3: Arrhythmias and Antiarrhythmic Drugs

Arrhythmias and Antiarrhythmic Drugs

• Lecture 3 covers arrhythmias and antiarrhythmic drugs.
• Learning objectives include describing various arrhythmias (sinus bradycardia, ventricular bradycardia, sinus tachycardia, atrial tachycardia/fibrillation, premature ventricular complexes, and ventricular tachycardia) and recognizing them on ECGs.
• Objectives also include understanding how abnormal automaticity and reentry cause arrhythmias.
• Identifying causes of abnormal conduction, utility/limitations of the Vaughn-Williams classification scheme, and specific drug effects on ion channels and conduction are also included.
• The lecture details how drugs (adenosine, atropine, and ivabradine) are used in treating arrhythmias.

Abnormal Heart Rates

• Abnormal heart rates include bradycardia (rates below 60 bpm) and tachycardia (rates above 100 bpm). These can be normal or pathological.
• Bradycardia:
  • Physiological causes: Highly trained athletes can exhibit resting heart rates as low as 40 bpm.
  • Pathological causes: SAN ischemia, excessive vagal tone, electrolyte disorders, and drug use (beta-blockers, calcium channel blockers) are common.
• Tachycardia:
  • Physiological causes: Exercise, acute stress (sympathetic activation).
  • Pathological causes: Chronic stress, hyperthyroidism, fever/infections, structural/ischemic heart disease, and anemia.

Bradycardia (Rate < 60 bpm)

• Atrial (sinus) bradycardia:
  • Physiological causes: highly trained athletes.
  • Pathological causes: ischemia of the sinoatrial node (SAN), excessive vagal tone, electrolyte imbalances, and some medications.
• Ventricular bradycardia:
  • Pathological: SA nodal failure, second-degree AV block (2° AV block), and third-degree AV block (3° AV block), often related to damage or degeneration of the His-Purkinje system.
• Treatment: addressing underlying causes (if possible), chronotropic drugs (like atropine, beta-agonists), or pacemaker implantation.

Tachycardia (Rate > 100 bpm)

• Sinus tachycardia:
  • Physiological causes: Exercise, acute stress
  • Pathological causes: Stress, hyperthyroidism, fever, infections, and structural/ischemic heart disease.
• Atrial tachycardia -Atrial flutter (250-350 bpm) -Causes: Structural/ischemic heart disease , Electrolyte disorders, thyroid disorders, medications/drugs/alcohol, Genetic diseases. -Atrial fibrillation (rapid, random depolarizations within atria). -Causes: Structural/ischemic heart disease, thyroid disease, excess catecholamines, medications & drugs/alcohol, and genetic diseases.
• Premature ventricular complex (PVC): -Spontaneous firing of ventricular ectopic foci. -Produces early/premature ventricular contraction. -Wide, atypical QRS complex.
• Ventricular tachycardia: -Pathological causes: Chronic stress, hyperthyroidism, fever/infection, structural/ischemic heart disease, and anemia. -Mechanism of electrophysiology includes rapid spontaneous firing of ectopic ventricular sites/afterdepolarization, and reentry (local/global).

Abnormal Conduction

• Prolonged PR interval, QRS, or QT interval often indicates problems with conduction pathways.
• Ischemic injuries to coronary arteries or severe hyperkalemia can affect conduction by altering cell depolarization and conduction velocity, often in non-nodal tissues.
• Abnormal pacemaker sites (like ectopic foci) and excessive vagal activation can also cause disruptions in conduction patterns.

Antiarrhythmic Drugs

• Vaughan-Williams classification categorizes antiarrhythmic drugs.
  • Class I (sodium channel blockers: IA, IB, IC, ID).
  • Class II (beta-blockers).
  • Class III (potassium channel blockers).
  • Class IV (calcium channel blockers).
• Drugs like adenosine, atropine, and ivabradine do not fit into these classes.

Class I Drugs

• These drugs block sodium channels in the heart, decreasing conduction velocity.
•   Different classes (IA, IB, IC, ID) exhibit varying degrees of fast sodium channel blockade, altering action potential duration, effective refractory period, and conduction velocity.

Class II Drugs (Beta-blockers)

• Block sympathetic activation
• Slow ventricular rate by depressing AV nodal conduction
• Suppress abnormal automaticity and reentry arrhythmias
• Decrease slope of phase 4 and conduction velocity.

Class III Drugs

• Structurally diverse drugs that delay repolarization (phase 3) and raise action potential duration and effective refractory periods (ERP).
• Very effective in supraventricular and ventricular tachycardia caused by reentry.
• Increased Q-T interval can lead to potentially dangerous torsades de pointes (TdP).

Class IV Drugs (Calcium Channel Blockers)

• Block L-type calcium channels, primarily in SA and AV nodes.
• Reduce conduction velocity and lengthen action potential duration.
• Effective in supraventricular tachycardias involving AV nodal reentry.

Drugs Not Fitting into Vaughan-Williams

• Adenosine: Rapidly suppresses supraventricular tachycardia caused by AV nodal reentry.
• Atropine: Used to reverse AV block by blocking excessive vagal influences on nodal tissues, increasing SA node heart rate, and AV nodal conduction velocity.
• Ivabradine: Blocks sinoatrial funny currents, reducing heart rate without affecting other crucial heart functions.

This quiz covers Lecture 3 on arrhythmias and antiarrhythmic drugs. It addresses different types of arrhythmias, their recognition on ECGs, and the mechanisms behind abnormal heart rates. Additionally, it explores the Vaughn-Williams classification and the application of specific drugs in treatment.