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Questions and Answers
What effect does PKC phosphorylation have on sodium current?
What effect does PKC phosphorylation have on sodium current?
- It completely blocks sodium current.
- It reduces the sodium current. (correct)
- It has no effect on the sodium current.
- It increases the sodium current.
Which medication is classified as a sodium channel blocker?
Which medication is classified as a sodium channel blocker?
- Isoproterenol
- Verapamil
- Lidocaine (correct)
- Nifedipine
What is the effect on phase 0 of the action potential if the sodium current is reduced?
What is the effect on phase 0 of the action potential if the sodium current is reduced?
- The repolarization occurs slower.
- The depolarization occurs faster.
- There is no change to phase 0.
- The depolarization occurs slower. (correct)
What is an effect of PKA on calcium current?
What is an effect of PKA on calcium current?
Which of the following drugs is a calcium channel blocker?
Which of the following drugs is a calcium channel blocker?
What initiates the depolarization phase of the myocyte action potential?
What initiates the depolarization phase of the myocyte action potential?
In which phase does a brief early repolarization occur?
In which phase does a brief early repolarization occur?
Which current flows more rapidly during the action potential upstroke?
Which current flows more rapidly during the action potential upstroke?
Which of the following currents is specifically responsible for early repolarization in myocytes?
Which of the following currents is specifically responsible for early repolarization in myocytes?
At approximately what membrane potential does the depolarization phase trigger?
At approximately what membrane potential does the depolarization phase trigger?
What ion movement occurs during the depolarization phase of a cardiac action potential?
What ion movement occurs during the depolarization phase of a cardiac action potential?
Which ion channels primarily influence automaticity in cardiac cells?
Which ion channels primarily influence automaticity in cardiac cells?
What best describes the escape phenomenon in non-pacemaker cells?
What best describes the escape phenomenon in non-pacemaker cells?
What is the status of the ion channels during the repolarization phase of the cardiac action potential?
What is the status of the ion channels during the repolarization phase of the cardiac action potential?
Which ion exchangers are involved in cardiac cellular electrophysiology?
Which ion exchangers are involved in cardiac cellular electrophysiology?
During which phase of a cardiac action potential are both sodium and potassium channels inactive?
During which phase of a cardiac action potential are both sodium and potassium channels inactive?
What is the effect of increased potassium ion concentration on cardiac action potentials?
What is the effect of increased potassium ion concentration on cardiac action potentials?
What describes the state of ion channels during the resting potential of cardiac cells?
What describes the state of ion channels during the resting potential of cardiac cells?
What happens to phase 2 of the action potential if the calcium current is reduced or delayed?
What happens to phase 2 of the action potential if the calcium current is reduced or delayed?
During which phase does the Na+-K+-ATPase show its highest activity?
During which phase does the Na+-K+-ATPase show its highest activity?
If the inward rectifying potassium channel (IK1) is inhibited, what is likely to occur?
If the inward rectifying potassium channel (IK1) is inhibited, what is likely to occur?
How does enhancing Ito affect the phases of the action potential?
How does enhancing Ito affect the phases of the action potential?
Which ion's current contributes to the early repolarization during phase 2 of the action potential?
Which ion's current contributes to the early repolarization during phase 2 of the action potential?
What effect does suppressing the Na+-K+-ATPase due to low ATP availability have on cardiac cells?
What effect does suppressing the Na+-K+-ATPase due to low ATP availability have on cardiac cells?
What happens to the action potential phases when an ion current is modified?
What happens to the action potential phases when an ion current is modified?
What is the role of L-type calcium currents during the action potential?
What is the role of L-type calcium currents during the action potential?
What characterizes the absolute refractory period?
What characterizes the absolute refractory period?
Why is the action potential during the relative refractory period typically smaller?
Why is the action potential during the relative refractory period typically smaller?
What is a significant difference between cardiac and skeletal muscle action potentials?
What is a significant difference between cardiac and skeletal muscle action potentials?
What happens to ion channels during Phase 3 of the cardiac action potential?
What happens to ion channels during Phase 3 of the cardiac action potential?
What role does the annulus fibrosus play in cardiac conduction?
What role does the annulus fibrosus play in cardiac conduction?
How does cardiac muscle differ from skeletal muscle regarding force generation?
How does cardiac muscle differ from skeletal muscle regarding force generation?
What happens if ion current changes during the cardiac action potential?
What happens if ion current changes during the cardiac action potential?
Which mechanism is crucial in understanding cardiac arrhythmias?
Which mechanism is crucial in understanding cardiac arrhythmias?
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Study Notes
Cardiac Action Potentials
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Cardiac action potentials have five phases:
- Phase 0: Depolarization (upstroke) due to fast voltage-gated sodium channel opening, creating INa.
- Phase 1: Brief rapid early repolarization, as INa slows.
- Phase 2: Plateau phase, resulting from a balance between slow inward calcium current (ICaL) and outward potassium currents (IK1).
- Phase 3: Repolarization, as ICaL declines and outward potassium currents increase.
- Phase 4: Resting membrane potential, maintained by IK1.
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Sodium, calcium, and potassium channel activity determines the shape and duration of each phase.
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Automaticity: The ability of some cardiac cells to spontaneously generate action potentials.
- Modified by specific ion channels, mainly the inward If (funny) current.
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Escape: When a non-pacemaker cell spontaneously generates action potentials due to altered electrophysiological conditions.
Sodium Current
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Sodium current is essential for rapid depolarization (Phase 0).
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Can be regulated by:
- Protein Kinase C (PKC) phosphorylation: Reduces sodium current.
- Sodium channel blockers: Reduce sodium current, examples include:
- Tetrodotoxin (TTX)
- Lidocaine
- Ranolazine
- Quinine
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Inhibiting sodium current slows depolarization, delaying action potential initiation.
Calcium Current
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Calcium current contributes to plateau phase (Phase 2) and is involved in early repolarization (Phase 1).
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Regulated by:
- Protein Kinase A (PKA): Increases calcium current.
- Calcium Channel Blockers: Decrease calcium current, examples include:
- Verapamil
- Nifedipine
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Enhancing calcium current alters Phase 1 and 2. Decreasing calcium current reduces plateau phase and may affect early repolarization.
Non-voltage-gated Channels
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Na+-K+-ATPase: Maintains resting membrane potential (Phase 4) by exchanging sodium and potassium ions.
- Impairment of Na+-K+-ATPase affects resting membrane potential maintenance.
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Key to understanding ion current effects:
- Consider the phases where the current is most active (channels are open).
- Think about the direction of ion movement – potassium out = polarization, sodium and calcium in = depolarization.
Differences between Myocytes
- There are variations in ion channel expression and activity among different myocytes, leading to variations in action potential characteristics.
Refractory Period
- Absolute refractory period: No action potential can be generated due to channel inactivation.
- Relative refractory period: Some channels are starting to close, but not all are ready to reopen, resulting in weaker action potentials.
- Importance of refractory period for cardiac electrophysiology:
- Essential for understanding arrhythmias and conduction abnormalities.
Cardiac vs. Skeletal Muscle
- Skeletal muscle: Can be tetanized (multiple depolarizations lead to force summation).
- Cardiac muscle: Cannot be tetanized due to differences in action potentials and ion channels.
- This prevents sustained contraction and allows for normal heart function.
Conduction
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Sequence of activation:
- Atria and ventricles mainly composed of myocytes connected by gap junctions.
- Annulus fibrosus isolates atria from ventricles, preventing direct conduction between chambers.
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Different cardiac cell types:
- Have different activation sequences, conduction velocities, pacemaker rates.
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