Please Help with Care plan

You are definitely thinking in right direction. Most patients who are septic from an infection or bacteremia are vasodilated due to the release of inflammatory mediators (a response to an overwhelming infection). Even with fluid resuscitation these patients still present with perfusion problems and require multiple pressors. Inflammatory mediators also cause capillary leakage which you mentioned in your nursing diagnosis. Some other factors to think about: Does your patient have a temperature, increased respiratory rate, increased WBC, evidence of organ dysfunction (i.e. Acute kidney injury)? These are just a few other things to think about and possibly include in your diagnosis. I will list a few simple nursing diagnoses related to sepsis:

* Ineffective tissue perfusion related to decreased vascular tone.

* Ineffective tissue perfusion related to hyopvolemia, fluid shifts, and vasopressors.

* Interrupted family processes related to sudden critical illness.

* Decreased cardiac output related to inadequate volume, inadequate cardiac contractility, inadequate vascular tone, dysrhythmias.

* Risk for electrolyte imbalance related to fluid shifts and potential hemolysis.

Hope this helps!

i think you've made a pretty good start on your own, and tnt1985 has given you a number of other possibilities.

think a bit about where all that leaking fluid is going and what happens to the places it leaks into. if she is already acidotic (metabolic), what will her body want to do to compensate for that, and will she be able to do that? why or why not?

Thank you for replying. I think I'm going to go with decreased CO. If we just fix the fluid deficit she'll still have problems....I like the tissue perfusion I just don"t know if I have enough evidence to support it.

Decreased cardiac output r/t inadequate volume, inadequate cardiac contractility, inadequate vascular tone, dysrhythmias AEB low blood pressure 89/55, sinus tach., tachypnea (RR 33), MAP 65.

Thank you so much for your help!

i think you might want to reconsider that. interestingly, many people in sepsis have very high cardiac output, at least for awhile, even though their bps are low. did you learn that in your reading about sepsis? why is that, do you think? did they do direct cardiac output measurements on her?

if you answer that, you will know why she can have high co and poor tissue perfusion, and that will tell you a lot about why people in sepsis get into such trouble. you will need to know that to really understand what's happening here, which is, of course, the idea your faculty is trying to get you to discern.

We have not had a lecture in class on sepsis yet so this has been very difficult for me. I really appreciate your help. I have been researching it and am having a hard time understanding it all. I'm now understanding why her symptoms didn't match exactly with some of the reading. She did have a low blood pressure, tachycardic, tachypnic, shallow breathing, strong pulses, warm extremities, good cap refill, mild edema and a CVP of 14 (which really threw me off). These symptoms are all seen in the early stage of septic shock. And no, they didn't check her cardiac output. I just assumed low bp means low CO...Now I know, it does not. And her warm extremities and good pulses also indicate her CO was not low.

I was wanting to use impaired tissue perfusion but I'm not sure if I have the correct evidence to support it. Just from the reading I know that an elevated lactic acid is due to tissue hypoxia. Her lactic acid was elevated at 3.8 (highest reading), and I read that that only a level greater than 5 is indicative of tissue hypoxia. She was in mild metabolic acidosis, pH 7.34, PaCO2 36, HCO3 20, PaO2 92. Her Pa02 might be so high because she is compensating w/ a RR of 33...If the metabolic acidosis is severe enough that cans cause arterial muscle relaxation and the vasodilation dramatically decrease total peripheral vascular resistance. It also makes capillaries more permeable causing leakage and fluid shifting into tissues causing third spacing.

I feel like I'm all over the place with this. If I'm way off please let me know. I think I'm having a hard time with this because this was my patients first day in CCU , so she was still going to get worse. I just saw her go from acute pancreatitis to being septic within a few hours.

Thanks for your time!

"i was wanting to use impaired tissue perfusion but i'm not sure if i have the correct evidence to support it. just from the reading i know that an elevated lactic acid is due to tissue hypoxia. her lactic acid was elevated at 3.8 (highest reading), and i read that that only a level greater than 5 is indicative of tissue hypoxia. she was in mild metabolic acidosis, ph 7.34, paco2 36, hco3 20, pao2 92. her pa02 might be so high because she is compensating w/ a rr of 33...if the metabolic acidosis is severe enough that cans cause arterial muscle relaxation and the vasodilation dramatically decrease total peripheral vascular resistance. it also makes capillaries more permeable causing leakage and fluid shifting into tissues causing third spacing. "

you're on the right track, so let me clear up some things for you. she is acidotic, and it is metabolic, with increased lactic acid, indicating that there is tissue hypoxia going on. how does your body try to right the ship if it's listing towards metabolic acidosis? by excreting co2, of course-- so hyperventilation is a compensatory move. her abg tells you that her co2 is in the low end of normal, because her resps are fast.

if you remember, a gas diffuses from an area of higher concentration (pressure) to an area of lower concentration (pressure). this is how the co2 in the pulmonary capillary leaves the blood there and goes to the alveolus for exhalation, because inspired air has very little co2 in it. everybody thinks that getting oxygen in is the lungs' primary job, but it isn't-- because of the variable production of co2 over a range of physical activity and the fact that co2 levels can be easily altered with nothing more than an increased amount of air moved in and out, the body uses the lungs to regulate ph (co2 is an acid for purposes of this discussion). you can drive your blood co2 way, way, way down with increased respiratory rate. this is why hyperventilation makes you feel tingly, for example, and why they have you rebreathe your exhaled air until the co2 level in it rises to normal levels.

now, to oxygen. there's a formula to calculate what the actual pressure of oxygen is at the alveolar level, and unless you really want it i won't bore you with it here, though it's pretty simple. because alveolar oxygen is higher than pulmonary capillary oxygen, oxygen diffuses into the blood there driven by that pressure. this is the short answer of why arterial oxygen pressure (torr) ought to be about the same as alveolar oxygen pressure. more rapid respiration does not change this, because of that simple fact. remember that rapid resps will "wash out" co2, because there's less co2 in the alveolus than in the blood. but you cannot get more os in your blood by breathing faster, because max blood oxygen level is determined by the oxygen content of inspired air.

those capillaries don't have to wait until acidosis is much worse to be leaking- the byproducts of the sepsis itself will make them leak. later acidosis will just make it worse.

Thank you so much for clearing that up for me! I GREATLY appreciate your time and help.

Great reply GrnTea!!! I work on a stepdown and am hopefully transferring to CVICU in a few months, and your explanation was better than my Critical Care textbook. =D

:::looking around for the "blushing" smilie::: my pleasure.