Cardiac question

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I'm a novice RN student, so bear with me. I'm studying the heart right now, and was wondering if the SA node "firing" is subsequent volume of the atria? Or does it send impulses regardless of volume of blood in the heart? Digoxin, for instance, is a vasodilater used to treat conditions like angina, and it decreases the workload on the heart by decreasing preload and afterload. If the SA node is "firing" as usual while taking digoxin, instead of slowing down (like the blood is), then it would seem to me that eventually there would be decreased filling of the atriiums and ventricles further decreasing CO and then eventually that would cause the body to accumulate toxins, it would lower O2 sats, and so on..... Could you please set me straight. Thanks.

The electrical impulse (SA node and entire cardiac conduction system) is separate from the volume being pumped and from the muscular strength of the pump itself. You can run into problems with the conduction, the volume or the pump. Think of a boiler heating system that forces hot water through pipes up to radiators to heat a house. You need electricity to power the pump, but you also need a working pump to force the water up through the pipes. Problems with your heating system can be caused by a problem with the electricity (cardiac conduction), the pump (cardiac muscle), the pipes (vascular system), or a lack of water in the heating system (hypovolemia).

You might find some videos online that are helpful in illustrating this concept, sometimes it can be hard to picture when you are just reading the text.

Thank you. That analogy seemed to pull it all together for me. I'll take your advise and find some videos to solidify.

I just saw the rest of your post... not sure if you updated it or if I missed the part about Digoxin the first time I read it. To the best of my knowledge, digoxin is not a vasodilator. It is a positive inotrope and a negative chronotrope, so it slows conduction/heart rate while also increasing the contractility- it makes the heart pump more effectively so that it doesn't have to work as hard. Stroke volume should increase while the heart rate decreases. It might be used with a vasodilator.

Digoxin increases intracellular calcium and thus increases contractility. It also increases parasympathetic activity, which slows down the rate by a mechanism that I'm not immediately aware of. Think of it this way though...

Anecdotally, if you increase contractility, you increase cardiac output and thus you increase perfusion. If you increase perfusion, there are various mechanisms (RAAS, baroreceptors, etc.) that will decrease sympathetic activity and lower HR.

Katyq82 is correct that they are 2 different systems. However, they are heavily interconnected. You just need to understand the mechanisms by which they communicate.

If you want to really understand how cardiac conduction works, read Dale Dubins Rapid Interpretation of EKGs. It's an easy read and does a GREAT job of breaking it all down.

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