SVR too low!!

altusjg · Sep 1, 2010

Hello Melissa,

I've been a CVICU/MICU nurse for 5 years now and have recovered my share of post cabg pts. I've had the same problem from time to time but must admit i've never had an svr in the 200's. I like to keep mine between 800-1400. In reference to SVR, I generaly stick with the old saying High is Tight and Low is Loose. Two ways to increase your SVR are: 1. increase volume and/or 2. increase vascular squeeze. Since you were low it would appear that you were loose. Seeing as how you had the pt on a substantial amount of pressors and inotropes I'm willing to bet that what you needed was volume. What was your CVP as it is used as an indicator of the pts vascular volume? I generally like to keep my post cabg pt's CVP around 10-12. Now i'll move on to why your blood pressure dropped as your SVR came up. When you squeeze down on your vasculature, your heart has to pump against that squeeze/pressure in the vasculature. My guess is your pts already sick heart could not pump sufficiently against the pressure in the vessels and therefore could not maintain an adequate bp. I'm sure that if you would have opened up a liter or 2 of NS and slowly titrated down the pressors and inatropes as tolerated, you would have seen your SVR and BP come up as well as seen your CO and CI come down a bit to within normal range. You have to think about the whole picture and consider the intire cardiovascular system not just the heart or just the vessels. If you have not yet studied up on preload and afterload, i would recomend doing so. As a side note, I dont mind saying that 3 yrs of ER experience does not qualify you to recover an open heart and your facility should not have put you in that position without having a proper CCU preceptorship and orientation to recovering post CABG pt's. I hope thats not what happened. I wish you luck in your future endeavors and hope this post helped you wrap your mind around the problem a bit.

-Altus

HeartRN80 · Sep 1, 2010

To begin.... My CVP 16 was with a PAWP of 28. I had obviously tried fluid before flogging a sick heart with pressors (Crytalloid, colloid, and Blood Products). I do understand what the SVR is and means.....what I was asking is WHY was my patient soooooo dialated and non responsive to fluids and pressors.

I had a 3 month oreintation before recovering hearts on my own. I also had my charge nurse and fellow co workers in the room to see if they could see a piece of the puzzle I was missing during this recovery.

Although I appreciate a response to my question, I have to admit that I am rather offened by your tone and implications of my ER nursing background

I was seeking some supportive advice about a patients situation, not an assesment of my nursing skills.

tri-rn · Sep 1, 2010

Hello Melissa,
Now i'll move on to why your blood pressure dropped as your SVR came up. When you squeeze down on your vasculature, your heart has to pump against that squeeze/pressure in the vasculature. My guess is your pts already sick heart could not pump sufficiently against the pressure in the vessels and therefore could not maintain an adequate bp.

Wouldn't her CO and CI have been lower if this were the case?

aCRNAhopeful · Sep 1, 2010

Wouldn't her CO and CI have been lower if this were the case?

I agree that CO and CI would be much lower. A sick cardiogenic-shocked heart wont produce a hyperdynamic circulatory state IMO.

To answer the question about the low SVR: Was there a long CPB time? It sounds like SIRS which could be induced by a long period of time on pump. Which brings me to my next question.. Why did they place the IABP? You certainly didn't need afterload reduction, you needed the exact opposite. I do have one other theory which would make sense as to why they placed the IABP. Was there any way the patient developed a ventricular septal rupture? I would certainly think you would have known about it if they did but its still a thought. A VSD would cause left to right shunting and a falsely elevated CO, CI, and SvO2 and could make a falsely low SVR. Again, I'm sure you would have known about it if they did develop a ventricular septal rupture but it was just a thought for discussion.

HeartRN80 · Sep 2, 2010

I like the idea about the SIRS and I think that the surgeons only put in the IABP as a last resort. Because as you said the patient didn't need any afterload reduction, however the IABP can help increase the blood flow to the coronary arteries...maybe that was the thought behind it. We did a stat echo after the IABP no rupture or major abnormalities.....

rickard · Sep 2, 2010

The condition you are referring to is Vasoplegic syndrome.

Vasoplegic syndrome - Wikipedia, the free encyclopedia

Vasoplegic Syndrome after Off-Pump Coronary Artery Bypass Surgery

Vasoplegic syndrome--the role of methylene blue

Ganesh Shanmugam *

Department of Cardiac Surgery, Royal Hospital for Sick Children, Dalnair Street, Glasgow G3 8SJ, UK

Received 15 May 2005; received in revised form 27 July 2005; accepted 29 July 2005.

Vasoplegic syndrome is a recognized complication following cardiac surgery using cardiopulmonary bypass and is associated with increased morbidity and mortality. In several patients profound post-operative vasodilatation does not respond to conventional vasoconstrictor therapy. Methylene blue has been advocated as an adjunct to conventional vasoconstrictors in such situations. There is limited data pertaining to the use of methylene blue and a number of reports have been anecdotal observations. This article reviews the incidence and problems associated with the vasoplegic syndrome, the mechanism of action of methylene blue, its effects and adverse reactions and the literature supporting its intra-operative and post-operative use.

In cases where first-line therapy fails, the use of methylene blue seems to be a potent approach to refractory vasoplegia. The early use of methylene blue may halt the progression of low systemic vascular resistance even in patients responsive to norepinephrine and mitigate the need for prolonged vasoconstrictor use. However, dosing regimens and protocols need to be clearly defined before widespread routine use. Whether methylene blue should be the first line of therapy in patients with vasoplegia is a matter of debate, and there is inadequate evidence to support its use as a first line drug. More scientific evidence is needed to define the role of MB in the treatment of catecholamine refractory vasoplegia.

grandmawrinkle · Sep 3, 2010

I have had a few like this. I wasn't aware it was called "vasoplegic syndrome" but did know that occasionally this is a complication and it's from CPB. It acts just like septic shock. Basically you want to make sure your tank is full (which yours was) and squeeze the crap out of them with pressors (as you were) and wait it out. From what I've seen, it's usually a 24-48-72 hour turn around.

Most of the ones I have seen that do this develop some degree of ARF as end organ perfusion suffers ... sometimes severe, sometimes not so much.

HeartRN80 · Sep 3, 2010

:yeah:Thank you rikard for the article. It was very helpfull...in fact I am going to print it out and take it into work.

fiveofpeep · Sep 3, 2010

Two ways to increase your SVR are: 1. increase volume and/or 2. increase vascular squeeze.

why would increasing volume increase your systemic vascular resistance? I can see increased volume increasing preload and thus increasing CO and BP but not SVR.

Very interesting about the vasoplegia. Ive had some bizarre hours of critically low SVR with my limited experience with OHs. I need to be less green before I take the fresh ones, and Ive always chalked it up to infection/sepsis because it happened to be concurrent.

TakeBack · Sep 3, 2010

Aside from what you've mentioned, consider adreonocortical insufficiency, particularly in patients taking steroids preoperatively.

highlandlass1592, BSN, RN · Sep 4, 2010

I have recently transfered to a CCU after doing ER nursing for 3 years. I had a fresh open heart patient the other night. The patient came back with a CO 14.6 and a CI 7.1 with an SVR 246, and a SBP in the 80's..... this was on 3 mcg of dopamine and 8 mcg of EPI. Throughout the night I had the pt up to 10 mcg of EPI, 200 mcg of NEO, 3 mcg of Dopamine, and 0.04 units an hr of Vassopressin....... To get me to an SVR of 496 and an SBP crashing in the 70's. Needless to say we did an emergent IABP at bedside.
Now for my questions.... why couldn't I get an SVR??? My white count actually decreased throughout the night going from 22 to 18, kinda ruling out sepsis. My patient was an emergent CABG so I if anything I would actually expect cardiogenic shock with a high SVR????
Just looking for some ideas from experienced CCU nurses...Thanks!!
Melissa

As someone else has linked to vasoplegia syndrome, I'll share that there was a GREAT presentation at NTI for critical care nurse this past May in Washington D.C. The speaker was awesome, here is a link to her presentation:

http://www.aacn.org/wd/nti2009/nti_cd/data/papers/main/28850.pdf

I can't begin to tell you how inspiring she was..and what a wonderful speaker. You may want to give a look to her risk factors for vasoplegia syndrome and see if your pt had any of these listed..I know I've found that to be the case with some of my pt's.