atrial tachycardia, atrial flutter, atrial fibrillation and junctional tachycardias.
SVTs are usually distinguished from ventricular tachycardias by the presence of narrow QRS complexes with the same morphology as sinus beats because they are conducted through the normal ventricular conduction pathway. However, if there is aberrant ventricular conduction (such as a bundle branch block, partial refractoriness of the conducting system secondary to tachycardia, or in some cases of ventricular pre-excitation), or severe ventricular hypertrophy, the QRS complexes can appear wide and mimic a ventricular tachycardia, complicating their diagnosis (Santilli et al, 2012).
Focal atrial tachycardias result from an ectopic focus within the atria but outside of the sinus node and can be caused by a micro re-entrant circuit, abnormal excitability, triggered activity, or a combination of these (Roberts-Thomson et al, 2006). Atrioventricular reciprocating tachycardias are a particular type of SVT which depend on the presence of an accessory pathway between the atria and the ventricles. Accessory pathways are aberrant myocardial bundles that bridge the fibrous tissue between the atria and ventricles, creating a potential electrical connection outside of the normal conduction system, in addition to the normal atrioventricular node pathway (Kent, 1893). In some cases, they allow a macro re-entrant pathway to be established, with repeated rapid depolarisation of atria and ventricles similar to an electrical ‘short circuit’ (Figure 4).
Without an electrophysiological study, the mechanism of the SVT (focal atrial tachycardia or accessory pathway-mediated) could not be determined in this case. The slurred upstroke of the R wave during the tachycardia (Figure 1) could have either been a result of aberrant conduction through the ventricular Purkinje system, or anterograde conduction through an accessory pathway (rather than the retrograde conduction seen during an orthodromic atrioventricular reciprocating tachycardia). Rapid tachycardias may leave inadequate time for complete repolarisation of ventricular conduction pathways, resulting in them being partially refractory when the next electrical impulse arrives. This can result in altered conduction through the ventricles, that changes the morphology of the QRS complex on the ECG. Either an orthodromic atrioventricular reciprocating tachycardia or focal atrial tachycardia may have been present with this form of aberrant conduction caused by the tachycardia, both of which would appear very similar on a surface ECG. The presence of an accessory pathway is another possible explanation for the slurred upstroke in the R wave, as a result of a supraventricular beat being conducted with ventricular pre-excitation (delta wave, Box 1). If both a focal atrial tachycardia and an accessory pathway were present, the focal atrial tachycardia may be conducted to the ventricles through both the accessory pathway and atrioventricular node, resulting in a delta wave. However, in this case, the accessory pathway is just incidental and not part of the actual tachycardia mechanism. A final differential diagnosis for the presenting ECG is antidromic atrioventricular reciprocating tachycardia with an accessory pathway located very near the normal atrioventricular node conduction system. In antidromic atrioventricular reciprocating tachycardia, the macro re-entrant circuit goes in the opposite direction to that of orthodromic atrioventricular reciprocating tachycardia, with the descending impulse travelling antegrade through the accessory pathway and retrograde back up the atrioventricular node. To the author's knowledge, this has never been described in a dog but is well documented in people (Bardy et al, 1984). Normally, in antidromic atrioventricular reciprocating tachycardia, the QRS is wide and abnormal because of the electrical impulse travelling though the myocardium via slow cell-to-cell transmission, rather than through the rapid budle of His–Purkinje fibres. However, it is possible that an accessory pathway was near the normal conduction pathway, and the impulse, after brief but slow cell-to-cell conduction (ventricular pre-excitation), can ‘jump’ back into the normal conduction pathway and the QRS can appear nearly normal during antidromic atrioventricular reciprocating tachycardia.
Box 1.Ventricular pre-excitationDuring sinus rhythm, the atrial depolarisation will reach the atrioventricular node and accessory pathway almost simultaneously. The depolarisation that travels down the atrioventricular node is slowed by the physiological conduction delay, while the depolarisation that travels down the accessory pathway is not, and will therefore reach the ventricles first. This results in the impulse reaching the ventricles quicker than if it had travelled through the atrioventricular node (pre-excitation – seen on the ECG as a short P-R interval) and at a different site in the ventricles (seen as a delta wave on the ECG, which may result in mild prolongation of the QRS duration) (Figure 6). Morphology of the delta wave and subsequent QRS can vary within the same patient, as it is dependent on accessory pathway conduction properties and location relative to the atrioventricular node, autonomic tone, and anti-arrhythmic medications. Although ventricular preexcitation indicates the presence of an accessory pathway, it is still a sinus rhythm (heart rate and rhythm still initiated and controlled by the sinoatrial node) and does not require anti-arrhythmic treatment itself.
Studies suggest the majority of accessory pathways allow retrograde (from ventricles to atria) conduction, and this may be seen as ectopic P waves (P’) within the ST segment or T wave (Figure 6) (Santilli et al, 2007). However, these P’ waves can be difficult to identify because they can be small or obscured by the rapid heart rate. Some accessory pathways can also allow antegrade (from atria to ventricles) conduction, and this may be seen on an ECG during sinus rhythm as a short P-R interval (ventricular pre-excitation) and abnormal QRS morphology (delta wave) (Box 1). Not all accessory pathways cause SVTs and are thus clinically insignificant in some dogs (Atkins et al, 1995).
In dogs, the most common reciprocating tachycardia is orthodromic atrioventricular reciprocating tachycardia (Oliveira, 2018). In this instance, the electrical depolarisation wave travels down the atrioventricular node (in the normal/antegrade direction), ventricular depolarisation occurs, the depolarisation wave then reaches the accessory pathway and is conducted retrograde back up to the atria. The depolarisation wave then travels through the atria and back down the atrioventricular node to the ventricles again, thus completing the circuit (Figure 4). Orthodromic atrioventricular reciprocating tachycardia is seen as a fast, narrow complex SVT, but has some features that may help distinguish it from other tachycardias, particularly a focal atrial tachycardia which can appear very similar (Box 2) (Santilli et al, 2007; Finster et al, 2008).
Box 2.Distinguishing ECG Features of orthodromic atrioventricular reciprocating tachycardia
- Rapid heart rate, often >300 bpm (but some other tachycardias can reach these rates)
- Electrical alternans (more common with orthodromic atrioventricular reciprocating tachycardia than focal atrial tachycardia)
- Negative P’ in early ST/T segments (but can be difficult to identify at higher heart rates)
- An RP’/P'R ratio of <1 (because P’ to R conduction is via the slower atrioventricular node, while R to P’ conduction is via the faster accessory pathway tissue)
- Sudden initiation and termination (rather than wind-up/wind-down)
- Termination with a blocked P wave (and persistence of P’ waves without QRS waves excludes orthodromic atrioventricular reciprocating tachycardia as the ventricular conduction is a necessary part of the circuit)
- Initiation/termination by an ectopic beat
- Narrow QRS complexes (distinguishes most supraventricular tachycardias from ventricular tachycardia)
- Regular rhythm (distinguishes from atrial fibrillation)
Orthodromic atrioventricular reciprocating tachycardias are always sudden in onset and offset (because the re-entrant circuit is either ‘on’ or ‘off’). They are often initiated by a premature atrial or ventricular beat because these are more likely to reach the accessory pathway when it is in an excitable, rather than refractory, state. An atrial or ventricular ectopic beat will also terminate the rhythm by breaking the circuit in the atria or ventricles respectively (Oliveira, 2018). Altered conduction because of medication or vagal tone at any point in the circuit (atria, atrioventricular node, ventricle or accessory pathway) can also break the re-entrant circuit.
Labrador retrievers are predisposed to accessory pathways (Finster et al, 2008; Wright et al, 2018) and detection of a SVT in a young Labrador is suspicious of an orthodromic atrioventricular reciprocating tachycardia. It is hypothesised this is because of the breed's predisposition towards tricuspid valve dysplasia (de Madron et al, 1987; Wright et al, 1996; Famula et al, 2002). Other dog breeds overrepresented in the literature with accessory pathways and orthodromic atrioventricular reciprocating tachycardia include Golden Retrievers, Boxers and Bulldogs (Foster et al, 2006; Santilli et al, 2012; Wright et al, 2018; Romito et al, 2019).
Consequences of sustained SVT can be life threatening. Tachycardia-induced cardiomyopathy can result, causing myocardial failure leading to signs of both left and/or right sided congestive heart failure (Shinbane et al, 1997). It can be difficult during initial assessment of such cases to distinguish between primary heart disease (such as dilated cardiomyopathy) with a secondary tachycardia, or a primary tachycardia with secondary tachycardia-induced cardiomyopathy. This is in part because of the rapid heart rate not allowing for complete diastolic filling, making echocardiographic dimensions and systolic function difficult to interpret. However, with cessation of the SVT, the tachycardia-induced cardiomyopathy changes are often reversible over several weeks (Shinbane et al, 1997). The very rapid improvement in systolic function in this case suggests that the apparent dysfunction was primarily a result of poor ventricular filling secondary to the tachycardia, and not tachycardia-induced cardiomyopathy.
Regardless of the type of SVT, emergency medical treatment usually aims to slow atrioventricular node conduction to block some of the SVT beats reaching the ventricles (rate control), or terminate the tachycardia (rhythm control) by disrupting an orthodromic atrioventricular reciprocating tachycardia circuit or suppressing a focal atrial tachycardia ectopic focus. Attempts can be made with a precordial thump (inducing an ectopic beat) or a vagal manoeuvre (increase vagal tone) to break the tachycardia, but in practice these are often ineffective. Even if a vagal manoeuvre only temporarily breaks a tachycardia, this may still help to reveal features to identify the arrhythmia. It is important to note that a precordial thump should not be attempted unless it is certain the rhythm is not a ventricular tachycardia, when it may induce fatal ventricular fibrillation.
Class IV antiarrhythmics (such as diltiazem) block calcium channels which slows depolarisation of atrioventricular nodal cells, thus slowing conduction in the atrioventricular node (Talajic et al, 1990). In doing so, the rapid conduction circuit of an orthodromic atrioventricular reciprocating tachycardia can be broken, resulting in spontaneous return to sinus rhythm. In the case of a focal atrial tachycardia, diltiazem can also block some of the premature beats from reaching the ventricles or suppress the atrial ectopic focus by altering myocyte calcium handling. Class I anti-arrhythmics (such as lidocaine), have been shown to be effective at terminating accessory pathway-mediated SVTs in dogs (Johnson et al, 2006; Wright et al, 2019), probably by altering conduction in the ventricles or accessory pathway itself (because it is also comprised of ventricular myocardium). However, the exact mechanism is still unknown. In this case, lidocaine was administered for control of a multiform ventricular tachycardia rather than treatment of the SVT. Generally, only haemodynamically unstable (weak or hypotensive) SVTs require immediate IV anti-arrhythmic treatment – cardiovascularly stable patients (usually those with lower rate tachycardias) can be managed with oral medications (Figure 7). It is worth noting that IV diltiazem is only available by special import to the UK. Verapamil (another class IV anti-arrhythmic) is more readily available, but is very negatively inotropic and long-lasting, so caution is advised with its use.
Following emergency medical stabilisation, an electrophysiology study and radiofrequency catheter ablation should be considered if an accessory pathway is suspected. Radiofrequency catheter ablation involves selective destruction of the accessory pathway, thereby eliminating the re-entrant circuit. Success rates are generally excellent, with first attempt success in up to 98% of cases (Santilli et al, 2018; Wright et al, 2018). However, the number of veterinary hospitals capable of performing radiofrequency catheter ablation are extremely limited because of the equipment and expertise required. For cases where radiofrequency catheter ablation is not an option, medical treatment is usually successful but sometimes requires combinations of anti-arrhythmics to maintain sinus rhythm.
This case demonstrates the successful emergency treatment and long-term medical management of an SVT in a young Labrador Retriever. Owing to the patient signalment and characteristic ECG findings, an accessory pathway and atrioventricular reciprocating tachycardia was a differential diagnosis. However, without an electrocardiographic study for a definitive diagnosis, this cannot be certain, and a focal atrial tachycardia with aberrant conduction or incidental accessory pathway that responded to medical management is an alternative possibility.
KEY POINTS
- Supraventricular tachycardias are fast heart rhythms originating from the sinus node, atrial tissue, or atrioventricular junctional tissue.
- Labrador Retrievers are predisposed to accessory pathways and the diagnosis of a supraventricular tachycardia should raise suspicion for a possible accessory pathway causing an atrioventricular reciprocating tachycardia.
- Characteristic electrocardiographic features can aid in the diagnosis of tachyarrhythmias
- Emergency medical management of supraventricular tachycardias involves diltiazem to slow conduction through the atrioventricular node to break the re-entrant circuit.
- Electrophysiological studies and radiofrequency catheter ablation are required to definitively diagnose, and ultimately cure, accessory pathways and associated tachyarrhythmias