Arrhythmia

• Cardiac dysrhythmia (arrhythmia) is characterized by abnormal electrical activity of the heart
• The heart cells spontaneously generate action potential (impulses), with the highest frequency in the SA node
• Excitability is the ability of heart cells to respond to impulses, with the impulse from the SA node activating neighboring cells
• Conductivity involves the rapid propagation of the impulse from the SA node to the entire conduction system and then more slowly through the working myocardium
• Contractility is the ability of the working myocardium to contract, as it contains myofibrils (muscle fibers)
• The conduction system of the heart includes the supraventricular conduction system (SA node, Bachmann's bundle, Internodal pathways) and the ventricular conduction system (Right bundle branch, Left bundle branch, Left anterior fascicles, Left posterior fascicles, Purkinje fibers)
• The phases of cardiac action potential include Phase 0 (rapid depolarization), Phase 1 (K+ channels), Phase 2 (plateau), Phase 3 (rapid repolarization), and Phase 4 (resting potential)
• Etiology of arrhythmias can be due to factors such as ischemia, ion imbalance, heart diseases, autonomic nervous system dysbalance, thyroid diseases, toxins/drugs, genetic mutations, and age
• Mechanisms of tachyarrhythmias include increased automaticity (normal and abnormal), triggered activity (early afterdepolarization, delayed afterdepolarization), and reentry
• Inherited arrhythmias like Long QT syndrome and Brugada syndrome are caused by mutations in ion channel genes and can lead to serious symptoms like ventricular tachycardia, syncope, and sudden cardiac death
• Signs of arrhythmias can manifest as changes in the ECG, alterations in hemodynamic parameters like preload and minute heart output, and specific symptoms like syncope, cardiac arrest, nightmares, and fever
• Bradycardia leads to decreased minute cardiac output
• Tachycardia results in increased minute cardiac output, but intensive tachycardia (>200/min) can lead to decreased minute cardiac output due to diastole shortening (insufficient chamber filling)
• Clinical symptoms of cardiac arrhythmias include syncope, palpitations, and sudden cardiac death
• Classification of cardiac arrhythmias based on mechanism includes disorders of impulse generation, disorders of impulse conduction, and a combination of both
• Cardiac arrhythmias can originate from different sites:

  • Supraventricular:
  • Sinus
  • Atrial
  • Junctional
  • Ventricular
• Sinus arrhythmias:

  • Sinus tachycardia:
  • Rate > 100 beats/min
  • Physiological causes: newborns, children, physical activity, stress, pain
  • Drug-induced causes: catecholamines, caffeine
  • Disease-related causes: hyperthyroidism, anemia, fever, sepsis, hypokalemia
  • Sinus bradycardia:
  • Rate < 60 beats/min
  • Physiological causes: athletes at rest, during sleep, elderly
  • Disease-related causes: hypothyroidism, hypothermia, hyperkalemia
  • Drug-induced causes: digitalis, beta-blockers
  • Premature sinus contraction (Sinus extra beat, extrasystole):
  • Common in young people
• • Can lead to Morgagni-Adams-Stokes syndrome: asystole, syncope, skeletal muscle cramps
• Sinus arrhythmia (sinus respiratory arrhythmia):

  • Physiological rhythm associated with breathing
  • Effect of vagus nerve on SA node automaticity
  • ↑ frequency during inspiration, ↓ frequency during expiration
  • Common in young people and sportsmen
  • Sick sinus syndrome:
  • Includes brady-tachy arrhythmias
  • Can be inherited or associated with coronary artery disease, hypertension, or idiopathic causes
  • Sinus arrest:
  • Causes: increased vagus activity, ischemia, inflammation, degeneration of SA node
  • Manifests as missing P-wave and QRS complex
• Atrial arrhythmias:

  • Premature atrial contraction (extra beat):
  • Impulse originates from an atrial ectopic focus
  • Changes in P-wave, QRS complex, and T wave are not significant
  • Atrial rhythm:
  • Rhythm generated by an ectopic focus in the atria
  • Atrial (supraventricular) tachycardia:
  • Involves reentry mechanism
  • Atrial flutter:
  • Associated with conditions like mitral stenosis, ICHS
  • Fast creation of impulses from a single ectopic focus in the atria (220-350/min)
  • Characterized by saw-toothed P-waves
  • AV node may filter impulses in ratios like 2:1, 3:1, 4:1
• • Atrial fibrillation:
  • Associated with conditions like mitral stenosis, hyperthyroidism, atrial septal defects
  • Can lead to thrombus formation and complications like stroke
  • Involves fast and uncoordinated impulses from multiple ectopic foci in the atria
  • AV node filters impulses irregularly, leading to irregular P-waves and QRS complexes
• Junctional arrhythmias (from AV node):

  • Premature junctional contraction (extra beat):
  • Impulse originates in the AV node and spreads to atria and ventricles
  • Different patterns of P-wave and QRS complex based on the location of the ectopic focus
  • Junctional rhythm
  • Junctional (supraventricular) tachycardia:
  • Involves reentry mechanism
• Ventricular arrhythmias:

  • Premature ventricular contraction (extra beat, extrasystole, VEX):
  • Impulse originates from a ventricular ectopic focus
  • ECG changes include variable shapes, shorter RR intervals, missing P-waves, wide QRS complexes, and abnormal T-waves
  • Unifocal and multifocal VEXs
  • Ventricular escape rhythm:
  • Involves abnormal ventricular pacemaker
  • Accelerated idioventricular rhythm:
  • Frequency < 100/min
  • Ventricular tachycardia:
  • Originates from a ventricular ectopic focus
  • Frequency > 100/min
  • Polymorphic ventricular tachycardia:
• • Includes ventricular flutter and Torsades de pointes
  • High risk of ventricular fibrillation
• Heart blocks (AV blocks):

  • 1st degree:
  • Every impulse is conducted with prolonged PR interval (>0.2 s)
  • 2nd degree:
  • Type 1 (Mobitz I, Wenckebach): Progressive prolonged conduction in AV node leading to occasional non-conducted impulses
  • Type 2 (Mobitz II): Some impulses are conducted while others are not
  • 3rd degree:
  • Complete AV block with independent atrial and ventricular activation leading to ventricular escape rhythm
• Bundle branch blocks:

  • Desynchronization of ventricular depolarization and repolarization
  • Right bundle branch block:
  • Delayed activation of the right ventricle
  • Produces secondary R wave (R’) in right precordial leads and wide, slurred S wave in lateral leads
  • Left bundle branch block:
  • Reversal of normal septal depolarization direction
  • Leads to tall R waves in lateral leads and deep S waves in right precordial leads with left axis deviation
• Wolff-Parkinson-White syndrome:

  • Preexcitation syndrome with an accessory pathway between atria and ventricles
  • Bundle of Kent: Abnormal accessory conduction pathway
  • ECG changes include widened QRS complex, shorter PR interval (delta wave)
  • Symptoms may include palpitations, dizziness, dyspnea, syncope