Decreased cardiac output r/t CABG - Graded care plan HELP!!

[gikg]

Hi, I am writing my graded care plan and need some help. I know that risk for decreased cardiac output is the most important nursing diagnosis for me to use. I am just trying to understand why CABG can lead to decrease cardiac output.

A little hx of my pt:

74 y.o. male pt with hx of CAD, HTN, hyperlipidemia, and R carotid stenosis was brought to the hospital after c/o increased SOB. CABG was performed since 3 vessel were found to be occluded.

On my clinical day he was post-op day 5. BP averaging at 130/80, HR varying between 95-105. sinus tacky. RR 18. O2 95% RA. c/o SOB. Crackles on lower lobes (CXR was done and showed pleural effusion).

So I was thinking in writting: decreased cardiac output r/t depressed cardiac function and increase systemic vascular resistance 2nd to CABG.

Does that makes sense? Why cardiac function and systemic vascular resistance is changed after CABG?

Thanks a lot :-)

[MendedHeart]

^^^awesome explanation! !

[Esme12, ASN, BSN, RN]

It isn't hard people just make it sound that way....LOL

[gikg]

Esme12 that is an awesome explanation. Thank you so much!!!

[nurseprnRN, BSN, RN]

Hi, I am writing my graded care plan and need some help. I know that risk for decreased cardiac output is the most important nursing diagnosis for me to use. I am just trying to understand why CABG can lead to decrease cardiac output.

A little hx of my pt:

74 y.o. male pt with hx of CAD, HTN, hyperlipidemia, and R carotid stenosis was brought to the hospital after c/o increased SOB. CABG was performed since 3 vessel were found to be occluded.

On my clinical day he was post-op day 5. BP averaging at 130/80, HR varying between 95-105. sinus tacky. RR 18. O2 95% RA. c/o SOB. Crackles on lower lobes (CXR was done and showed pleural effusion).

So I was thinking in writting: decreased cardiac output r/t depressed cardiac function and increase systemic vascular resistance 2nd to CABG.

Does that makes sense? Why cardiac function and systemic vascular resistance is changed after CABG?

No, it doesn't. None of the assessment data you have say anything about increased systemic vascular resistance. So you have no data to support that as a cause.

I'm looking right now at the NANDA-I 2012-2014 nursing diagnosis of decreased cardiac output. There are a LOT of defining characteristics for this, of which increased SVR is only one. There are only six causes (related factors), and they are: Altered afterload (there's your SVR), altered contractility (why might someone who needed a CABG have less-than-decent contractility?), altered heart rate, altered preload (do you know what that means? It's less venous return for the ventricle to play with), altered rhythm, and altered stroke volume ( that's a result of altered contractility or, sometimes, some other things).

[MendedHeart]

Couldnt the blood pressure indicate increased SVR?

[Esme12, ASN, BSN, RN]

Not always......depending on the heart. The SVR might be elevated but the heart and body in it's attempt to maintain hemodynamic stability will attempt to compensate and work harder against the resistance/constriction to maintain the "normal" B/P. It is after the heart tries and tries to compensate and is beginning to fail and get tired will you see the reflection of this strain reflected in the patients vital signs (HTN) in the absence of invasive lines.

In the presence of shock.....while they all are hypotensive......depending on the type of shock.....the SVR will vary. For example. In Septic shock....the patient is hypotensive due to the histamine response and vasodilitation there fore the CO is abnormally elevated in the bodies attempt to perfuse the body and you need to administer huge amounts of volume to "fill" up these dilated vessels and administer vasoconstrictors to restore hemodynamic stability.

In the presence of cardiogenic shock...there is vasoconstriction (elevation of the SVR) in order to compensate for the failing hearts (low output) inability to perfuse the vital organs so the body constricts the vessels in an attempt to achieve hemodynamic stability....making it harder on the hearts workload...so the goal is to rest the heart, support output and vasodilate to allow the heart to function more effectively/efficiently.

This is a great site!

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