Arrhythmias

Re-entry occurs when there is a unidirectional block in a branch of the electrical circuit that can only be passed by passing on the other side of the circuit. If the previously blocked area becomes excitable (unblocked) by the time the impulse arrives again, it will pass it and circle back, creating a loop. This loop will continue until it encounters tissue that cannot be depolarised.

Re-entry can be classified as either anatomical or functional re-entry:

• Anatomical re-entry - the blocking in this instance is an anatomical structure, such as the tricuspid valve. In this instance, the impulse will circle around the myocardial cells around the tricuspid valve. These are fixed and stable re-entry circuits.

• Functional re-entry - in this case there is no anatomical defining border of the blockage. Instead the blockage is due to variations in the electrophysiology of some myocardial cells which are not excitable. This will cause the circuit to circulate around it and emit impulses into the core (inwards) of the circuit and also outwards. The core of the circuit then becomes overwhelmed and refractory to depolarisation, thus becoming the barrier around which the circuit continues to propagate itself. These re-entry circuits are more unstable and may give rise to further re-entry circuits.

Re-entry is responsible for:

1. Paroxysmal SVTs
1. AV re-entrant (AVRT) - in AVRT there is an anatomical accessory pathway known as the bundle of Kent which creates a pathway between the atria and ventricles. This is what is seen in Wolff-Parkinson-White syndrome. The bundle of Kent can create 1 of 2 pathways:
1. Orthodromic AVRT - orthodromic means that the impulse is travelling in the normal direction of the nerve fibre, i.e. from the AV node → ventricles. As the ventricles contract at the same time, it presents as a narrow complex tachycardia.
2. Antidromic AVRT - antidromic means that the impulse is travelling in the opposite direction of the nerve fibre, i.e. from ventricles → AV node. As the ventricles depolarise at different times, it presents as a widened QRS complex tachycardia.
2. AV nodal re-entry (AVNRT) - in AVNRT, it is usually scarring or fibrosis of myocardial tissue that leads to a disturbance in the regular conduction of the myocardium. This creates 2 pathways, a slow pathway and a fast pathway. The difference in the pathway speeds means that the fast pathway becomes refractory while the slow pathway depolarises. The impulse from the slow pathway will then travel back up the fast pathway when it becomes excitable, thus establishing a re-entry circuit.

2. Atrial flutter

Atrial flutter is most often caused by an anatomical re-entrant circuit that is facilitated by the cavotricuspid isthmus which enables the action potential to return to the atria.

3. Atrial fibrillation

The entirety of the pathophysiology of AF can be found in the page on atrial fibrillation. In short, it is due to multiple foci that spontaneously fire action potentials, creating re-entry circuits that enter the AV node and travel to the ventricles.

4. Ventricular tachycardia

This is from a single focus found in the ventricles that fires an action potential which creates a re-entry circuit. Ventricular tachycardias may be monomorphic (MVT) or polymorphic (PVT). A specific type of PVT is Torsades de Pointes (TdP) which has a distinct “twisting” morphology. We will discuss these in depth later on.

5. Ventricular fibrillation

Similar to AF, where there are multiple foci firing action potentials, creating multiple re-entrant circuits. However, VF is much more dangerous and is fatal.

This is a regular, narrow complex tachycardia with the focus originating in the SA node (as it normally should be). It is defined as a sinus rhythm with a resting heart rate >100bpm in adults.

It is the most common type of tachycardia as it is a normal physiological response to stimuli.

What are some causes of sinus tachycardia?

These are all “appropriate” causes of sinus tachycardia.

Inappropriate sinus tachycardia is a primary condition in which there is persistent sinus tachycardia without an underlying cause.

🧰 Management

• Appropriate sinus tachycardia → manage underlying cause.
• Inappropriate sinus tachycardia → generally we can leave it alone. However, we can also give ß-blockers or ivabradine which have a negative chronotropic effect on the heart.

Atrial flutter is a type of SVT with a highly organised electrical circuit within the right atrium. It’s pathophysiology is as described above (re-entry due to the cavotricuspid isthmus). The direction in which the circuit travels can be either clockwise or anti-clockwise (anti-clockwise is more common).

In atrial flutter the atria contract at very high rates. However, it is important to note that the heart rate we count on an ECG is reflective of the ventricular contractions (as we typically count the R-waves which depicts ventricular apex depolarisation). In atrial flutter, the atrial rate typically varies from 250-320bpm.

The ventricular rate is not the same, however. It is only a fraction of the atrial rate, and the rate that is conducted through the AV node is dependent on the degree of “AV block” associated with it. The term AV block in this context is actually wrong as the AV node functions normally. It simply refers to the physiological response that the AV node exhibit is which prevents passage of all the electrical impulses from the atria to the ventricles. This is due to the relatively long refractory period that the AV node has.

Let’s look at an example:

If the atrial rate is contracting at 300bpm:

• 2:1 block - the ventricular rate will be 300 ÷ 2 = 150bpm. 2:1 block is the most common AV block associate with atrial flutter.
• 3:1 block - the ventricular rate will be 300 ÷ 3 = 100bpm.
• 4:1 block - the ventricular rate will be 300 ÷ 4 = 75bpm.

3:1 block and 4:1 block usually occur in the setting of underlying cardiac disease or with medications that block the AV node (ABCD - adenosine, ß-blockers, CCBs, digoxin). Sometimes atrial flutter may not be as regular. This is known as atrial flutter with variable block (for example, there is 3:1 block followed by 2:1 block).

⚠️ Causes

• In most patients it will occur due to acute illness.
• Treating patients with Wolff-Parkinson-White syndrome with AV nodal blocking medication can cause 1:1 flutter.
• Atrial fibrillation - it may convert to atrial flutter due to alterations in the atrial activity. The ECG may show fluctuations between both rhythms in the same patient.

🚨 Conversely, atrial flutter may lead to atrial fibrillation due to stretching of the atria which can then precipitate atrial fibrillation.

🧰 Management

🔪 If it is chronic atrial flutter or refractory atrial flutter then the definitive management is ablation of the cavotricuspid isthmus which yields a 90% success rate. It is important to note that ablation does not prevent the patient from developing atrial fibrillation.

AVNRT is a paroxysmal, narrow-complex, regular tachycardia with a heart-rate of 140-280bpm. The term paroxysmal refers to spontaneous attacks that may reoccur again and again. It may be spontaneous or it may be provoked (with exertion, caffeine, alcohol, ß-agonists, sympathomimetics).

It is the most common cause of palpitations with normal heart structures and is not life-threatening.

There are 3 variants of AVNRT :

1. Slow-fast AVNRT - makes up 80-90% of cases.
2. Fast-slow AVNRT
3. Slow-slow AVNRT

We won’t be discussing the features of fast-slow and slow-slow in the ECG findings, rather focusing on slow-fast AVNRT.

⚠️ Risk factors

• Female gender - about 75% of cases occur in women.
• Chronic heart disease - although it may occur in young and healthy patients.

😷 Presentation

• Rapid, regular palpitations
• Presyncope/syncope
• Chest pain
• Dyspnoea
• Anxiety
• Polyuria - this is rare but may be due to elevated atrial pressures which can cause atrial natriuretic peptide to be released (increasing natriuresis).