Cardio questions...

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ihatescience

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Could someone explain the answers to these two questions please 🙂?

1) Which of the following produce(s) an increase in contractility: decreased heart rate; increased phosphorylation of phospholamban; increased action potential duration

2) If, simultaneously, there is an increased rate of phase 4 depolarization and hyperpolarization of the threshold potential, will there be an increase, decrease, or no change in heart rate?

Answers...

1) increased phosphorylation of phospholamban; increased action potential duration

2) increased heart rate

For #1, I understand the phospholamban, but not the increased action potential duration...

Thanks so much!
 
Could someone explain the answers to these two questions please 🙂?

1) Which of the following produce(s) an increase in contractility: decreased heart rate; increased phosphorylation of phospholamban; increased action potential duration

2) If, simultaneously, there is an increased rate of phase 4 depolarization and hyperpolarization of the threshold potential, will there be an increase, decrease, or no change in heart rate?

Answers...

1) increased phosphorylation of phospholamban; increased action potential duration


2) increased heart rate

For #1, I understand the phospholamban, but not the increased action potential duration...

Thanks so much!

#1
Phosphorylating phospholamban inhibits its inhibition of SERCA, so more Ca2+ is taken up into the SR for use during subsequent contractiton (positive inotropy). Increased action potentials means less time b/t contractions. Since SERCA is more efficient at pumping Ca2+ into the SR than the Ca2+-ATPase is at pumping it out into the ECF, again you get more Ca2+ in the SR (positive inotropy)


#2
My take is just that as long as there isn't a great enough hyperpolarization to completely negate an action potential then that will not have an effect on the rate of action potentials as long as the phase 4 depolarization rate increases. The "hump" of phase 4 depolarization is still going to cross the threshold at the same rate regardless of whether the threshold is hyperpolarized a bit.
 
Could someone explain the answers to these two questions please 🙂?

1) Which of the following produce(s) an increase in contractility: decreased heart rate; increased phosphorylation of phospholamban; increased action potential duration

2) If, simultaneously, there is an increased rate of phase 4 depolarization and hyperpolarization of the threshold potential, will there be an increase, decrease, or no change in heart rate?

Answers...

1) increased phosphorylation of phospholamban; increased action potential duration

2) increased heart rate

For #1, I understand the phospholamban, but not the increased action potential duration...

Thanks so much!

With respect to 1, an increased AP duration provides a longer duration of depolarization. This longer period of depolarization will allow for more Ca-induced Ca-release (calcium channels on the plasma membrane will allow more calcium into the cell which will activate ryanodine calcium channels on the sarcoplasmic reticulum to release calcium into the cell), thus causing more calcium to bind to troponin-C, shifting tropomyosin out of the way and leading to increased cross-bridge cycling, with the net effect of increasing contractility.

kdburton, your AP explanation is assuming an increase in the frequency of APs (i.e., a higher HR). I do not believe this was what the answer choice was trying to capture...
 
With respect to 1, an increased AP duration provides a longer duration of depolarization. This longer period of depolarization will allow for more Ca-induced Ca-release (calcium channels on the plasma membrane will allow more calcium into the cell which will activate ryanodine calcium channels on the sarcoplasmic reticulum to release calcium into the cell), thus causing more calcium to bind to troponin-C, shifting tropomyosin out of the way and leading to increased cross-bridge cycling, with the net effect of increasing contractility.

kdburton, your AP explanation is assuming an increase in the frequency of APs (i.e., a higher HR). I do not believe this was what the answer choice was trying to capture...


Actually that is how it works. Action potentials in cardiac pacemaker cells (i.e. in the SA node) will have a direct positive relationship with the heart rate until a critical level is met in which case the AV node is refractory and you have a relative heart block. If you increase the heart rate there is more Ca2+ retained in the sarcoplasmic reticulum and you get stronger contractions. Theres a name for the phenomenon which is fundamental to cardiac phys, but I can'tt think of it off the top of my head

Edit: its called the Treppe Phenomenon
 
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Actually that is how it works. Action potentials in cardiac pacemaker cells (i.e. in the SA node) will have a direct positive relationship with the heart rate until a critical level is met in which case the AV node is refractory and you have a relative heart block. If you increase the heart rate there is more Ca2+ retained in the sarcoplasmic reticulum and you get stronger contractions. Theres a name for the phenom, but I can'tt think of it off the top of my head

Yes, it is called the Treppe phenomenon. Your explanation is correct for a situation in which you have a greater frequency of AP's. However, the original poster's answer choices did not include this answer choice. If you look back up the answer choice listed is an increase in AP duration.
 
Yes, it is called the Treppe phenomenon. Your explanation is correct for a situation in which you have a greater frequency of AP's. However, the original poster's answer choices did not include this answer choice. If you look back up the answer choice listed is an increase in AP duration.

Touche. I mistook it for increased rate of AP not an increased duration 🙂 In that case I think the answer is wrong unless we're assuming the patient is on a cardiac glycoside in which case they could have a prolonged AP/decreased HR and greater contraction force
 
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