Fiche de révision : Cardiac Electrical Physiology and Arrhythmias

📋 Course Outline

1. Conduction Pathway
2. Cardiac Action Potential
3. Refractory Periods
4. Excitation–Contraction Coupling
5. SA Node Pacemaker
6. ECG Waves and Intervals
7. ECG Vector Principles
8. Cardiac Axis Deviations
9. Arrhythmias and Causes
10. Channelopathies and QT Prolongation
11. Hyperkalaemia Effects

📖 1. Conduction Pathway

🔑 Key Concepts & Definitions

• Conduction Pathway: The sequence of electrical activation in the heart, ensuring coordinated contraction.
• SA Node (Sinoatrial Node): The heart's natural pacemaker that initiates electrical impulses, setting the rhythm.
• Atrial Conduction: Spread of electrical activity through the atria, leading to atrial contraction.
• AV Node (Atrioventricular Node): Delays conduction to allow atrial contraction before ventricles contract.
• Bundle of His: The pathway transmitting impulses from AV node to bundle branches.
• Bundle Branches: Right and left pathways that conduct impulses to respective ventricles.
• Purkinje Fibers: Network of fibers that rapidly distribute impulses throughout the ventricles, causing synchronized contraction.

📝 Essential Points

• The conduction sequence: SA node → atria → AV node → Bundle of His → bundle branches → Purkinje fibers → ventricles.
• Conduction speeds vary: slow in atria (allows atrial emptying), very slow in AV node (ventricular filling), very fast in His-Purkinje system (coordinated ventricular contraction).
• AV delay is crucial for cardiac efficiency, ensuring atria contract before ventricles.
• Disruption in this pathway can cause arrhythmias, such as AV block or re-entry circuits.

💡 Key Takeaway

The heart's conduction pathway is a precisely timed electrical sequence that ensures effective and coordinated cardiac contractions, with specific delays like the AV node critical for optimal heart function.

📖 2. Cardiac Action Potential

🔑 Key Concepts & Definitions

• Phases of Cardiac Action Potential: Sequential stages (0-4) that describe voltage changes during a cardiac cell's electrical activity.
• Depolarisation (Phase 0): Rapid influx of Na⁺ ions through fast sodium channels, causing a sharp rise in membrane potential.
• Plateau (Phase 2): Sustained depolarisation due to Ca²⁺ influx via L-type calcium channels balancing K⁺ efflux.
• Repolarisation (Phase 3): Outflow of K⁺ ions through delayed rectifier channels returning the membrane potential to resting.
• Refractory Period: Time during which a cell cannot initiate another action potential; includes absolute and relative refractory periods.
• Excitation–Contraction Coupling: Process linking electrical depolarisation to muscle contraction, involving Ca²⁺ dynamics.

📝 Essential Points

• Phases and Ion Movements:
  • Phase 0: Na⁺ influx → rapid depolarisation.
  • Phase 1: Transient K⁺ outflow → brief repolarisation.
  • Phase 2: Ca²⁺ influx balances K⁺ efflux → plateau.
  • Phase 3: K⁺ outflow dominates → repolarisation.
  • Phase 4: Resting potential maintained by K⁺ leak channels.
• Plateau Significance:
  • Ensures sustained contraction.
  • Prevents tetany, allowing the heart to relax and fill.
• Refractory Periods:
  • Prevents premature contractions and re-entry arrhythmias.
  • Absolute RP: no new AP possible.
  • Relative RP: stronger stimulus needed.
• ECG Correlation:
  • P wave: atrial depolarisation.
  • QRS complex: ventricular depolarisation.
  • T wave: ventricular repolarisation.
• Autonomic Modulation:
  • Sympathetic ↑ Ca²⁺ entry → stronger, faster contractions.
  • Parasympathetic ↓ HR via K⁺ efflux.

💡 Key Takeaway

The cardiac action potential's phases coordinate to produce a controlled electrical and mechanical response, with the plateau phase playing a crucial role in sustaining contraction and preventing arrhythmias. Proper timing of depolarisation, repolarisation, and refractory periods ensures effective and safe heart function.

📖 3. Refractory Periods

🔑 Key Concepts & Definitions

• Refractory Period (RP): The time during which cardiac cells cannot initiate a new action potential or require a stronger-than-normal stimulus to do so. It ensures proper timing of heart contractions.
• Absolute Refractory Period: The phase in which no new action potential can be generated, regardless of stimulus strength. Corresponds mainly to phases 0, 1, and part of 2 of the cardiac action potential.
• Relative Refractory Period: The phase following the absolute RP during which a stronger-than-normal stimulus can initiate a new action potential. Corresponds to late phase 2 and phase 3.
• Effective Refractory Period (ERP): The period during which the heart cannot be re-excited, preventing premature contractions.
• Functional Significance: Refractory periods prevent abnormal rhythms such as back-propagation of impulses and tetanic contractions, maintaining coordinated heart activity.

📝 Essential Points

• The absolute refractory period overlaps with the plateau phase (phase 2) of the ventricular action potential, where Ca²⁺ influx sustains contraction.
• The relative refractory period occurs during repolarization (phase 3), when some Na⁺ channels are recovered but the cell is still less excitable.
• The length of refractory periods varies across cardiac tissue; it is longest in the AV node to allow proper conduction delay.
• Prevention of re-entry circuits: Refractory periods are crucial in preventing abnormal re-excitation that can cause arrhythmias.
• Clinical relevance: Shortened refractory periods can predispose to tachyarrhythmias; prolonged periods may cause conduction blocks.

💡 Key Takeaway

Refractory periods are vital for ensuring the heart beats in a coordinated, rhythmic manner by preventing premature or abnormal electrical impulses, thus maintaining effective cardiac function.

📖 4. Excitation–Contraction Coupling

🔑 Key Concepts & Definitions

• Excitation–Contraction Coupling (ECC): The physiological process linking electrical stimulation (action potential) of cardiac muscle cells to mechanical contraction.
• L-type Calcium Channels: Voltage-gated channels on the cell membrane that allow Ca²⁺ entry during the action potential, initiating ECC.
• Sarcoplasmic Reticulum (SR): Intracellular Ca²⁺ store that releases Ca²⁺ in response to triggers, facilitating muscle contraction.
• Troponin: Regulatory protein on actin filaments that binds Ca²⁺, enabling cross-bridge formation and contraction.
• SERCA (Sarcoplasmic/Endoplasmic Reticulum Ca²⁺-ATPase): Pump responsible for re-sequestering Ca²⁺ into the SR during relaxation.
• Sympathetic Modulation (PKA pathway): Enhances Ca²⁺ influx and SR Ca²⁺ uptake, increasing contraction strength and relaxation speed.

📝 Essential Points

• The process begins with an action potential (AP) that depolarizes the cardiac cell membrane.
• Depolarization opens L-type Ca²⁺ channels, allowing Ca²⁺ to enter the cell.
• The influx of Ca²⁺ triggers the release of additional Ca²⁺ from the SR via ryanodine receptors (calcium-induced calcium release).
• Increased cytosolic Ca²⁺ binds to troponin, causing conformational changes that enable actin-myosin cross-bridge formation, resulting in contraction.
• Relaxation occurs when Ca²⁺ is pumped back into the SR by SERCA and expelled from the cell via other mechanisms.
• Sympathetic stimulation (via PKA) increases Ca²⁺ entry and SR Ca²⁺ reuptake, producing a stronger and faster contraction and relaxation.
• Proper timing of Ca²⁺ cycling is crucial for effective cardiac function and prevention of arrhythmias.

💡 Key Takeaway

Excitation–Contraction Coupling in the heart translates electrical signals into mechanical force through regulated Ca²⁺ movements, with sympathetic modulation enhancing cardiac performance.

📖 5. SA Node Pacemaker

🔑 Key Concepts & Definitions

• SA Node (Sinoatrial Node): The primary pacemaker of the heart located in the right atrium; initiates electrical impulses that set the heart rate.
• Pacemaker Potential: The gradual depolarisation that occurs in pacemaker cells due to the "funny current" (If), leading to spontaneous firing.
• Funny Current (If): A slow, inward Na⁺ current activated during hyperpolarisation, responsible for the spontaneous depolarisation in SA node cells.
• Autonomic Regulation: Modulation of heart rate via sympathetic (↑ HR) and parasympathetic (↓ HR) nervous systems acting on the SA node.
• Absence of Stable Resting Potential: Unlike other cardiac cells, SA node cells do not have a true resting potential; they continuously depolarise toward threshold.

📝 Essential Points

• Pacemaker Activity: The SA node depolarises spontaneously due to If, leading to rhythmic action potentials without external stimuli.
• Control of Heart Rate: Sympathetic stimulation increases cAMP, enhancing If and increasing HR; parasympathetic stimulation decreases cAMP and increases K⁺ efflux, reducing HR.
• Automaticity: The SA node's ability to generate impulses independently, ensuring continuous heartbeat.
• Threshold and Firing: Once depolarisation reaches threshold (~-40 mV), voltage-gated Ca²⁺ channels open, producing the action potential.
• Clinical Relevance: Dysfunction can lead to arrhythmias such as sinus bradycardia or sinus tachycardia.

💡 Key Takeaway

The SA node's unique ability to spontaneously depolarise via the funny current, modulated by autonomic input, makes it the heart's natural pacemaker, controlling the rhythm and rate of cardiac contractions.

📖 6. ECG Waves and Intervals

🔑 Key Concepts & Definitions

• P wave: Represents atrial depolarisation, the electrical activity initiating atrial contraction.
• PR interval: Time from the start of atrial depolarisation (P wave) to the start of ventricular depolarisation (QRS complex); reflects AV nodal delay.
• QRS complex: Represents ventricular depolarisation, leading to ventricular contraction.
• ST segment: The plateau phase of ventricular action potential; indicates early ventricular repolarisation.
• T wave: Represents ventricular repolarisation, restoring the resting state.
• Normal intervals:
  • PR: 0.12–0.20 seconds
  • QRS: 0.08–0.12 seconds
  • QT: 0.25–0.45 seconds

📝 Essential Points

• ECG waves correspond to specific electrical events in the cardiac cycle.
• Intervals measure the time between waves, indicating conduction times and repolarisation duration.
• Depolarisation toward the electrode produces positive deflections; depolarisation away produces negative deflections.
• Normal ECG axis is downwards and to the left; deviations indicate axis deviations (left or right).
• Refractory periods prevent abnormal rhythms; the absolute refractory period blocks any new impulses, while the relative RP allows a strong stimulus to evoke a response.
• Arrhythmias such as sinus arrhythmia, AV block, ventricular tachycardia, are identified by changes in wave morphology and intervals.
• Channelopathies (e.g., Long QT syndrome) involve ion channel dysfunctions affecting repolarisation, increasing arrhythmia risk.
• Hyperkalaemia causes partial depolarisation, inactivating Na⁺ channels, leading to conduction issues and arrhythmias.

💡 Key Takeaway

ECG waves and intervals provide a window into the heart’s electrical activity, with specific waveforms corresponding to distinct phases of cardiac depolarisation and repolarisation; understanding these patterns is essential for diagnosing conduction abnormalities and arrhythmias.

📖 7. ECG Vector Principles

🔑 Key Concepts & Definitions

• Electrical Vector: A representation of the direction and magnitude of electrical activity during cardiac depolarisation or repolarisation, depicted as an arrow in a 2D plane.
• Depolarisation Vector: The direction of electrical current flow during the activation of cardiac tissue, influencing ECG waveforms.
• Positive Deflection: An upward wave on ECG when the depolarisation vector moves toward the recording electrode.
• Negative Deflection: A downward wave when the depolarisation vector moves away from the electrode.
• Perpendicular Vector: When the electrical activity is at a 90° angle to the electrode, resulting in a small deflection.
• Cardiac Axis: The overall direction of the heart's electrical depolarisation in the frontal plane, typically oriented downward and to the left.

📝 Essential Points

• The ECG records the vector sum of electrical activity from millions of cardiac cells, not individual cell activity.
• The direction of depolarisation determines the deflection: toward the electrode = positive; away = negative.
• The cardiac axis reflects the general orientation of the heart's electrical activity; normal axis is downward-left.
• Deviations in the axis (left or right axis deviation) are identified by the polarity of leads II, III, and I:
  • Left axis deviation: Lead II & III negative.
  • Right axis deviation: Lead I negative.
• Understanding the vector principle helps interpret ECG abnormalities, such as hypertrophy or conduction blocks.

💡 Key Takeaway

The ECG vector principle explains how the direction of electrical depolarisation influences waveform deflections, enabling accurate assessment of cardiac electrical activity and axis deviations.

📖 8. Cardiac Axis Deviations

🔑 Key Concepts & Definitions

• Cardiac Axis: The overall direction of the heart's electrical depolarization during ventricular contraction, represented as an angle in the frontal plane on an ECG.
• Normal Axis: The mean electrical vector points downward and to the left, typically between -30° and +90°.
• Left Axis Deviation (LAD): The mean axis shifts more leftward, beyond -30°, indicating abnormal depolarization.
• Right Axis Deviation (RAD): The axis shifts more rightward, beyond +90°, indicating abnormal depolarization.
• Electrical Axis: The average direction of ventricular depolarization, inferred from the QRS complex in leads I and aVF.
• Lead I & aVF: Standard ECG leads used to determine the direction of the cardiac axis based on the polarity of the QRS complex.

📝 Essential Points

• The normal cardiac axis is between -30° and +90°, reflecting typical ventricular depolarization.
• Left axis deviation suggests conditions like left anterior fascicular block, left ventricular hypertrophy, or inferior myocardial infarction.
• Right axis deviation indicates right ventricular hypertrophy, pulmonary hypertension, or lateral myocardial infarction.
• To determine the axis:
  • Check the QRS polarity in leads I and aVF.
  • If QRS is positive in both, axis is normal.
  • If QRS is negative in lead I and positive in aVF, axis is rightward (RAD).
  • If QRS is positive in lead I and negative in aVF, axis is leftward (LAD).
• Extreme axis deviation (northwest axis) is rare and indicates severe conduction abnormalities or ventricular rhythms.

💡 Key Takeaway

The cardiac axis reflects the predominant direction of ventricular depolarization, and deviations from the normal axis can indicate underlying cardiac pathology or conduction abnormalities. Correct interpretation involves analyzing the QRS polarity in leads I and aVF to determine the axis shift.

📖 9. Arrhythmias and Causes

🔑 Key Concepts & Definitions

• Arrhythmia: An abnormal heart rhythm resulting from irregular electrical activity in the heart. It can be too fast (tachyarrhythmia), too slow (bradyarrhythmia), or irregular.
• Re-entry circuit: A self-perpetuating electrical loop that causes abnormal rapid rhythms, often responsible for tachyarrhythmias like ventricular tachycardia.
• AV block: Impaired conduction between the atria and ventricles, classified into first, second, and third degree, leading to delayed or dissociated ventricular activation.
• Ventricular fibrillation: Disorganized electrical activity in the ventricles causing ineffective contractions, leading to sudden cardiac death if untreated.
• Channelopathies: Genetic or acquired disorders affecting ion channels, disrupting normal cardiac repolarization or depolarization, e.g., Long QT syndrome.
• Hyperkalaemia: Elevated extracellular potassium levels that depolarize cardiac cells, impairing conduction and increasing arrhythmia risk.

📝 Essential Points

• Mechanisms of arrhythmias:
  • Abnormal automaticity: Increased or abnormal pacemaker activity outside the SA node.
  • Triggered activity: Early or delayed afterdepolarizations that initiate abnormal impulses.
  • Re-entry: Most common cause, involving a circuit where an impulse re-enters tissue due to unidirectional block and slowed conduction.
• Common causes:
  • Ischemia, electrolyte disturbances (hyperkalaemia, hypokalemia), drugs (e.g., QT-prolonging medications), structural heart disease, and channelopathies.
• ECG features:
  • Sinus arrhythmia: Normal variation with breathing.
  • AV block: Prolonged PR interval (1st degree), dropped QRS (2nd degree), complete dissociation (3rd degree).
  • Ventricular tachycardia: Wide QRS, rapid rate.
  • Ventricular fibrillation: Chaotic, irregular waveforms.
• Clinical significance:
  • Some arrhythmias are benign (sinus arrhythmia), while others are life-threatening (ventricular fibrillation).
  • Treatment depends on the type, cause, and hemodynamic stability.

💡 Key Takeaway

Arrhythmias arise from disturbances in the heart’s electrical conduction or automaticity, often caused by re-entry circuits or ion channel dysfunctions, and can range from benign to immediately life-threatening conditions requiring prompt diagnosis and management.

📖 10. Channelopathies and QT Prolongation

🔑 Key Concepts & Definitions

• Channelopathy: A disorder caused by dysfunctional ion channels affecting cardiac electrical activity, often leading to arrhythmias.
• QT interval: The time from the start of ventricular depolarisation (Q wave) to the end of repolarisation (T wave) on ECG; reflects total ventricular electrical activity.
• Long QT syndrome (LQTS): A condition characterized by an abnormally prolonged QT interval, increasing risk of torsades de pointes and sudden cardiac death.
• HERG (Human Ether-à-go-go-Related Gene) channels: Potassium channels responsible for phase 3 repolarisation; blockade causes QT prolongation.
• Early afterdepolarisations (EADs): Abnormal depolarisations during the repolarisation phase, triggered by delayed repolarisation, leading to arrhythmias.
• Re-entry circuit: An abnormal electrical loop that can cause tachyarrhythmias, often facilitated by prolonged repolarisation.

📝 Essential Points

• Mechanism of Long QT: Reduced function of K⁺ channels (especially HERG) delays repolarisation, prolonging the QT interval.
• Drug-induced QT prolongation: Many medications block HERG channels, increasing risk of torsades de pointes; a common reason for drug withdrawal.
• Genetic LQTS: Mutations affecting ion channels (e.g., KCNQ1, KCNH2) impair repolarisation, predisposing to arrhythmias.
• Consequences of QT prolongation: Delayed repolarisation fosters EADs, which can trigger re-entry circuits, leading to torsades de pointes and ventricular fibrillation.
• Hyperkalaemia: Elevated extracellular K⁺ depolarizes RMP, inactivates Na⁺ channels, and predisposes to conduction abnormalities and arrhythmias.
• ECG features: Prolonged QT interval (>0.45s in females, >0.44s in males), risk of torsades, characteristic notches or biphasic T waves in some cases.

💡 Key Takeaway

Prolongation of the QT interval due to channelopathies disrupts normal repolarisation, increasing the risk of dangerous arrhythmias like torsades de pointes and ventricular fibrillation, especially when triggered by drugs or electrolyte disturbances.

📖 11. Hyperkalaemia Effects

🔑 Key Concepts & Definitions

• Hyperkalaemia: Elevated serum potassium levels, typically >5.0 mmol/L, which can disrupt normal cardiac electrical activity.
• Resting Membrane Potential (RMP): The electrical potential across the cell membrane when the cell is at rest; in cardiac cells, normally around -90 mV.
• Inactivation of Na⁺ Channels: A state where sodium channels become non-conductive due to sustained depolarisation, impairing action potential initiation.
• Arrhythmia: Abnormal heart rhythm resulting from disrupted electrical conduction.
• Repolarisation: The process of returning the cardiac cell membrane potential to its resting state after depolarisation, primarily via K⁺ efflux.
• ECG Changes in Hyperkalaemia: Characteristic alterations such as peaked T waves, widened QRS complexes, and eventual sine wave pattern indicating severe hyperkalaemia.

📝 Essential Points

• Mechanism of Hyperkalaemia: Increased extracellular K⁺ reduces the gradient across the cell membrane, leading to partial depolarisation of cardiac cells.
• Effect on Resting Membrane Potential: Elevated serum K⁺ causes the RMP to become less negative (less polarized), approaching the threshold for activation.
• Impact on Sodium Channels: Partial depolarisation inactivates fast Na⁺ channels, impairing the initiation and conduction of action potentials.
• Consequence for Cardiac Conduction: Slowed or blocked conduction pathways, increasing the risk of arrhythmias such as ventricular fibrillation.
• ECG Manifestations:
  • Peaked T waves (early sign)
  • Prolonged PR interval
  • Widened QRS complex
  • Sine wave pattern in severe cases
• Clinical Significance: Hyperkalaemia is a medical emergency; rapid treatment is essential to prevent life-threatening arrhythmias.

💡 Key Takeaway

Hyperkalaemia depolarises cardiac cells by reducing the potassium gradient, leading to Na⁺ channel inactivation, slowed conduction, and characteristic ECG changes that can progress to fatal arrhythmias if untreated.

📊 Synthesis Tables

⚠️ Common Pitfalls & Confusions

1. Confusing absolute and relative refractory periods; absolute RP is during phases 0-2, relative during late phase 2-3.
2. Misinterpreting the ECG waves: P wave (atrial depolarisation), QRS (ventricular depolarisation), T wave (repolarisation).
3. Assuming the conduction delay only occurs at the AV node; it also occurs in atria and bundle branches.
4. Overlooking the plateau phase (Phase 2) as a period of repolarisation; it actually sustains depolarisation.
5. Mistaking the "funny current" (If) in pacemaker cells for sodium channels; it's primarily mixed Na⁺/K⁺ current.
6. Believing all arrhythmias are due to conduction block; some are caused by automaticity or re-entry.
7. Confusing hyperkalaemia effects with hypokalaemia; hyperkalaemia causes peaked T waves and conduction delays.
8. Overgeneralizing the ECG axis deviations without considering individual patient context.

✅ Exam Checklist

• Describe the conduction pathway of the heart and its components.
• Explain the phases of the cardiac action potential and their ionic basis.
• Differentiate between absolute and relative refractory periods and their significance.
• Outline the process of excitation–contraction coupling in cardiac myocytes.
• Identify the SA node as the primary pacemaker and describe its pacemaker potential.
• Interpret ECG waves and intervals, including their normal durations and clinical significance.
• Explain the principles of ECG vector analysis and how it relates to the cardiac axis.
• Recognize signs of axis deviations and their possible causes.
• List common arrhythmias, their ECG features, and underlying mechanisms.
• Discuss channelopathies affecting repolarisation, such as Long QT syndrome, and their implications.
• Describe the effects of hyperkalaemia on cardiac electrophysiology and ECG.
• Understand the clinical implications of conduction delays, blocks, and re-entry circuits.