HARD QUIZ CARDIAC ELECTROPHYSIOLOGY
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Questions and Answers

What is a key difference between non-pacemaker and pacemaker action potentials?

  • Pacemaker cells are located in atrial and ventricular myocytes.
  • Non-pacemaker cells have spontaneous depolarization.
  • Non-pacemaker cells exhibit rapid depolarization with a plateau phase. (correct)
  • Pacemaker cells have a true resting potential.

    • Which ions primarily influence the resting membrane potential in cardiac cells?

  • K+ and SO4^2-
  • Na+, Ca++, and K+ (correct)
  • Cl- and HCO3-
  • Na+ and Mg2+

    • What role do ion transport pumps play in the generation of membrane potentials in the heart?

  • They promote spontaneous depolarization in pacemaker cells.
  • They maintain ion concentration gradients. (correct)
  • They initiate action potentials.
  • They directly affect the duration of action potentials.

    • Which statement about the cardiac action potential is true?

    <p>It has a duration that is significantly longer than that in skeletal muscle. (C)</p> Signup and view all the answers

    How does the autonomic nervous system affect pacemaker cell activity?

    <p>It inhibits the depolarization rate. (A)</p> Signup and view all the answers

    Which of the following cells are classified as non-pacemaker cells?

    <p>Ventricular contracting myocytes (A)</p> Signup and view all the answers

    Which type of AV block causes complete dissociation between atrial and ventricular depolarizations?

    <p>3° AV block (B)</p> Signup and view all the answers

    What is a common effect of excessive vagal activation on the AV node?

    <p>Decreases conduction velocity (D)</p> Signup and view all the answers

    What triggers reentry in a cardiac conduction pathway?

    <p>Unidirectional block and critical timing (A)</p> Signup and view all the answers

    In ventricular ectopic foci, why is there a wide QRS complex observed?

    <p>Normal conduction pathways are not followed (B)</p> Signup and view all the answers

    Which condition is associated with a high risk of supraventricular tachycardia due to reentry?

    <p>Wolff-Parkinson-White syndrome (C)</p> Signup and view all the answers

    What is a characteristic feature of junctional pacemaker sites in the presence of AV block?

    <p>Rate of 30-40 bpm (C)</p> Signup and view all the answers

    What primarily initiates the spontaneous depolarization in pacemaker action potentials?

    <p>Pacemaker funny current (If) driven by slow inward Na+ (C)</p> Signup and view all the answers

    During which phase of non-pacemaker action potentials does rapid depolarization occur?

    <p>Phase 0 (A)</p> Signup and view all the answers

    What effect does sympathetic activation have on nodal action potentials?

    <p>Increases the slope of phase 4 (B)</p> Signup and view all the answers

    Which channel's activity is primarily responsible for K+ dependence during the repolarization phase of pacemaker action potentials?

    <p>Delayed rectifier potassium channels (A)</p> Signup and view all the answers

    What is the primary reason for the phase 2 'plateau phase' in non-pacemaker action potentials?

    <p>Increased Ca++ influx (D)</p> Signup and view all the answers

    Which factor primarily influences the sinoatrial node's (SA node) firing rate at rest?

    <p>Parasympathetic nervous system activity (C)</p> Signup and view all the answers

    What happens during the inactivation of sodium channels in cardiac action potentials?

    <p>Current can no longer flow, preventing depolarization (D)</p> Signup and view all the answers

    What is the role of gap junctions in cardiac action potential conduction?

    <p>To allow electrical impulse conduction between adjacent cells (C)</p> Signup and view all the answers

    What is the primary function of the atrioventricular node (AVN) in the conduction system?

    <p>Delays conduction into the ventricles (B)</p> Signup and view all the answers

    Which receptor activation increases conduction velocity in cardiac cells?

    <p>β1 receptors (D)</p> Signup and view all the answers

    What effect does increased vagal tone have on conduction velocity within the heart?

    <p>Decreases conduction velocity through calcium channel blockade (C)</p> Signup and view all the answers

    Which structure has the fastest conduction speed in the heart?

    <p>Purkinje fibers (B)</p> Signup and view all the answers

    What mechanism can cause a decreased phase 0 slope in AVN cells?

    <p>Calcium channel blockade (B)</p> Signup and view all the answers

    Which of the following conditions is associated with conduction blocks in the heart?

    <p>Myocardial ischemia (D)</p> Signup and view all the answers

    Which ion mechanism contributes to decreased conduction velocity in non-nodal cells?

    <p>Sodium channel inactivation (D)</p> Signup and view all the answers

    How does autonomic nerve activity generally influence heart conduction?

    <p>It regulates conduction speed depending on sympathetic or parasympathetic balance (D)</p> Signup and view all the answers

    What characterizes the conduction through the Bundle of His?

    <p>Fast conduction speed (A)</p> Signup and view all the answers

    What is a potential cause for ectopic foci in the heart?

    <p>Electrolyte imbalances (B)</p> Signup and view all the answers

    Flashcards

    Resting Membrane Potential

    The voltage difference across a cell's membrane when the cell is not active, influenced by ion concentrations and channel functions.

    Pacemaker Action Potentials

    Electrical signals generated by pacemaker cells that control heart rhythm; these cells have spontaneous depolarization without a true resting phase.

    Non-Pacemaker Action Potentials

    Action potentials in atrial and ventricular myocytes characterized by a true resting potential and distinct phases of rapid depolarization and prolonged plateau.

    Ion Concentration Gradients

    Differences in ion concentrations (Na+, Ca++, K+) across a membrane that generate electrical activity in cells.

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    Electrogenic Ion Pumps

    Membrane proteins that move ions to maintain gradients and contribute to the resting membrane potential of cardiac cells.

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    Electrical Conduction Pathways

    Pathways in the heart that allow for the conduction of electrical signals, essential for coordinated heart contractions.

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    Electrogenic ion transport

    Transport of ions across membranes that generates an electrical potential.

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    Pacemaker potential

    The slow depolarization in pacemaker cells initiating heartbeats.

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    Types of cardiac action potentials

    Fast-response and slow-response action potentials in the heart.

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    Phase 4 in pacemaker cells

    Resting phase, maintains pacemaker potential before depolarization.

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    Role of sympathetic activation

    Increases heart rate and decreases time to threshold in pacemaker cells.

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    Non-pacemaker action potential phases

    Sequence: Phase 4 resting, Phase 0 rapid depolarization, Phases 1-3 repolarization.

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    Gap junctions function

    Connections that allow the electrical impulse to spread between cardiac cells.

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    Calcium's role in cardiac action potentials

    Calcium influx is critical during depolarization and plateau phases.

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    Sinoatrial Node (SAN)

    The primary pacemaker of the heart that initiates heartbeats.

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    Atrioventricular Node (AVN)

    A specialized node that slows conduction to allow ventricular filling.

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    Bundle of His

    Conducts electrical impulses from the AVN to the bundle branches.

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    Purkinje Fibers

    Fibers that rapidly conduct impulses throughout the ventricles.

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    Positive Dromotropy

    Increase in conduction velocity in the heart, primarily through sympathetic activation.

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    Negative Dromotropy

    Decrease in conduction velocity due to parasympathetic activation.

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    Calcium Channel Blockers

    Medications that decrease conduction velocity by blocking calcium channels.

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    Ectopic Foci

    Abnormal pacemaker sites outside the SAN that can cause irregular heartbeats.

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    Ion Channel Inactivation

    The prevention of ions from entering or exiting cells, affecting conduction speed.

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    Conduction Blocks

    Disruptions in the normal electrical conduction system of the heart.

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    Functional Abnormalities

    Alterations that affect heart conduction, such as ischemic injury or hyperkalemia.

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    AV Block

    A delay or complete block in electrical impulses through the atrioventricular node.

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    Reentry Circuits

    Circuits that can cause tachyarrhythmias due to unidirectional blocks.

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    Bradycardia

    Slow heart rate due to AV block causing distal pacemaker activation.

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    Autonomic Influence on Heart

    Nervous system modulation affecting heart rate and conduction velocity.

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    Study Notes

    Cardiac Electrophysiology Lecture Notes

    • The lecture is about cardiac electrophysiology, specifically focusing on action potentials and conduction pathways within the heart.
    • Learning objectives include explaining how ion concentrations, ion channel function, and electrogenic pump activity affect resting membrane potential.
    • Objectives also include describing the electrophysiological basis for cardiac pacemaker and non-pacemaker action potentials.
    • Identifying and describing normal pathways for electrical conduction within the heart is also noted.

    Cardiac Action Potentials

    • Cardiac action potentials differ in duration from nerve and muscle action potentials. They last longer than action potentials in nerve and skeletal muscle.
    • Cardiac action potentials are not initiated by nerves or neurotransmitters.
    • Some cardiac cells possess spontaneous pacemaker activity.

    Non-Pacemaker vs. Pacemaker Action Potentials

    • Non-pacemaker cells (fast-response) include atrial and ventricular myocytes and Purkinje fibers.
    • These cells exhibit a true resting potential, followed by rapid depolarization with a prolonged plateau phase followed by repolarization.
    • Pacemaker cells (slow-response) include sinoatrial and atrioventricular nodes.
    • They do not have a resting potential and exhibit spontaneous depolarization and repolarization.

    Membrane Potential Generation

    • Membrane potentials in the heart are generated by ion movement across membranes (ion currents).
    • Ion concentration gradients are maintained by ion transport pumps.
    • Ion conductances are calculated using the Goldman-Hodgkin-Katz equation.
    • Electrogenic ion transport contributes via Na+/K+-ATPase, Na+/Ca2+ exchangers, and Ca2+-ATPase.

    Cardiac Ion Channels

    • Different ion channels influence various phases of cardiac action potentials.
    • Sodium channels (fast and slow) are involved in phase 0 depolarization.
    • Potassium channels (inward rectifier, transient outward, and delayed rectifier) contribute to repolarization.
    • Calcium channels (L-type and T-type) play a role in both non-pacemaker and pacemaker action potentials.

    Pacemaker Action Potentials

    • Pacemaker potentials are slow-response action potentials found in the sinoatrial and atrioventricular nodes.
    • Phase 4, the pacemaker potential, is driven by the "funny" current (If).
    • Phase 0 depolarization is largely Ca++-dependent.
    • Phase 3 repolarization is primarily K+-dependent.

    Location of Pacemaker Cells

    • Sinoatrial (SA) node: primary pacemaker (60-100 bpm).
    • Atrioventricular (AV) node: secondary pacemaker (40-60 bpm).
    • Purkinje fibers: secondary pacemaker (30-40 bpm).

    SA Nodal Firing Rate Regulation

    • Sympathetic activation increases firing rate (positive chronotropy) via β1-adrenergic receptors.
    • Parasympathetic activation (vagal) decreases firing rate (negative chronotropy) via muscarinic (M2) receptors.

    Autonomic Regulation of Nodal Action Potentials

    • Sympathetic activation decreases time to reach threshold, increases the slope of phase 4, and decreases action potential duration.
    • Vagal activation increases time to reach threshold, decreases the slope of phase 4, and increases action potential duration.

    Factors Affecting Pacemaker Activity

    • Hormones (e.g., thyroxine, catecholamines) affect pacemaker activity.
    • Potassium ions, ischemia, and hypoxia influence the rate.
    • Various drugs affect pacemaker activity.

    Non-Pacemaker Action Potentials

    • These action potentials are present in atrial and ventricular myocytes and Purkinje fibers.
    • They generally involve fast Na+-dependent depolarization and repolarization, involving significant K+ currents.
    • Some phases display a plateau which is calcium current-mediated.

    Sodium Channels - Timing of Activation and Inactivation

    • Activation occurs during phase 0 depolarization due to rapid depolarization to threshold.
    • Inactivation occurs during phases 2 and 3, when the cell is unresponsive to further stimulation.
    • Resting states exist during phase 4, enabling the cell to be re-excited.

    Fast Response Action Potentials

    • Fast-response action potentials are typically suppressed by pacemaker activity.
    • Specialized cells in the His-Purkinje system may exhibit slow spontaneous depolarization in some cases.
    • Removal of the overdrive suppression (e.g., during a 3rd degree heart block) may allow for slow, spontaneous activity in these cells.

    Conduction of Action Potentials within the Heart

    • Cardiac action potentials are conducted from cell to cell.
    • Conduction is facilitated by specialized pathways and low-resistance gap junctions.
    • These junctions allow current flow between cells, enabling the coordinated contraction of the heart.

    Cardiac Conduction System

    • Sinoatrial (SA) node initiates the heartbeat and triggers action potential spread.
    • Internodal pathways propagate signals through the atria.
    • Atrioventricular (AV) node slows conduction to allow atrial contraction(s) to complete.
    • Bundle of His and Purkinje fibers rapidly conduct signals through the ventricles for coordinated contraction.

    Factors Affecting Conduction Velocity

    • Sympathetic activation increases conduction velocity (positive dromotropy).
    • Parasympathetic activation decreases conduction velocity (negative dromotropy).
    • Certain ions (e.g., potassium) and drugs influence conduction velocity.

    Abnormal Conduction

    • Conduction blocks and ectopic foci can disrupt normal conduction pathways.

    • Ischemia/hypoxia and drugs can disrupt conduction.

    AV Block

    • AV blocks can lead to ventricular bradycardia.
    • Different degrees of AV block cause variable delays in ventricular depolarization.

    Ectopic Foci

    • Ectopic foci generate abnormal action potentials outside the normal conduction pathways.
    • These foci lead to wide QRS complexes. These result from dysrhythmic depolarization/contraction. This can lead to ventricular dysrhythmia.

    Reentry

    • Reentry requires: partial depolarization of a conduction pathway, unidirectional block and critical timing.
    • Changes in autonomic function can initiate or stop reentry by altering conduction velocity and ERP.

    Summary of Major Concepts

    • Cardiac cell membrane potentials are primary influenced by Na+, K+, and Ca++.
    • SAN pacemaker activity and conduction velocity are contingent on autonomic nerves, hormones, electrolytes, and afterdepolarizations.
    • Specialized conduction pathways ensure rapid activation.
    • AvN blocks disrupt coordinated atrial and ventricular contractions.
    • Reentry can cause tachycardia.

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    Cardiac Electrophysiology Lecture 01 PDF

    Description

    This quiz covers key concepts in cardiac electrophysiology, focusing on action potentials and conduction pathways in the heart. It includes learning objectives related to ion concentrations, channel functions, and the differences between pacemaker and non-pacemaker action potentials. Test your understanding of how these elements work together to regulate heart function.

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