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Questions and Answers
What primarily drives changes in transmembrane potential in myocardial cells?
What primarily drives changes in transmembrane potential in myocardial cells?
- Oxygen levels in the blood
- Changes in temperature
- Variation in heart rate
- Movement of ions across the membrane (correct)
If a cardiac muscle cell membrane were only permeable to potassium ions (K+), what would the membrane potential be approximately?
If a cardiac muscle cell membrane were only permeable to potassium ions (K+), what would the membrane potential be approximately?
- -90 mV (correct)
- +130 mV
- +60 mV
- 0 mV
What happens to the transmembrane voltage when there is a balance in current flow across the membrane?
What happens to the transmembrane voltage when there is a balance in current flow across the membrane?
- It reaches zero
- It becomes unstable
- It increases indefinitely
- It remains constant (correct)
During an action potential, what primarily changes the membrane's relative permeability?
During an action potential, what primarily changes the membrane's relative permeability?
Which of the following ions contributes positively to the resting membrane potential of a cardiac muscle cell?
Which of the following ions contributes positively to the resting membrane potential of a cardiac muscle cell?
What is the Nernst potential for sodium ions (Na+) in a myocardial cell?
What is the Nernst potential for sodium ions (Na+) in a myocardial cell?
Which scenario indicates that an action potential is likely to occur in myocardial cells?
Which scenario indicates that an action potential is likely to occur in myocardial cells?
What is the significance of ion permeability changes during the cardiac action potential?
What is the significance of ion permeability changes during the cardiac action potential?
What characterizes the supranormal period (SNP) in ventricular tissue?
What characterizes the supranormal period (SNP) in ventricular tissue?
What triggers the upstroke in the action potential of the SA and AV nodal cells?
What triggers the upstroke in the action potential of the SA and AV nodal cells?
What is the maximum diastolic potential approximately in SA nodal cells?
What is the maximum diastolic potential approximately in SA nodal cells?
How does the action potential amplitude in SA and AV nodal cells compare to fast fibers?
How does the action potential amplitude in SA and AV nodal cells compare to fast fibers?
What is one consequence of the slower rate of depolarization in SA and AV nodal fibers?
What is one consequence of the slower rate of depolarization in SA and AV nodal fibers?
What can result from the generation of abnormally timed action potentials during the SNP?
What can result from the generation of abnormally timed action potentials during the SNP?
Which phase is absent in the SA and AV nodal action potential?
Which phase is absent in the SA and AV nodal action potential?
At what threshold level do L-type calcium channels open during the action potential phase?
At what threshold level do L-type calcium channels open during the action potential phase?
What role do inward rectifying potassium channels (Kir 2.1) play in cardiac muscle cells?
What role do inward rectifying potassium channels (Kir 2.1) play in cardiac muscle cells?
During which phase of the cardiac action potential do the inward rectifying potassium channels (Kir 2.1) close?
During which phase of the cardiac action potential do the inward rectifying potassium channels (Kir 2.1) close?
What is the primary effect of K+ currents flowing out of cardiac cells during repolarization?
What is the primary effect of K+ currents flowing out of cardiac cells during repolarization?
What is the function of delayed rectifying K+ channels (lK) during the cardiac action potential?
What is the function of delayed rectifying K+ channels (lK) during the cardiac action potential?
How does the closure of inward rectifying potassium channels (Kir 2.1) affect the plateau phase of the cardiac action potential?
How does the closure of inward rectifying potassium channels (Kir 2.1) affect the plateau phase of the cardiac action potential?
What is the approximate membrane potential (Em) at rest due to the high K+ conductance from Kir 2.1 channels?
What is the approximate membrane potential (Em) at rest due to the high K+ conductance from Kir 2.1 channels?
What triggers the opening of delayed rectifying K+ channels (lK)?
What triggers the opening of delayed rectifying K+ channels (lK)?
How many distinct types of K+ channels are present in cardiac muscle that facilitate outward K+ current?
How many distinct types of K+ channels are present in cardiac muscle that facilitate outward K+ current?
What phenomenon occurs when myocardial cells outside specialized fibers develop automaticity?
What phenomenon occurs when myocardial cells outside specialized fibers develop automaticity?
Which mechanism does acetylcholine utilize to slow the intrinsic pacemaker activity in the heart?
Which mechanism does acetylcholine utilize to slow the intrinsic pacemaker activity in the heart?
What is the effect of the vagus nerve on heart rate?
What is the effect of the vagus nerve on heart rate?
How does decreased cAMP affect the phase 4 depolarization in the SA node?
How does decreased cAMP affect the phase 4 depolarization in the SA node?
What type of receptors does acetylcholine act on in the heart to exert parasympathetic effects?
What type of receptors does acetylcholine act on in the heart to exert parasympathetic effects?
What change in action potentials occurs as a result of increased parasympathetic stimulation?
What change in action potentials occurs as a result of increased parasympathetic stimulation?
What current is affected by acetylcholine in the SA node, leading to slower depolarization?
What current is affected by acetylcholine in the SA node, leading to slower depolarization?
Which of the following is NOT a consequence of acetylcholine's actions in the heart?
Which of the following is NOT a consequence of acetylcholine's actions in the heart?
What property allows the SA node to be the primary pacemaker of the heart?
What property allows the SA node to be the primary pacemaker of the heart?
What happens to secondary and tertiary pacemakers when the SA node generates action potentials?
What happens to secondary and tertiary pacemakers when the SA node generates action potentials?
How does the pacemaker potential affect the heart rate?
How does the pacemaker potential affect the heart rate?
What occurs if the SA node fails?
What occurs if the SA node fails?
What is the intrinsic firing rate of AV nodal cells?
What is the intrinsic firing rate of AV nodal cells?
Which of the following correctly describes the Purkinje fibers?
Which of the following correctly describes the Purkinje fibers?
What is 'overdrive suppression' in the context of heart pacemakers?
What is 'overdrive suppression' in the context of heart pacemakers?
What distinguishes the electrical activity of the SA node from other cardiac cells?
What distinguishes the electrical activity of the SA node from other cardiac cells?
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Study Notes
Cardiac Action Potentials Overview
- Myocardial cells have an electric potential due to charge distribution across their membranes, enabling current flow.
- Changes in transmembrane potential relate directly to current movement; a balanced current keeps voltage constant.
- Cardiac contractions originate from action potentials, involving ion flow through specific channels: Na+, K+, and Ca2+.
Membrane Potential Dynamics
- Membrane potential varies based on permeability to ions:
- If only Na+ permeable, potential approaches +60 mV (Nernst for Na+).
- If only K+ permeable, potential approaches -90 mV (Nernst for K+).
- Ca2+ permeability results in a potential of +130 mV (Nernst for Ca2+).
- During action potentials, membrane permeability shifts, causing depolarization and subsequent repolarization.
Potassium Current in Cardiac Action Potentials
- Outward K+ currents contribute to repolarization, making the interior of the cell more negative.
- At rest, ungated K+ channels maintain high permeability, holding the membrane potential near EK+ (-90 mV).
- Four K+ channels contribute to varying outward K+ currents:
- Inward rectifying potassium channels (Kir 2.1)
- Transient outward potassium channels (Ito)
- Delayed rectifying K+ currents (IK) classified into:
- Rapid component (IKr)
- Slow component (IKs)
Inward Rectifying Potassium Channels (Kir 2.1)
- Voltage-gated channels that maintain K+ conductance under resting conditions.
- Close near depolarization end and reopen during repolarization.
- Closure during plateau phase is critical for preventing premature repolarization.
Delayed Rectifying K+ Channels (IK)
- Closed at resting membrane potential; open gradually during depolarization.
- More rapid opening near end of plateau phase to initiate repolarization.
Supranormal Period (SNP)
- Occurs when ventricular tissue is depolarized, leading to a hyper-excitable state.
- Results in a decreased action potential amplitude but may still elicit propagated responses.
- Can cause rhythm abnormalities due to mis-timed action potentials.
Ionic Basis of SA and AV Node Action Potentials
- Pacemaker cells in the SA and AV nodes exhibit automatic action potentials and lack a true resting membrane potential.
- Maximum diastolic potential reaches around -60 mV.
- The SA node generates action potentials at 60-100 beats per minute, making it the primary pacemaker.
Setting Heart Rate
- SA node cells enable the heart to beat independently due to intrinsic electrical activity.
- Phase 4 depolarization progressively approaches the threshold for action potential generation.
- AV node and Purkinje fibers exhibit slower intrinsic rates (40-60 and 20-40 beats per minute, respectively).
Overdrive Suppression
- Faster pacing from the SA node suppresses other pacemaker cells, ensuring a unified heart rate.
- Should the SA node fail, backup pacemakers take over based on their intrinsic rates.
Automaticity and Ectopic Beats
- Cardiac tissue injury can lead to ectopic beats due to the development of automaticity in non-specialized myocardial cells.
Effects of Parasympathetic Nervous System on Heart Rate
- The vagus nerve stimulates the heart, releasing acetylcholine, which lowers pacemaker activity through M2 cholinergic receptors.
- Activation of M2 receptors decreases the If current, causing a slower depolarization rate.
- Reduced cAMP levels lead to a less steep phase 4 depolarization, decreasing action potentials per unit time, thus lowering heart rate.
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