These factors will result in prostaglandin synthesis by the kidneys
Renal ischemia, renal hypotension, and physiological stress
This common drug used for post-op pain relief should be avoided in those at risk for medullary ischemia. Why?
Ketorolac (Toradol) This is because it is a powerful NSAID, which drastically reduces prostaglandin synthesis, putting the kidneys at risk for ischemia
Low dose dopamine will do this, but not this
Will have positive inotropic effects, which increase UO. Will not decrease the incidence of ARF, dialysis, or mortality
The kidneys are able to autoregulate over this range of MAPs
80-180 Some say up to 200 Either way, kidneys are very sensitive to a reduction in MAP Also, may be higher than 80 if the patient has chronic HTN
Surgical stimulation can cause release of this hormone
ADH This will cause a drop in UO
This will cause aldosterone release
baroreceptor response to volume depletion
In hypotension, blood will be shunted (towards/away) from the kidneys
Away from the kidneys! Towards the vital organs
What ion are we concerned about in renal failure?
Floride. Free fluoride ions cause tubular injury and loss of concentrating ability (can result in ARF)
Ranking of volatile agent effects on the kidney
Methoxy>Enflu>Sevo>Iso>Des>Halo (MESID H)
We prefer the use of these IAs in renal failure patients
Iso and des These have negligible effects on renal function
This is the minimum amount of gas flow that should be given with Sevo
2L to prevent compound A formation
BUN > ___ is indicative of decreased GFR
These factors may cause GFR to rise despite a normal GFR
High protein diet GI bleed Febrile illness Dehydration
What is the most common cause of high BUN
CHF secondary to the reabsorption of BUN Low CO causes lows kidney perfusion. Kidneys try to correct perceived fluid deficit by reabsorbing urea.
There is a __-__ hour lag time after a change in GFR before the increase creatinine levels are seen
8 - 17
What test is the most reliable estimate of GFR?
Why is anemia common in renal failure?
1) Decreased EPO production 2) Build-up of toxins decreases the lifespan of RBCs
Chronic renal patients will usually have an increased or decreased CO?
Increased to compensate for the anemia
Hemoglobin levels as low as __-__ are common for renal patients, so don't freak out
Renal patients usually have fucked up coags. Which coags are fucked up and why?
PT, PTT, and bleeding time. These are fucked up because they have shitty vWF. Treat this by replacing vWF.
How can you treat the fucked up coags seen in renal dysfunction?
Replace the vWF! 1) Desmopressin .3-.4mg/kg over 30 min) - Desmopressin will increase the release of vWF from endothelial cells 2) Cryoprecipitate (remember that this contains factor VIII, XIII, fibrinogen, and whaddup --> vWF!)
The hyperkalemia seen in RF can result in these EKG changes
Peaked T waves, ST depression, prolonged PR interval and QRS complex, heart block, and V-fib
Hypermagnesemia resulting from RF can cause
Coma and CNS depression Prolongs the duration of NMBs
Why do we use a microdripper to give fluids in renal patients?
To make sure we don't fluid overload them
Why does RF cause HTN?
1) Renin release by the diseases kidney 2) High intravascular fluid volume d/t inappropriate handling of sodium and water
RF can lead to ____ pericarditis and cause
uremic pericarditis tamponade
Hypocalcemia causes this on EKG
Digitalis toxicity produces this on EKG
Shortened QT and depressed ST
These meds are excreted via the kidneys unchanged and are contraindicated in RF
Gallamine (100% renal elimination) and phenobarbital
Is UO predictive of post-op renal insufficiency?