First off thank you to everyone who I've been emailing back and forth - I haven't had the chance to personally thank you.
My EKG skills are slowly improving, Thanks.
We are currently studying Acute & Chronic Renal failure. I am having the hardest time grasping how lab values will manifest.
Acute Renal Failure may be caused by 3 methods:
Prerenal - basically factors outside the kidney itself. These factors (Hemorrhage, Hypovolemia, Decreased cardiac output) can all contribute to decreased renal blood flow. Eventually this will lead to renal ischemia
Intrarenal - Direct damage eventually causing the nephron dysfunction. The damage may be caused by (ABX like aminoglycosides, contrast media, etc.) The point is the damage (insult) is direct.
Postrenal - I will automatically think some form of mechanical obstruction. Reflux of urine into the renal pelvis eventually causes kidney dysfunction. Examples are (BPH, tumors, etc.)
Renal Failure is further divided into phases.
Oliguric Phase: This is the phase I am confused and need HELP
MY BOOK SAYS: That damaged tubules can't conserve Na+ and therefore urinary excretion of Na+ will INCREASE
and thusly the Laboratory data will show a Normal to decreased
level of Na+. My book lastly warns against high sodium consumption as it can cause fluid expansion and CHF.
However; if the insult is due to decreased renal perfusion as in CHF or blood loss (as in Prerenal); wouldn't it make sense that the body would detect the decrease in blood pressure and initiate Angiotensin I > Angiotensin II (which help of ACE). Angiotensin II will then cause release of aldosterone from the adrenal cortex; consequently water and sodium retention will occur.
SO is the elevated SODIUM in the urine ALWAYS true? Wouldn't NOT be applicable to Prerenal etiology? (Unless prolonged ischemia occurred? So perhaps initially we would see normal Na+ levels in urine then as it progresses increased levels?)
It sounds like high Na+ in the urine would be more for Intrarenal. (Where the nephrotoxic agents can damage the tubules).
IN both cases we would see the fluid ret (JVD+, Edema, Bounding pulse, Tachycardic, CVP of 8 or greater, increased BP... correct?). We would see Hyperkalemia and it could be expressed in the EKG as a tall peaked T wave (treatment for hyperkalemia could be kayexalate which will rid the K+ via the stool).
I don't know if I'm along the right lines in regard to sodium in water. I was always taught that where sodium goes; water goes. So that concept is also conflicting with me.
NOTE: Is there a way I could post this in the critical care section and the nursing student assistance section for more answers?
Jul 22, '13
I moved to critical care for best response....I am on the run and will be back...and get more response here.
My favorite resource is medscape you have to register but it is FREE!!!!!!!!!
Last edit by Esme12 on Jul 22, '13