physiological mechanisms of arrhythmias

• cardiac arrhythmias - abnormality in cardiac rhythm

  • May cause sudden death, syncope, heart failure, chest pain, dizziness, palpitations or no symptoms at all

  two main types of arrhythmia:

  • Bradycardia: heart rate is slow (<60b.p.m. during the day or <50b.p.m. at night)

  • Tachycardia: the heart rate is fast (>100b.p.m.).
• • Tachycardias are more symptomatic when arrhythmia is fast and sustained

  Tachycardias are subdivided into:

  • supraventricular tachycardias (SVT), which arise from the atrium or the AV junction

  • ventricular tachycardias, which arise from the ventricles
• • Some arrhythmias occur in patients with apparently normal hearts or originate from diseased tissue (scar) because of underlying structural heart disease

  • When myocardial function is poor, arrhythmias are more symptomatic and are potentially life-threatening.
• Sinus arrhythmia - Fluctuations of autonomic tone result in phasic changes of the sinus discharge rate

  • During inspiration, parasympathetic/vagal tone falls, and heart rate quickens; on expiration, the heart rate falls

  • This variation is normal in children and young adults

  •Typically, sinus arrhythmia results in predictable irregularities of the pulse.
• sinus bradycardia - <60bpm at day or <50bpm at night, usually asymptomatic unless really slow, normal in athletes due to increased vagal tone
• mechanisms of arrhythmia production:

  • disturbances in impulse generation: 1) disorder in automaticity, 2) Triggered activity (EADs and DADs)
  • disturbances in impulse propagation: 1) Re-entery, 2) Conduction Block, 3) Both (Atrial flutter)

  both can cause either bradycardia or tachycardia
• •Sinus bradycardia is a result of abnormally slow automaticity while bradycardia due to AV block is caused by abnormal conduction within the AV node or the intraventricular conduction system.
• 1. disorder of automaticity: give examples

  Increased (accelerated) automaticity due to reduced threshold potential or an increased slope of phase 4 depolarisation.

  
• 2) Triggered Activity:

   Triggered activity due to early (E) or delayed (D) ‘after-depolarizations’ reaching threshold potential

  
• Early Afterdepolarizations (EADs):

  • occur during repolarization phase of the cardiac action potential
  • Normally, during repolarization, potassium channels open, allowing potassium ions to leave the cell, leading to repolarization.
  • EADs occur when certain ion channels are reactivated, typically calcium channels, during the repolarization phase causing additional small depolarization before completion of repolarization.
  • Associated with conditions like long QT syndrome and potentially lead to life-threatening arrhythmias (e.g., torsades de pointes)
• Delayed After depolarizations (DADs):

  • occur after repolarization, during diastole
  • typically triggered by abnormal calcium release from sarcoplasmic reticulum leading to additional depolarization, can trigger premature heartbeats.
  • associated with conditions like heart failure, ischemia, and certain medications
• Torsades de pointes - type of ventricular tachycardia, potentially life-threatening

  Key features:

  1. Irregular Rhythm: polymorphic ventricular tachycardia with changing amplitude and twisting appearance of the QRS complexes around the baseline on the ECG.
  2. Prolonged QT Interval: associated with prolonged QT interval which increases the risk of torsades de pointes.
  3. Triggered by Early Afterdepolarizations (EADs)
• Risk Factors for torsades de pointes: Conditions that prolong QT interval or disrupt electrolyte balance, such as certain medications (e.g., antiarrhythmics, antipsychotics), electrolyte abnormalities (e.g., hypokalemia), and congenital long QT syndrome
• Torsades de pointes can lead to syncope (fainting) or ventricular fibrillation. If untreated, can result in sudden cardiac arrest.

  Management: addressing underlying causes or triggers - discontinue medications, correcting electrolyte imbalances, and managing contributing medical conditions. Acutely, antiarrhythmic medications or electrical cardioversion may be used
• Unlike defibrillation, which is used in cardiac arrest patients, synchronized cardioversion is performed on patients that still have a pulse but are hemodynamically unstable. It is used to treat both hemodynamically unstable ventricular and supraventricular rhythms.
• what does the image show?


  Mechanism of circus movement or re-entry. In panel 1 the impulse passes down both limbs of the potential tachycardia circuit. In panel 2 the impulse is blocked in one pathway (α) but proceeds slowly down pathway β, returning along pathway α until it collides with refractory tissue. In panel 3 the impulse travels so slowly along pathway β that it can return along pathway α and complete the re-entry circuit, producing a circus movement tachycardia.

  
• Accelerated automaticity

  • normal spontaneous cardiac rhythmicity is slow depolarization during diastole until the threshold potential is reached and the action potential of the pacemaker cells takes off

  • This may be accelerated by increasing rate of diastolic depolarization or changing the threshold potential

  • For example, sympathetic stimulation releases adrenaline, which enhances automaticity

  • Such changes are thought to produce sinus tachycardia, escape rhythms and accelerated AV nodal (junctional) rhythms.
• Triggered activity:

  • Myocardial damage can result in ‘after-depolarizations’, which may reach threshold potential and produce an arrhythmia

  • If occur before reaches threshold (end of phase 3), they are EADs

  • When they develop after the transmembrane potential is completed, they are called DADs
• EADs and DADs:

  • exaggerated by pacing, catecholamines, electrolyte disturbances, hypoxia, acidosis and some medications, which may then trigger an arrhythmia

  • atrial tachycardias produced by digoxin toxicity are due to triggered activity

  • ventricular arrhythmia in the long QT syndrome may be caused by this mechanism.
• causes of EADs:

  • slow HR
  • prolonged action potentials
  • medications like quinine which prolong action potential

  causes of DADs:

  • increased serum Ca -> increases activity of 3Na+/2Ca+ exchanger
  • increased adrenaline
  • myocardial infarctions
  • drug toxicity like digoxin
• what can EADs cause?

  here

  
• what can DADs cause?

  here

  
• Re-entry (or circus movements)

  • ‘ring’ of cardiac tissue surrounds an inexcitable core (e.g. scarred myocardium)

  • Tachycardia initiated if an ectopic beat finds one limb refractory, resulting in unidirectional block, and the other limb excitable

  • Provided conduction through the excitable limb (β) is slow enough, the other limb (α) will have recovered, allowing retrograde activation to complete the re-entry loop

  • If time to conduct around the ring is longer than refractory periods of the tissue within the ring, re-entry producing tachycardia

  
• Re-entry

  •The majority of regular paroxysmal tachycardias are produced by this mechanism
• re-entry summary:

  • Two possible routes for electrical impulse to flow down

  Fast-pathway -> Long RP

  Slow-pathway -> Short RP

  • Impulse flows down one pathway, back up the other, and gets caught in a loop.

  • Slower pathway/route can be caused by:

  1. Central area of block e.g. scar tissue, refractory cells
  2. 2.Area/path of variable blocking e.g. dead myocyte, myocytes with different RP/conduction speed
• •Sinus bradycardia is due either to extrinsic factors that influence a relatively normal sinus node, or to intrinsic sinus node disease.

  •The mechanism can be acute and reversible, or chronic and degenerative.
• Common extrinsic causes of bradycardia:

  • hypothermia, hypothyroidism, cholestatic jaundice and raised intracranial pressure

  • drug therapy with beta-blockers, digitalis and other antiarrhythmic drugs

  • neurally mediated syndromes (carotid sinus syndrome, vasovagal attacks)

  Common intrinsic causes:

  • acute ischaemia and infarction of the sinus node (as a complication of acute myocardial infarction)

  • chronic degenerative changes, such as fibrosis of the atrium and sinus node (sick sinus syndrome)
• sick sinus syndrome/sinoatrial diesease:

  • caused by idiopathic fibrosis of the sinus node

  • Other causes of fibrosis - ischaemic heart disease, cardiomyopathy or myocarditis

  • episodes of sinus bradycardia or sinus arrest and commonly experience paroxysmal atrial tachyarrhythmias (tachy–brady syndrome) owing to diffuse atrial disease.

  
• Heart block

  • Block in either the AV node or the His bundle results in AV block

  • Block lower in the conduction system produces bundle branch block

  3 forms:

  1.First-degree

  2.Second-degree

  3.Third-degree
• First-degree AV block:

  •The PR interval is uniformly prolonged more than 0.20sec. Every atrial depolarization is followed by conduction to the ventricles but with delay

  
• Second-degree AV block

  2nd degree is characterized by intermittently “dropped” QRS complexes. There are two major subtypes of second-degree AV block: Mobitz type I (AV Wenckebach) and Mobitz type II
• Mobitz I block (Wenckebach block phenomenon)

  •Sinus rhythm is present

  •The PR interval lengthens progressively with successive beats

  •Until one P wave is not conducted at all

  •The PR interval before the blocked P wave is much longer than the PR interval after the blocked P wave

  
• mobitz I block / Wenckebach block phenomenon:

  With Mobitz type I, the classic AV Wenckebach pattern , each stimulus from the atria encounters progressively more “difficulty” in traversing the AV node en route to the ventricles (i.e., the node becomes increasingly refractory). Finally, an atrial stimulus is not conducted at all, such that the expected QRS complex is blocked (“dropped QRS”). This cycle is followed by recovery of the AV node, and then the whole cycle starts again.
• Mobitz II block:

  • Sinus rhythm is present

  • The PR interval is consistent

  • One P wave is not conducted at all

  • Dropped QRS complex is NOT preceded by PROGRESSIVE PR interval prolongation

  • Usually, the QRS complex is wide (>0.12sec).

  
• Progressive PR interval prolongation = Mobitz 1

  consistent PR interval with sudden drop = type II
• 2:1 or 3:1 (advanced) block

  • Occurs when every second or third P wave conducts to the ventricles

  • The PR interval prior to the dropped P wave is always the same

  • This form of second-degree block is neither Mobitz I nor Mobitz II

  • 2:1 in bold because it is more prominent

  • May flick between 2:1 and 3:1

  
• second degree type I vs type II:

  
• Third-degree (complete) AV block

  • independent atrial (P) and ventricular (QRS complex) activity
  • Sending signals without communicating with each other - the waves overlap
  • May be buried in QRS or T wave

  
• Third-degree (complete) AV block

  • Atrial rate faster than ventricular rate

  • PR intervals are completely variable

  • Some P waves fall on the T wave, distorting its shape

  • Others may fall in the QRS complex and be “lost.”•Notice that the QRS complexes are of normal width, indicating that the ventricles are being paced from the atrioventricular junction.
• Third-degree (complete) AV block

  • Atrial rate faster than ventricular rate

  • PR intervals are completely variable• Some P waves fall on the T wave, distorting its shape• Others may fall in the QRS complex and be “lost.”•Notice that the QRS complexes are of normal width, indicating that the ventricles are being paced from the atrioventricular junction.