Arrythmias Flashcards
Pacemakers
Pacemakers deliver controlled electrical impulses to specific areas of the heart to improve heart function. They consist of a pulse generator (the pacemaker box) and the pacing leads, which carry electrical impulses to the relevant part of the heart. The box is implanted under the skin (most commonly in the left anterior chest wall). The wires fed into the left subclavian vein and through the venous system to the relevant chambers of the heart.
Patients with a pacemaker are followed up regularly to download information from the pacemaker, check everything is working ok, and decide when the battery needs replacing. They are given an identity card and bracelet.
Pacemakers do not interact with most day-to-day electrical activities. However, they may be incompatible with MRI scans (due to powerful magnets), TENS machines (used for pain management) and diathermy (used during surgical procedures). Many modern pacemakers are MRI-compatible. Some smartphones may interact with pacemakers if held too close. Devices with strong magnets (e.g., handheld security scanners at airports) can affect the pacemaker function.
TOM TIP: Pacemakers must be removed before cremation in deceased patients. On the cremation form, one of the most critical tasks is to confirm whether the body has a pacemaker and whether it has been removed. You may hear stories about pacemakers “blowing up” crematoriums (this is a dramatic exaggeration, but they can explode, causing significant damage).
Indications
Indications for a pacemaker include:
Symptomatic bradycardias (e.g., due to sick sinus syndrome)
Mobitz type 2 heart block
Third-degree heart block
Atrioventricular node ablation for atrial fibrillation
Severe heart failure (biventricular pacemakers)
Single-chamber
Single-chamber pacemakers have leads in a single chamber, either the right atrium or the right ventricle.
They are placed in the right atrium if the issue is with the sinoatrial node and conduction through the atrioventricular node is normal. This way, they stimulate depolarisation in the right atrium, and this electrical activity passes to the left atrium and ventricles.
They are placed in the right ventricle if conduction through the atrioventricular node is abnormal. They stimulate the ventricles directly.
Dual-chamber
Dual-chamber pacemakers have leads in both the right atrium and right ventricle. The pacemaker coordinates the contraction of the atria and ventricles.
Biventricular (Triple-Chamber) Pacemaker
Biventricular pacemakers have leads in the right atrium, right ventricle and left ventricle.
They are usually in patients with severe heart failure. They coordinate the contraction of these chambers to optimise heart function. This is referred to as cardiac resynchronisation therapy (CRT).
Implantable Cardioverter Defibrillators
Implantable cardioverter defibrillators (ICDs) continually monitor the heart and apply a defibrillator shock if they identify ventricular tachycardia or ventricular fibrillation.
Implantable cardioverter defibrillators are used in patients at risk of ventricular tachycardia or fibrillation, for example:
Previous cardiac arrest
Hypertrophic obstructive cardiomyopathy
Long QT syndrome
ECG Changes
The pacemaker intervention can be seen as a sharp vertical line on all leads on the ECG trace. A line before each P wave indicates a lead in the atria. A line before each QRS complex indicates a lead in the ventricles. Therefore:
A line before either the P wave or QRS complex but not the other indicates a single-chamber pacemaker
A line before both the P wave and QRS complex indicates a dual-chamber pacemaker
TOM TIP: It is worth ensuring you can identify the type of pacemaker on an ECG, as this is common in exams.
Cardiac Arrest Rhythms
These are the four possible rhythms in a pulseless patient. They are either shockable (meaning defibrillation may be effective) or non-shockable (meaning defibrillation will not be effective).
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)
Narrow Complex Tachy
Narrow complex tachycardia refers to a fast heart rate with a QRS complex duration of less than 0.12 seconds. On a normal 25 mm/sec ECG, 0.12 seconds equals 3 small squares. Therefore, the QRS complex will fit within 3 small squares in narrow complex tachycardia.
There are four main differentials of a narrow complex tachycardia:
Sinus tachycardia (treatment focuses on the underlying cause)
Supraventricular tachycardia (treated with vagal manoeuvres and adenosine)
Atrial fibrillation (treated with rate control or rhythm control)
Atrial flutter (treated with rate control or rhythm control, similar to atrial fibrillation)
Patients with life-threatening features, such as loss of consciousness (syncope), heart muscle ischaemia (e.g., chest pain), shock or severe heart failure, are treated with synchronised DC cardioversion under sedation or general anaesthesia. Intravenous amiodarone is added if initial DC shocks are unsuccessful.
Broad Complex Tachy
Broad complex tachycardia refers to a fast heart rate with a QRS complex duration of more than 0.12 seconds or 3 small squares on an ECG.
The resuscitation guidelines break down broad complex tachycardia into:
Ventricular tachycardia or unclear cause (treated with IV amiodarone)
Polymorphic ventricular tachycardia, such as torsades de pointes (treated with IV magnesium)
Atrial fibrillation with bundle branch block (treated as AF)
Supraventricular tachycardia with bundle branch block (treated as SVT)
Patients with life-threatening features, such as loss of consciousness (syncope), heart muscle ischaemia (e.g., chest pain), shock or severe heart failure, are treated with synchronised DC cardioversion under sedation or general anaesthesia. Intravenous amiodarone is added if initial DC shocks are unsuccessful.
Atrial Flutter
Normally the electrical signal passes through the atria once, stimulating a contraction, then disappears through the atrioventricular node into the ventricles. Atrial flutter is caused by a re-entrant rhythm in either atrium. The electrical signal re-circulates in a self-perpetuating loop due to an extra electrical pathway in the atria. The signal goes round and round the atrium without interruption. The atrial rate is usually around 300 beats per minute.
The signal does not usually enter the ventricles on every lap due to the long refractory period of the atrioventricular node. This often results in two atrial contractions for every one ventricular contraction (2:1 conduction), giving a ventricular rate of 150 beats per minute. There may be 3:1, 4:1 or variable conduction ratios.
Atrial flutter gives a sawtooth appearance on the ECG, with repeated P wave occurring at around 300 per minute, with a narrow complex tachycardia.
Treatment is similar to atrial fibrillation, including anticoagulation based on the CHA2DS2-VASc score. Radiofrequency ablation of the re-entrant rhythm can be a permanent solution.
Prolonged QT
The QT interval is from the start of the QRS complex to the end of the T wave. The corrected QT interval (QTc) estimates the QT interval if the heart rate were 60 beats per minute. It is prolonged at:
More than 440 milliseconds in men
More than 460 milliseconds in women
A prolonged QT interval represents prolonged repolarisation of the heart muscle cells (myocytes) after a contraction. Depolarisation is the electrical process that leads to heart contraction. Repolarisation is a recovery period before the muscle cells are ready to depolarise again. Waiting a long time for repolarisation can result in spontaneous depolarisation in some muscle cells. These abnormal spontaneous depolarisations before repolarisation are known as afterdepolarisations. These afterdepolarisations spread throughout the ventricles, causing a contraction before proper repolarisation. When this leads to recurrent contractions without normal repolarisation, it is called torsades de pointes.
Torsades de pointes is a type of polymorphic ventricular tachycardia. It translates from French as “twisting of the spikes”, describing the ECG characteristics. On an ECG, it looks like standard ventricular tachycardia but with the appearance that the QRS complex is twisting around the baseline. The height of the QRS complexes gets progressively smaller, then larger, then smaller, and so on.
Torsades de pointes will terminate spontaneously and revert to sinus rhythm or progress to ventricular tachycardia. Ventricular tachycardia can lead to cardiac arrest.
Causes of prolonged QT include:
Long QT syndrome (an inherited condition)
Medications, such as antipsychotics, citalopram, flecainide, sotalol, amiodarone and macrolide antibiotics
Electrolyte imbalances, such as hypokalaemia, hypomagnesaemia and hypocalcaemia
Management of a prolonged QT interval involves:
Stopping and avoiding medications that prolong the QT interval
Correcting electrolyte disturbances
Beta blockers (not sotalol)
Pacemakers or implantable cardioverter defibrillators
Acute management of torsades de pointes involves:
Correcting the underlying cause (e.g., electrolyte disturbances or medications)
Magnesium infusion (even if they have normal serum magnesium)
Defibrillation if ventricular tachycardia occurs
Ventricular Ectopics
Ventricular ectopics are premature ventricular beats caused by random electrical discharges outside the atria. Patients often present complaining of random extra or missed beats. 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).
Ventricular ectopics appear as isolated, random, abnormal, broad QRS complexes on an otherwise normal ECG.
Bigeminy refers to when every other beat is a ventricular ectopic. The ECG shows a normal beat (with a P wave, QRS complex and T wave), followed immediately by an ectopic beat, then a normal beat, then an ectopic, and so on.
Management involves:
Reassurance and no treatment in otherwise healthy people with infrequent ectopics
Seeking specialist advice in patients with underlying heart disease, frequent or concerning symptoms (e.g., chest pain or syncope), or a family history of heart disease or sudden death
Beta blockers are sometimes used to manage symptoms
Heart Block
First-degree heart block occurs where there is delayed conduction through the atrioventricular node. Despite this, every atrial impulse leads to a ventricular contraction, meaning every P wave is followed by a QRS complex. On an ECG, first-degree heart block presents as a PR interval greater than 0.2 seconds (5 small or 1 big square).
Second-degree heart block is where some atrial impulses do not make it through the atrioventricular node to the ventricles. There are instances where P waves are not followed by QRS complexes. There are two types of second-degree heart block:
Mobitz type 1 (Wenckebach phenomenon)
Mobitz type 2
Mobitz type 1 (Wenckebach phenomenon) is where the conduction through the atrioventricular node takes progressively longer until it finally fails, after which it resets, and the cycle restarts. On an ECG, there is an increasing PR interval until a P wave is not followed by a QRS complex. The PR interval then returns to normal, and the cycle repeats itself.
Mobitz type 2 is where there is intermittent failure of conduction through the atrioventricular node, with an absence of QRS complexes following P waves. There is usually a set ratio of P waves to QRS complexes, for example, three P waves for each QRS complex (3:1 block). The PR interval remains normal. There is a risk of asystole with Mobitz type 2.
A 2:1 block is where there are two P waves for each QRS complex. Every other P wave does not stimulate a QRS complex. It can be difficult to tell whether this is caused by Mobitz type 1 or Mobitz type 2.
Third-degree heart block is also called complete heart block. There is no observable relationship between the P waves and QRS complexes. There is a significant risk of asystole with third-degree heart block.
Bradycardia
Bradycardia refers to a slow heart rate, typically less than 60 beats per minute. A heart rate under 60 can be normal in healthy fit patients without causing any symptoms. There is a long list of causes of bradycardia, including:
Medications (e.g., beta blockers)
Heart block
Sick sinus syndrome
Sick sinus syndrome encompasses many conditions that cause dysfunction in the sinoatrial node. It is often caused by idiopathic degenerative fibrosis of the sinoatrial node. It can result in sinus bradycardia, sinus arrhythmias and prolonged pauses.
Asystole refers to the absence of electrical activity in the heart (resulting in cardiac arrest). There is a risk of asystole in:
Mobitz type 2
Third-degree heart block (complete heart block)
Previous asystole
Ventricular pauses longer than 3 seconds
Management of unstable patients and those at risk of asystole involves:
Intravenous atropine (first line)
Inotropes (e.g., isoprenaline or adrenaline)
Temporary cardiac pacing
Permanent implantable pacemaker, when available
Options for temporary cardiac pacing are:
Transcutaneous pacing, using pads on the patient’s chest
Transvenous pacing, using a catheter, fed through the venous system to stimulate the heart directly
Atropine is an antimuscarinic medication and works by inhibiting the parasympathetic nervous system. Inhibiting the parasympathetic nervous system leads to side effects of pupil dilation, dry mouth, urinary retention and constipation.
Superventricular Tachycardia
Supraventricular tachycardia (SVT) refers to when abnormal electrical signals from above (supra-) the ventricles cause a fast heart rate (tachycardia).
Pathophysiology
Normally, the electrical signals of the heart start in the sinoatrial node. The sinoatrial node is the heart’s natural pacemaker, dictating when the heart beats. It is located at the junction between the superior vena cava and the right atrium. The electrical signal travels through the right and left atrium, causing the atria to contract. Then it travels through the atrioventricular (AV) node, which is the pathway between the upper part (atria) and lower part (ventricles) of the heart, down to the ventricles, causing the ventricles to contract. The electrical signal in the heart can only go in one direction, from the atria to the ventricles. Normally, electrical activity cannot travel from the ventricles to the atria.
Supraventricular tachycardia is caused by the electrical signal re-entering the atria from the ventricles. The electrical signal finds a way from the ventricles back into the atria. Once the signal is back in the atria, it again travels through the atrioventricular node to the ventricles, causing another ventricular contraction. This causes a self-perpetuating electrical loop without an endpoint, resulting in narrow complex tachycardia. It is described as a “narrow complex”, as the QRS complex has a duration of less than 0.12 seconds.
Paroxysmal SVT describes a situation where SVT reoccurs and remits in the same patient over time.
Narrow Complex Tachycardia
Narrow complex tachycardia is a fast heart rate with a QRS complex duration of less than 0.12 seconds. On a standard 25 mm/sec ECG, 0.12 seconds equals 3 small squares. Therefore, the QRS complex will fit within 3 small squares in SVT. On an ECG, SVT looks like a QRS complex followed immediately by a T wave, QRS complex, T wave and so on.
There are four main differentials of a narrow complex tachycardia. There are key ECG features that will help you differentiate these:
Sinus tachycardia
Supraventricular tachycardia
Atrial fibrillation
Atrial flutter
Sinus tachycardia will take the normal P wave, QRS complex and T wave pattern. Sinus tachycardia is not an arrhythmia and is usually a response to an underlying cause, such as sepsis or pain.
Atrial fibrillation can be identified on an ECG by:
Absent P waves
Narrow QRS complex tachycardia
Irregularly irregular ventricular rhythm (as opposed to SVT, which causes a regular rhythm)
In atrial flutter, the atrial rate is usually around 300 beats per minute and gives a saw-tooth pattern on the ECG. A QRS complex occurs at regular intervals depending on how often there is conduction from the atria. This often results in two atrial contractions for every one ventricular contraction, giving a ventricular rate of 150 beats per minute.
Supraventricular tachycardia looks like a QRS complex followed immediately by a T wave, then a QRS complex, then a T wave, and so on. There are P waves, but they are often buried in the T waves, so you cannot see them. It can be distinguished from atrial fibrillation by the regular rhythm and atrial flutter by the absence of a saw-tooth pattern.
It can be tricky to distinguish SVT from sinus tachycardia. SVT has an abrupt onset and a very regular pattern without variability. Sinus tachycardia has a more gradual onset and more variability in the rate. The history is also important, where sinus tachycardia usually has an explanation (e.g., pain or fever), while SVT can appear at rest with no apparent cause.
Sometimes it can be difficult to distinguish between the different causes, so always seek help from an experienced person when in doubt.
TOM TIP: SVT can cause a broad complex tachycardia if the patient also has a bundle branch block. Therefore, consider this differential in patients with tachycardia and wide QRS complexes. The most important thing to remember is that SVT causes a narrow complex tachycardia.
Types
There are three main types of SVT, based on the source of the abnormal electrical signal.
Atrioventricular nodal re-entrant tachycardia is where the re-entry point is back through the atrioventricular node. This is the most common type of SVT.
Atrioventricular re-entrant tachycardia is where the re-entry point is an accessory pathway. An additional electrical pathway, somewhere between the atria and the ventricles, lets electricity back through from the ventricles to the atria. Having an extra electrical pathway connecting the atria and ventricles is called 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 from abnormally generated electrical activity in the atria.
Wolff-Parkinson-White Syndrome
Wolff-Parkinson-White syndrome (WPW) is caused by an extra electrical pathway connecting the atria and ventricles. It is also called pre-excitation syndrome. Normally, only the atrioventricular (AV) node connects the atria and ventricles. The extra pathway in Wolff-Parkinson-White syndrome may be called the Bundle of Kent. The additional pathway allows electrical activity to pass between the atria and ventricles, bypassing the atrioventricular node. This electrical pathway might not cause any symptoms, or it might cause episodes of SVT.
ECG changes in Wolff-Parkinson-White syndrome are:
Short PR interval, less than 0.12 seconds
Wide QRS complex, greater than 0.12 seconds
Delta wave
The delta wave appears as a slurred upstroke in the QRS complex. It is caused by the electricity prematurely entering the ventricles through the accessory pathway.
The definitive treatment for Wolff-Parkinson-White syndrome is radiofrequency ablation of the accessory pathway.
In someone with 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, which is a life-threatening medical emergency. The heart rate can get above 200, or even 300, beats per minute, and ventricular fibrillation and cardiac arrest can follow. Most anti-arrhythmic medications (e.g., beta blockers, calcium channel blockers, digoxin and adenosine) increase this risk by reducing conduction through the AV node and promoting conduction through the accessory pathway. Therefore, they are contra-indicated in patients with WPW that develop atrial fibrillation or flutter.
Acute Management
Management here summarises the Resuscitation Council UK guidelines (2021) to help with exam preparation. Get experienced senior support and refer to local and national guidelines when managing patients.
The patient should have continuous ECG monitoring during management.
Management of supraventricular tachycardia in patients without life-threatening features involves a stepwise approach, trying each step to see whether it works before moving on.
Step 1: Vagal manoeuvres
Step 2: Adenosine
Step 3: Verapamil or a beta blocker
Step 4: Synchronised DC cardioversion
Patients with life-threatening features, such as loss of consciousness (syncope), heart muscle ischaemia (e.g., chest pain), shock or severe heart failure, are treated with synchronised DC cardioversion under sedation or general anaesthesia. Intravenous amiodarone is added if initial DC shocks are unsuccessful.
Patients with Wolff-Parkinson-White syndrome (pre-excitation syndrome) with possible atrial arrhythmias (e.g., atrial fibrillation or atrial flutter) should not have adenosine, verapamil or a beta blocker, as these block the atrioventricular node, promoting conduction of the atrial rhythm through the accessory pathway into the ventricles, causing potentially life-threatening ventricular rhythms. Sometimes it can be difficult to distinguish this from SVT, so the involvement of experienced seniors is essential. In this scenario, the usual management is procainamide (which does not block the AV node) or electrical cardioversion (if unstable).
Vagal Manoeuvres
Vagal manoeuvres stimulate the vagus nerve, increasing the activity in the parasympathetic nervous system. This can slow the conduction of electrical activity in the heart, terminating an episode of supraventricular tachycardia.
Valsalva manoeuvres involve increasing the intrathoracic pressure. This can be achieved by having the patient blow hard against resistance, for example, blowing into a 10ml syringe for 10-15 seconds.
Carotid sinus massage involves stimulating the baroreceptors in the carotid sinus by massaging that area on one side of the neck (not both sides at the same time). Carotid sinus massage is avoided in patients with carotid artery stenosis (e.g., with a carotid bruit or previous TIA).
The diving reflex involves briefly submerging that patient’s face in cold water.
Adenosine
Adenosine works by slowing cardiac conduction, primarily through the AV node. It interrupts the AV node or accessory pathway during SVT and “resets” it to sinus rhythm. The half-life of adenosine is less than 10 seconds, meaning it is very quickly metabolised and stops having an effect. It needs to be given as a rapid bolus to ensure it reaches the heart with enough impact to interrupt the pathway for a short period. It will often cause a brief period of asystole or bradycardia that can be scary for the patient and doctor. However, it metabolises quickly, and sinus rhythm will return.
Adenosine is avoided in patients with:
Asthma
COPD
Heart failure
Heart block
Severe hypotension
Potential atrial arrhythmia with underlying pre-excitation
Adenosine must be given as a rapid IV bolus into a large proximal cannula (e.g., grey cannula in the antecubital fossa). The patient should be warned about the scary feeling of dying or impending doom when it is injected. This feeling quickly passes.
Three doses are attempted until sinus rhythm returns:
Initially 6mg
Then 12mg
Then 18mg
Synchronised DC Cardioversion
Synchronised DC (direct current) cardioversion involves an electric shock applied to the heart to restore normal sinus rhythm. A defibrillator machine monitors the electrical signal, particularly identifying the R waves. An electric shock is synchronised with a ventricular contraction, at the R wave on the ECG. If successful, the shock will be followed by sinus rhythm.
Synchronised cardioversion is used in patients with a pulse to avoid shocking the patient during a T wave. Delivering a shock during a T wave can result in ventricular fibrillation and, subsequently, cardiac arrest.
During a cardiac arrest scenario with pulseless ventricular tachycardia or ventricular fibrillation, where the patient does not have organised electrical activity or a pulse, there is no need for the shock to be synchronised.
Management of Paroxysmal SVT
Patients with recurrent episodes of supraventricular tachycardia can be treated to prevent further episodes. The options are:
Long-term medication (e.g., beta blockers, calcium channel blockers or amiodarone)
Radiofrequency ablation
Radiofrequency Ablation
Catheter ablation is performed in a catheter laboratory, often called a “cath lab”. It involves a general anaesthetic or sedation. A catheter is inserted into a femoral vein and fed through the venous system under x-ray guidance to the heart.
Once in the heart, the catheter tip is placed against different areas to test the electrical signals. The operator attempts to identify the location of any abnormal electrical pathways. Once identified, radiofrequency ablation (heat) is applied to burn the abnormal electrical pathway. This leaves scar tissue that does not conduct electrical activity. Destroying the abnormal electrical pathway aims to remove the source of the arrhythmia.
Radiofrequency ablation can permanently resolve certain arrhythmias caused by abnormal electrical pathways, including:
Atrial fibrillation
Atrial flutter
Supraventricular tachycardias
Wolff-Parkinson-White syndrome
