confused about cardiac output....

[IHeartPeds87]

Hi everyone,

can someone please read the following and either tell me i'm correct or explain why I'm wrong?

Am I understanding the following concepts properly? I'm most confused about preload.

Heart rate: bradycardia can decrease cardiac output (if the heart isn't pumping fast enough then cardiac output can go down). Tachycardia can decrease cardiac output (if the heart is pumping too fast, the heart doesn't have time to fill and then cardiac output can go down). That's why you want the heart rate in the "sweet spot" of 60-100 bpm.

Afterload is the resistance the left ventricle has to fight to push the blood out, and is a combination of systemic ventricular pressure and aortic pressure. Increasing afterload would decrease cardiac output, correct? So vasodilation decreases afterload, correct?

Contractictility of the heart is how strong/intensity of the contraction is...you want a strong contraction to push more blood to the body so increasing contractility of the heart (done with inotrope medications) increases cardiac output, correct?

How does preload factor in to this? I've heard people refer to preload as stretch....I don't totally get that. My understanding is that preload is the volume of blood in the right ventricle at the end of diastole....meaning it is the volume of blood that gets "left behind" in the heart and doesn't get to the body where it needs to be....meaning that decreasing preload would increase cardiac output? Is that correct? How would preload ever get increased? would we ever want preload increased?

Your help is much appreciated!

[Carpediem1012, BSN, RN]

Love these threads!

And hi Esme!! Nice to see you :)

[vuphan86]

i know angiotensin is released by Kidney to constrict the vessels, so it increase Blood pressure. Angiotensin receptor blocker is angiotensin antagonist. it blocks the angiotensin receptors so that it cant cause vasoconstricton. It helps to decrease Blood pressure. How can it help for afterload? that part i need your help?

According to my understanding, afterload is the pressure of LV or the amount of blood leftover in LV after systole or before diastole.

The reason i asked you is i kind of misunderstand that how can the drugs ARB can reduce the afterload? i tried to look up on my pharm book and internet but they do not give detail explaination about it. Before the article, i dont understand afterload and preload. after reading your reply to someone that misunderstood like me, i am better understanding the process of reducing preload but not for afterload.

[vuphan86]

.......

[nurseprnRN, BSN, RN]

Afterload is not the pressure in the LV, nor is it the amount of blood left in the LV at the end of systole. That's the reason for your confusion, so thanks for explaining. Afterload is the pressure the LV has to overcome in systole-- the pressure in the aorta that's holding the aortic valve shut after systole so it can prevent blood from flowing backwards into the ventricle again.

So. Now that you know the ARB (angiotensin receptor blocker) makes for relaxation in the arteries by preventing angiotensin from making them tighter, reducing afterload, you can see how that would make the ventricles' job easier. They don't have to push so hard to open the door, as it were. (Don't forget the RV -- it has to work with its own preload and afterload conditions).

[vuphan86]

let me clearify what i understand about your saying.

afterload is the pressure in RV or LV during systole to overcome the pressure of Pulmonary veins or Arotic so that the Pulmonay valve or Aortic valve will be opened and blood is ejected to Lungs or body and close to prevent to backward to RV or LV due to the pressure of RV and LV decrease after ejecting the blood, right?

Am I right that Preload is the pressure of RA or LA to overcome the pressure of RV or LV to open the AV valve so that blood can pass down to RV and LV?

[Natasha A., CNA, LVN]

Is this correct. ...becaus its a decrease cardiac output in the kidney system therefore nitogenous accumulaion occur causing the blood not to filtrae properly leading to octuria right? And this is because of lack of blood flow right?