Questions and Answers
What primarily drives changes in transmembrane potential in myocardial cells?
If a cardiac muscle cell membrane were only permeable to potassium ions (K+), what would the membrane potential be approximately?
What happens to the transmembrane voltage when there is a balance in current flow across the membrane?
During an action potential, what primarily changes the membrane's relative permeability?
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Which of the following ions contributes positively to the resting membrane potential of a cardiac muscle cell?
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What is the Nernst potential for sodium ions (Na+) in a myocardial cell?
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Which scenario indicates that an action potential is likely to occur in myocardial cells?
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What is the significance of ion permeability changes during the cardiac action potential?
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What characterizes the supranormal period (SNP) in ventricular tissue?
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What triggers the upstroke in the action potential of the SA and AV nodal cells?
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What is the maximum diastolic potential approximately in SA nodal cells?
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How does the action potential amplitude in SA and AV nodal cells compare to fast fibers?
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What is one consequence of the slower rate of depolarization in SA and AV nodal fibers?
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What can result from the generation of abnormally timed action potentials during the SNP?
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Which phase is absent in the SA and AV nodal action potential?
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At what threshold level do L-type calcium channels open during the action potential phase?
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What role do inward rectifying potassium channels (Kir 2.1) play in cardiac muscle cells?
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During which phase of the cardiac action potential do the inward rectifying potassium channels (Kir 2.1) close?
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What is the primary effect of K+ currents flowing out of cardiac cells during repolarization?
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What is the function of delayed rectifying K+ channels (lK) during the cardiac action potential?
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How does the closure of inward rectifying potassium channels (Kir 2.1) affect the plateau phase of the cardiac action potential?
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What is the approximate membrane potential (Em) at rest due to the high K+ conductance from Kir 2.1 channels?
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What triggers the opening of delayed rectifying K+ channels (lK)?
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How many distinct types of K+ channels are present in cardiac muscle that facilitate outward K+ current?
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What phenomenon occurs when myocardial cells outside specialized fibers develop automaticity?
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Which mechanism does acetylcholine utilize to slow the intrinsic pacemaker activity in the heart?
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What is the effect of the vagus nerve on heart rate?
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How does decreased cAMP affect the phase 4 depolarization in the SA node?
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What type of receptors does acetylcholine act on in the heart to exert parasympathetic effects?
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What change in action potentials occurs as a result of increased parasympathetic stimulation?
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What current is affected by acetylcholine in the SA node, leading to slower depolarization?
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Which of the following is NOT a consequence of acetylcholine's actions in the heart?
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What property allows the SA node to be the primary pacemaker of the heart?
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What happens to secondary and tertiary pacemakers when the SA node generates action potentials?
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How does the pacemaker potential affect the heart rate?
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What occurs if the SA node fails?
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What is the intrinsic firing rate of AV nodal cells?
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Which of the following correctly describes the Purkinje fibers?
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What is 'overdrive suppression' in the context of heart pacemakers?
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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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Description
Explore the dynamics of cardiac action potentials in myocardial cells. This quiz covers the role of membrane potential, ion flow, and the significance of Na+, K+, and Ca2+ currents in cardiac function. Test your knowledge on how these elements contribute to cardiac contractions and repolarization.