Cardiac Action Potential Duration Question

In summary: Therefore, decreasing Ca++ concentration can effectively limit the heart rate and prevent it from firing at fast rates. In summary, decreasing the concentration of Ca++ can inhibit atrial muscle contraction, SA node pacemaker activity, and AV node conduction, all of which can result in the increase of APD and refractory time, making it more difficult for the cardiac cell to fire action potentials at fast rates. This effect can be achieved by the release of acetylcholine from the vagal nerve, which reduces Ca++ concentration and slows down the upstroke of the action potential.
  • #1
John Larkin
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What does the APD (Action potential duration) determine in a cardiac cell and how can it be changed (do I need to effect any of the phases of the AP)?

For example, if the vagal nerve releases acetylcholine here are its effects:

Inhibits Atrial Muscle Contraction- Negative inotropic effect (contract less vigorously)
Why- We lost Ca++ which causes weak muscle contractions

Inhibits SA Node Pacemaker activity- slows heart rate, lengthens R-R interval and P-P interval; Negativie Chronotropic
Why- We hyper-polarized and now it takes more time to get up to the threshold!

Inhibits AV Node Conduction (not Pacemaker it’s not firing): lengthens P-R internal; Negative Dromotorpic
Why- Any tissues that uses Ca++ for AP will now have a slower conduction as we have decreased the amount of Ca++ going through the L-type channels (decreased upstroke slope)

So did this effect increase the APD in all these cases therefore increasing the refractory time so that AP could not be fired at fast rates?
 
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  • #2
Yes, decreasing the concentration of Ca++ will increase the APD (action potential duration) and also increase the refractory time, making it harder for the cell to fire action potentials at a fast rate. This is because decreasing the concentration of Ca++ reduces the speed of the upstroke in the action potential, which increases the total duration of the action potential. Furthermore, as the action potential takes longer to complete, the refractory time is increased, making it more difficult for the cell to generate another action potential.
 

FAQ: Cardiac Action Potential Duration Question

1. What is the cardiac action potential duration?

The cardiac action potential duration refers to the length of time it takes for a cardiac muscle cell to depolarize and repolarize during an action potential. It is an important measure of the electrical activity of the heart and can be affected by various factors such as hormones, medications, and diseases.

2. How is the cardiac action potential duration measured?

The cardiac action potential duration can be measured using an electrocardiogram (ECG) or by recording the electrical activity directly from a cardiac muscle cell using a microelectrode. The duration is typically measured from the beginning of the QRS complex to the end of the T wave on an ECG.

3. What factors can influence the cardiac action potential duration?

The cardiac action potential duration can be influenced by various factors, including heart rate, electrolyte levels, hormones, and medications. For example, a higher heart rate can lead to a shorter action potential duration, while low levels of potassium or calcium can prolong the duration.

4. Why is it important to understand cardiac action potential duration?

Understanding cardiac action potential duration is crucial for diagnosing and treating various heart conditions. Abnormalities in the duration can indicate underlying cardiac issues, such as arrhythmias and heart failure. It can also help guide the use of medications and treatments to manage these conditions.

5. Can the cardiac action potential duration be modified?

Yes, the cardiac action potential duration can be modified by various factors as mentioned earlier. Additionally, certain medications can also directly affect the duration. For example, antiarrhythmic drugs can prolong the duration, while beta-blockers can shorten it. These modifications can have significant implications for the functioning of the heart and its response to different stimuli.

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