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Questions and Answers
What is the primary role of the Bundle of His in the cardiac conduction system?
What is the primary role of the Bundle of His in the cardiac conduction system?
What is the estimated time taken for impulse to travel from the bundle branches to the Purkinje fibers?
What is the estimated time taken for impulse to travel from the bundle branches to the Purkinje fibers?
What is the primary barrier that prevents impulses from moving directly from the atria to the ventricles?
What is the primary barrier that prevents impulses from moving directly from the atria to the ventricles?
Which receptor is involved in the hyperpolarization of nodal tissue when cholinergic vagal fibers are stimulated?
Which receptor is involved in the hyperpolarization of nodal tissue when cholinergic vagal fibers are stimulated?
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What is the effect of sympathetic stimulation on the cardiac conduction system?
What is the effect of sympathetic stimulation on the cardiac conduction system?
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What change occurs in intracellular cAMP levels when M2 receptors are activated?
What change occurs in intracellular cAMP levels when M2 receptors are activated?
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How long does it take for impulse transmission from initial bundle branches to the ventricles in a normal heart?
How long does it take for impulse transmission from initial bundle branches to the ventricles in a normal heart?
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What is the velocity of transmission of impulses in ventricular muscle fibers?
What is the velocity of transmission of impulses in ventricular muscle fibers?
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What is the primary role of the sinoatrial (SA) node in the heart?
What is the primary role of the sinoatrial (SA) node in the heart?
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What triggers the spontaneous depolarization in the SA node?
What triggers the spontaneous depolarization in the SA node?
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What is the threshold membrane potential for action potential generation in the SA node?
What is the threshold membrane potential for action potential generation in the SA node?
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What causes the delay in conduction at the AV node?
What causes the delay in conduction at the AV node?
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What is the normal firing rate of the SA node?
What is the normal firing rate of the SA node?
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How long does it take for the impulse to travel from the SA node to the AV node?
How long does it take for the impulse to travel from the SA node to the AV node?
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Which structures serve as latent pacemakers if the SA node is suppressed?
Which structures serve as latent pacemakers if the SA node is suppressed?
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What is the primary mechanism for repolarization of the SA node action potential?
What is the primary mechanism for repolarization of the SA node action potential?
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What defines an ectopic pacemaker in the heart?
What defines an ectopic pacemaker in the heart?
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What is a primary cause for the shift of the pacemaker from the SA node?
What is a primary cause for the shift of the pacemaker from the SA node?
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Why is the AV nodal delay important in cardiac function?
Why is the AV nodal delay important in cardiac function?
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What is the resting membrane potential of normal cardiac muscle?
What is the resting membrane potential of normal cardiac muscle?
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What primarily causes the plateau phase in the action potential of ventricular cardiac muscle?
What primarily causes the plateau phase in the action potential of ventricular cardiac muscle?
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During which phase of the cardiac action potential does rapid K+ efflux occur?
During which phase of the cardiac action potential does rapid K+ efflux occur?
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What mechanism restores the resting potential after cardiac muscle depolarization?
What mechanism restores the resting potential after cardiac muscle depolarization?
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What happens during Phase 3 of the action potential of cardiac muscle cells?
What happens during Phase 3 of the action potential of cardiac muscle cells?
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What occurs during the plateau phase of the action potential in cardiac muscle?
What occurs during the plateau phase of the action potential in cardiac muscle?
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What is the function of the absolute refractory period in cardiac muscle?
What is the function of the absolute refractory period in cardiac muscle?
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Which statement best describes the mechanism of cardiac muscle contraction?
Which statement best describes the mechanism of cardiac muscle contraction?
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What causes the rapid outflux of potassium at the end of the action potential?
What causes the rapid outflux of potassium at the end of the action potential?
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During which phase is the cardiac muscle most difficult to excite?
During which phase is the cardiac muscle most difficult to excite?
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What is a characteristic feature of the sinoatrial (SA) node's action potential?
What is a characteristic feature of the sinoatrial (SA) node's action potential?
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What differentiates the relative refractory period from the absolute refractory period?
What differentiates the relative refractory period from the absolute refractory period?
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What is the duration of the absolute refractory period in cardiac muscle?
What is the duration of the absolute refractory period in cardiac muscle?
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What is the primary function of the sarcoplasmic reticulum in cardiac muscle?
What is the primary function of the sarcoplasmic reticulum in cardiac muscle?
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How does the action potential reach the interior of cardiac muscle cells?
How does the action potential reach the interior of cardiac muscle cells?
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What structural feature distinguishes the T tubules in cardiac muscle from those in skeletal muscle?
What structural feature distinguishes the T tubules in cardiac muscle from those in skeletal muscle?
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What is the relationship between calcium concentration in extracellular fluid and cardiac muscle contraction strength?
What is the relationship between calcium concentration in extracellular fluid and cardiac muscle contraction strength?
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Where are T tubules located in relation to the sarcomere in cardiac muscle?
Where are T tubules located in relation to the sarcomere in cardiac muscle?
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What difference exists in calcium ion diffusion between cardiac and skeletal muscle?
What difference exists in calcium ion diffusion between cardiac and skeletal muscle?
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What is a characteristic of the sarcoplasmic reticulum in cardiac muscle compared to skeletal muscle?
What is a characteristic of the sarcoplasmic reticulum in cardiac muscle compared to skeletal muscle?
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What role do mucopolysaccharides play in the T tubules of cardiac muscle?
What role do mucopolysaccharides play in the T tubules of cardiac muscle?
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Study Notes
### Cardiac Conduction System
- Bundle of His conducts impulses from the AV node to its left and right branches. This unidirectional conduction from atria to ventricles is crucial except during unusual circumstances
- A fibrous barrier separates the atrial and ventricular muscles, preventing impulse transmission between them except through the AV bundle
- The AV bundle travels down the ventricular septum for 5 to 15 mm and divides into left and right branches, delivering impulses to both ventricles
- The branches further divide into Purkinje fibres, which connect with cardiac muscle fibres, facilitating rapid impulse distribution throughout the ventricles
- The impulse travels from the bundle branches to Purkinje fibres in 0.03 seconds, and then spreads rapidly through the ventricular muscle fibres
- The velocity of impulse transmission in ventricular muscle fibers is between 0.3 and 0.5 m/s, first spreading along the endocardial surface and then to the epicardial surface, taking about 0.03 seconds
- The total time for impulse transmission from the initial bundle branches to the ventricles in a normal heart is 0.06 seconds
### SA Node as Pacemaker
- The SA node is the heart's primary pacemaker, with an unstable resting potential and exhibiting phase 4 depolarization, also known as automaticity
- The AV node and His-Purkinje system can act as latent pacemakers if the SA node is suppressed, exhibiting their own automaticity
- The SA node has the fastest intrinsic rate of depolarization, followed by the AV node and then the His-Purkinje system
### Pacemaker Potential
- The SA node fires spontaneously at approximately 70 to 80 times per minute under the influence of vagal tone
- SA node cells do not maintain a resting membrane potential like neurons or skeletal muscle cells
- Instead, SA node cells exhibit a gradual spontaneous depolarization called the pacemaker potential (prepotential) during diastole
- This self-excitation is due to the inherent leakiness of SA nodal fibers to Ca +2 ions, resulting in Ca+2 influx
- The membrane potential begins at about (–60 mV) and slowly depolarizes to (–40 mV), which is the threshold for generating an action potential in these cells
- This spontaneous depolarization is driven by Ca+2 diffusion through specific slow calcium channels
- Once the threshold level of depolarization is reached, fast calcium channels open, leading to rapid Ca+2 influx into the cells
### Repolarization
- Repolarization occurs through opening of K+ gates and outward diffusion of K+, similar to other excitable tissues
- After repolarization to –60 mV, a new pacemaker potential begins, culminating in a new action potential at the end of diastole
### Internodal Tracts and AV Node
- Three pairs of internodal tracts connect the SA node to the AV node fibers
- The impulse travels from the SA node to the AV node within 0.03 seconds
- At the AV node, a delay of 0.09 seconds occurs, with an additional delay of 0.04 seconds in the ‘bundle of His’ (total delay of 0.13 seconds)
### AV Nodal Delay - Causes
- Transitional fibers, very small fibers connecting the internodal tract and AV node, conduct the impulse at a very slow rate (0.02 to 0.05 m/s)
- The velocity of impulse conduction in AV nodal fibers is also slow (0.05 m/s)
- There are limited gap junctions connecting successive fibers in the pathway
### Contraction Duration
- Atrial muscle contraction duration is 0.1 seconds, while ventricular muscle contraction duration is 0.3 seconds
### Ectopic Pacemaker
- When the pacemaker is located outside the SA node (e.g., AV node or Purkinje fibers), it is called an ectopic pacemaker
- An ectopic pacemaker leads to an abnormal sequence of contraction in different parts of the heart
### Causes of Pacemaker Shift
- Shifts in the pacemaker from the SA node to other sites can occur if:
- The discharge rate of other parts of the heart becomes higher than the SA node
- Impulses fail to properly transmit from the SA node to the AV node
### Importance of AV Nodal Delay
- The AV nodal delay allows for the atria and ventricles to be excited and contract at different times
### Resting Membrane Potential of Cardiac Muscle
- The resting membrane potential of normal cardiac muscle is −85 to –95 mV
### Ventricular Cardiac Muscle Fiber Action Potential
- Phases of the action potential of the ventricular cardiac muscle fiber cell:
- Phase 0 (upstroke): Rapid depolarization with an overshoot to about +20 mV due to opening of voltage-gated Na+ channels and rapid Na+ influx
- Phase 1 (partial repolarization): Initial rapid repolarization due to K+ efflux (K+ outflow) following the closure of Na+ channels when the voltage reaches nearly +20 mV
- Phase 2 (plateau): Prolonged plateau due to slow and prolonged opening of voltage-gated Ca+2 channels with Ca+2 influx, prolonging membrane depolarization.
- Phase 3 (rapid repolarization): Final repolarization due to opening of voltage-gated K+ channels at zero voltage with rapid K+ outflow (K+ efflux) followed by the closure of Ca+2 channels, restoring the resting potential.
- Phase 4 (complete repolarization): The membrane potential returns to the resting level (- 90 mV) through the Na+-K+ pump, which moves excess K+ in and excess Na+ out.
### Plateau in Cardiac Muscle Action Potential - Cause
-
Plateau is due to:
- Opening of slow voltage-gated calcium and sodium channels, allowing these ions to continue to diffuse into the fiber, extending depolarization
- Decreased permeability of the membrane for potassium at the onset of action potential (about fivefold decrease), reducing potassium outflux during the action potential plateau and preventing repolarization
- When slow calcium and sodium channels close after 0.2 to 0.3 seconds, membrane permeability for potassium rapidly increases, leading to rapid potassium outflux
- This rapid potassium outflux causes the membrane potential to return to the resting level (repolarization)
### Inward Na+ Current Result
- The inward Na+ current is responsible for the upstroke of the action potential in both the sinoatrial (SA) node and Purkinje fibers
### Refractory Period
- Absolute refractory period (ARP): During this interval, no action potential can be generated, regardless of stimulus intensity. It lasts from the upstroke to mid-repolarization (about -50 to -60 mV), for approximately 0.25 to 0.30 seconds. This period prevents wave summation and tetanus. Prevents re-excitation during systole and early diastole.
- Relative refractory period (RRP): This interval makes it more difficult to excite the muscle, but it can still be excited by a strong signal. It lasts about 0.05 seconds, from the end of the ARP (mid-repolarization) to shortly before complete repolarization, occurring during diastole.
### Cardiac Muscle Structure
-
Myocardial cell structure:
- Sarcomere: The contractile unit of the myocardial cell, similar to skeletal muscle. It runs from Z line to Z line. Contains thick filaments (myosin) and thin filaments (actin, troponin, tropomyosin). It shortens according to the sliding filament model, where thin filaments slide along thick filaments.
### Sliding Filament Mechanism
- Cardiac muscle shortens during contraction due to the sliding of thick and thin filaments past one another.
- Myosin heads attach to and move along the thin filaments at both ends of a sarcomere, pulling the thin filaments toward the M line, resulting in muscle contraction.
### Excitation-Contraction Coupling in Cardiac Muscle
- The sarcoplasmic reticulum (SR) in cardiac muscle is less well-developed than in skeletal muscle.
- It exists as a network of tubules surrounding the myofibrils and has dilated terminals (cisternae) located near the external cell membrane and T tubules
- The SR and cisternae hold high concentrations of ionic calcium.
- T tubules are invaginations of the cell membrane, conducting action potentials to the interior of the cell.
- They are well-developed in the ventricles, but poorly developed in the atria.
- T tubules form dyads with the SR.
- When an action potential travels across the cardiac muscle membrane, it goes into the muscle cells through T tubules.
- The action potential causes immediate calcium release from the longitudinal sarcoplasmic tubules, which diffuses into the myofibrils to catalyze the chemical reactions necessary for the sliding of actin and myosin filaments, resulting in muscle contraction.
- Extra calcium ions also diffuse into the sarcoplasm from T tubules in cardiac muscle (unlike skeletal muscle).
- T tubules of cardiac muscle contain mucopolysaccharides with negative charges, binding a large store of calcium ions.
- These calcium ions come directly from extracellular fluid, as T tubules open to the exterior.
- Therefore, the strength of cardiac muscle contraction depends heavily on the calcium concentration in the extracellular fluid, unlike skeletal muscle contraction.
- The SR stores and releases Ca2+ for excitation–contraction coupling.
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Description
This quiz covers the essentials of the cardiac conduction system, detailing the roles of key components such as the Bundle of His and Purkinje fibres. Understand how electrical impulses travel through the heart to ensure coordinated contraction, and learn about the implications of impulse transmission. Test your knowledge of this vital aspect of cardiovascular physiology.