Albumin/fluids and svr

Specialties CCU

Published

Ok, open heart RN's. Does Albumin increase SVR? Do isotonic solutions increase SVR? I was under the thinking that Albumin does, but was assured otherwise. Thank you guys and girls:)

Specializes in Cardiac &Medical ICU, Emergency Medicine.
Thank you.

My patient had very low SVR-so likely vasodilatated. I figured some albumin would bump the svr, but some people disagreed. Eventualy levo fixed the issue.

haha yea usually levo does fix the issue :)

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Specializes in Critical Care, ED, Cath lab, CTPAC,Trauma.
Thank you.

My patient had very low SVR-so likely vasodilatated. I figured some albumin would bump the svr, but some people disagreed. Eventualy levo fixed the issue.

If the patient was vasodilated.....just adding fluid to try to fill a big pipe will not really work. YOu need to make the pipe smaller in volume so it takes less to fill it to the poper volume. Also albumin can cause diuresis further increasing the hypovolemia.

http://tinyurl.com/6ht3lso Here is a link to several good sites.....:heartbeat

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Sure, vasodilation decreases SVR and there is an inverse relationship b/n CO and SVR. I would agree giving some Albumin but only if pt' Hct is only > 30 otherwise I would give 1 Unit of PRBC's. This pt. has gotten a dose of lasix in OR, could he be dry intravascularly may be? Norepi would be my first choice after volume expander is given prn.

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Specializes in Post Anesthesia.

Hypovolemia causes a HIGH SVR- correcting the problem by adding fluid will reduce the SVR. Low cardiac output with high SVR is the hallmark of hypovolemia. Colloid corrects the problem for longer than crystaloid since the fluid dosen't 3rd space out as quickly. Low CO/CI with a normal or low SVR is an indication for a inotrope. High cardiac output with a low SVR and poor perfusion pressure is an indication for pressors. High SVR with elevated filling pressures is an indication for a vasodialator. If you drop someones SVR without adequate fluid volume they are going to crash or go tachycardic to compensate for the greater vascular space.

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Sure, vasodilation decreases SVR and there is an inverse relationship b/n CO and SVR. I would agree giving some Albumin but only if pt' Hct is only > 30 otherwise I would give 1 Unit of PRBC's. This pt. has gotten a dose of lasix in OR, could he be dry intravascularly may be? Norepi would be my first choice after volume expander is given prn.

-I've had one anesthesiologist give lasix in the OR but it is not common in my experience. BUT....every practice differs. Cardiac pts suck up volume so it would be an odd choice to diurese during that period.

-Transfusing to a hct of 30 is a thing of the past. Cardiac pts as a whole can tolerate hgbs down to 7. In anemic pts who are not actively bleeding I use albumin for oncotic pressure. If bleeding or sig. anemic and shocky, then PRBCs.

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Giving fluid will more than likely decrease your SVR even further because the vasculature dilates in response to increased volume within the system. The reason open heart patients "suck up volume" according to TakeBack is because opening the thoracic cavity completely eliminates the intrathoracic pressure which is generally around -4. This in and of itself significantly reduces the hearts ability to fill so you have to drastically increase the mean systemic filling pressure (above the normal value of 7 mm Hg) to compensate and maintain cardiac output.

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The main reason they require volume is due to the massive third spacing from cardiopulmonary bypass/inflammatory response, and the use of vasodilating agents for anesthesia and postoperative sedation. The thoracic pump mechanism you are suggesting would really only applies to the chest when it is open, during the case, not afterward.

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It is really difficult to say that volume loading will have any absolute effect on SVR. Resistance results from the interplay of flow (CO) and vascular tone. With fixed tone and CO the SVR would increase with IVF. However EVERY pt responds differently- the degree of change in the SV (ventricular compliance variability), vasodilation (vascular compliance variability) and HR response (chronotropic variability) makes it nearly impossible to predict. Experts on hemodynamics tend to agree that it is a bedside, case-by-case titration model which requires constant feedback to determine the individual results.

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They tend to run our hearts dry; so immediate post-op they often need albumin to help with preload, cardiac output, or hypotension; of course blood is best! You could try some with high SVR, but we tend not to treat the SVR in general unless its sky high. We also tend not to give Levophed or Neo on this patient population; we use Dopamine, Epi, & even Vasopressin. I think it's the preference of the surgeon though. Oh, some the anesthesiologists give Lasix or mannitol at the end of the case if they ran wet instead.

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TakeBack - Your definition regarding flow is a misconstrued deviation of Ohms law that actually incorporates resistance twice (V=IR). Tone is generally referred to as resistance and if examined separately is still the driving force of resistance (increase vascular tone = increase resistance). Additionally, your hypothetical situation involving Delta P = CO X SVR (V=IR) is nothing more than that. A textbook definition can use these types of variables in order to describe a particular situation but that is generally not the case in the real world. Stating that someone has "fixed tone and CO" is similar to describing the effects of an increased preload by stating that it will increase stroke volume, increase end diastolic volume, etc. and neglecting to include the response of the right atrium (Bainbridge reflex, ANP release, etc.).

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I think we're getting at the same idea from different sides.It's impossible to predict the result of one intervention (say, volume loading/increased SV) when the other variables are not fixed. It sounds like we agree that textbook scenarios don't uniformly apply to real pts.

Regarding resistance, I am referring to both the static and dynamic aspects. The isolated contstrictive state of the VSM will have a dynamic effect on the flow generated by the CO (producing what we measure as the SVR). The degree of vasoconstriction produces the variable SVR in our calculations (using CO and MAP).

Analagous to peak and plateau airway pressures.

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Please I just want to know, what is the aim of these questions?

providing information , brain storming, or discussion ?

thank you

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