Supraventricular Tachycardia Overview
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Questions and Answers

What are the three principal types of supraventricular tachycardia?

Atrioventricular nodal re-entrant tachycardia (AVNRT), atrioventricular re-entrant tachycardia (AVRT), and atrial tachycardia.

Describe the mechanism of AVNRT.

AVNRT is caused by a re-entry circuit involving the AV node and its two pathways: a superior ‘fast’ pathway and an inferior ‘slow’ pathway.

What is the typical heart rate range observed in patients with AVNRT?

The heart rate typically ranges from 120 to 240 beats per minute.

List two management options for acute attacks of AVNRT.

<p>Carotid sinus massage and intravenous adenosine.</p> Signup and view all the answers

What characterizes the concealed accessory pathway in AVRT?

<p>The concealed accessory pathway conducts only in the retrograde direction, not altering the ECG in sinus rhythm.</p> Signup and view all the answers

How does the presence of an accessory pathway affect the PR interval in AVRT?

<p>It shortens the PR interval and may result in a delta wave on the ECG.</p> Signup and view all the answers

What is a potential risk when atrial fibrillation occurs in the context of AVRT?

<p>It may produce a dangerously rapid ventricular rate due to the accessory pathway lacking rate-limiting properties.</p> Signup and view all the answers

What treatment approach is recommended for recurrent AVNRT?

<p>Catheter ablation is recommended, with a success rate of more than 90%.</p> Signup and view all the answers

What is the primary emergency treatment for pre-excited atrial fibrillation?

<p>DC cardioversion is the primary emergency treatment.</p> Signup and view all the answers

Describe the characteristic ECG findings associated with atrial flutter.

<p>The ECG shows saw-tooth flutter waves, often difficult to identify due to AV block.</p> Signup and view all the answers

What medications are typically used for rate control in atrial flutter?

<p>Digoxin, β-blockers, and verapamil are typically used for rate control.</p> Signup and view all the answers

What is the most effective treatment for patients with persistent symptoms of atrial flutter?

<p>Catheter ablation is the most effective treatment for persistent symptoms.</p> Signup and view all the answers

What type of ventricular ectopic beats are characterized by identical beats arising from a single ectopic focus?

<p>Unifocal PVCs are characterized by identical beats from a single ectopic focus.</p> Signup and view all the answers

What is the main symptom that patients with frequent ventricular premature beats (VPBs) may experience?

<p>Patients may experience an irregular heartbeat or missed beats.</p> Signup and view all the answers

Identify a common setting where ventricular tachycardia (VT) occurs.

<p>VT commonly occurs following an acute myocardial infarction (MI).</p> Signup and view all the answers

What is one important ECG characteristic of ventricular tachycardia?

<p>VT is characterized by broad, abnormal QRS complexes.</p> Signup and view all the answers

What is the management protocol for hemodynamically unstable VT?

<p>DC cardioversion is required for hemodynamically unstable VT.</p> Signup and view all the answers

What action should be taken when a patient with VT is hemodynamically stable?

<p>An intravenous amiodarone bolus followed by maintenance should be administered.</p> Signup and view all the answers

What are premature ventricular complexes (PVCs) more likely to manifest in?

<p>PVCs are more prominent at rest and can disappear with exercise.</p> Signup and view all the answers

Why are Class Ic anti-arrhythmic drugs contraindicated in patients with structural heart disease?

<p>They risk slowing the flutter circuit, potentially causing hemodynamic compromise.</p> Signup and view all the answers

In patients experiencing bigeminy, how are ectopic beats defined?

<p>Bigeminy is characterized by alternating normal and ectopic beats.</p> Signup and view all the answers

What role does catheter ablation play in the management of PVCs?

<p>Catheter ablation can be useful in refractory cases of symptomatic PVCs.</p> Signup and view all the answers

What is a common trigger for torsade de pointes?

<p>Hypokalaemia</p> Signup and view all the answers

Which medication is contraindicated in patients with long QT syndrome?

<p>Isoprenaline</p> Signup and view all the answers

What is the correct duration of a prolonged QT interval in women?

<blockquote> <p>0.46 sec</p> </blockquote> Signup and view all the answers

What ECG characteristic is seen in Brugada syndrome?

<p>Right bundle branch block</p> Signup and view all the answers

What is a primary management strategy for torsade de pointes?

<p>Overdrive atrial pacing</p> Signup and view all the answers

What condition is indicated by a prolonged PR interval?

<p>First-degree atrioventricular block</p> Signup and view all the answers

Patients with congenital long QT syndrome should be considered for which intervention in high-risk cases?

<p>Implantable defibrillator</p> Signup and view all the answers

What often triggers arrhythmias in long QT type 2 patients?

<p>Sudden noise</p> Signup and view all the answers

What phenomenon is characterized by the progressive lengthening of successive PR intervals in Mobitz type I second-degree AV block?

<p>Wenckebach phenomenon</p> Signup and view all the answers

What is a potential risk for patients with Mobitz type II second-degree AV block?

<p>Asystole</p> Signup and view all the answers

In third-degree AV block, what is the term used to describe the independent beating of the atria and ventricles?

<p>AV dissociation</p> Signup and view all the answers

Which condition is typically associated with high vagal tone and may lead to physiological second-degree AV block?

<p>Athletic young adults</p> Signup and view all the answers

In cases of symptomatic second- or third-degree AV block, what is an initial treatment option commonly used?

<p>IV Atropine</p> Signup and view all the answers

What is the most reliable treatment for Mobitz type II or third-degree AV block if it is not due to a reversible cause?

<p>Permanent pacing</p> Signup and view all the answers

What heart rate can typically be observed in cases of complete AV block?

<p>25–50/min</p> Signup and view all the answers

What clinical feature may occur due to prolonged asystole in patients with severe heart block?

<p>Syncope</p> Signup and view all the answers

What is a common trigger for torsade de pointes?

<p>Administration of QT-prolonging medications</p> Signup and view all the answers

Which management strategy is effective for preventing syncope in patients with congenital long QT syndrome?

<p>Beta-blockers</p> Signup and view all the answers

What is a characteristic ECG finding in Brugada syndrome?

<p>Right bundle branch block and ST elevation in V1 and V2</p> Signup and view all the answers

In the context of torsade de pointes, what is the normal duration of a prolonged QT interval in men?

<blockquote> <p>0.44 sec</p> </blockquote> Signup and view all the answers

Which condition is indicated by a prolonged PR interval greater than 0.20 sec?

<p>First-degree atrioventricular block</p> Signup and view all the answers

What is the function of intravenous isoprenaline in the treatment of torsade de pointes?

<p>Rate-dependent shortening of the QT interval</p> Signup and view all the answers

Which type of atrioventricular block is characterized by dropped beats due to some impulses failing to conduct to the ventricles?

<p>Second-degree AV block type I</p> Signup and view all the answers

What genetic defect is associated with Brugada syndrome?

<p>Sodium channel function defect</p> Signup and view all the answers

What characterizes Mobitz type I second-degree AV block?

<p>Progressive lengthening of successive PR intervals</p> Signup and view all the answers

What distinguishes Mobitz type II second-degree AV block from Mobitz type I?

<p>Presence of consistent PR intervals with some dropped beats</p> Signup and view all the answers

In cases of third-degree AV block, what maintains ventricular activity?

<p>An escape rhythm from the AV node or bundle of His</p> Signup and view all the answers

What is a common clinical feature of severe heart block?

<p>Cannon waves visible in the neck</p> Signup and view all the answers

What treatment option may be used for symptomatic second- or third-degree AV block?

<p>Atropine administration</p> Signup and view all the answers

What can trigger transient AV block in the context of acute inferior myocardial infarction?

<p>Right coronary artery involvement</p> Signup and view all the answers

What is the typical heart rate in complete AV block?

<p>25–50 beats per minute</p> Signup and view all the answers

What is a possible consequence of prolonged asystole in patients experiencing severe heart block?

<p>Fainting spells</p> Signup and view all the answers

Study Notes

Supraventricular Tachycardia (SVT)

  • Three main types: atrioventricular nodal re-entrant tachycardia (AVNRT), atrioventricular re-entrant tachycardia (AVRT), and atrial tachycardia.
  • Term "SVT" technically incorrect, as ventricles often part of re-entry circuit.

Atrioventricular Nodal Re-entrant Tachycardia (AVNRT)

  • Caused by re-entry in a circuit involving the AV node and its two right atrial input pathways: a superior 'fast' pathway and an inferior 'slow' pathway.
  • Occurs in patients with structurally normal hearts.
  • ECG: Narrow complex, rate 120-240 bpm, rate-dependent bundle branch block may occur.
  • Symptoms: Palpitations lasting seconds to hours.

Management of AVNRT

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

Atrioventricular Re-entry Tachycardia (AVRT)

  • Involves an abnormal band of conducting tissue connecting atria and ventricles (accessory pathway).
  • Accessory pathway comprises rapidly conducting fibers resembling Purkinje tissue.
  • In about 50% of cases, this pathway only conducts retrograde (ventricles to atria).
  • This is known as a concealed accessory pathway, and doesn't alter ECG appearance in sinus rhythm.
  • In the remaining cases, the pathway also conducts antegrade (atria to ventricles), distorting the QRS complex in sinus rhythm.
  • Premature ventricular activation through the accessory pathway shortens the PR interval and causes initial slurring of QRS (delta wave), known as a manifested pathway.
  • WPW pattern/WPW syndrome: Result of an accessory pathway with different refractory periods and conduction velocities than the AV node, leading to a re-entry circuit.

Management of AVRT

  • Narrow complex arrhythmia (retrograde conduction): Intravenous adenosine and carotid sinus massage.
  • Wide complex arrhythmia (antegrade conduction): Class 1c antiarrhythmics with beta-blockers.
  • Atrial fibrillation (AF) with AVRT: May cause dangerously rapid ventricular rate due to lack of rate-limiting properties in accessory pathway.
    • Pre-excited AF can cause collapse, syncope, and even death.
    • Treated as an emergency, typically with DC cardioversion.
  • Catheter ablation: Highly successful and curative in most cases.

Atrial Flutter

  • Characterized by a large (macro) re-entry circuit, usually within the right atrium encircling the tricuspid annulus.
  • Atrial rate is approximately 300/min, often associated with 2:1, 3:1, or 4:1 AV block (corresponding heart rates of 150, 100, or 75/min).
  • Rarely, every flutter wave conducted, producing a 300/min rate and possible hemodynamic compromise.
  • ECG: Shows saw-tooth flutter waves. Difficult to identify buried in QRS complexes and T waves when there's regular 2:1 AV block.
  • Suspect when there is a narrow complex tachycardia of 150/min.
  • Carotid sinus pressure or intravenous adenosine: Can help establish diagnosis by temporarily increasing AV block and revealing flutter waves.

Management of Atrial Flutter

  • Medical Management: Digoxin, β-blockers, or verapamil can control ventricular rate.
    • Direct current (DC) cardioversion may be preferable to restore sinus rhythm.
  • Post cardioversion: β-blockers or amiodarone prevent recurrent episodes.
  • Class Ic anti-arrhythmic drugs (flecainide): Contraindicated due to risk of slowing flutter circuit and paradoxically causing extreme tachycardia and hemodynamic compromise.
  • Catheter Ablation: Highly effective, offering >90% chance of cure. Treatment of choice for persistent symptoms.
  • Anticoagulation Management: Identical to patients with atrial fibrillation.

Premature Ventricular Ectopics (PVE)

  • Frequently found in healthy people, prevalence increases with age.
  • More prominent at rest and disappear with exercise in patients with otherwise normal hearts.
  • May be a manifestation of subclinical coronary artery disease or cardiomyopathy.
  • Also occur in patients with established heart disease, especially after myocardial infarction (MI).
  • Most patients asymptomatic, but some have irregular heart beat, missed beats, or strong beats due to increased cardiac output from the post-ectopic sinus beat.
  • ECG: Shows broad and bizarre complexes due to sequential ventricular activation.
    • May be unifocal (identical beats from a single ectopic focus) or multifocal (varying morphology with multiple foci).
    • 'Couplet' and 'triplet' refer to two or three successive ectopic beats.
    • Bigeminy is a run of alternating sinus and ventricular ectopics.

Management of PVE

  • Symptomatic patients: Beta-blockers helpful to control symptoms.
  • Refractory cases: Catheter ablation can be useful.
  • Frequent PVCs in patients with structural heart disease (MI, cardiomyopathy): Common, associated with worse prognosis. Treatment should target underlying heart disease.
    • Anti-arrhythmic medication doesn't improve prognosis except beta-blockers in cases of MI and heart failure.

Ventricular Tachycardia (VT)

  • Most common settings: Acute MI, chronic coronary artery disease, cardiomyopathy.
  • Associated with extensive ventricular disease, impaired left ventricular function, ventricular aneurysm.
  • May cause hemodynamic compromise or degenerate into ventricular fibrillation.
  • Caused by abnormal automaticity or triggered activity in ischemic tissue, or by re-entry within scarred ventricular tissue.
  • Symptoms: Palpitations, dyspnea, lightheadedness, syncope.
  • ECG: Shows tachycardia and broad, abnormal QRS complexes with a rate >120/min.
  • Difficult to distinguish VT from SVT with bundle branch block or preexcitation (WPW syndrome) on ECG. Features favoring VT listed in Box 16.25.
  • 12-lead ECG or electrophysiology study can help establish diagnosis.
  • Idioventricular rhythm ('slow' VT): Patients recovering from MI sometimes have periods of idioventricular rhythm at a rate slightly above preceding sinus rate, but below 120/min.
    • May reflect reperfusion of infarct territory and be a good sign.
    • Usually self-limiting, asymptomatic, and don't require treatment.
  • Normal heart VT: Occurs in otherwise healthy hearts, usually due to abnormal automaticity in the right ventricular outflow tract or one of the fascicles in the left bundle branch.

Management of VT

  • Hemodynamically unstable VT: Requires DC cardioversion (chest pain, dizziness, raised JVP, bibasal crackles).
  • Hemodynamically stable VT: Intravenous amiodarone bolus and maintenance.
  • Intravenous lidocaine: Can be used for chemical cardioversion of VT, but may cause hypotension, convulsion, and myocardial depression.
  • VT prevention: Beta-blockers and amiodarone. Class IC anti-arrhythmics contraindicated in patients with structural heart disease (CAD, cardiomyopathy).
  • ICD implantation: Consider in high-risk patients.

Torsades de Pointes

  • A type of polymorphic ventricular tachycardia (VT) that is a complication of prolonged ventricular repolarization (prolonged QT interval).
  • Characterized by rapid, irregular complexes that "twist" around the baseline as the mean QRS axis changes.
  • Usually non-sustained and repetitive, but may degenerate into ventricular fibrillation.
  • ECG shows a prolonged QT interval (> 0.44 sec in men, > 0.46 sec in women, corrected to a heart rate of 60 bpm).
  • More common in women.
  • Often triggered by a combination of factors, such as QT-prolonging medications and hypokalemia.
  • Congenital Long QT Syndromes: a family of genetic disorders caused by mutations in genes coding for cardiac sodium or potassium channels.
    • Long QT Type 1: triggered by vigorous exercise.
    • Long QT Type 2: triggered by sudden noise.
    • Long QT Type 3: arrhythmias more common during sleep.
  • Management:
    • Intravenous magnesium (8 mmol over 15 mins, 72 mmol over 24 hours) for all patients.
    • Overdrive atrial pacing to suppress arrhythmia through rate-dependent shortening of the QT interval.
    • Intravenous isoprenaline as an alternative to atrial pacing (contraindicated in long QT syndrome).
    • Beta-blockers for preventing syncope in patients with congenital long QT syndrome.
    • Implantable defibrillator may be considered for patients with extreme QT prolongation (> 500 msec) or high-risk genotypes.
    • Left stellate ganglion block for resistant arrhythmias.

Brugada Syndrome

  • Related genetic disorder that can present with polymorphic VT or sudden death.
  • Characterized by a defect in sodium channel function and an abnormal ECG (right bundle branch block and ST elevation in V1 and V2, but not usually prolongation of the QT interval).
  • Only known effective treatment is an implantable defibrillator.

Atrioventricular Block

  • First-degree AV block: AV conduction is delayed, leading to a prolonged PR interval (> 0.20 sec).
    • Rarely causes symptoms and usually doesn't require treatment.
  • Second-degree AV 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, then repeats.
      • Usually due to impaired conduction in the AV node.
      • Can be physiological and occurs in some athletic young adults with high vagal tone.
    • Mobitz type II: Constant PR interval, but some P waves are not conducted.
      • Usually caused by disease of the His-Purkinje system and carries a risk of asystole.
  • Third-degree AV block (Complete AV block): Complete conduction failure; atria and ventricles beat independently (AV dissociation).
    • Ventricular activity maintained by an escape rhythm from AV node/bundle of His (narrow QRS) or distal Purkinje tissues (broad QRS).
    • Produces a slow (25-50/min), regular pulse that doesn't vary with exercise.
    • Compensatory increase in stroke volume, leading to a large-volume pulse.
    • Cannon waves may be visible in the neck.

Clinical Features

  • Syncope (Adams-Stokes attacks): Sudden loss of consciousness without warning, resulting in collapse.
    • Prolonged asystole may lead to brief anoxic seizures.
    • Characterized by pallor, a death-like appearance during the attack, and flushing when the heart beats again.

Treatment of Heart Block

  • First-degree and Mobitz type I second-degree AV block: Usually asymptomatic.
  • Mobitz type II second-degree AV block and third-degree AV block:
    • Acute inferior MI often complicated by transient AV block due to the right coronary artery (RCA) supplying the AV node.
    • If the patient remains well, no treatment is required.
    • Symptomatic cases may respond to atropine (0.6 mg IV) or temporary pacing.
    • Usually resolves within 7-10 days.

Lines in the Management of Arrhythmias

  • Drugs
  • DC shock (cardioversion and defibrillation)
  • Implantable devices (pacemakers and ICDs)
  • Catheter ablation

Torsade de Pointes

  • A type of polymorphic ventricular tachycardia (VT) caused by prolonged ventricular repolarization (QT interval)
  • ECG shows rapid irregular complexes, appearing to twist around the baseline as the QRS axis changes.
  • Usually non-sustained and repetitive, but can degenerate into ventricular fibrillation.
  • Prolonged QT interval (>0.44 sec in men, >0.46 sec in women when corrected to a heart rate of 60 bpm) during sinus rhythm is a key indicator.
  • More common in women and often triggered by QT-prolonging medications and hypokalaemia.
  • Congenital long QT syndromes are caused by mutations in genes responsible for cardiac sodium or potassium channels
  • Adrenergic stimulation, like vigorous exercise, triggers arrhythmias in long QT type 1.
  • Sudden noises can trigger arrhythmias in long QT type 2.
  • Arrhythmias more common during sleep in type 3.

Management of Torsade de Pointes

  • Intravenous magnesium (8 mmol over 15 mins, 72 mmol over 24 hours) should be given in all cases.
  • Overdrive atrial pacing can suppress arrhythmia by shortening the QT interval.
  • Intravenous isoprenaline is an alternative to atrial pacing but contraindicated in long QT syndrome.
  • Beta-blockers prevent syncope in patients with congenital long QT syndrome.
  • Implantable defibrillator may be considered for high-risk patients or those with extreme QT prolongation (>500 msecs).
  • Left stellate ganglion block may be helpful for resistant arrhythmias.

Brugada Syndrome

  • Genetic disorder presenting with polymorphic VT or sudden death.
  • Defective sodium channel function and abnormal ECG with right bundle branch block and ST elevation in V1 and V2 (not usually prolonged QT interval).
  • Only effective treatment is an implantable defibrillator.

Atrioventricular Block

  • First-degree AV block: Delayed AV conduction leading to a prolonged PR interval (>0.20 sec). Rarely symptomatic and usually doesn't require treatment.
  • Second-degree AV block: Some atrial impulses fail to conduct to ventricles, resulting in dropped beats. Two subtypes:
    • Mobitz type I (Wenckebach): Progressive lengthening of PR intervals culminating in a dropped beat. Often physiological, observed in athletic youth with high vagal tone.
    • Mobitz type II: Constant PR interval with non-conducted P waves. Caused by disease of the His-Purkinje system, carrying risk of asystole.
  • Third-degree AV block (Complete AV block): Complete conduction failure, atria and ventricles beat independently (AV dissociation).
    • Escape rhythms, originating in the AV node or bundle of His (narrow QRS) or distal Purkinje tissues (broad QRS), maintain ventricular activity.
    • Complete AV block results in a slow, regular pulse that doesn't vary with exercise.
    • Produces large-volume pulse and Cannon waves in the neck.

Clinical Features: Syncope

  • Adam Stokes attacks are sudden, unexpected losses of consciousness leading to collapse.
  • Prolonged asystole can lead to brief anoxic seizures.
  • Pallor and death-like appearance during attack, followed by characteristic flushing upon cardiac recovery.

Management of Heart Block

  • First-degree and Mobitz type I second-degree AV block are usually asymptomatic.
  • Mobitz type II second-degree and third-degree AV block:
    • Acute inferior MI often results in transient AV block due to RCA involvement.
    • Symptomatic cases may be treated with atropine (0.6 mg IV, repeated as necessary).
    • Temporary pacemaker if atropine fails.
    • Usually resolves within 7-10 days.
  • Second- or third-degree AV block during acute anterior MI reflects extensive ventricular damage, indicating poor prognosis.
  • Mobitz type II or third-degree AV block, even asymptomatic, not due to reversible causes, requires pacing.

Lines in the Management of Arrhythmias

  • Drugs
  • DC shock (cardioversion and defibrillation)
  • Implantable devices:
    • pacemakers
    • ICD (Implantable Cardiac Defibrillator)
  • Catheter ablation.

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Description

This quiz covers the essential aspects of supraventricular tachycardia, including its major types like AVNRT and AVRT. It explores the underlying mechanisms, symptoms, and management strategies for acute and recurrent cases of AVNRT. Test your knowledge on this important cardiac condition.

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