Electrolytes Flashcards
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?
hyperPO4
causes:
Manifestations:
- massive cellular lysis
- renal dysfunction
- parathyroid dysfunction
- similar to hypocalcemia (inverse relation)
- increased cell membrane excitability, anxiety, irritable twitching
- decreased cardiac contractility and prolonged QT
how do you treat hyperPO4
correct hypocalcemia , limit intake, ensure adequate renal function
Mg - location ***
functions
ICF
function: supports the Na/K pump
- facilitates cardiac function **
- important for neuromuscular activity: conduction of nerve impulses, helps Ca move into muscle, promotes vasodilation
- cofactor in intracellular enz actions (ATP)
- protein and DNA synthesis
Mg regulation
- we eat it and get rid through vomit, urine and feces
hypoMg *****
causes
clinical manifestations
cause: inadequate intake or poor absorption
- GI loss: vomit, diarrhea, loss- diuretics
Manifest: neuromuscular overstim, muscle cramps, twitching, hyperrefexia
In severe: resp muscle weakness/paralysis, altered mental status, coma, dysrhythmias, N/V ***?
Treat HypoMg
increase intake and replace losses
HyperMg
Causes
Manifest
cause: high intake and renal dysfunction
Manifest: neuromuscular depression; decreased muscle activity, hypoactive reflexes, general weakness
- flushing and mild hypotension
treating hyperMg
minimize intake, ensure adequate fluid vol to support urine output, dialysis
Calcium
found?
functions?
99% bones, 1% in ECF
Ionized- active free floating
Bound- albumin and competes with H+ for sites
Fnctn: cell permeability, membrane stability
- skeletal and heart muscle contraction
- blood coagulation
Ca regulation **
- diet
- excrete urine
- parathyroid horm mobilizes Ca from bones, promote GI absorption, decrease renal excretion
- Ca influences pH and albumin levels ***
(more H in the plasma than bound to alb = acidotic, more Ca in plasma than bound to alb = alkalosis) - calcitonin decreases absorption and increases renal excretion
- uptake Ca influenced by PO4 and Vit D levels
** Ca and PO4 have an inverse relationship**
hypocalcemia **
causes
manifestations
cause:
- inadequate intake, GI malabsorption (when PO4 is elevated in gut, fight for uptake), blood transfusion (citrate binds with Ca)
- thyroid cancer, increased renal losses
manifest: increased cell membrane excitability, reduced stability
- anxiety, confusion, irritable, twitch, cramp
- muscle spasms: laryngeal, abd, bronchial
- prolonged QT, decreased cardiac contractility
- impaired coagulation process
hypoCa treatment *****
- correct albumin levels and acid/base imbalance
- replace losses (IV CaCl, Cagluc)
HyperCalcemia
causes
Manifestations
cause: cancer (esp with bone mets), renal dysfunction (excreted by kidneys)
manifest: decreased cell membrane excitability
- fatigue, confusion, depression
- muscle weakness, hyporefexia
- dysrhythmias, short QT, short ST
hyperCa treatment
- correct PO4 levels (inverse), ensure adequate vol to support urine output
- correct acid/base balance
- diuretic/dialysis
Chloride
where?
function
regulation
in the ECF
- along with Na helps regulate serum osmolality
- helps maintain acid/base balance
reg: ingested, reabsorbed/excrete by kidneys to maintain acid/base balance
- has inverse relation with HCO3
Hypochloremia
causes
manifestations
cause: Na deficit, excess HCO3
- GI losses (vomit-hydrochloric acid, diarrhea)
- increased renal losses (diuetics)
man: signs of alkalosis (confusion, twitching, nausea, lightheaded, numbness), incld low Na or low K
- overexcitability, crams, twitch, seizure, coma
- dysrhythmias
hypoCl treating
- correct underlying cause, usually acid/base imbalance (alkalosis), ensure adequate hydration
hyperchloremia
cause
manifest
cause: Na excess, HCO3 deficit, acidosis
man: signs of metabolic acidosis (tachypnea, lethargy, weakness)
- dysrhythmias, decreased CO
- deceased LOC, coma
- role in acid/base balance will also affect Na and K levels
hyperCl treatment
correct cause, usually acid/base imbalance (acidosis)
explain pH and K+ relation **
too many H+ = acidosis in ECF and moves into ICF and pushes K out causing = hyperkalemia
consider if it is a deficit or if K+ has just shifted before you treat
explain glucose/insulin affect on pH****
insulin drives glucose into cells (ICF) taking with it K+ and PO4 making the ECF alkalotic
explain influencing factors albumin, pH, and Ca*******
serum exists in 2 forms
ionized- active free in serum
bound- Ca fights H for binding to albumin. if there is more Ca bound to albumin than H+, then there is more H+ in serum = acidotic
explain chloride and pH relation
chloride depletion is one of the most common causes of metabolic alkalosis in critical illness
- from diuretic use
- Na and Cl are inhibited and excreted
- hydrochloric acid is depleted in gastric secretions (vomit/NG)
Metabolic acidosis- from hyperchloremia when HCO3 is lost from body from severe diarrhea or lack of retention from kidneys
OR large/rapid infusion NaCl
metabolic acidosis can rise from?
maybe*****
- lactic acidosis (inadequate cell O2)
- renal dysfunction (alter HCO3 regulation)
- loss HCO3 from diarrhea, or fistula
metabolic acidosis wide-ranging effects**
- often in septic PTs, the HCO3 gets eaten up
- decreased cardiac contractility –> reduced CO
- vasodilation–> hypotension
- pulm vasoconstriction –> impaired gas exchange
- reduces effectiveness of vasoactive drugs (epi, levo), esp when pH falls below 7.2 (think about parameters re; permissive hypercapnia
- cardiac dysrhythmias
- LOC changes
- shift Oxy/Hgb curve to the right
- increase inflam response
- impairs immune response
- decreased response to insulin/increased insulin resistance
- decreased ATP production
- vasopressin doesnt cause vasoconstrict to pulm vasculature
