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Questions and Answers
What is the primary cause of the rapid upstroke spike of the action potential in ventricular muscle fibers?
What occurs during the plateau phase of the ventricular action potential?
Which channels become inactivated to help prevent constant depolarization during the action potential?
What is hyperpolarization in the context of action potentials?
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At the termination of the action potential, what membrane potential is typically reached?
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Which ion channels remain open for a few tenths of a second after the action potential terminates?
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What key process occurs in the sinus node that initiates the action potential?
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During which phase of the action potential does the influx of positive calcium and sodium ions stop?
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What is the total delay in the A-V nodal and A-V bundle system before the excitatory signal reaches the contracting muscle of the ventricles?
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What primarily causes the slow conduction in the transitional, nodal, and penetrating A-V bundle fibers?
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How does the action potential from the sinus node affect the atrial muscle mass?
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What is the approximate conduction velocity in most atrial muscle?
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What occurs as part of the hyperpolarization process after an action potential?
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What is the resting membrane potential in the sinus nodal fiber?
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What happens to potassium channels after an action potential in the sinus nodal fiber?
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What is the primary function of the atrioventricular node in cardiac conduction?
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Why is hyperpolarization not maintained indefinitely in sinus nodal fibers?
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What is the main consequence of the A-V node's delay in impulse conduction?
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What is the characteristic feature of the 'funny' current in sinus nodal fibers?
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What type of fibers are responsible for rapidly conducting impulses in the ventricles?
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Which of the following channels is primarily inactivated during hyperpolarization in sinus nodal fibers?
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Which characteristic of the A-V node is crucial for normal heart function?
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What effect does the cardiac impulse delay at the A-V node have on ventricular filling?
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What primarily causes the slow rise in the resting membrane potential of sinus nodal fibers between heartbeats?
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At what voltage does the activation of L-type calcium channels occur in sinus nodal fibers?
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What primarily prevents the sinus nodal fibers from continuously remaining depolarized?
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Which part of the heart's conduction system is responsible for delaying the impulse before it reaches the ventricles?
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Which statement accurately describes the process of impulse conduction in the heart?
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What role do funny currents play in the functioning of nodal fibers?
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What is the effect of high sodium ion concentration in the extracellular fluid on nodal fibers?
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What characterizes the self-excitation of sinus nodal fibers?
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How does hyperpolarization affect cardiac muscle fiber function?
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Which of the following describes the role of the atrial internodal pathways?
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What role does the sinoatrial node primarily serve in the cardiac conduction system?
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Which of the following statements accurately describes A-V node delay?
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What is the significance of conduction barriers in the sinoatrial pacemaker complex?
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How do HCN channels contribute to cardiac rate control?
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What is a primary mechanism through which hyperpolarization can affect cardiac cells?
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What is the primary pathway for impulse conduction from the atria to the ventricles?
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Which cell types are primarily responsible for the intrinsic rhythm of the heart?
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Which of the following mechanisms contributes to arrhythmogenesis at the tissue level?
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What is the primary consequence of impaired conduction pathways in the heart?
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Which statement best describes the interaction between local innervation and atrial fibrillation?
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What is the primary function of the sinus node in the heart?
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What is a significant feature of the sinus nodal fibers?
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How does ischemia affect the heart's conduction system?
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What allows simultaneous contraction of the ventricular chambers in the heart?
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What is primarily affected by damage to the heart's conductive system?
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What causes the slow rise in the resting membrane potential in sinus nodal fibers between heartbeats?
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At what voltage do L-type calcium channels become activated in sinus nodal fibers?
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What primarily prevents continuous depolarization of sinus nodal fibers despite sodium and calcium ion leakiness?
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What is the primary reason that sinus nodal fibers exhibit self-excitation?
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Why does the resting membrane potential not remain depolarized in sinus nodal fibers?
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What is the primary location of the A-V node?
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How long does the total delay last from the sinus node to the A-V nodal system before the impulse enters the ventricles?
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What happens after the impulse reaches the A-V node?
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What is the potential achieved at the threshold level for discharge in the A-V node?
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Which structures are involved in the conduction pathway through the A-V node?
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Which part of the heart system is primarily responsible for delaying impulse transmission to the ventricles?
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What are the approximate intervals between the sinus node impulse and its appearance in the A-V nodal system?
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What initiates the self-excitation process within the cardiac conduction system?
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What is the primary function of the A-V bundle in the cardiac conduction system?
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Why is it important for the A-V node to delay the transmission of impulses?
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The total delay in the A-V nodal and A-V bundle system is approximately 0.16 seconds.
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The conduction velocity in most atrial muscle is about 1 m/sec.
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The hyperpolarization process occurs after the action potential in cardiac muscle fibers.
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Gap junctions in the A-V bundle tissue are increased to enhance conduction speed.
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Atrial muscle fibers connect directly with the endings of the sinus nodal fibers.
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The opening of L-type calcium channels contributes to the hyperpolarization phase of the action potential in ventricular muscle fibers.
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Potassium channels remain open for a few tenths of a second after the action potential to assist in returning the membrane potential to its resting level.
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The inactivation of fast sodium channels begins approximately 250 milliseconds after they open.
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During the plateau phase of the ventricular action potential, calcium and sodium ions continue to enter the fiber.
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The resting membrane potential after an action potential in ventricular muscle fibers typically reaches around -70 to -80 millivolts.
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The barrier in the heart functions as a conductor to allow the cardiac impulse to pass freely between atrial and ventricular muscle.
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In rare cases, an abnormal muscle bridge can connect the atria and ventricles outside of the A-V bundle.
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The total elapsed time for the cardiac impulse to travel through the bundle branches until it reaches the Purkinje fibers is approximately 0.1 seconds.
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The left and right bundle branches of Purkinje fibers spread upward toward the base of the heart.
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The Purkinje fibers terminate approximately two-thirds of the way into the muscle mass of the ventricles.
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Cardiac arrhythmias can result from the re-entry of the cardiac impulse into the atria from the ventricles.
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The Purkinje fibers primarily conduct impulses within the atrial muscle mass.
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The A-V bundle is crucial for carrying the cardiac impulse from the ventricles to the atria.
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The cardiac impulse spreads immediately throughout the entire ventricular muscle mass once it enters the Purkinje conductive system.
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The A-V bundle divides after passing downward in the ventricular septum.
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Match the parts of the heart's conduction system with their functions:
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Match the ion channels with their role in cardiac muscle:
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Match the types of fibers with their characteristics:
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Match the components with their recorded potentials:
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Match the conditions with their effects on cardiac function:
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Match the following terms with their descriptions regarding the cardiac conduction system:
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Match the following phases with their respective time durations in the A-V nodal and A-V bundle system:
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Match the following cardiac conduction features with their characteristics:
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Match the following terms regarding heart impulse conduction with their roles:
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Match the following components of the cardiac conduction system with their velocities:
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Study Notes
Sinus Nodal Fiber Action Potentials
- Sinus nodal fibers have a less negative resting potential (-55 millivolts) compared to ventricular muscle fibers (-90 millivolts).
- The less negative resting potential in sinus nodal fibers allows for the influx of sodium and calcium ions, resulting in self-excitation.
- This "leaky" nature causes a slow rise in the resting membrane potential between heartbeats.
- When the potential reaches -40 millivolts, L-type calcium channels activate, initiating an action potential.
Action Potential Termination
- The action potential terminates due to the inactivation of L-type calcium channels and the opening of potassium channels.
- Inactivation of calcium channels prevents further calcium and sodium ion influx.
- Potassium channels allow potassium ions to outflow, reducing the intracellular potential back to its resting level.
- The outward flow of potassium causes a brief period of hyperpolarization (increased negativity inside the fiber) after the action potential.
Recovery from Hyperpolarization
- The hyperpolarization state is not maintained because potassium channels close over time.
- The inward "funny" current of sodium and calcium ions, along with the leakiness of the sinus nodal fiber, overcomes the outward potassium flow.
- This causes the resting potential to gradually rise back towards the threshold for another action potential.
Internodal and Interatrial Pathways
- The sinus node transmits the action potential to the atrial muscle fibers through direct connection.
- The atrial muscle fibers, in turn, spread the action potential throughout the atria.
- Conduction velocity is generally 0.3 m/sec in atrial muscle, but some specialized bands conduct more rapidly at 1 m/sec.
- These pathways ultimately transmit the impulse to the atrioventricular (AV) node.
Atrioventricular Node delays Impulses
- The AV node acts as a delay mechanism, preventing rapid transmission of the impulse from atria to ventricles.
- This delay allows the atria to empty blood into ventricles before ventricular contraction.
- The delay is caused by fewer gap junctions between cells in the AV nodal and bundle fibers.
- The reduced gap junctions create high resistance to ion flow, slowing down conduction.
- The total delay in the AV node and AV bundle is approximately 0.13 seconds.
- When combined with the initial delay from the sinus node to the AV node (0.03 seconds), the overall delay is 0.16 seconds.
Rapid Transmission in Purkinje Fibers
- The Purkinje fibers of the ventricles are specialized fibers that facilitate rapid conduction of the action potential.
- They are responsible for transmitting the impulse throughout the ventricle walls, enabling coordinated contraction.
- Their rapid conduction ensures that the ventricles contract effectively and efficiently to pump blood to the body.
The Heart's Rhythmic System
- The human heart beats approximately 100,000 times per day, or 3 billion times in a lifetime.
- This rhythmic contraction is driven by a specialized system that generates electrical impulses, initiating and conducting them through the heart for coordinated contraction.
- The system ensures atrial contraction before ventricular, allowing for ventricle filling before blood is pumped to the lungs and body.
- This system's efficiency allows for simultaneous ventricular contraction, crucial for effective blood pressure generation.
- The system is susceptible to damage from heart disease, particularly ischemia (inadequate blood flow), which can lead to abnormal heart rhythms.
Sinus Node and its Function
- The sinus node, located in the right atrium, is responsible for generating electrical impulses.
- This node has specialized fibers with low contractile capacity but are directly connected to atrial muscle fibers for rapid conduction of impulses.
Automatic Electrical Rhythmic of the Sinus Fibers
- The sinus node exhibits self-excitation: the ability to generate its own rhythmic electrical impulses.
- This is due to the high extracellular sodium concentration and the presence of open sodium channels, facilitating slow, positive sodium ion influx between heartbeats.
- This influx causes a gradual rise in the resting membrane potential, eventually reaching a threshold of -40 millivolts, which activates L-type calcium channels, triggering an action potential.
The Atrioventricular (A-V) Node
- The A-V node, located in the posterior wall of the right atrium, acts as a barrier, ensuring the cardiac impulse travels only in a forward direction from atria to ventricles via the A-V bundle.
- This delay is important to coordinate atrial and ventricular contraction.
- The A-V node delays the transmission of the electrical impulse from the sinus node for approximately 0.09 seconds before it reaches the ventricles.
The Purkinje Fibers
- The Purkinje fibers, a network of specialized conducting cells, rapidly distribute the electrical impulses throughout the ventricles.
- The A-V bundle divides into the left and right bundle branches, which further divide into smaller branches, effectively traversing the ventricular walls.
- These fibers connect with the ventricular muscle, ensuring rapid and coordinated contraction.
Significance of the Conduction System
- The organized structure of the cardiac conduction system facilitates rapid and efficient spread of electrical impulses throughout the heart, resulting in coordinated contractions for efficient blood pumping.
- Any disruption in the system, such as damage from heart disease, can lead to arrhythmias (abnormal heart rhythms).
Summary of the Heart's Conduction System
- The sinus node generates electrical impulses for heart contraction.
- The A-V node delays transmission, ensuring atrial contraction before ventricular.
- The Purkinje fibers distribute impulses rapidly throughout the ventricles for coordinated muscle contraction.
- This integrated system is crucial for normal heart rhythm and function.
Action Potential in Ventricular Muscle
- Opening of fast sodium channels results in rapid upstroke spike of action potential due to sodium ion influx.
- Plateau of the action potential is caused by slower opening of sodium-calcium channels lasting for approximately 0.3 seconds.
- Potassium channel opening allows potassium ion efflux, returning membrane potential to resting level.
Rhythmical Discharge of Sinus Nodal Fiber
- L-type calcium channels inactivate after 100-150 milliseconds.
- Increase in potassium channels opening at the same time as inactivation of calcium channels leads to a decrease in intracellular potential.
- Hyperpolarization occurs due to continued potassium efflux for a few tenths of a second, resulting in a more negative intracellular potential.
Conduction of Cardiac Impulses Through the Atria
- Sinus nodal fibers connect directly with atrial muscle fibers, transmitting action potentials.
- Action potential spreads through atrial muscle mass, reaching the AV node.
- Conduction velocity in atrial muscle is approximately 0.3 m/sec, with faster conduction (1 m/sec) in certain atrial fiber bands.
AV Node and AV Bundle
- AV node delays conduction of the cardiac impulse by approximately 0.03 seconds.
- AV Bundle, composed of multiple fascicles, further delays conduction by 0.04 seconds.
- Total delay between sinus node and ventricular muscle is 0.16 seconds.
Cause of Slow Conduction in AV Node and Bundle
- Fewer gap junctions between cells in the conducting pathways increase resistance to ion conduction.
Rapid Transmission of Cardiac Impulse Through Ventricles
- Purkinje fibers, after passing through the fibrous tissue, divide into left and right bundle branches.
- Branches spread to the apex of the ventricle and course around the ventricular chambers.
- Purkinje fibers penetrate muscle mass and connect with cardiac muscle fibers.
- Cardiac impulse travels through the Purkinje fiber system within 0.03 seconds.
Sympathetic Stimulation of the Heart
- Increases heart rate.
- Enhances excitability of the heart.
- Increases contractile force of atrial and ventricular muscle.
- Increases permeability of muscle fiber membranes to sodium and calcium ions.
- Increases rate of diastolic membrane potential drift towards threshold in sinus node, accelerating self-excitation and increasing heart rate.
- Reduces conduction time from atria to ventricles by increasing sodium-calcium permeability in AV node and bundle.
- Increases calcium ion permeability contributing to stronger cardiac contraction.
Parasympathetic (Vagal) Stimulation of the Heart
- Decreases heart rate.
- Reduces excitability of AV junctional fibers, slowing transmission of cardiac impulses to ventricles.
- Increases potassium permeability of conductive fibers, causing hyperpolarization and reduced excitability.
- Strong vagal stimulation can block transmission of cardiac impulses from atria to ventricles.
Mechanism of Vagal Effects
- Acetylcholine released at vagal nerve endings increases potassium permeability of conductive fibers.
- Potassium efflux results in hyperpolarization, making the tissue less excitable.
Ventricular Escape
- Weak vagal stimulation slows heart rate, while strong stimulation can block conduction from the atria to the ventricles.
- In case of complete block, some area in the Purkinje fibers develops its own rhythm, leading to ventricular contraction at 15-40 beats per minute.
Fibrous Barrier
- Normally prevents passage of the cardiac impulse between atrial and ventricular muscle.
- Allows for selective transmission through the AV bundle.
- In rare cases, accessory pathways may penetrate the barrier, leading to re-entry of impulses and cardiac arrhythmias.
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Description
Explore the intriguing mechanisms behind sinus nodal fiber action potentials and their role in cardiac physiology. This quiz covers the resting potentials, ion influx, and the termination of action potentials due to channel inactivation. Test your understanding of these vital concepts in heart function.