Question about contractility of heart?

  • #1
663
3

Main Question or Discussion Point

1.Increased heart rate- Increase contraction in a step wise manner, by accumulating calcium.
2. Post extrasystolic potentiation- The beat that occurs after an extrasystolic beat has increased the force of contraction because extra "Ca 2+" enters the cell duing extrasystole.
3. Also hypoxia and hypercapnea, acidosis depress myocardial contractility.
First point I can understand somewhat. Since many contractions, with out much pause, would accumulate Calcium. Second point I'm assuming is saying the same thing, but I don't understand the terminology. Can anyone explain it clearly. Also hypoxia and hypercapnea directly stimulate vasomotor centre so how does it depress myocardial contractility Thanks :smile:
 
Last edited:

Answers and Replies

  • #2
bobze
Science Advisor
Gold Member
647
18
First point I can understand somewhat. Since many contractions, with out much pause, would accumulate Calcium. Second point I'm assuming is saying the same thing, but I don't understand the terminology. Can anyone explain it clearly. Also hypoxia and hypercapnea directly stimulate vasomotor centre so how does it depress myocardial contractility Thanks :smile:
1. Because in the heart, electromechanical coupling is dependent on Ca for depolarization, then accumulation of intracellular Ca increases contractility and heart rate.

Ca gets sequestered in the sarcoplasmic reticulum, "more than normal" means when the Ca-channels on the SR open more is dumped into the cell. This activates more myosin through the myosin binding proteins (ie; troponin) and provides stronger contractions (ie; increase contractility).

Having more Ca around makes depolarization faster as well.

2. A post-extrasystole beat is normally generated by latent pacemaker cells. This isn't a complete depolarization and muscle tension generated is less than normal. On the next "normal" beat, extra Ca has been accumulated in the SR because of the extra beat, so more Ca is released intracellularly during the next "normal" beat.

3. Hypoxia and hypercapnea (acidosis in general) increase heart rate as your breathing rate increases because your body is trying to "blow off" CO2. Because the increased heart rate, this leads the heart not being able to achieve its full force-development, thus lowering contractility while raising heart rate.

I believe the mechanism for increasing HR has to do with changes in blood flow in the pulmonary-cardiac circuit. I'll have to double check for you when I have time.
 
  • #3
663
3
1. Because in the heart, electromechanical coupling is dependent on Ca for depolarization, then accumulation of intracellular Ca increases contractility and heart rate.

Ca gets sequestered in the sarcoplasmic reticulum, "more than normal" means when the Ca-channels on the SR open more is dumped into the cell. This activates more myosin through the myosin binding proteins (ie; troponin) and provides stronger contractions (ie; increase contractility).

Having more Ca around makes depolarization faster as well.

2. A post-extrasystole beat is normally generated by latent pacemaker cells. This isn't a complete depolarization and muscle tension generated is less than normal. On the next "normal" beat, extra Ca has been accumulated in the SR because of the extra beat, so more Ca is released intracellularly during the next "normal" beat.

3. Hypoxia and hypercapnea (acidosis in general) increase heart rate as your breathing rate increases because your body is trying to "blow off" CO2. Because the increased heart rate, this leads the heart not being able to achieve its full force-development, thus lowering contractility while raising heart rate.

I believe the mechanism for increasing HR has to do with changes in blood flow in the pulmonary-cardiac circuit. I'll have to double check for you when I have time.
Thanks for the reply :smile: However with the last point, if increase in heart rate accummulates calcium how does it affect force relationship, isn't it contradictory? I'm assuming you are telling that end diastolic volume decreases with increased heart rate, then why do we consider heart rate as a inotropic agent.
 
  • #4
bobze
Science Advisor
Gold Member
647
18
Thanks for the reply :smile: However with the last point, if increase in heart rate accummulates calcium how does it affect force relationship, isn't it contradictory? I'm assuming you are telling that end diastolic volume decreases with increased heart rate, then why do we consider heart rate as a inotropic agent.
No, because its not an isolated increase in heart rate but rather sustained. If we were talking about 5 beats out of a hundred or something (just making up numbers here) then yes, you'd increase contractility because the basal beats would be able to take advantage of that increased sequestered calcium.

But a sustained increase in heart rate, past a certain point, means the heart doesn't get to fully develop the muscle tension it could generate at a lower level.

Remember the equation SW brought up on the other topic;
CO= HRxSV,

So high changes in heart rate with little changes in CO (cardiac output) result in decreased SV. Remember that SV is EDV-ESV, so your difference would be a smaller number (so yes, in this case a decreased EDV).

An inotropic agent affects contractility, HR is affected by chronotropic agents (and for the trifecta a dromotropic agent affects the conduction velocity through the AV node).

Inotropes are things like Ca, Digoxin, Catecholamines, etc
 
  • #5
663
3
No, because its not an isolated increase in heart rate but rather sustained. If we were talking about 5 beats out of a hundred or something (just making up numbers here) then yes, you'd increase contractility because the basal beats would be able to take advantage of that increased sequestered calcium.

But a sustained increase in heart rate, past a certain point, means the heart doesn't get to fully develop the muscle tension it could generate at a lower level.

Remember the equation SW brought up on the other topic;
CO= HRxSV,

So high changes in heart rate with little changes in CO (cardiac output) result in decreased SV. Remember that SV is EDV-ESV, so your difference would be a smaller number (so yes, in this case a decreased EDV).

An inotropic agent affects contractility, HR is affected by chronotropic agents (and for the trifecta a dromotropic agent affects the conduction velocity through the AV node).

Inotropes are things like Ca, Digoxin, Catecholamines, etc
Then let's say heart rate was increased very slightly and maintaind at that level. Would that cause postive inotropism even though it is not an isolated increase, due to accumulation of calcium. I can understand how heart rate increased too much, would decrease contractility as you have mentioned but the book says increased heart rate has shown to increase contractility, and takes it as an example of positive inotropism.
 
  • #6
bobze
Science Advisor
Gold Member
647
18
Then let's say heart rate was increased very slightly and maintaind at that level. Would that cause postive inotropism even though it is not an isolated increase, due to accumulation of calcium. I can understand how heart rate increased too much, would decrease contractility as you have mentioned but the book says increased heart rate has shown to increase contractility, and takes it as an example of positive inotropism.
What book? Can you quote exactly what it says? HR in and of itself wouldn't be an inotropic factor. Maybe they are talking about changes in [Ca], or sympathetic innervation that increases the HR.

Things which affect contractility alter the amount of activated myosin binding in the heart muscle, so there must be an underlying biochemical basis for it.
 
  • #7
663
3
What book? Can you quote exactly what it says? HR in and of itself wouldn't be an inotropic factor. Maybe they are talking about changes in [Ca], or sympathetic innervation that increases the HR.

Things which affect contractility alter the amount of activated myosin binding in the heart muscle, so there must be an underlying biochemical basis for it.
This is what book says.

1. Factors that increase contractility (positive inotropism)

a. Increased heart rate
When more action potentials occur per unit time, more Ca2+ enters myocardial cells during action potential plateus, more Ca2+ is released from SR, and greater tension is produced during contraction.

Examples of the effect of increase heart rate are,
1.Positive staircase or Bowditch stair case. Increased heart rate increases the force of contraction in a step wise fashion as the intracellular Ca2+ increases cumulatively over several beats.
2.Post extrasystolic potentiation

:smile:
 
  • #8
bobze
Science Advisor
Gold Member
647
18
This is what book says.

1. Factors that increase contractility (positive inotropism)

a. Increased heart rate
When more action potentials occur per unit time, more Ca2+ enters myocardial cells during action potential plateus, more Ca2+ is released from SR, and greater tension is produced during contraction.

Examples of the effect of increase heart rate are,
1.Positive staircase or Bowditch stair case. Increased heart rate increases the force of contraction in a step wise fashion as the intracellular Ca2+ increases cumulatively over several beats.
2.Post extrasystolic potentiation

:smile:

Right so, its not really the increase in HR that its saying is the inotropic effect, rather the change in Ca available intracellularly.

So with Bowditch effect you accumulate more Ca as the HR increases, but this eventually plateaus off.

I want to go back to what you said initially,
Also hypoxia and hypercapnea directly stimulate vasomotor centre so how does it depress myocardial contractility Thanks
So I said I thought the reason was; "I believe the mechanism for increasing HR has to do with changes in blood flow in the pulmonary-cardiac circuit. I'll have to double check for you when I have time. "

This is incorrect. The correct reason has to do with changes during an acidosis that occur in K+ levels. Increasing the extracellular H+ results in increases in K+. K+ levels affect the cardiac action potential. So I'm not sure if you're familiar with the phases of the cardiac action potential so I'll go through them real fast.

So phase 0 is the depolarization, where voltage-gated (VG) Na channels open.
Phase 1 is the early repolarization phase, where transient K channels open.
Phase 2 is the Ca and Delayed K channels, which starts as a plateau. Phase 3 is where the delayed K channels fully open and phase 4 is where the VG K channels open that restore membrane potential.

As the increased extracellular H+ rises, intracellular H+ rises to compensate. To maintain electrical neutrality K+ leaves increasing the resting membrane potential. Increasing the RMP decreases cell's excitability.

This decreases repolarization and prolongs the refractory period, which means less muscle cells can be recruited during contraction--Or in other words, it decreases contractility.

Now I also read that in severe cases of acidosis, the decreased pH can also affect catecholamines--reducing their effectiveness on the heart, thus further reducing contractility (remember that catecholamines are positive inotropic agents).

Hope that clears it up for you!
 

Related Threads on Question about contractility of heart?

Replies
3
Views
13K
Replies
3
Views
7K
Replies
2
Views
3K
Replies
1
Views
3K
  • Last Post
Replies
9
Views
236
Replies
4
Views
3K
  • Last Post
Replies
2
Views
18K
  • Last Post
Replies
7
Views
3K
  • Last Post
Replies
9
Views
3K
Top