Sepsis case

Published

Pt arrived to unit in respiratory distress, was intubated and put on CMV 80% FiO2. B/P low on arrival in 70's-80's and pt got 500ml NS bolus.

B/P remained low in 70's after bolus (boluses were given over 1 hr)

HR 130-138

Temp 40.2 C

RR maybe 16-22

0 urine out for 2 hours upon arrival (until started on pressors)

report states pt has hx of HTN, CHF, and possible UTI and PE

Pt got bolus of 500ml NS, B/P still low with MAP about 50-52.

Started another 500ml bolus but B/P remained low, medicated for temp, and started on Vaso 0.04units/minute to achieve MAP> 65.

>>>>Would you argue that Phenylephrine should have been started first?

The Vaso combined with continuous bolusing of 250ml NS per hour achieved MAPs in 65-70's and Syst B/P 90's. o2 sat stayed 97% the whole time (even with weaning Fio2 to 50%) Neo was added later to assist B/P

Pt on Heparin gtt, then determined to have definite DVT in leg. PE undetermined bc poor kidney functioning. Creat 6.3

When checking labs, lactate came back 1 something, and the ICU fellow states "pt is not septic-they don't even have an elevated lactate"

>>>>>I have not found anywhere that lactate level is a determinant of sepsis or MODS.

PLEASE COMMENT!

Specializes in Critical Care Nursing.

Definately had SIRS but is there something else going on that is causing the hypotenson and high fluid requirments. My Docs tend to echo most patients these days and would definately echoed this one because of the history of CHF, ongoing high fluid requirments and possible PE.

In most of the studies I've seen Norepinephrine is the first line however There are some new ones that suggest Vaso may work better. Like someone said it depends on which doc is on. I think the sepsis goal is a cvp of at least 8. I like looking at urine lytes in the face of low uop and rising creat. It usually comfirms pre renal and gives some ammo for fluid. Hope the pt is doing well.

Specializes in Critical Care.

In sepsis, with a patient on a vent, you should shoot for a CVP of 12-15. This is because the high positive intrathoracic pressure decreases venous return to the heart, thus significantly decreasing preload and cardiac output. A higher CVP offset that with higher right heart pressures. I agree that the renal failure is prerenal. Our sepsis protocol kicks in with a lactate of 2.2, but with severe hypotension and MSOF, who cares if its low. You have to treat the shock first, and assume he's septic and treat with ABT. At our hospital we use Levo as a first line pressor in shock then add Dopamine and Vasopressin. I don't think I've seen any of the intesivists order Neo. I'm not sure why. This patient also needs alot more fluid, like 2000ml over an hour. Thats my opinion, but I realize there is more than one right way to do things too.

Specializes in here and there.

Im new to ICU , I have been told that Levo is the drug of choice for patients in septic shock but I will be concerned about starting the patient on levo due to the already elevated heart rate.

as posted in other parts of this topic, this pt had CHF- so we weren't trying to flood his lungs all at once- he got a few 500ml boluses, each over an hour, then ordered to continue giving 250 bolus/ hr if cvp

Specializes in Med/Surg ICU.

Did you have a scvo2?

hal no! this guy just dot a triple lumen as soon as i got there, thank God! and, THAT was asking a bit! it's a good thing he got the line when he did, since the pressors were started only an hour hour and a half after i got there!

Specializes in Med/Surg ICU.

Well if you did or heck last ditch try dobutamine.

at the end of the day, vaso and neo were stopped concurrently while dobutamine was started. the only problem was his cvp still had not climbed up much; it was about 7-8 at the end of the day.

Specializes in CTICU.
Im new to ICU , I have been told that Levo is the drug of choice for patients in septic shock but I will be concerned about starting the patient on levo due to the already elevated heart rate.

Levophed does not really elevate heart rate - it acts on alpha 1 and 2 adrenergic receptors to cause vasoconstriction and increase SVR.

Thanks for your comment, but Levophed's mechanism of action is stimulation ofalpha- and beta1-adrenergic receptors.

:coollook:

http://128.240.24.212/cgi-bin/omd?receptors,+adrenergic,+beta-1

http://www.cvpharmacology.com/cardiostimulatory/beta-agonist.htm

Also, the key here was to not increase the heart rate further and increase potential for arrhythmia. For this reason, Vaso and then Neo, then later dobutamine, were chosen.

Specializes in CTICU.

In 12 years, I have *never* seen norepi lead to an arryhthmia. Epi, maybe, but not norepi.

Did you read the link you wrote? It says " Reflex bradycardia masks direct stimulatory effects on sinoatrial node".

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