Electrolytes Flashcards
(49 cards)
what does RAAS do?
decreased renal perfusion to kidneys:
Angiotensin II –>
1. vasoconstricts (increase vol and afterload)
2. releases Aldosterone : water (increase vol and preload)
3. triggers the production of Vasopressin (ADH) (water: volume)
Aldosterone
acts on kidneys to reabsorb water and Na to increase volume
Volume only!
ADH
vasopressin secreted from the post-pit.
- primary controller of the ECF volume. By osmolality (tonicity)
- feedback from osmoreceptors
- water ONLY
ANP
where does it come from and what does it do
from cells in the heart.
from stretch receptors from increasing volume
ANP blocks aldosterone and ADH produciton
= excretes H2O and Na
whats the cardinal rule re Na **
where Na goes, H2O follows
what is Hct
the ratio of vol of blood expressed as a percent
what happens to solutes from blood sample if the PT had 2L fluid bolus
the concentration would go down from earlier labs
where is Na ICF or ECF
what are a few functions
ECF
- ECF osmolality/tonicity
- fluid balance
- cellular depolarization
- contributes to acid/base balance
what is Na influenced by? hormones
aldosterone and ANP
clinical manifestation of hyponatremia?
- too dilute
- confusion, irritable, seizure
- headache, muscle weakness
how do you treat hyponatremia
fluid restriction, possible admin hypertonic sol 3% Nacl
Hypernatremia
clinical manifestations
- dehydrated/water def
- confused, twitch, seizures, coma, thirst, flushed
how to treat hypernatremia
Slowly replace H2O with D5W
- limit Na intake
- free water to enteral feeds
where is K+ located
function?
ICF
- essential for nerve impulses conduction and muscle contraction
- acid/base balance
how is K+ influenced by acid/base balance
-when the serum pH is low, there are more H+ ions. These H+ go into the ICF, which pushes the K+ out =
Hyperkalemia
Hypokalemia causes:
clinical manifestations
cause: inadequate intake, GI loss, diurese, shift in cells (acid/base or from glucose/insulin)
- flattened T, dysrhythmias, skeletal muscle weakness
how does insulin and glucose influence K+ and what else does it influence?
what would you do in an emergency?
- insulin shifts glucose into cells and K+ and PO4 follows, reducing serum K+ and phos
hyperkalemia emerg: give D50 IV followed by insulin to shift K + into cells
- can help of delay lethal arrhythmias while waiting for other interventions (dialysis)
hypokalemia treatment
- replace loss, treat acid/base imbalance, food, reconsider meds (diuretics)
Hyperkalemia cause:
Manifestation
high intake, renal dysfunction, acidosis, cell injury
Manifestation: ECG changes, peaked T, bradycardia and blocks , skeletal muscle weakness, cramps, nausea
hyperkalemia treatment
- resolve acid/base, remove with diuretics, kayexalate, dialysis
phosphate PO4 ****
where is it?
Functions?
80% bones, 20% ICF
- cell mem structure
- formation of ATP and 2,3 DPG **
- cofactor in enzyme reactions
PO4 regulation *****
- absorbed in GI tract
- competes with Ca for absorbtion
- PO4 and Ca++ have inverse relationship ***
- influenced by acid/base
when insulin moves glucose into cells, PO4 and K+ go with
hypophosphatemia*** causes
manifestations
- intake, shift into cells (alkalosis/insulin), poor absorption, diarrhea, renal loss
man: loss ATP = muscle weak, irritable, confusion, poor contractility
Low 2,3 DPG (stabilizes deoxygenated form of Hgb) - left shift curve, decreased O2 delivery
hypoPO4
treatment
- replace loss
- correct alkalosis, treat diarrhea, diuretic?
