Electrical Properties of the Heart Flashcards
[…] cells make up the atrial and ventricular tissue
Contractile
What do contractile cells do?
These cells are the ones actually doing the contraction. Therefore, they are involved in propogating action potentials, contracting, and generating force (pressure) within the chambers of the heart.
[…] cells make up the SA and AV node tissues, internodal tracts, bundle of his and purkinje fibers.
Conducting
What is the function of conducting cells?
Rapidly spread action potentials over entire myocardium
What is the significance of intercalated discs?
For the purposes of review, explain the resting membrane potential and a standard action potential curve.
RMP is ~ -70mV. Threshold for depolarization and generation of an AP is ~ -50mV. In order to reach threshold, depolarizing stimuli (EPSPs) act on the tissue leading to some small opening of sodium channels. If enough of these channels open (strong enough stimuli or summation of many smaller stimuli) then Na+ can enter causing depolarization to threshold (1) and then that will trigger opening of voltage gated Na+ channels that generates an AP (2). Once the membrane potential reaches ~ +30mV (3), voltage gated Na+ channels begin closing and voltage gated K+ channels open leading to efflux of K+ from the cell. This causes MP to drop closer to the Nernst potential of K+ and leads to hyperpolarization (4). Na+/K+ ATPase channels restore RMP by pumping K+ back in and Na+ out.
What kind of cells do purkinje fibers consist of?
What significance does this have for the heart?
Purkije fibers consist of specialized cardiomyocytes that are able to conduct cardiac action potentials more quickly and efficiently than any other cells in the heart. Purkinje fibers allow the heart’s conduction system to create synchronized contractions of its ventricles, and are, therefore, essential for maintaining a consistent heart rhythm.
What does Nernst potential mean? For example, if I say the Nernst potential of Na+ is +67mV, what does that actually mean?
Let’s say that you have a cell whose RMP is 0mV and that cell only expresses leak sodium channels. If you add Na+ to the environment, Na+ will leak into that cell through the leak channels until the RMP of the cell was +67mV. Therefore, the nernst potential is the membrane potential at which there is no more net movement of this ion across the membrane. It is (+) to reflect the fact that the inside of the cell would be more positive relative to the outside of the cell.
If the nernst potential of Na+ is +67mV and voltage gated Na+ channels are responsible for depolarization of the membrane during an AP, why doesn’t the depolarization go all the way to the Nernst potential of Na+ (i.e. why does it only go to about +30mV instead of +67mV)?
- Voltage gated Na+ channels rapidly inactivate via the “ball and chain” that is attached to the cytoplasmic side of the channel –> unable to allow enough Na+ to enter to reach that +67mV.
- K+ channels open and repolarize the membrane causing a decrease in membrane potential. Na+ channels are inactivated until the membrane repolarizes.
Which of the following lacks a K+ leak channel, leading to unstable resting membrane potential?
A) Purkinje fibers and bundle of his in ventricles
B) Internodal fibers in atria
C) SA node
C
What is different about the typical action potential curve in cardiac tissue?
- Final depolarization voltage is lower
- The amount of time spent with voltage gated K+ channels open
Why do action potentials of the atria and ventricles exhibit a long action potential depolarization phase?
During the action potential depolarization, there is decreasing [K+] due to K+ leaving the cell through voltage gated K+ channels, but there is also an influx of Ca2+. This prolongs the time and increases the width of the action potential curve.
What is happening at each of these points on the graph?
How does Ca2+ affect the cardiac action potential and function of the cardiac myocyte?
Extracellular calcium ions enter the cell through L-type calcium channels. Ca2+ entry sustains the depolarization of cardiac muscle cells for a longer duration. These channels are long-acting and open more slowly than Na+ channels. They slowly inactivate so they remain open longer. This calcium stimulates calcium induced calcium release (CICR) from intracellular stores (SR) via the RYR2.