Cardiac Output variables... question about contractility factors

[BlondeCookie]

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There are several factors that increase heart contractility, but I was confused by two factors listed in First Aid. To quickly summarize...
Increased heart contractility

• increased intracellular Ca++
• decreased extracellular Na++

Having a hard time conceptualizing this. How or why does a change in those ions increase heart contractility? These ions play a role in the cardiac muscle and cardiac nodal action potentials, but I don't understand why they affect heart contractility the way they do.

 

[ZonaRidicularis]

z

 

[FutureInternist]

Okay here is my take on it...

Increased Ca2+ results in increased contractility because of basic cardiac muscle physiology... high amounts of intracellular Ca2+ increase the binding of the filaments.

Decreased extracellular Na2+ will increase contractility because... if you remember there is a Na-Ca exchanger in the heart... so if you decrease the amount of extracellular Na2+ it will slow down the exchanger and allow more Ca2+ to stay inside the cell.... more calcium = more contractility.

Please correct me if I am wrong.. b/c that is how I understand it. 🙂

Both of these are right as far as I know. The 2nd one took a while for me to get as well during class. Pg 241 of FA 2006 explains it well (Digoxin has this MOA)

 

[kdburton]

Zona is correct for both. For the first part I'd just add that when you have higher intracellular Ca2+ in general then the amount of trigger calcium in the SR becomes larger since the Ca-ATPase on the SR does more pumping relative to the fewer Ca-ATPase's and the Ca/Na antiport on the sarcolemma. So the next time you have signal calcium coming in to trigger the Ca-induced-Ca-release you're going to have more Ca released for that contraction.

 

[BlondeCookie]

Zona is correct for both. For the first part I'd just add that when you have higher intracellular Ca2+ in general then the amount of trigger calcium in the SR becomes larger since the Ca-ATPase on the SR does more pumping relative to the fewer Ca-ATPase's and the Ca/Na antiport on the sarcolemma. So the next time you have signal calcium coming in to trigger the Ca-induced-Ca-release you're going to have more Ca released for that contraction.

Ahh! Thanks guys. I forgot that Ca++ is basic in muscle contractions, i.e. binding of troponin to remove the tropomyosin from the actin, allowing blah, blah, blah for more cross-bridge cycling and thus contraction! Thanks Zona, Future, and kdburton.

Oh wait. kdburton, what do you mean by signal calcium doing its thing? I understand what you are saying about higher intracellular Ca++ leading to higher "trigger" Ca++ loaded into the SR and that leading to a higher contraction once the trigger calcium is released by the SR, but I don't what you meant with the signal calcium. Anyways, not too big of a deal. I get the basic idea, but if you or anyone could clarify the signal calcium thing that would be good. Thanks.

 

[kdburton]

Ahh! Thanks guys. I forgot that Ca++ is basic in muscle contractions, i.e. binding of troponin to remove the tropomyosin from the actin, allowing blah, blah, blah for more cross-bridge cycling and thus contraction! Thanks Zona, Future, and kdburton.

Oh wait. kdburton, what do you mean by signal calcium doing its thing? I understand what you are saying about higher intracellular Ca++ leading to higher "trigger" Ca++ loaded into the SR and that leading to a higher contraction once the trigger calcium is released by the SR, but I don't what you meant with the signal calcium. Anyways, not too big of a deal. I get the basic idea, but if you or anyone could clarify the signal calcium thing that would be good. Thanks.

Signal Ca++ is the EXTRACELLULAR calclium that comes in from outside the cell. For example an action potential in a cardiac myocyte will cause the L-type [voltage-dependent] Ca++ channels to open up and let a relatively small amount of "signal calcium" to come in. This signal Ca++ is what activates the Ryanodine receptors on the sarcoplasmic reticulum of that cardiac myocyte which release a relatively large amount of activator pool Ca++ aka "trigger Ca++" (this is the INTRACELLULAR Ca++). It is this relatively large amount of intracellular "trigger Ca++" that has the predominant effect in muscle contraction. Does that clear it up?