Cardiac Arrhythmia and Tachycardia Mechanisms

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Questions and Answers

What are the three main mechanisms of tachycardia?

Increased automaticity, re-entry, and triggered activity.

How do supraventricular rhythms differ from ventricular rhythms in terms of QRS complexes?

Supraventricular rhythms produce narrow QRS complexes, while ventricular rhythms produce broad, bizarre QRS complexes.

What is an escape rhythm and where can it originate from?

An escape rhythm is when a distal part of the conducting system assumes the role of pacemaker, originating from the AV node, His bundle, or the ventricles.

Describe the symptoms associated with sustained tachycardia.

Sustained tachycardia may cause palpitations, dizziness, chest discomfort, breathlessness, and syncope. Signup and view all the answers

What clinical features are commonly associated with bradycardia?

Bradycardias typically cause symptoms like fatigue, lightheadedness, and syncope. Signup and view all the answers

What are the key features of atrioventricular nodal reentry tachycardia (AVNRT) seen on an ECG?

The ECG shows a narrow complex with a heart rate ranging from 120 to 240 bpm, potentially with rate-dependent bundle branch block. Signup and view all the answers

What are the first-line management options during an acute AVNRT attack?

Carotid sinus massage, Valsalva maneuver, intravenous adenosine, intravenous verapamil, or a beta blocker. Signup and view all the answers

How does an accessory pathway contribute to the development of atrioventricular reentry tachycardia?

It creates a reentry circuit that allows rapid conduction between the atria and ventricles, often involving both antegrade and retrograde pathways. Signup and view all the answers

Describe the cardioversion approach for treating pre-excited atrial fibrillation due to an accessory pathway.

DC cardioversion is utilized as an emergency treatment to stabilize patients experiencing pre-excited atrial fibrillation. Signup and view all the answers

What characterizes the rhythm and anatomy of atrial flutter, and how is it typically represented on an ECG?

Atrial flutter is marked by a macro re-entry circuit usually around the tricuspid annulus, producing a consistent atrial rate of approximately 300/min. Signup and view all the answers

What ECG pattern is typically seen in atrial flutter?

Saw-tooth flutter waves. Signup and view all the answers

What is the rate of ventricular response in atrial flutter with every flutter wave conducted?

300 beats per minute. Signup and view all the answers

Which medications are commonly used for medical management of atrial flutter?

Digoxin, β-blockers, or verapamil. Signup and view all the answers

What is a potential adverse effect when using Class Ic anti-arrhythmic drugs like flecainide in atrial flutter?

It may facilitate 1:1 AV nodal conduction and produce extreme tachycardia. Signup and view all the answers

What diagnostic maneuver may temporarily increase AV block and help visualize flutter waves?

Carotid sinus pressure or intravenous adenosine. Signup and view all the answers

What is the chance of complete cure with catheter ablation for persistent atrial flutter symptoms?

Greater than 90%. Signup and view all the answers

How do premature ventricular beats (VPBs) typically present in healthy individuals?

They are often asymptomatic and increase with age. Signup and view all the answers

What ECG characteristics define a VPB?

Broad and bizarre complexes. Signup and view all the answers

What terms describe two or three successive ectopic beats?

'Couplet' for two beats and 'triplet' for three beats. Signup and view all the answers

What role does anticoagulant management play in patients with atrial flutter?

It is identical to that of patients with atrial fibrillation. Signup and view all the answers

What is a common trigger for Torsade de Pointes in patients with congenital long QT syndrome?

Exposure to loud noises Signup and view all the answers

What is the recommended intravenous magnesium dosage for treating Torsade de Pointes?

8 mmol over 15 minutes Signup and view all the answers

What condition is characterized by mutations in genes coding for cardiac sodium or potassium channels?

Congenital long QT syndrome Signup and view all the answers

In the management of Torsade de Pointes, under what circumstance is intravenous isoprenaline contraindicated?

In patients with long QT syndrome Signup and view all the answers

Which clinical feature is commonly associated with Brugada syndrome?

ST elevation in V1 and V2 Signup and view all the answers

What is the first-line therapeutic approach for patients with extreme QT interval prolongation over 500 msecs?

Implantable defibrillator Signup and view all the answers

What is the mechanism primarily responsible for most tachyarrhythmias?

Re-entry circuits Signup and view all the answers

What symptom is most commonly associated with sustained tachycardia?

Chest discomfort Signup and view all the answers

In the context of cardiac arrhythmias, what is meant by 'escape rhythm'?

A rhythm initiated by the AV node during sinus arrest Signup and view all the answers

Which of the following is a characteristic of ventricular rhythms compared to supraventricular rhythms?

Broad and bizarre QRS complexes Signup and view all the answers

What might triggered activity in the heart result in?

Ventricular arrhythmias Signup and view all the answers

How do symptoms of bradycardia typically manifest?

Symptoms indicative of low cardiac output Signup and view all the answers

What is the primary purpose of rate control in managing atrial fibrillation?

To decrease heart rate to a manageable level Signup and view all the answers

Which approach to rhythm control is recommended when atrial fibrillation has been present for less than 3 months?

Electrical cardioversion Signup and view all the answers

Which medication is often combined with flecainide to prevent atrial fibrillation episodes?

A rate-limiting beta-blocker Signup and view all the answers

What essential test is performed if atrial fibrillation onset is unknown and has lasted more than 48 hours?

Transesophageal echocardiogram (TEE) Signup and view all the answers

Which of the following statements about cardioversion is true?

Electrical cardioversion is utilized in cases of hemodynamic instability. Signup and view all the answers

Which class of antiarrhythmic medications is known for its effectiveness in preventing recurrence of atrial fibrillation but has side effects that restrict its use to when other treatments fail?

Class III Signup and view all the answers

For patients presenting with atrial fibrillation and no history of structural heart disease, which pharmacological agent can be administered for cardioversion?

Flecainide Signup and view all the answers

What is a common outcome after electrical cardioversion for atrial fibrillation within one year?

25% chance of relapse Signup and view all the answers

When performing rate control in atrial fibrillation, which medication is typically less effective during exercise versus beta-blockers?

Digoxin Signup and view all the answers

What is the preferred first-line treatment strategy if a patient presents with hemodynamically unstable atrial fibrillation?

Electrical cardioversion Signup and view all the answers

What is the heart rate threshold that defines sinus bradycardia?

Less than 60 beats per minute Signup and view all the answers

Which condition is NOT commonly associated with sinus tachycardia?

Hypoglycemia Signup and view all the answers

What is the expected ECG finding in a premature atrial beat?

Normal QRS complex with an abnormal P wave morphology Signup and view all the answers

In what scenario is pacing generally NOT indicated?

Asymptomatic bradycardia Signup and view all the answers

Which of the following statements about atrial fibrillation is true?

It is the most common sustained cardiac arrhythmia in adults Signup and view all the answers

What may the absence of sinus arrhythmia indicate?

Potential diabetic neuropathy or increased sympathetic drive Signup and view all the answers

What is a common symptom experienced during sinus node dysfunction?

Palpitations and dizziness Signup and view all the answers

Which treatment is indicated for significant symptoms caused by frequent premature atrial beats?

Beta blockers Signup and view all the answers

Study Notes

Cardiac Arrhythmia

A disturbance of the electrical rhythm of the heart.
Often a manifestation of structural heart disease, but can also occur in otherwise healthy hearts due to conduction or depolarisation issues.

Mechanisms of Tachycardia

Increased Automaticity: Spontaneous depolarisation of an ectopic focus in the atria, atrioventricular junction, or ventricles, often triggered by catecholamines.
Re-entry: Initiated by an ectopic beat sustained by a re-entry circuit. The most common cause of tachyarrhythmias.
Triggered Activity: Can cause ventricular arrhythmias in patients with coronary artery disease. A secondary depolarisation from an incompletely repolarised cell membrane.

Supraventricular vs Ventricular Rhythms

Supraventricular Rhythms: Usually produce narrow QRS complexes due to normal depolarisation of the ventricles.
Ventricular Rhythms: Produce broad, bizarre QRS complexes due to abnormal activation of the ventricles.

Escape Rhythms

Occur if the sinus rate becomes too slow.
Can occur in the AV node or His bundle (junctional rhythm) or the ventricles (idioventricular rhythm).

Clinical Features

Arrhythmia: Can be asymptomatic. Sustained tachycardia can cause palpitations, dizziness, chest discomfort, breathlessness, syncope.
Bradycardia: Tend to cause symptoms of low cardiac output, including fatigue, lightheadedness, and syncope.

Management of AVNRT (Atrioventricular Nodal Re-entrant Tachycardia)

Acute Attack: Carotid sinus massage, Valsalva maneuver, intravenous adenosine, intravenous verapamil, intravenous beta-blocker, intravenous flecainide, or amiodarone.
Recurrent AVNRT: Catheter ablation is indicated with a success rate exceeding 90%.

Atrioventricular Re-entry Tachycardia (AVRT)

Involves an abnormal band of conducting tissue connecting the atria and ventricles.
This "accessory pathway" conducts rapidly and can be concealed (only retrograde conduction), or manifested (both antegrade and retrograde conduction).
Manifestation of the accessory pathway can shorten the PR interval and result in a "delta wave" on the ECG.
The accessory pathway and AV node have different refractory periods and conduction velocities, leading to re-entry circuits.

Management of AVRT

Narrow complex arrhythmia, retrograde conduction: Intravenous adenosine and carotid sinus massage.
Wide complex arrhythmia, antegrade conduction: Class Ic antiarrhythmic with beta-blockers.
Atrial fibrillation: Can produce a rapid ventricular rate due to the absence of the rate-limiting properties of the AV node. This is called pre-excited atrial fibrillation and may cause collapse, syncope, or death. Treatment involves DC cardioversion.
Catheter ablation: Highly effective treatment, considered curative, with a success rate over 90%.

Atrial Flutter

Characterized by a large re-entry circuit within the right atrium, usually surrounding the tricuspid annulus.
Atrial rate is about 300 beats per minute, typically associated with 2:1, 3:1, or 4:1 AV block.
ECG shows saw-tooth flutter waves.
Suspect atrial flutter in narrow-complex tachycardia of 150 beats per minute.

Management of Atrial Flutter

Medical Management: Digoxin, β-blockers, or verapamil can control the ventricular rate.
DC Cardioversion: May be preferable to restore sinus rhythm.
Prevention of Recurrence: β-blockers or amiodarone are used after cardioversion.
Class Ic Antiarrhythmic Drugs (flecainide): Contraindicated due to the risk of slowing the flutter circuit and producing paradoxical tachycardia.
Catheter Ablation: Highly effective treatment, offering a greater than 90% chance of cure.
Anticoagulation: Managed identically to atrial fibrillation patients.

Premature Ventricular Ectopics (VPBs)

Commonly found in healthy individuals and their prevalence increases with age.
In individuals with normal hearts, ectopic beats are more prominent at rest and disappear with exercise.
Can be a manifestation of subclinical coronary artery disease or cardiomyopathy, or occur in patients with established heart disease following an MI.
Most patients are asymptomatic, but some may experience an irregular heartbeat, missed beats, or abnormally strong beats due to increased cardiac output of the post-ectopic sinus beat.
ECG shows broad and bizarre complexes due to sequential activation of the ventricles.
Complexes can be unifocal (identical beats from a single focus) or multifocal (varying morphology from multiple foci).

Management of VPBs

VT Prevention: Beta-blockers and amiodarone can prevent VT. Class Ic antiarrhythmics are contraindicated in patients with structural heart disease (CAD, cardiomyopathy).
Consider ICD Implantation: Depending on the severity and risk of ventricular arrhythmias.

Torsades de Pointes

A form of polymorphic ventricular tachycardia, a complication of prolonged ventricular repolarisation (prolonged QT interval).
ECG shows rapid, irregular complexes that appear to twist around the baseline as the mean QRS axis changes.
Usually non-sustained and repetitive, but can degenerate into ventricular fibrillation.
ECG during sinus rhythm will reveal a prolonged QT interval (> 0.44 sec in men, > 0.46 sec in women when corrected to a heart rate of 60 bpm).

Factors Contributing to Torsades de Pointes

More common in women.
Often triggered by a combination of factors including QT-prolonging medications and hypokalaemia.
Congenital Long QT Syndromes: Genetic disorders caused by mutations in genes coding for cardiac sodium or potassium channels.

Management of Torsades de Pointes

Intravenous Magnesium: 8 mmol over 15 minutes, 72 mmol over 24 hours, in all patients with torsades de pointes.
Overdrive Atrial Pacing: Can suppress arrhythmia by rate-dependent shortening of the QT interval.
Intravenous Isoprenaline: Alternative to atrial pacing, but contraindicated in long QT syndrome.
Beta-Blockers: Effective in preventing syncope in patients with congenital long QT syndrome.
Implantable Defibrillator: Considered for patients with extreme QT interval prolongation (>500 msec) or high-risk genotypes.
Left Stellate Ganglion Block: May be beneficial for resistant arrhythmias.

Brugada Syndrome

A related genetic disorder with polymorphic VT or sudden death.
Characterized by sodium channel dysfunction and abnormal ECG (right bundle branch block and ST elevation in V1 and V2, but not usually QT interval prolongation).
Effective treatment is implantable defibrillation.

Atrioventricular Block

First-Degree Atrioventricular Block: AV conduction is delayed, resulting in a prolonged PR interval (> 0.20 sec).
- Rarely causes symptoms, not usually requiring treatment.
Second-Degree Atrioventricular Block: Dropped beats occur because some atrial impulses fail to conduct to the ventricles.
- Mobitz Type I (Wenckebach): Progressive lengthening of successive PR intervals culminating in a dropped beat.
  - Often due to impaired conduction in the AV node.
  - Can be physiological and seen in athletic young adults with high vagal tone.
- Mobitz Type II: PR interval of conducted impulses remains constant, but some P waves are not conducted.
  - Usually caused by disease of the His–Purkinje system and carries a risk of asystole.
Third-Degree Atrioventricular Block (Complete AV Block): Conduction fails completely, atria and ventricles beat independently (AV dissociation).
- Ventricular activity is maintained by an escape rhythm originating in the AV node or bundle of His (narrow QRS) or distal Purkinje tissue (broad QRS).
- Produces a slow (25–50/min), regular pulse that doesn't change with exercise.
- Compensatory increase in stroke volume produces a large-volume pulse.
- Cannon waves may be visible in the neck, and first heart sound intensity varies due to loss of AV synchrony.

Clinical Features of Complete AV Block (CHB)

Syncope
Adam-Stokes attacks: Sudden loss of consciousness without warning, resulting in collapse.
- Brief anoxic seizures can occur if there is prolonged asystole.
- Pallor and a death-like appearance during the attack.
- Characteristic flushing when heartbeat resumes.

Cardiac Arrhythmia

Cardiac arrhythmia is a disturbance of the heart's electrical rhythm.
It can be caused by structural heart disease or abnormal conduction/depolarisation in a healthy heart.
Tachycardia can be caused by increased automaticity, re-entry, and triggered activity.
Increased automaticity leads to spontaneous depolarisation of ectopic foci in the atria, atrioventricular junction, or ventricles.
Re-entry is initiated by an ectopic beat and sustained by a re-entry circuit.
Triggered activity causes ventricular arrhythmias in patients with coronary artery disease.
Supraventricular rhythms produce a narrow QRS complex due to normal depolarisation of the ventricles.
Ventricular rhythms produce a broad QRS complex due to abnormal ventricular depolarisation.
Supraventricular tachycardia can mimic ventricular tachycardia due to bundle branch block or accessory pathways.
Escape rhythms can occur in the AV node or His bundle (junctional rhythm) or the ventricles (idioventricular rhythm).
Clinical Features:
- Asymptomatic
- Symptomatic: Palpitation, Dizziness, Chest discomfort, Breathlessness, Syncope (tachycardia)
- Fatigue, lightheadedness, syncope (bradycardia)
- Extreme bradycardia or tachycardia can lead to sudden death or cardiac arrest.
Investigations:
- 12-lead ECG
- Ambulatory ECG
- Patient-activated loop recorder

Sinus Arrhythmia

Cyclical alteration of heart rate during respiration, increasing during inspiration and decreasing during expiration.
Normal phenomenon, pronounced in children.
Absence of variation can indicate diabetic neuropathy, autonomic involvement in peripheral nerve diseases, or increased sympathetic drive.
No treatment required.

Sinus Bradycardia

HR less than 60 beats per minute.
Can occur in normal individuals, common in athletes.
Asymptomatic bradycardia requires no treatment.
Treatment options: Atropine, Pacing (temporary or permanent).

Sinus Tachycardia

Usually due to increased sympathetic activity during exercise, emotion, and pregnancy.
Healthy young adults can reach 200 beats/min during intense exercise.
Treatment is not usually required but may indicate underlying disease.

Sinus Node Dysfunction

Caused by ischemia, fibrosis, and degenerative changes of the SA node.
Presents with palpitation, dizzy spells, or syncope due to intermittent tachycardia, bradycardia, or pauses.
May benefit from a permanent pacemaker for symptomatic bradycardias, or bradycardias induced by antiarrhythmic drugs.
Atrial pacing can prevent atrial fibrillation episodes.
Pacing improves symptoms but not prognosis.

Premature Atrial Beat (Atrial Ectopic)

Often asymptomatic, or may feel like a missed or strong beat.
ECG shows a premature but otherwise normal QRS complex with an abnormal P wave morphology.
No treatment typically required.
Frequent ectopics can herald the onset of atrial fibrillation.
Beta-blockers can be used for significant symptoms.

Atrial Fibrillation

Most common sustained cardiac arrhythmia, with 0.5% prevalence in the UK.
Investigations:
- 12-lead ECG
- Echocardiography
- Thyroid function tests (TFT)
- Treadmill test (TMT) and coronary angiogram if ischemic heart disease (IHD) is suspected.
Management:
- Rate control
- Rhythm control
- Prevention of recurrence
- Prevention of thromboembolism

Rate Control (AF)

Beta-blockers
Calcium channel blockers
Digoxin
AV node ablation and permanent pacemaker implantation (pace and ablate strategy)
Beta-blockers and calcium antagonists are more effective than digoxin for controlling heart rate during exercise.

Rhythm Control (AF)

Cardioversion (pharmacological or electrical) is initially successful but relapse is frequent.
Electrical cardioversion is used for hemodynamic instability or no response to pharmacological cardioversion.
If AF onset is less than 48 hours, cardioversion can be given with intravenous heparin.
If onset is unknown or more than 48 hours, a transesophageal echocardiogram (TEE) should be performed to rule out left atrial appendage (LAA) thrombus.
Anticoagulation with warfarin or NOACs should be given for 4 weeks before cardioversion.
Intravenous flecainide can be used for pharmacological cardioversion in stable patients with no structural heart disease.
Intravenous amiodarone can be given for patients with structural heart disease.
"Pills in pocket" regimen using oral flecainide can be used to restore sinus rhythm in young patients without structural heart disease.
AF catheter ablation (pulmonary vein isolation) can be performed.

Prevention of Recurrence (AF)

Class IC drugs (propafenone or flecainide) can prevent episodes.
Flecainide is usually combined with a rate-limiting beta-blocker.
Class III drugs (amiodarone) are highly effective but side effects limit their use.
Ventricular tachycardia (VT) can be prevented with beta-blockers, amiodarone.
Class IC antiarrhythmics are contraindicated in patients with structural heart disease.
Consider implantable cardioverter-defibrillator (ICD) implantation.

Torsades de Pointes

Polymorphic ventricular tachycardia (VT) due to prolonged ventricular repolarisation (prolonged QT interval).
ECG shows rapid irregular complexes "twisting" around the baseline.
Usually non-sustained and repetitive, but can degenerate into ventricular fibrillation.
ECG during sinus rhythm shows prolonged QT interval (> 0.44 sec in men, > 0.46 sec in women).
More common in women and often triggered by QT-prolonging medications, hypokalaemia.
Congenital long QT syndromes are caused by genetic mutations in sodium or potassium channel genes.
Exercise can trigger long QT type 1 arrhythmias, while sudden noise can trigger type 2 arrhythmias.
Type 3 arrhythmias are more common during sleep.

Management (Torsades de Pointes)

Intravenous magnesium should be given to all patients.
Overdrive atrial pacing suppresses arrhythmia through rate-dependent shortening of the QT interval.
Intravenous isoprenaline is an alternative to atrial pacing but contraindicated in long QT syndrome.
Beta-blockers prevent syncope in congenital long QT syndrome.
Consider ICD implantation for high-risk patients.
Left stellate ganglion block can be used for resistant arrhythmias.

Brugada Syndrome

Genetic disorder presenting with polymorphic VT or sudden death.
Defect in sodium channel function with abnormal ECG (right bundle branch block and ST elevation in V1 and V2).
Treatment involves only implantable defibrillators.

Atrioventricular Block

First-degree: Conduction delay with prolonged PR interval (>0.20 sec), rarely causes symptoms, no treatment usually required.
Second-degree: Some impulses from the atria fail to conduct to the ventricles, leading to dropped beats.
- Mobitz Type I: Progressive lengthening of PR intervals culminating in a dropped beat, usually due to impaired AV nodal conduction.
- Mobitz Type II: Constant PR interval but some P waves are not conducted, usually caused by His-Purkinje system disease, carries a risk of asystole.
Third-degree (Complete AV Block): Complete conduction failure, atria and ventricles beat independently (AV dissociation).
- Ventricular activity maintained by escape rhythm in the AV node or bundle of His (narrow QRS complex) or distal Purkinje tissues (broad QRS complex).
- Complete AV block produces a slow (25-50/min) regular pulse that does not vary with exercise, except in congenital cases.

Clinical Features (Complete AV Block)

Syncope.
Adam-Stokes attacks are sudden, warningless collapses with possible anoxic seizures.
Pallor and death-like appearance during the attack followed by characteristic flushing after the heart resumes beating.

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Description

This quiz explores the complex mechanisms behind cardiac arrhythmias, specifically focusing on tachycardia. It covers key concepts such as increased automaticity, re-entry circuits, and the distinctions between supraventricular and ventricular rhythms. Test your understanding of how these mechanisms affect heart rhythm and health.