4th May 2025

Cardiac Arrhythmias

Supraventricular Tachycardia

The term Supraventricular Tachycardia (SVT) refers to any tachycardia that is not ventricular in origin. SVT is an umbrella term which includes Atrioventricular Nodal Reentry Tachycardia (AVNRT) and Atrioventricular Reentry Tachycardia (AVRT). AVNRT is used synonymously with the term SVT.

Atrioventricular Nodal Reentry Tachycardia (AVNRT)

AVNRT typically occurs in younger people. It is usually paroxysmal and may occur spontaneously. It may have a trigger such as alcohol intoxication, nicotine, stress, concurrent illness, caffeine or stimulants such as amphetamines.

Brief pathophysiology of ‘Slow-Fast AVNRT’

AVNRT results from having dual AV nodal pathways within the AV node itself. There is a fast pathway which conducts rapidly but has a long refractory period, and there is a slow pathway which conducts slowly but a short refractory period. During normal sinus rhythm, electrical impulses travel down both pathways simultaneously and cancel each other out.

However, a premature atrial contraction disrupts this as while the fast pathway is still in a refractory period, electrical impulses would then have to solely travel down the slow pathway as it is no longer in refractory period. By the time the premature impulses reach the distal end of the slow pathway, the fast pathway is no longer in a refractory period which allows impulses to travel retrogradely up the fast pathway.

Hence, a ‘re-entrant’ circuit is created as impulses are now continuously cycling around both pathways activating the bundle of His anterogradely and the atria retrogradely.

Clinical manifestations

Symptoms arise from the tachycardia generated and they include:

Palpitations
Chest pain
Light-headedness or dizziness
Syncope or presyncope
Breathlessness
Anxiety

ECG features

P waves hidden within QRS complexes
Late P waves resulting in Pseudo R wave/second R wave

ECG showing AVNRT

Image Source: Wikimedia Commons (2020), ECG AVNRT, Licenced under a creative commons licence. Available for free at: https://commons.wikimedia.org/wiki/File:ECG_AVNRT_181_bpm.jpg (Accessed: 1 May 2025).

Medical management

The principle in managing AVNRT is inhibiting AV nodal activity as this is the driver for the tachycardia. This can be achieved via vagal manoeuvres and medication. Vagal manoeuvres work by increasing vagal parasympathetic tone. DCCV is rarely required unless the patient is haemodynamically unstable or refractory to medical cardioversion.

1st line therapy: Vagal manoeuvres:

Blowing into an empty 10ml syringe
Carotid sinus massage (contraindicated in carotid disease due to the risk of stroke)
Modified Valsalva Manoeuvre: head down, legs up

2nd line therapy: Adenosine

This is given IV 6mg, then 12mg and then followed by 18mg
Contraindicated in asthma due to bronchoconstriction
Safe to give in pregnancy as does not significantly cross the placenta
Dipyridamole enhances the effect of adenosine, whereas Theophylline is a potent adenosine receptor antagonist

3rd line therapy: Beta blockers or Calcium channel blockers

IV Metoprolol or Verapamil
If 3rd line treatment ineffective, DCCV should be attempted with appropriate sedation and anaesthetic support

Accessory Pathways

Background

Wolff-Parkinson-White (WPW) Syndrome is caused by an accessory conduction pathway between the atria and the ventricles leading to an atrioventricular reentry tachycardia (AVRT). This accessory pathway is also called the bundle of Kent which allows electrical impulses generated by the Sino-atrial node to bypass the AV node. This accessory pathway allows electrical impulses to be conducted quicker than the AV node, resulting in a shorter PR interval which brings about the characteristic Delta wave seen in ECGS. WPW has an incidence of 0.1-0.3 per 1000.

accessory pathway in WPW Syndrome

Image Source: Wikimedia Commons (2011). Wolf, Parkinson and White. Licenced under a creative commons licence. Available for free at: https://commons.wikimedia.org/w/index.php?search=wolf+parkinson+white&title=Special:MediaSearch&go=Go&type=image (Accessed: 1 May 2025).

Associations with WPW syndrome

Hypertrophic Cardiomyopathy (HCM)
Mitral valve prolapse
Ebstein’s Anomaly

Clinical manifestations

Most patients who present with an arrhythmia will present with one or more of the following symptoms:

Palpitations
Chest pain
Light-headedness or dizziness
Syncope or presyncope
Sudden cardiac death

ECG features in WPW

Short PR interval <120ms
Slurred upstroke of a wide QRS complex – ‘delta wave’
Prolonged QRS >110ms

CG features of WPW in sinus rhythm

Image Source: Wikimedia Commons (2020). Delta Wave, Licensed under a creative commons licence. Available for free at: https://upload.wikimedia.org/wikipedia/commons/thumb/e/e9/DeltaWave09.JPG/640px- DeltaWave09.JPG (Accessed: 1 May 2025).

Arrhythmias associated with WPW

Atrial Fibrillation is seen in about 10-30% of patients with WPW syndrome. The presence of an accessory pathway in WPW allows the rapid conduction of atria signals to the ventricles as it bypasses the AV node. This results in rapid ventricular rates that may result in VT or VF.

Medical management

The general principle in managing patients with WPW is to prevent electrical impulses from travelling through the accessory pathway. Hence any AV nodal blocking drugs such as Adenosine, Beta blockers and Calcium channel blockers are contraindicated as blocking the AV node will allow uncontrolled electrical impulses down the accessory pathway potentially leading to VT/VF and cardiac arrest.

Drugs used to treat WPW include

Flecainide (In the absence of structural heart disease)
Amiodarone
Procainamide

Surgical management

Definitive treatment options include Catheter ablation or Surgical ablation. Efficacy of catheter- based ablation is around 85%to 95% but this is mainly dependent on the location of the accessory pathway.

Wide QRS Complex Tachycardias

Ventricular Tachycardia

Background

Ventricular tachycardia (VT) is a broad complex tachycardia originating from the ventricles. It is also defined by having a cardiac rhythm with a rate >100bpm and a QRS width >120ms.

VT occurs as there are regions of slowed conduction in the ventricle allowing the opportunity to develop reentrant arrhythmias. This process can be caused by any structural abnormality in the ventricle. In post myocardial infarction patients, ventricular scars from infarction or fibrosis provide a substrate for this process.

Risk factors for developing Monomorphic VT

Coronary ischaemic heart disease (especially prior MI)
Hypertrophic cardiomyopathy
Dilated cardiomyopathy
Arrhythmogenic right ventricular cardiomyopathy

ECG features

ECG Wide QRS complex Tachycardia

Image Source: Wikimedia Commons (2020). Lead Generated Ventricular Tachycardia, Licensed under a creative commons licence. Available for free at: https://upload.wikimedia.org/wikipedia/commons/thumb/4/45/12_lead_generated_ventricular_tachycardia.JPG/640px-12_lead_generated_ventricular_tachycardia.JPG (Accessed 1 May 2025).

Features suggestive of VT rather than SVT with aberrancy

RSR’ complexes with a taller “left rabbit ear”
Very broad QRS complex >160ms
AV dissociation
Positive or negative concordance in precordial leads
Fusion or capture beats
Marked left axis deviation
Absence of typical RBBB or LBBB morphology

Even with the use of algorithms, differentiating VT vs SVT with aberrancy can still be challenging. Therefore, in an emergency, broad complex tachycardias are to be treated as ventricular in origin.

* Verapamil should NOT be given in a broad complex Tachycardia, as it may precipitate Ventricular Fibrillation in patients with VT * As this may precipitate electrical impulses travelling down an aberrant pathway in SVT’s with a bundle branch block.

Medical management

Unstable patients

Synchronised DCCV

Stable patients

Amiodarone
Lidocaine
Procainamide

Polymorphic VT

Background

Polymorphic VT is defined as an unstable rhythm with a continuously varying QRS complex morphology. A subtype of polymorphic VT is Torsades de Pointes (Twisting of the points) and is often precipitated by prolongation of the QT interval. Torsades de Pointes if left untreated can lead to Ventricular fibrillation.

Image Source: Wikimedia Commons (2011). Torsades converted by AICD ECG Strip Lead, Licensed under a creative commons licence. Available for free at: https://upload.wikimedia.org/wikipedia/commons/thumb/e/ed/Torsades_converted_by_AICD_ECG_strip_Lead_II.JPG/640px-Torsades_converted_by_AICD_ECG_strip_Lead_II.JPG (Accessed: 1 May 2025).

Causes of Long QT interval

Congenital

Jervell-Lange-Nielsen syndrome (deafness)
Romano-Ward syndrome (no deafness)
Long QT syndrome

Drugs

Sotalol, Amiodarone
SSRIs (Citalopram)
Tricyclic antidepressants (Amitriptyline)
Antipsychotics (Haloperidol, Quetiapine, Risperidone)
Azithromycin
Ondansetron
Methadone

Other

Subarachnoid haemorrhage
Hypokalaemia
Hypomagnesaemia
Hypocalcaemia
MI
Myocarditis

Medical management

Unstable patients (haemodynamic compromise) need urgent shocking as for patients with monomorphic VT
Pharmacological management is the same as that of monomorphic VT
Correct underlying cause
IV Magnesium Sulphate

Ventricular Fibrillation

VF is defined as rapid disorganised ventricular activity. This results in no uniform ventricular contractions and as a result leads to loss of cardiac output.

ECG shows a rapid ventricular rate of 300-400bpm. Over time, the amplitude of these irregular deflections decreases. (Coarse VF to fine VF).

ECG showing VF

Image Source: Wikimedia Commons (2020). Ventricular Fibrillation, Licensed under a creative commons licence. Available for free at: https://upload.wikimedia.org/wikipedia/commons/thumb/f/f1/Ventricular_fibrillation.png/640px-Ventricular_fibrillation.png (Accessed 1 May 2025).

Management

Prompt defibrillation
Reversal of underlying cause * Tricyclic Antidepressant overdose is treated with Sodium Bicarbonate solution*

Cardiac Arrest

In cardiac arrest situations, following a systematic approach is crucial. Resuscitation council UK has given clear Advanced Life Support guidelines in cardiac arrest situations.

Once VF/Pulseless VT is identified on the monitor, the treatment would be delivering an immediate shock of 150-200J for the first shock. After 3 shocks via the defibrillator, Amiodarone 300mg IV and Adrenaline 1mg IV is given alongside cardio-pulmonary resuscitation.

Tachyarrhythmia algorithm