Cardiac Arrhythmias Quiz

Arrhythmias

• Arrhythmia is an abnormality in the heart's rhythm.
• Arrhythmias can cause serious health problems, including sudden death, syncope, heart failure, dizziness, palpitations.
• Some people have no symptoms.
• Two main types are bradycardia (slow heart rate) and tachycardia (fast heart rate).

Lecture Plan

• Electrical conduction in the heart involves action potentials in myocardial and nodal cells, as recorded by ECG.
• Arrhythmias include bradycardia and tachyarrhythmias (supraventricular and ventricular).
• Mechanisms of arrhythmias include automaticity, triggered activity, and re-entry.
• Treatment and anti-arrhythmic drugs like Class I-IV are discussed.
• Atrial fibrillation is a specific type of arrhythmia addressed here.

Normal Physiology

• Heart impulses originate regularly at 60-100 beats per minute.
• The SA node sets the heart's rhythm (pacemaker).
• The AV node delays the electrical signal to the heart apex.
• The bundle of His and Purkinje fibers transmit the impulse for contraction throughout the ventricles.
• The SA node is the fastest pacemaker in the heart.
• The AV node ensures the atria contract fully before the ventricles, which is important for efficient blood pumping.

Myocardial Cell Action Potential

• Phase 4: Resting membrane potential.
• Phase 0: Depolarization - Na+ channels open.
• Phase 1: Initial repolarization - Na+ channels close, K+ channels open.
• Phase 2: Plateau - Ca2+ channels open, K+ channels slowly open, but still slow to open and allow the plateau to occur.
• Phase 3: Repolarization- Ca2+ channels close, K+ channels fully open.
• Voltage-gated channels regulate ion movement, influencing membrane potential changes.

Auto-rhythmic Cells Action Potential

• Pacemaker potential is an unstable resting potential that initiates each heartbeat.
• It's driven by the slow inward movement of Ca2+ (funny current) and a subsequent outward current of K+.
• This differs from action potentials in contractile cells, where Na+ channels trigger depolarization.
• The pacemaker potential reaches threshold, triggering an action potential.
• Pacemaker potentials regulate heart rhythm and contractility.

Cardiac Arrhythmias

• Abnormal heart rhythms are called cardiac arrhythmias.
• Bradycardia (slow heart rate) is less than 60 beats per minute, while tachycardia (fast heart rate) is greater than 100 beats per minute.

Arrhythmia Causes (multiple factors)

• Acid-base imbalances
• Cellular hypoxia (lack of oxygen)
• Congenital heart defects
• Connective tissue disorders
• Degeneration of conductive tissue
• Drug toxicity
• Electrolyte imbalances
• Emotional stress
• Hypertrophy of the heart muscle
• Myocardial ischemia or infarction (heart attack)
• Organic heart disease

Tachyarrhythmias (supraventricular and ventricular)

• Supraventricular:
  • Sinus tachycardia (SA node fires too quickly)
  • Atrial tachycardia
  • Focal atrial tachycardia
  • Multifocal atrial tachycardia
  • Atrial flutter (re-entry)
  • Atrioventricular nodal re-entry tachycardia (AVNRT)
  • Atrioventricular re-entry tachycardia (AVRT)
• Ventricular:
  • Ventricular tachycardia (monomorphic and polymorphic)
  • Torsades de pointes (prolonged QT interval)
  • Ventricular fibrillation

Bradycardia

• Sinus bradycardia (slowed SA node firing)
• Heart block (1st, 2nd, and 3rd degree)
• Sick sinus syndrome

Mechanisms

• Automaticity
• Triggered activity
• Re-entrant circuit
• Parasystole

Automaticity (Bradycardia and Tachycardia)

• Bradycardia: Increased vagal tone, drug effects (beta-blockers, calcium channel blockers, digoxin), decreased metabolic activity (hypothermia, hypothyroidism). Increased intracranial pressure
• Tachycardia: Increased sympathetic activity, hypovolemia, hypoxia (COPD, pulmonary embolism), sympathomimetics (e.g., cocaine), pain/anxiety, increased metabolic activity (fever, hyperthyroidism).

Triggered Activity

• EAD (Early After Depolarization): Occurs shortly after the previous action potential, caused by decreased levels of K+, Ca2+, and Mg2+.
• DAD (Delayed After Depolarization): Follows the previous action potential with a longer delay, possibly due to ischaemia, hypoxia, inflammation, stretch, increased sympathetic activity, or digoxin toxicity.

EAD Causes

• Decreased levels of K+, Ca2+, Mg2+.
• Drugs: anti-arrhythmics, antibiotics, psychotics, depressants, emetics.

QT Elongation

• Prolonged QT interval can lead to torsades de pointes, potentially fatal cardiac arrhythmia.
• Blockade to potassium current (I_k) affects the action potential duration.

Torsades de Pointes

• Prolonged QT interval
• Can lead to ventricular fibrillation
• Treat with magnesium sulfate
• Some drugs like terfenadine block potassium channels and are linked to the condition.

DAD Causes

• Ischaemia
• Hypoxia
• Inflammation (myocarditis)
• Stretch
• Increased sympathetic activity
• Digoxin toxicity

Re-entry

• Cyclical activation in a part of the heart causing tachycardia.
• Often involves a slow and a fast pathway causing an impulse and repeating process.
• Often associated with supraventricular tachycardia (e.g., atrial fibrillation, atrial flutter) and ventricular tachycardia

AVNRT and AVRT

• Functional and anatomical re-entry pathways.

ECG in Arrhythmias

• ECGs (electrocardiograms) help diagnose arrhythmias by visualizing the electrical activity of the heart.
• Key features to look for include P waves, QRS complexes, and heart rate patterns.

Anti-arrhythmic Agents

• Classified by their mechanism of action, such as Class Ia, Ib, Ic, II, III, IV, and other medications.

Class I

• Na+ channel blockers.
• Quinidine, Lidocaine, Flecainide.

Class II

• β-adrenergic blockers.
• Block sympathetic stimulation to slow down heart rate and conduction..
• Propranolol, atenolol, metoprolol

Class III

• K+ channel blockers.
• Ibutilide
• Amiodarone.
• Sotalol is a mixed-class II and III anti-arrhythmic.
• Drugs block repolarization and lengthen the effective refractory period.

Class IV

• Ca2+ channel blockers.
• Verapamil and Diltiazem.
• They preferentially reduce conduction in SA and AV nodes.
• They prolong repolarization and reduce AV conduction velocity by blocking calcium channels.

Anti-arrhythmic Agents - Other

• Adenosine stimulates P₁ purinergic receptors, opening K+ channels, inhibiting SA and AV node conduction, and reducing Ca²+ dependent action potentials.
• Digoxin increases force of contraction and vagal activity. Some effects are on the Na+/K+ -ATPase pump

Digoxin Toxicity

• Gastrointestinal distress, hyperkalemia, life-threatening arrhythmias (including increased automaticity and AV nodal blockade).
• Chronic toxicity is more prevalent in the elderly and those with renal impairment.

Non-Pharmacological Treatments

• Vagal maneuvers (e.g., valsalva, carotid massage) to slow the heart rate might be used.
• Cardioversion (electrical shock) can be used to reset the heart rhythm.
• Ablation, surgically destroying parts of the heart, helps correct abnormal electrical pathways.

Atrial Fibrillation (AF)

• Cardiac (e.g. hypertension, valvular) or systemic causes (e.g., alcohol intake, hyperthyroidism).

Atrial Fibrillation Symptoms

• Breathlessness, palpitations, chest discomfort, syncope, decreased exercise tolerance, malaise, or polyuria, stroke, transient ischemic attack, heart failure.

Atrial Fibrillation Diagnosis

• 12-lead ECG—shows no P waves and an irregular heart rate.

Atrial Fibrillation Treatment

• Rate control (drugs like beta-blockers or calcium channel blockers)
• Rhythm control (drugs like amiodarone or cardioversion)
• Anticoagulation (drugs like warfarin or DOACs).

Cardioversion

• Electrical shock to reset the heart rhythm; a treatment for atrial fibrillation.

Test your knowledge on various types of cardiac arrhythmias and their characteristics. This quiz covers the mechanisms, drugs, and conditions related to heart rhythm disorders, providing insights into the complex world of cardiac electrophysiology. Perfect for students and professionals in the medical field.