Cardiac Physiology and ECG Interpretation Quiz

Cardiology: Dysrhythmias and Basic ECG's

• This is a BMS200 week 9 course content on cardiology concerning dysrhythmias and basic electrocardiograms (ECGs).
• Learning outcomes include analysis of ECG characteristics, pathophysiology of dysrhythmias, description of supraventricular and ventricular dysrhythmias, conduction blocks, ECG findings related to cardiac ischemia, mechanisms of anti-arrhythmic medications, and the role of chronic inflammation and myocardial fibrosis in dysrhythmia development.
• Students will learn to analyze a normal ECG, including heart rate and determination of rhythm, P-R, QRS, and Q-T intervals, and normal waveforms in P, QRS, and T waves.
• The student will understand the etiology, pathophysiology, clinical features, ECG findings, and prognosis of atrial fibrillation, atrial flutter, sinus tachycardia, and paroxysmal supraventricular tachycardia, premature ventricular contraction, idioventricular rhythm, ventricular tachycardia, ventricular fibrillation, torsades de pointes, 1st-degree heart block, 2nd-degree heart block, and 3rd-degree heart block.
• Basic ECG findings related to cardiac ischemia and correlation with vascular territories will be discussed.
• The pharmacological mechanisms of action and adverse effects of common anti-arrhythmic medications.
• The student will also understand the contribution of chronic inflammation and myocardial fibrosis to dysrhythmia development.

Learning Outcomes (Detailed)

• Analyzing normal ECG characteristics (heart rate, rhythm, P-R, QRS, Q-T intervals, waveforms).
• Describing how triggered activity, abnormal automaticity, and re-entry contribute to the pathophysiology of common dysrhythmias.
• Outlining the epidemiology, pathogenesis, clinical features, ECG findings, and prognosis of various supraventricular and ventricular dysrhythmias (e.g., atrial fibrillation, atrial flutter, sinus tachycardia, PVCs, VT).
• Describing the ECG findings in cardiac ischemia and correlating them to vascular territories.
• Discussing the mechanism of action and adverse effects of common anti-arrhythmic medications.
• Examining the role of chronic inflammation and myocardial fibrosis in dysrhythmia development.

Pre-Assessment Questions

• Question 1: What electrical event occurs during the Q-T interval of an ECG ?

  • Repolarization of the ventricular myocyte

• Question 2: Where in the heart are the cells responsible for the cardiac pacemaker located?

  • The right atrium, close to the entrance of the superior vena cava

Review: Electrocardiogram (ECG)

• ECG records electrical impulses produced by heart muscle depolarization and repolarization.

• The amplitude of ECG waves reflects the amount of electrical activity. Larger waves correspond to larger areas of activated myocardial tissue.

• Upward deflections indicate electrical impulse movement toward the electrode; downward deflections suggest movement away.

• Conducting tissues (SA node, AV node, bundle branches) generate less electrical activity than myocardial tissue, making them less prominent on an ECG.

• ECG primarily reflects activity of larger myocardial cells that contract and pump blood.

• The duration of waves (P, QRS, T) provides information about timing of electrical events. Example: a prolonged QRS may indicate delayed ventricular conduction.

• ECG leads measure the extracellular current that travels from depolarized cells to polarized (resting) cells.

• ECG leads only "notice" changes in membrane potential.

• "Plateaus" do not register as waves (phase 4, 2 of a myocyte).

• ECG lead placement (coronal, cross-sectional) gives a 3-dimensional view of heart's electrical activity.

• Bipolar leads compare voltage changes between two leads (e.g., lead I compares right and left arms). Unipolar/precordial leads compare voltage changes between a lead and center of the heart.

• The x-axis of an ECG represents time in seconds; the y-axis depicts voltage in mV.

Approach to Interpreting ECG

• Determine heart rate.
• Methods: Divide 300 by the number of large boxes between R waves.
• Determine the rhythm (regular or irregular).
• Identify the origin of impulses (is there a P wave before the QRS?).
• Regular, or regularly irregular, or irregularly irregular rhythms.

Step 3-Intervals (1)

• Examine intervals for widening or shortening; this can indicate conduction system problems.
• Major intervals of interest: P-R interval (prolongation = AV nodal dysfunction), QRS interval (delay in ventricular excitation), QT interval (repolarization abnormalities).

Step 3- Intervals (2)

• Evaluate intervals to understand conduction pathway problems.

Step 4 - Waves

• Examine the positioning and morphology of waves (upward or downward).
• Compare wave sizes to normal.
• Check for abnormal waves or variations in appearance

Step 4 - Q-Waves

• Abnormal Q waves suggest possible prior myocardial infarction (MI). Significant Q waves typically are wide, large, and measurable, and present in leads V1–V3.

Step 4 - ST Segments

• Evaluate ST segments to identify possible MI or other conditions.

Steps 4 - T-Waves

• Examine T-wave morphology (shape & position).
• Determine presence of abnormal T waves (e.g., increased or decreased amplitude, inverted, elevated or depressed segments). These abnormalities might indicate problems/ conditions like hypokalemia, hyperkalemia.

Steps 4 - P-Waves

• Examine P-wave shape & position
• Determine the presence of absent or multiple P-waves
• Characterize the atrial axis.

General Pathophysiology of Dysrhythmias (1)

• Re-entry occurs when a depolarization wave enters a damaged area where conduction is slower than normal.
  • This damaged tissue results in the wave taking an alternative/slower pathway leading to re-excitation, resulting in tachycardia.

General Pathophysiology of Dysrhythmias (2)

• Ectopic foci can be caused by local changes in electrolyte concentration in scar tissue, a phenomenon called abnormal automaticity.
• Inhibition of Na+/K+ pump, leading to accumulation of Na+ and Ca2+ resulting in partial depolarization, leading to abnormal cell activity.

General Pathophysiology of Dysrhythmias (3)

• Triggered activity is an abnormal depolarization of ventricular myocytes that occurs before the original action potential has completed its course, an example being PVCs.
• Conditions like Bradycardia and reduced or prolonged phase 3 of the action potential duration favor triggering activity..

Chronic Inflammation and Myocardial Fibrosis and Dysrhythmias

• Immune cells (macrophages, mast cells, T-cells) promote myocardial repair or fibrosis based on conditions.
• Myocardial fibrosis promotes re-entry.

Supraventricular Dysrhythmias

• Atrial fibrillation is the most common type of arrhythmia, often linked to chronic lung or heart disease.

• Risk factors for atrial fibrillation include age, hypertension, chronic lung and/ or heart disease.

• Other supraventricular dysrhythmias include atrial flutter, sinus tachycardia (can be normal or a problem), and paroxysmal supraventricular tachycardia.

Atrial Fibrillation ECG - (1, 2)

• Narrow complex, regularly irregular rhythm, no distinguishable P waves.

Supraventricular Dysrhythmias - Atrial Flutter

• Very common and characterized by a regular atrial rhythm, usually with a fast atrial rate (300 bpm).
• The ventricular rate can be regular or irregular.

Supraventricular Dysrhythmias - Sinus Tachycardia

• Normal rhythm but a fast heart rate (150 - 250 bpm), resulting from increased cardiac output.
• Can be normal or pathological, as often an indication of elevated catecholamines due to exercise, pain, or anxiety.

Supraventricular Dysrhythmias - Paroxysmal Supraventricular Tachycardia (SVT)

• Intermittent/ sudden episodes of supraventricular tachycardia
• Can originate in the atria or AV node resulting in regular or irregular rhythms.
• Many causes, including hyperthyroidism, anxiety, cocaine, structural heart disease.

Ventricular Dysrhythmias - Premature Ventricular Contractions (PVCs)

• Starts with a heartbeat arising from the ventricle before the next expected.
• Can be in isolation (single PVC), doublets, or triplets (normal heart beat (QRS) followed by 2 (PVCs), or followed by 3 (PVCs) followed by a normal heart beat.
• Etiology is often unknown, caffeine, anxiety, sleep deprivation.

Ventricular Dysrhythmias - Idioventricular Rhythm

• Slow, regular ventricular rhythm with a rate below 50 bpm and no P waves.
• Usually, the result of failing SA and AV nodes.

Ventricular Dysrhythmias - Ventricular Tachycardia (VT)

• Characterized by three or more consecutive premature ventricular contractions, sometimes with a rate of 100-250 bpm.
• Etiology often linked to ischemic heart disease, can result in sudden cardiac death from progression to ventricular Fibrillation.

Ventricular Dysrhythmias - Ventricular Fibrillation

• Irregular electrical activity with ventricular rate exceeding 300 bpm.
• Life threatening requiring immediate treatment (defibrillator and CPR)
• Often related to cardiac ischemia, or other problems.

Ventricular Dysrhythmias - Torsades de Pointes

• A specific form of polymorphic ventricular tachycardia
• Often associated with QTc prolongation (lengthening of the QT interval), which can trigger arrhythmia.

Conduction Blocks - First-Degree AV Block

• Prolonged PR interval (>0.20 seconds), with each impulse conducted to the ventricles, usually asymptomatic.

Conduction Blocks - Second-Degree AV Block Type 1 (Wenckebach)

• Progressive lengthening of the PR interval until a QRS complex is dropped, usually asymptomatic.

Conduction Blocks - Second-Degree AV Block Type 2

• Fixed PR intervals with occasional dropped QRS complexes. More serious than Type I (Wenckebach), sometimes progressing to third-degree heart block.

Conduction Blocks - Third-Degree AV Block (Complete Heart Block)

• No impulse transmission from the atria to the ventricles which results in independent atrial and ventricular rates.
• Likely needs immediate treatment or a pacemaker.

Cardiac Ischemia and ECG

• Ischemia typically first shows as inverted T waves in any lead.
• ST elevation in leads matching the location of the injury.
• Q waves may be present with or without ST elevation in cases concerning old or previous myocardial infarction.

Anti-Arrhythmic Mechanism of Action

• Class 1: Bind and inhibit Na+ channels.
• Class 2: Beta-blockers.
• Class 3: Block K+ channels prolonging repolarization.
• Class 4: Block Ca2+ channels to reduce influx.

Additional Information:

• Cases from the class, and potential ECG abnormalities can arise from placing the ECG incorrectly, which can distort the information provided.