Arrhythmias

Question 1

These are the four possible rhythms that you will see in a pulseless unresponsive patient. They can be categorised into:

Answer 1

shockable (meaning defibrillation may be effective) and non-shockable (meaning defibrillation will not be effective and should not be used).

Shockable rhythms:
- Ventricular tachycardia
- Ventricular fibrillation

Non-shockable rhythms:
- Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse)
- Asystole (no significant electrical activity)

Question 2

Tachycardia management in the unstable patient:

Answer 2

Consider up to 3 synchronised shocks
Consider an amiodarone infusion

Question 3

Tachycardia management in a stable patient with a narrow QRS complex?

Answer 3

Narrow complex (QRS < 0.12s)

Atrial fibrillation – rate control with a beta blocker or diltiazem (calcium channel blocker)

Atrial flutter – control rate with a beta blocker

Supraventricular tachycardias – treat with vagal manoeuvres and adenosine

Question 4

Tachycardia management in a stable patient with a broad QRS complex?

Answer 4

Broad complex (QRS > 0.12s)

Ventricular tachycardia or unclear – amiodarone infusion

If known SVT with bundle branch block treat as normal SVT

If irregular may be AF variation – seek expert help

Question 5

What is atrial flutter?

Answer 5

Normally the electrical signal passes through the atria once, simulating a contraction then disappears through the AV node into the ventricles.

Atrial flutter is caused by a “re-entrant rhythm” in either atrium. This is where the electrical signal re-circulates in a self-perpetuating loop due to an extra electrical pathway.

The signal goes round and round the atrium without interruption. This stimulates atrial contraction at 300 bpm.

The signal makes its way into the ventricles every second lap due to the long refractory period to the AV node, causing 150 bpm ventricular contraction. It gives a “sawtooth appearance” on ECG with P wave after P wave.

Question 6

Associated Conditions of atrial flutter?

Answer 6

Hypertension
Ischaemic heart disease
Cardiomyopathy
Thyrotoxicosis

Question 7

Treatment of atrial flutter?

Answer 7

Treatment is similar to atrial fibrillation:

• Rate/rhythm control with beta blockers or cardioversion
• Treat the reversible underlying condition (e.g. hypertension or thyrotoxicosis)
• Radiofrequency ablation of the re-entrant rhythm
• Anticoagulation based on CHA2DS2VASc score

Question 8

What are supraventricular tachycardias (SVT)

Answer 8

Supraventricular tachycardia (SVT) is caused by the electrical signal re-entering the atria from the ventricles.

Normally the electrical signal in the heart can only go from the atria to the ventricles. In SVT the electrical signal finds a way from the ventricles back into the atria.

Once the signal is back in the atria it travels back through the AV node and causes another ventricular contraction.

This causes a self-perpetuating electrical loop without an end point and results in fast narrow complex tachycardia (QRS < 0.12). It looks like a QRS complex followed immediately by a T wave, QRS complex, T wave and so on.

Question 9

Paroxysmal SVT describes a situation where?

Answer 9

SVT reoccurs and remits in the same patient over time.

Question 10

There are three main types of SVT based on the source of the electrical signal:

Answer 10

“Atrioventricular nodal re-entrant tachycardia” is when the re-entry point is back through the AV node.

“Atrioventricular re-entrant tachycardia” is when the re-entry point is an accessory pathway (Wolff-Parkinson-White syndrome).

“Atrial tachycardia” is where the electrical signal originates in the atria somewhere other than the sinoatrial node. This is not caused by a signal re-entering from the ventricles but instead from abnormally generated electrical activity in the atria. This ectopic electrical activity causes an atrial rate of >100bpm.

Question 11

Acute Management of Stable patients with SVT

Answer 11

When managing SVT take a stepwise approach trying each step to see whether it works before moving on. Make sure they are on continuous ECG monitoring.

• Valsalva manoeuvre. Ask the patient to blow hard against resistance, for example into a plastic syringe.
• Carotid sinus massage. Massage the carotid on one side gently with two fingers.
• Adenosine
• An alternative to adenosine is verapamil (calcium channel blocker)
• Direct current cardioversion may be required if the above treatment fails

Question 12

Adenosine works by:

Answer 12

slowing cardiac conduction primarily though the AV node. It interrupts the AV node / accessory pathway during SVT and “resets” it back to sinus rhythm. It needs to be given as a rapid bolus to ensure it reaches the heart with enough impact to interrupt the pathway. It will often cause a brief period of asystole or bradycardia that can be scary for the patient and doctor, however it is quickly metabolised and sinus rhythm should return.

Question 13

A few key points on administering adenosine:

Answer 13

Avoid if patient has asthma / COPD / heart failure / heart block / severe hypotension

Warn patient about the scary feeling of dying / impending doom when injected

Give as a fast IV bolus into a large proximal cannula (e.g. grey cannula in the antecubital fossa)

Initially 6mg, then 12mg and further 12mg if no improvement between doses

Question 14

Long Term Management of patients with paroxysmal SVT

Answer 14

When patients develops recurrent episodes of SVT then measures can be taken to prevent these episodes. The options are:

• Medication (beta blockers, calcium channel blockers or amiodarone)
• Radiofrequency ablation

Question 15

Wolff-Parkinson White Syndrome is caused by?

Answer 15

an extra electrical pathway connecting the atria and ventricles. Normally there is only one pathway connecting the atria and ventricles called the atrio-ventricular node. The extra pathway that is present in Wolff-Parkinson White Syndrome is often called the Bundle of Kent.

Question 16

The definitive treatment for Wolff-Parkinson White syndrome is?

Answer 16

radiofrequency ablation of the accessory pathway.

Question 17

ECG Changes in Wolf-Parkinson White Syndrome?

Answer 17

Short PR interval (< 0.12 seconds)

Wide QRS complex (> 0.12 seconds)

“Delta wave” which is a slurred upstroke on the QRS complex

Question 18

Note: If the person has a combination of atrial fibrillation or atrial flutter and WPW there is a risk that the chaotic atrial electrical activity can pass through the accessory pathway into the ventricles causing a polymorphic wide complex tachycardia. Most antiarrhythmic medications (beta blockers, calcium channel blockers, adenosine etc) increase the risk of this by reducing conduction through the AV node and therefore promoting conduction through the accessory pathway – therefore they are contraindicated in patients with WPW that develop atrial fibrillation or flutter.

Question 19

What is Radiofrequency Ablation (RFA)?

Answer 19

Catheter ablation is performed in a electrophysiology laboratory, often called a “cath lab”. It involves local or general anaesthetic, inserting a catheter in to the femoral veins and feeding a wire through the venous system under xray guidance to the heart. Once in the heart it is placed against different areas to test the electrical signals at that point. This way the operator can hopefully find the location of any abnormal electrical pathways. The operator may try to induce the arrhythmia to make the abnormal pathways easier to find. Once identified, radiofrequency ablation (heat) is applied to burn the abnormal area of electrical activity. This leaves scar tissue that does not conduct the electrical activity. The aim is to remove the source of the arrhythmia.

Question 20

Radiofrequency ablation (RFA) can be curative for certain cases of arrhythmia caused by abnormal electrical pathways, including:

Answer 20

Atrial Fibrillation
Atrial Flutter
Supraventricular Tachycardias
Wolff-Parkinson-White Syndrome

Question 21

Torsades de pointes is a type of?

Answer 21

polymorphic (multiple shape) ventricular tachycardia

It translates from French as “twisting of the tips”, describing the ECG characteristics. It looks like normal ventricular tachycardia on an ECG however there is an appearance that the QRS complex is twisting around the baseline. The height of the QRS complexes progressively get smaller, then larger then smaller and so on. It occurs in patients with a prolonged QT interval.

Question 22

Torsades de pointes pathophysiology?

Answer 22

It looks like normal ventricular tachycardia on an ECG however there is an appearance that the QRS complex is twisting around the baseline. The height of the QRS complexes progressively get smaller, then larger then smaller and so on. It occurs in patients with a prolonged QT interval.

A prolonged QT interval is the ECG finding of prolonged repolarisation of the muscle cells in the heart after a contraction. Depolarisation is the electrical process that leads to the heart contraction. Repolarisation is a period of recovery before the heart muscle cells (myocytes) are ready to depolarise again. Waiting a longer time for repolarisation can result in random spontaneous depolarisation in some areas of heart myocytes. These abnormal spontaneous depolarisations prior to repolarisation are known as “afterdepolarisations”. These depolarisations spread throughout the ventricle, leading to a ventricular contraction prior to proper repolarisation occurring. When this occurs and the ventricles continue to stimulate recurrent contractions without normal repolarisation it is called Torsades de pointes.

When a patient develops Torsades de pointes it will either terminate spontaneously and revert back to sinus rhythm or progress in to ventricular tachycardia. Usually they are self limiting but if they progress to VT it can lead to a cardiac arrest.

Question 23

Causes of Prolonged QT

Answer 23

Long QT Syndrome (inherited)

Medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide antibiotics)

Electrolyte Disturbance (hypokalaemia, hypomagnesaemia, hypocalcaemia)

Question 24

Acute Management of Torsades de pointes

Answer 24

Correct the cause (electrolyte disturbances or medications)

Magnesium infusion (even if they have a normal serum magnesium)

Defibrillation if VT occurs

Question 25

Long Term Management of Prolonged QT Syndrome

Answer 25

Avoid medications that prolong the QT interval
Correct electrolyte disturbances
Beta blockers (not sotalol)
Pacemaker or implantable defibrillator

Question 26

What are ventricular ectopics?

Answer 26

premature ventricular beats caused by random electrical discharges from outside the atria. Patients often present complaining of random, brief palpitations (“an abnormal beat”). They are relatively common at all ages and in healthy patients however they are more common in patients with pre-existing heart conditions (e.g. ischaemic heart disease or heart failure).

They can be diagnosed by ECG and appear as individual random, abnormal, broad QRS complexes on a background of a normal ECG.

Question 27

what is Bigeminy?

Answer 27

This is where the ventricular ectopics are occurring so frequently that they happen after every sinus beat. The ECG looks like a normal sinus beat followed immediately by an ectopic, then a normal beat, then ectopic and so on.

Question 28

Management of ventricular ectopic beats?

Answer 28

Check bloods for anaemia, electrolyte disturbance and thyroid abnormalities

Reassurance and no treatment in otherwise healthy people

Seek expert advice in patients with background heart conditions or other concerning features or findings (e.g. chest pain, syncope, murmur, family history of sudden death)

Question 29

First degree heart block?

Answer 29

First-degree heart block occurs where there is delayed atrioventricular conduction through the AV node. Despite this, every atrial impulse leads to a ventricular contraction, meaning every p waves results in a QRS complex. On an ECG this presents as a PR interval greater than 0.20 seconds (5 small or 1 big square).

Question 30

Second degree heart block

Answer 30

Second-degree heart block is where some of the atrial impulses do not make it through the AV node to the ventricles. This means that there are instances where p waves do not lead to QRS complexes. There are several patterns of second-degree heart block described below:

Question 31

Wenckebach’s phenomenon (Mobitz Type 1)

Answer 31

This is where the atrial imputes becomes gradually weaker until it does not pass through the AV node. After failing to stimulate a ventricular contraction the atrial impulse returns to being strong. This cycle then repeats.

On an ECG this will show up as an increasing PR interval until the P wave no longer conducts to ventricles. This culminates in absent QRS complex after a P wave. The PR interval then returns to normal but progressively becomes longer again until another QRS complex is missed. This cycle repeats itself.

Question 32

Mobitz Type 2

Answer 32

This is where there is intermitted failure or interruption of AV conduction. This results in missing QRS complexes. There is usually a set ratio of P waves to QRS complexes, for example 3 P waves to each QRS complex would be referred to as a 3:1 block. The PR interval remains normal. There is a risk of asystole with Mobitz Type 2.

Question 33

2:1 Block

Answer 33

This is where there are 2 P waves for each QRS complex. Every second p wave is not a strong enough atrial impulse to stimulate a QRS complex. It can be caused by Mobitz Type 1 or Mobitz Type 2 and it is difficult to tell which.

Question 34

Third Degree Heart Block

Answer 34

This is referred to as complete heart block. This is no observable relationship between P waves and QRS complexes. There is a significant risk of asystole with third-degree heart block.

Question 35

Treatment for Bradycardias / AV Node Blocks: stable patient?

Answer 35

Observe

Question 36

Treatment for Bradycardias / AV Node Blocks: Unstable or risk of asystole (i.e. Mobitz Type 2, complete heart block or previous asystole)?

Answer 36

First line:
- Atropine 500mcg IV

No improvement:
- Atropine 500mcg IV repeated (up to 6 doses for a total to 3mg)
- Other inotropes (such as noradrenalin)
- Transcutaneous cardiac pacing (using a defibrillator)

Question 37

Treatment for Bradycardias/AV node blocks: In patients with high risk of asystole (i.e. Mobitz Type 2, complete heart block or previous asystole):

Answer 37

Temporary transvenous cardiac pacing using an electrode on the end of a wire that is inserted into a vein and fed through the venous system to the right atrium or ventricle to stimulate them directly

Permanent implantable pacemaker when available

Question 38

Note. Atropine is an antimuscarinic medication so…?

Answer 38

works by inhibiting the parasympathetic nervous system. This leads to side effects of pupil dilatation, urinary retention, dry eyes and constipation.