Endocrine Flashcards
non pulsatile flow may affect
flow distribution to organs and within organs
hypothermia effect on hormonal and biochemical rxn
decreased rate of biochemical rxn and disrupts hormonal response
hemodilution effect
disrupts concentrations of hormones and electrolytes
difficult to pinpoint source of
stress hormones. may be an increase post bypass
deeper levels of anesthesia appear to reduce
or eliminate endocrine responses and decreases morbidity
type of anesthesia that further reduces endocrine response
spinal and epidural
pituitary type of fxn
neural (posterior) and endocrine (anterior)
posterior pituitary is the _____ and secretes______
neurosecretory and is modified nervous tissue. ADH oxytocin (does not produce these)
high concentrations of ADH cause
INCREASE perpheral resis. decrease contractility, decrease coronary BF, REDUCES RENAL BF, increase von willbrand factor,
what causes adh release?
increase plasma osmolarity, decrease BF or decrease BP or percieved decrease Bp, hypoglycemia, angiotensin 2, stress , pain
huge ADH release may be initiated by
initiation of bypass and transient decrease in BP, VENTING
prevention of ADH release
diuretic, pulsatile flow decrease post op only no effect on u.o.,anesthesia with large doses of synthetic opioids (fentanyl 50ug/kg), regional anesthesia
adh concentrations increase regardless
of anesthesia pointless!!
anterior portion secretes trophic hormones
ACTH,TSH, ovaries and testes, HGH
pituitary apoplexy
most damaging complication to pituitary, rare and occurs with pituitary adenomas,
pituitary apoplexy symptoms
droopy eyelids, opthamoplegia, non reactive dilated pupils, decreased visual acuity, hormonal defects
high concentrations of vasopressin
increase peripheral vascular resistance, decrease contractility, decrease coronary BF, increase vascular resistance, reduce renal BF, stimulates release of von willebrand factor
what stimulate vasopressin release
increase in plasma osmolarity, decrease in BV OR BP, hypoglycemia, angiotensin , stress, pain
steps to ADH release form CPB (7)
- )Hypothalamus osmoreceptor cells detect increased serum osmolarity
- ) posterior pituitary releases ADH due to increase serum osmolarity
- )vasopressin binds to kidneys allowing increased water reabsorption from urine
- ) increases urine osmolarity and decreases its volume
- )decreases serum osmolarity and increases volume
- )decreased serum osmolarity is detected by osmoreceptors in hypothalamus and ADH is reduced
ADH may be initiated by bypass due to
decrease in CBV and BP. Venting keeps LAP low stimulating low CBV
can we prevent adh release
no but it can be reduced.
pulsatile flow adh release
No significant decrease during bypass but decreases it 48 hours after. U.O. does not change
anesthesia can reduce adh release by
giving large doses of synthetic opioids. fentanyl (50ug/kg)
regional anesthesia can reduce adh in
non cardiac procedures
adh concentrations increase during cpb irrespective
of anesthesia or perfusion technique
damage to pituitary usually blamed
on ischemia, hemorrhage, and edema of gland. HGH hypophysectomy
treatment of pituitary apoplexy
HGH / hypophysectomy
epinephrine concentration increases
10 fold
nore epinephrine concentration
4 fold
catecholmine secretion can be reduced
deep anesthesia vs. light, propofol infusion (4 mg/kg/hr) vs single bolus injection (.1mg/kg), high dose opioid general (fentanyl or sufentanil) general anesthesia with spinal block (bupivacaine) vs. general anesthesia
cortisol is released in reponse
to stress. increases stores of sugar in liver as glycogen. increases blood sugar
adrenocorticotropic hormone
promotes increased production and release of corticosteroids and cortisol. acts as appetite suppressant, anxietiomimetic and pro inflammatory
adrenal cortical hormones are increased and how is it attenuated
in the initiation of bypass. increase attenuated with deeper levels of anesthesia and addition of thoracic epidural
carbohydrate metabolism regulated by
insulin, glucagon, cortisol, growth hormone, epinephrine
hyperglycemia is worse with
hypothermia
hypoinsulinemia is worse with
hypothermia
type 1 dm do not require
insulin doses
type 2 dm do require
insulin doses
atrial natriuretic factor and is antagonist of what
incredibly efficacious vasodilator . antagonist of aldosterone
anf peptides released by
cardiac atria
anf release triggered by
atrial distension. b adrenergic stimulation, angiotensin 2, hypernatremia, endothelins
ANF physiologic causes
increase GFR, inhibits renin release, reduced plasma concentrations of aldosterone, antagonize renal vasoconstrictors, reduce ABP
ANF PREVENTS
scarring of ischemic myocardium and has other anti ischemic effects on cardiomyocytes and vascular endothelium
ANF cancentrations are reduced during
hypothermia and cross clamping
ANF conentrations rise during
rewarming and post bypass. mormal relation between factor conc. and pressure lost during bypass
renin angiotensin aldosterone regulates
atrial pressure, intravascular volume, electrolyte balance
what secretes renin
juxtaglomerular apparatus due to Na depletion, decreased BV, reduced renal perfusion
ACE inhibitors and ARBS temporarily
breaks the linkage between Renin angiotensin aldosterone and hypo or hypertension during immediately post bypass
eicosanoids metabolized by
lungs
prostaglandins mostly related to
inflammation
thromboxanes related to
injury
Endoperoxide prostaglandins H2 produces
PGE2, PGF2alpha, PGD2
prostacyclin (PGI2) or thromboxane (TXA2)
PGE
generally vasodilator
PGF2alpha, PGD2
pulmonary vasoconstrictor
PGI2
disaggregates platelets, potent vasodilator
TXA2
platelet aggregator, potent vasoconstrictor
Prostacyclin & thromboxane increase during bypass and
start to decrease after
Aprotinin
protease inhibitor – reduces increase in thromboxane – no effect on prostacyclin – better preservation of platelet function
“sick euthyroid syndrome
T3 and T4 levels are low but the thyroid gland is apparently “normal”
The result of disruption of the thyrotropic feedback loop
Mixed evidence whether giving thyroxine helps (trophic and pro-metabolic effects) or hurts (possible increased risk of MIs)
Many things stimulate histamine release like…
opioids (morphine / meperidine) muscle relaxants (tubocurarine) antibiotics heparin protamine
calcium con concentration
Ionized (50%), bound to protein (40%), chelated (10%)
calcium Blood concentration maintained by
parathormone and vitamin D (bones / kidney)
calcium changes during bypass attributed to
type of fluids used and addition calcium. parathormone secretion not affected by bypass
Give extra calcium only when the following three conditions are present
1) ready to terminate bypass
2) ionized calcium is reduced
3) need to increase contractility and blood pressure
magnesium key players in these enzyme finctions
transmembrane electrolyte gradients energy metabolism synthesis various messaging substances function of ion channels hormone secretion and action
mag concentrations
Ionized (55%), bound protein (30%), chelated (15%)
mag decreases during and is associated with
bypass. arrhythmias
mag benefits
direct myocardial membrane effect
direct / indirect effect on cellular sodium and potassium
antagonism of calcium entry into the cell
prevention of coronary arterial spasms
antagonism of catecholamine action
improves myocardial oxygen supply / demand ration
inhibition of calcium current during plateau phase of myocardial action potential
typical mag dose
2 grams post cross clamp
Changes in potassium concentration caused by
cardioplegia anesthetic drugs priming solutions renal function carbon dioxide tension arterial pH hypothermia (decrease as cool, increase as warm) insulin treatment of hyperglycemia moves glucose and potassium into cell)
Hyperkalemia not uncommon with
multi dose high k protocols
Hypokalemia may be increasing
as the use of Custodial CP increases
Albumin may help reduce
decrease in concentration