Brainy

I'm a nursing student and have been assigned a patient for which I will be providing total care. One of the things I have to do prior to going onto the floor is making a time plan outlining some important nursing diagnoses that pertain to this diagnosis. I believe this patient is on dialysis and thus urinary elimination problems is out of the question. However, what would be a nursing diagnosis for fluid volume excess? How do I word this? Also, what are some other important things I should add into my care plan?

correct, the carbonic acid is the temporary fix as it is using the basic HCO3 ions in the blood (so less freely roaming HCO3 so the bloods pH drops because of that, not because Carbonic Acid is actually acidic in itself)

The bloods pH is not made acidic by Carbonic Acid, rather by free hydronium (H+) ions in the blood. In order to compensate for the acute respiratory alkalosis, the already formed carbonic acid should be dissociating to form more HCO3 and H+ ions, thereby decreasing the pH. But i agree with your third statement "Eventually the kidneys start to compensate for the imbalance by increasing resorption of hydrogen ions and increasing excretion of HCO3 to maintain a balanced ratio. This results in a more pronounced compensatory reduction of HCO3."

the long one :)

desperately waiting for clarification still

Somebody please clarify this for me :$

Well her HCO3 level is not exactly normal so to say, it is on the low end (normal range is 21-28). Shouldn't the HCO3 levels be high instead in an attempt to compensate and bring the pH back down? Carbonic acid (H2CO3) should be dissociating in the blood to release more H+ and HCO3 into the blood to lower the pH back down (yet the HCO3 levels is not as high as it should be?)

In the case study, it does say that she has a pain score of 8/10. And I understand how that would relate to her tachypnea. Lastly, her HCO3 level is in normal range

This is the conclusion i am trying to make: Because the red blood cells take on a sickle shape and harden, they cannot easily pass through capillaries or other small vessels and can cause vascular occlusion, leading to acute or chronic tissue injury. The red blood cells cannot effectively carry out internal gas exchange which has lead to local hypoxia and hypocapnia. For the same reason, although her PaO2 is in range, it is still low. In an attempt to compensate, her respiratory rate has increased to 25 beats per minute. Is this correct?

If I can answer this question, everything else will make sense: why do sickle cell anemia patients have hypocapnia?

Hey guys. So I am doing a Sickle Cell Anemia research paper/case study and I seem to be stuck on this one question. "Discuss how these lab results are consistent with patients who have SCA". The lab results are as follows: white blood cell count (WBC) 18 x 109/L (higher than norms) red blood cell count (RBC) 3x1012/L (lower than norms) hemoglobin (Hgb) 75 g/L (lower than norms) hematocrit (Hct) 0.218 (lower than norms) reticulocyte count 0.23 (lower than norms) ABG'S pH 7.54 (alkalosis) PaCO2 32 (lower than norms) HCO3 22 (in range) PaO2 87 (in range, but on the low end) I understand why the RBC, Hgb, Hct, retic count, and WBC count are outside of norms considering the diagnosis, but I don't understand why the ABG's are affected. All thoughts are appreciated!

Our instructor sends us our patient assignment before coming into clinical so that we can prepare and create a timeplan ahead of time. I'm supposed to come up with some major assessments based on the patient's diagnosis.

Ok so tomorrow I have an 84 y.o patient diagnosed with AKI and right nephrectomy. I had a difficult time figuring out some appropriate assessments and making a timeplan. All help is appreciated

Hmm ok seems to make sense now, I was just confusing starvation ketoacidosis and hypoglycemic ketoacidosis. Thanks for the clarification.

I had read this before and it doesn't clarify anything, so I posted this instead -.-

Some1 please clarify this for me, I have a test coming up soon

I have read my book regarding Ketoacidosis and I understand why it is caused by diabetes type 1. However, one question that I still have unanswered is whether hypoglycemia and cause DKA or not. I know that hyperglycemia can cause it, but why can't hypoglycemia cause it too? If we have low blood sugar (hypoglycemic) and cannot use carbohydrates for fuel, the second option would be to break down triglycerides, which would produce ketones that are acidic. So why can't hypoglycemia cause ketoacidosis?????