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Help Understanding Pacemaker Action Potentials and ventricular/atrial action potentials


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I will attach the graphs.

 

Here is what I understand. Let me know if something is wrong

 

SA node/Pacemaker Potential (and AV node?)

 

 

The permeability of potassium decreases based on the graph and potassium is kept within the cell and less goes out of the cell. Then the fast gated calcium channels open for a rapid depolarization of the muscle cell. Then the calcium permeability increases so there is a lot of calcium rushing into the cell. The calcium permeability then decreases so less calcium is exciting the cell. Then during the repolarization the potassium channels open to help repolarize the cell. The permeability of potassium increases so potassium enters the cell. Is this one cycle? There is another hump and a slow depolarization and an action potential labeled on the graph and reaching threshold.

 

Can it reach threshold after the first hump in the graph or does it need two of them?

 

Are the large humps or peaks in the graph both an action potential?

 

 

Ventricular and Atrial

Atrial and ventricular rely on sodium (Na+), not potassium like pacemakers do. The sodium channels open and cause the depolarization of the cell. Then repolarization ooccurs because the NA+ gates close and Ca+ gates open. They have a slower refractory period due to the slow Ca+ gates (Ca+ enters slower).

 

The depolarization of pacemakers is slower compared to atrial and ventricular cells. The refractory period is slower for ventricular and atrial cells.

 

I few questions as my exam is tomorrow.

 

Ok. A couple of questions when I am reading from that diagram. Are both of the humps the same process of an SA node or pacemaker? Like just one is a pacemaker action potential? Also, when the Ca permeability decreases does that mean the calcium channels close? And do the potassium channels open and then the permeability increases so potassium rushes in from the cell from outside of the cell?

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Ok. A couple of questions when I am reading from that diagram. Are both of the humps the same process of an SA node or pacemaker? Like just one is a pacemaker action potential?

 

The pacemaker potentials initiate the action potentials of autorhythmic cells. So this is what is displayed in the diagram the first hump is the pacemaker potential the second is the action potential of the autorhythmic cell.

 

Also, when the Ca permeability decreases does that mean the calcium channels close? And do the potassium channels open and then the permeability increases so potassium rushes in from the cell from outside of the cell?

 

The membrane potential is a result of Na+ diffusing into the cell at a slow rate and the cell being permeable to K+ which causes the cell membrane interior to become more positive and less negative. It has a threshold of how positive it can get before the Ca 2+ channels open.When threshold is reached the Ca 2+ channels open. Ca 2+ moves into the extracellular space. This influx of calcium causes the rising phase of the action potential in the autorhythmic cell and reverses the membrane potential. The Ca 2+ channels are now closed. The cell then repolarizes and the process begins again with the cell becoming increasingly permeable to K+ and K+ moves into the cell. Repolarization completes and the K+ channels are closed reflecting decreased K+ permeability and the slow depolarization process.

 

The action potentials of autoarythmic cells act as the trigger for the heart's contractions they are found in 5 different areas.

1. Sinoatrial (SA) node

2. Atrioventricular (AV) node

3. Atrioventricular (AV) bundle (bundle of his)

4. Right + left bundle branches

5. Purkinje fibers

 

conduction.jpg

 

They have a slower refractory period due to the slow Ca+ gates (Ca+ enters slower).

 

At the atrioventricular node, the impulse is delayed slightly this delay reflects the smaller diameter of the fibers which conduct impulses more slowly than other parts of the system

Edited by fiveworlds
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About 20% of the calcium needed for the calcium pulse that triggers the contraction of skeletal and heart muscle enters from the extracellular space and once inside it stimulates the release of much larger amounts of Ca2+ from the sarcoplasmic reticulum. Ionic calcium is barred from entering nonstimulated cardiac fibers, but when sodium dependent membrane depolarization occurs the voltage change opens calcium channels that allow Ca 2+ entry from the extracellular space. These channels are called slow Ca2+ channels because channel opening is delayed a bit.

 

These make up the large majority of heart muscle and are not limited to atrial or ventricular. About 1% of the cardiac fibers are autorythmic.

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