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169 Cards in this Set

  • Front
  • Back
what is considered the best measure of renal function
GFR
what is normal GFR
~125 ml/min
what is a potentially misleading test of renal function
BUN
serum creatnine is produced how
at a relatively steady rate by hepatic conversion of skeletal muscle creatnine
how is serum creatnine filtered
freely at the glomerulus
what is the normal value for serum creatnine for a female
0.6-1.0 mg/dl
what is the normal value for serum creatnine for a male
0.8-1.3 mg/dl
why is serum creatnine decreased in the elderly
secondary to decreased muscle mass
what lab test is slow to reflect acute changes in GFR
serum creatnine
what lab test is the most reliable measure of GFR
creatnine clearance
what is the normal value of creatnine clearance for a female
85-125 ml/min
what is the normal value of creatnine clearance for a male
95-140 ml/min
creatnine clearance decreases with what
AGE
urine specfic gravity is a assessment of what
urine concentrating ability
urine specific gravity of what implies adequate concentrating ability
> 1.018
what is normal protenuria
</= 150 mg/day
what are causes of proteinuria
*glomerular damage
*failure of reabsorption
*excessive plasma proteins
*orthostatic proteinuria
*microalbuminuria
with urinary sodium what value reflects decreased ability of the tubules to conserve sodium
> 40 meq/l
what is glycosuria
tubules unable to reabsorb enough glucose to compensate for an increased load (typically r/t DM) and it is spilled into the urine
with neurohormonal regulation the body protects against hypovolemia and hypotension through what mechanisms
vasoconstriction and salt & water retention

(sympathoadrenal axis, renin-angiotension-aldosterone system, arginine vasopressin)
with neurohormonal regulation the body protects against hypervolemia and HTN through what mechanisms
vasodilation and salt and water excretion
(prostaglandins, bradykinins, ANP)
sx and trauma may produce significant vasoconstriction and salt and water retention lasting for several days leading to what
post-op oliguria and edema
the kidneys lack which innervation PS or sympathetic
PS
the predominately a-adrenergic renal effects of sympathoadrenal stimulation result in what
vasoconstriction from NE, epi, phenylephrine and high dose dopamine
the predominately b-adrenergic renal effects of sympathoadrenal stimulation result in what
*increase in renal blood flow secondary to increased CO

*unclear intrinsic renal effects from isoproteronol, dobutamine
renal effects of sympathoadrenal stimulation from dopaminergic agonists do what
*selectively increase RBF

*may oppose a-adrenergic induced vasoconstriction
aldosterone is released from where
adrenal cortex
aldosterone is released in response to what
*angiotension II

*hyponatremia

*hyperkalemia
aldosterone does what to blood volume
INCREASES it
how does aldosterone affect blood volume
*active sodium absorption

*passive H20 absorption
aldosterone acts via what
mRNA transcription
is the effect of aldosterone immediate or delayed
DELAYED 1-2 hrs
what is the function of arginine vasopressin
regulates urine volume and osmolality
where is arginine vasopressin synthesized
in the hypothalamus
where is arginine vasopressin stored
in the pituatary
arginine vasopressin is released in response to what
*increasing plasma osmolality

*decreased intravascular volume

*arterial hypotension
how does arginine vasopressin maintain adequate glomerular filtration
*constriction of EFFERENT arterioles

*little to no effect on AFFERENT arterioles
what do prostaglandins do in regards to the kidneys
*promote renal vasodilation

*maintain intrarenal hemodynamics

*enhance Na & H2o excretion
what do kinins do
*stimulate phospholipase a2

*act as vasodilators enhancing the action of prostaglandins
atrial natriuretic peptide is released when and why
from atrial myocytes in response to increased atrial volume and subsequent wall stretch
ANP does what to vascular smooth muscle
dilates via formation of cGMP
what does ANP do at phospholipase C receptor
*competively blocks NE

*non-competively blocks angiotension II
what does ANP inhibit
*renin secretion

*aldosterone secretion

*AVP secretion
dopamine may produce benefit by
*DA1 effects-increased RBF

*b-adrenergic effects-increased CO & renal perfusion
dopamines effectiveness is limited by what
it mixed adrenergic effects
dopamine is useful as an inotropic agent when
oliguria persists despite adequate intravascular volume
what is dopexamine
synthetic analog of dopamine
dopaxamine has found use in CHF producing what
*afterload reduction

*increased RBF
what is fenoldopam
selective DA1 receptor agonist
what is fenoldopam approved for
short term tx of severe HTN particulary renovascular
prostaglandins do what to the effects of NE and angiotension II
counteract the vascoconstrictive effects
prostaglandins do what to the inner cortex
maintain the perfusion
Ca channel blockers do what in HTN pts
increase RBF and GFR and induce natriuresis
decreased renal reserve is a GFR of what
60-75% of normal
renal insufficiency is a GFR of what
25-40% of normal
what are the symptoms and abnormal labs with renal insufficiency
*elevated creatnine and BUN

*nocturia may be the only symptom
what is the GFR with end stage renal dz
<25% of normal
what is the most severe form of chronic renal failure
uremic syndrome
what is the GRF with uremic syndrome
<10% normal
what are the s/s of uremic syndrome
*anorexia
*nausea
*vomiting
*pruritis
*anemia
*fatigue
*coagulopathy
what are the CV changes in chronic renal failure
*systemic HTN

*uremic pericarditis
what are the pulmonary changes seen with chronic renal failure
*low pressure pulm edema secondary to increased permeability of alveolar cap membranes

*peripheral vascular congestion appearing as a butterfly wing on CXR
what is the tx for chronic renal failure
*aggresive management of HTN
*aggressive management of DM
*dietary protein restriction <0.6g/kg/day
*tx of anemia w/ erythropoietin
*dialysis or transplant
what are the general goals with anesthetic drugs
*maintain renal blood flow with adequate perfusion pressure
*suppress vasoconstricting salt retaining response to sx stimulation and pain
*avoid or minimize nephrotoxic insults
sympathetic block of what areas effectively suppresses the sympathoadrenal stress response and release of catecholamines, renin and arginine vasopressin
T4-T10
with regional anesthesia renal blood flow and GFR remain adequate as long as what
perfusion pressure is maintained
with general anesthesia ALL anesthestic tech tend to reduce what
GFR and urine output
with general anesthesia what with the kidney is typically maintained
renal autoregulation
with volatile agents there is a mild to moderate reductions in what regarding the kidney that can be attenuated with fluid loading
RBF and GFR
what anesthetic tech has minimal effect on RBF and GFR
high dose opioid tech
what anesthetic tech is more effective than volatile in suppressing the vasoconstricting salt retaining effects of releasing catecholamines, angiotension, aldosterone and AVP
high dose opiod
IV induction agents with the exception of ketamine do what to RBF
produce small decreases
ketamine does what to RBF and urine output
*increases RBF

*decreased UO
peak flouride levels of what rarely produce injury
< 50
peak flouride levels of what have a high incidence of injury
>150
methoxyflurane can produce what fluoride levels
>100
enflurane can produce what fluoride levels
25
isoflurane can produce what fluoride levels
<4
desflurane has what kind of fluroride levels
MINIMAL
positive pressure ventilation and PEEP may do what in regards to the renal system
may decrease
*RBF
*GFR
*Na excretion
*UO
the effect that positive pressure ventilation and PEEP has on RBF, GFR, Na excretion and UO can be attenuated how
by adequate fluid load and maintenance of CO
with deliberate hypotension what renal changes are commonly seen
marked reduction in

*GFR

*UO
nipride does what regarding the renal system
*decreases renal vascular resistance but shunts blood away from the kidneys

*produces sig renin-angiotensin-aldosterone activation & catecholamine release
NTG does what regarding the renal system
produces less reduction in RBF than nipride
what kind of drug is fenoldopam
selective DA1 receptor agonist
what kind of effects does fenoldopam have regarding the renal system
NO reduction in RBF
what are the 2 major predictors of acute renal failure following aortic sx
*pre-existing renal dysfunction

*peri-op hemodynamic instability
with suprarenal or infrarenal aortic crossclamp RBF is decreased to what of normal
50%
with suprarenal or infrarenal aortic crossclamp following release of cross clamp what occurs with RBF
it increases to supranormal levels (reflex hyperemia)
with suprarenal or infrarenal aortic crossclamp following release of cross clamp what is GFR at 2 hrs
remains ~ 1/3 of control values
with suprarenal or infrarenal aortic cross clamp following release of cross clamp what is GFR at 24 hrs
still only ~ 2/3 of control values
with suprarenal or infrarenal aortic cross clamp, clamp times longer than 50-60 min may do what
produce prolonged decrease in GFR
pts with hepatic failure and obstructive jaundice are particularly susceptible to what other system dysfunction
RENAL
what system dysfunction may occur in up to 2/3 of pts following liver transplant
RENAL DYSFUNCTION
has low dose dopamine shown advantage over pre-op hydration in preventing renal dysfunction in pts with obstructive jaundice
NO
nephrotoxic acute renal failure is usually oliguric or non-oliguric with what kind of concentrating ability
*NON-OLIGURIC

*DECREASED concentrating ability
regarding nephrotoxic insults what drug class is directly related to high trough levels
AMINOGLYCOSIDES
with nephrotoxic insults and aminoglycosides toxicity may be reduced how
by once daily dosing
during stress what occurs with NSAIDs and the kidneys
during stress impaired prostaglandin activity d/t NSAIDs results in failure of their protective activity w/ subsequent decrease in RBF & GFR
what occurs with cyclosporin and a nephrotoxic insult
induces sympathetic hyperreactivity, HTN & renal vasoconstriction
with cyclosporin and nephrotoxicity what does concurrent use of Ca channel blockers do
may allow dosage reduction & reduce incidence of ATN
what is the mechanism of nephrotoxic insults with radiocontrast dyes
*microvascular obstruction

*direct tubular toxicity
with radiocontrast dyes nephrotoxic insults are markedly increased when
*in diabetic renal insufficiency
*hypovolemia
*CHF
*with a secondary insult (sx) in the 1st 3-5 days following contrast
what drugs may offer some protection when given prophylactically with radiocontrast dye
*n-acetylcysteine

*fenoldopam
what are the symptoms of pigment nephropathy
*rhabdomyalysis

*hemolysis

*jaundice
what occurs with hemolysis in pigment nephropathy
renal damage secondary to RBC stroma deposition
with jaundice with pigment nephropathy at conjugated bilirubin > 8 mg/dl what occurs
bile salt excretion ceases and portal septicemia occurs
with jaundice with pigment nephropathy circulating endotoxins do what
induce renal vasoconstriction
what are the general goals of anesthetic drugs with renal disease
*maintain renal blood flow w/ adequate perfusion pressure

*suppress vasoconstricting, salt retaining response to sx stimulation and pain

*avoid or minimize nephrotoxic insults
with renal dz what would cause a pt to have attenuated sympathetic nervous system activity
*anti-hypertensives

*uremia
with a renal pt with induction an exaggerated drop in BP may be seen secondary to what
*positive pressure ventilation
*position changes
*blood loss
*drug-induced myocardial depression
what volatile anesthetic should be AVOIDED in the maintenance for a pt with renal dz
SEVOFLURANE
what are the ADVANTAGES of using volatiles for the maintenance of anesthetic for pts with renal dz
*easily titratible

*allows reduction in dose of MR which might have prolonged duration
what are the DISADVANTAGES of using volatiles for the maintenance of anesthetic for pts with renal dz
*high incidence of concurrent hepatic dz

*risk of depression of CO
what are the ADVANTAGES of using an opioid tech for the maintenance of anesthesia for a pt with renal dz
*less myocardial depression

*avoid concerns over hepato- and nephrotoxicity
what are the DISADVANTAGES of using an opioid tech for the maintenance of anesthesia for a pt with renal dz
*less able to control BP elevations

*not as titratable
what would be an example of a TIVA tech for a pt with renal dz
propofol + remi + cisatracurium
what muscle relaxants HAVE renal excretion
*vecuronium

*rocuronium

*pancuronium
what reversal agents HAVE renal excretion
*neostigmine

*edrophonium

*pyridostigmine
what muscle relaxants are INDEPENDENT of renal excretion
*mivacurium

*atracurium

*cisactacurium
succinylcholine is safe to use with renal dz with what exceptions
*extensive neuropathy

*high or high-normal serum K+
what anti-hypertensives are UNAFFECTED by impaired renal function
*propranolol

*labetalol

*esmolol

*Ca channel blockers
what anti-hypertensives ARE affected by impaired renal function
*furosemide

*thiazide duiretics

*methyldopa

*guanethidine
with deliberate hypotension how is trimethaphan affected
UNCHANGED
with deliberate hypotension how is NTG affected
UNCHANGED
with deliberate hypotension how is nipride affected
potential for thiocyanate toxicity
with deliberate hypotension how is hydralazine affected
PROLONGED
with deliberate hypotension how is esmolol affected
UNCHANGED
which vasopressor has the greatest negative impact on renal vasculature
PHENYLEPHRINE
which vasopressors are preferrable with renal dz but may increase myocardial irritability
b-adrenergic agonists
what type of fluid should be AVOIDED in fluid management of renal pts
potassium containing fluids (LR)
with renal dz pts the most likely etilogy of decreased UO is what
inadequate circulating fluid volume
is intra-op UO predictive of post-op renal function
NO
with IV access in a renal pt veins where need to be avoided
veins in dominant arm
what are the ADVANTAGES of a brachial plexus block for shunt placement
*ideal sx conditions secondary to vasodilation
*good post-op analgesia
*avoids many concerns with GETA
what are the DISADVANTAGES of a brachial plexus block for shunt placement
*must assure adequate coagulation
*possible presence of diabetic or uremic neuropathies
*metabolic acidosis lowers sz threshold following intravascular injection
for post-op management of pts with renal dz they will need smaller doses of narcotics particularly which ones
*MS

*demerol
what are the most common causes of ESRD
*DM (#1)
*glomerulonephritis
*polycystic kidney dz
*systemic HTN
a kidney can be preserved, cold and perfused for how long
48 hrs
a donor kidney is placed where in the body
lower abd
a donor kidney get blood supply how
from iliac vessels
what things are critical in the anesthesia of a renal transplant
maintenance of euvolemia and adequate perfusion pressure
with a renal transplant osmotic diuresis with mannitol does what
facilitates urine formation by transplanted kidney without relying on renal tubular mech
release of vascular clamps with a renal transplant does what
*releases K+ and acid metabolites (vasodilating) into circulation

*addition of ~300 ml new capacity to intravascular space
hypotension after release of vascular clamps with a renal transplant usually responds to what
fluid bolus
acute renal failure is deterioration of renal function over hrs to days resulting in what
*inability to maintain fluid & electrolyte homeostasis

*inability to excrete nitrogenous wastes
what are the common definitions of acute renal failure
*increase in serum creatinine > 0.5 mg/dl
*50% decrease in creatnine clearance
*decreased renal fxn resulting in need for dialysis
what is oliguric acute renal failure
< 400 ml/day
what is non-oliguric acute renal failure
> 400 ml/day
who is at the highest risk for acute renal failure
elderly pts with DM and baseline renal insufficiency
what is PRERENAL acute renal failure
acute circulatory problems which impair renal perfusion
what is RENAL acute renal failure
caused by primary or secondary renal dz, toxins or pigments
what is POSTRENAL acute renal failure
caused by obstruction of the urinary tract
what is the management for acute renal failure
*supportive
*correct underlying causes
*fluid resuscitation
*vasopressors
*diuretics
*dialysis
what is the supportive care for acute renal failure
*limit further renal failure

*correct H2O, electrolyte & acid-base imbalances
what is the correction of underlying causes for acute renal failure
correct

*hypovolemia
*hypotension
*sepsis
what are vasopressors that can be used to tx acute renal failure
*norepi

*dopamine
in general attempts to convert oliguric to non-oliguric renal failure w/ diuretics are unsuccessful and potentially harmful w/ what EXCEPTIONS
*post transfusion ATN who receive mannitol w/ adequate hydration
*forced alkaline diuresis w/ mannitol useful in preventing ATN following renal crush injury
what may reduce ARF in high-risk pts who receive radiocontrast dye
N-acetylcysteine
what is the most common cause of new onset acute renal failure in the post-op period
SEPSIS
what happens to renal autoregulation with sepsis
it is IMPAIRED
what things may offer renal protection in sepsis
*anti-inflammatories
(U63557A, NSAIDs, high dose methylprednisolone)
*supranormal O2
*low dose dopamine
*norepi
*arginine vasopressin
how does U63557A offer renal protection in sepsis
protective effect against deterioration of creatinine clearance
how do NSAIDs offer renal protection in sepsis
decrease synthesis of renal vasodilating prostacyclin
what are the benefits of norepi in renal pts with sepsis
*increases stroke volume

*decreased HR

*increased GFR
norepi for renal protection in sepsis may be particularly advantageous in what pts
pts in whom high dose dopamine can be weaned by substitution with norepi
norepi in renal pts with sepsis may require high doses d/t the refractoriness of peripheral vasculature secondary to what
*massive release of NO

*vasopressin deficiency
what type of pts have very low levels of arginine vasopressin
*vasodilitory shock (hypotension, increased CI, decreased SVR)
arginine vasopressin deficiency is likely a result of what
excessive baroreceptor mediated release following sustained hypotension