electrolytes, fluid, acid/base Flashcards
- What are three main players involved in electrolyte balance?
- GI, renal, endocrine
- water is what % body weight?
ECF?
ICF?
- intracellular determined by what?
extracellular?
- 60% (75% if neonate)
20% ECF
40% ICF
- K
Na
- What is -volemia?
- what is effective circulating volume?
what is normal?
What is abnormal?
- changes in blood vol
- perfusion status of patient (fluid relative to capacity in vascular space)
dec perfusion is counteracted by CV adaptation, conservation of fluid/electrolytes
^vasc space (shock) or compromised compensation
How Does each of the following affect fluid and electrolyte balance (and how)?
- ADH
- Renin-angiotensin system
- aldosterone
- natriuretic peptides
- fluid retention (induce thirst, ^resorption from tubules)
- fluid retention (angiotensin II ^renal retention of Na)
- fluid retention (^Na resorption in exchange for K and H+)
- fluid loss (antagonize RAS, aldosterone)
(Dehydration)
- Example of hypotonic fluid loss?
- isotonic fluid loss?
- hypertonic fluid loss?
- panting, restricted water access
(protein and PCV also increase)
- hemorrhage
(TP and PCV variable depending on losses)
- heavy sweating in horses, some kinds of renal dz/diarrhea
(Assessment of Dehydration)
- usually done by physical exam
- What lab abnormalities? (remember they have LACK OF PREDICTIBILITY)
- pre-renal azotemia
^serum protein IF no protein loss
^PCV if no loss/dec prod of RBC
electrolyte changes variable depending on intake (K+ NOT Na/Cl)
(Increased Total Body Water)
- what is most common cause?
- iatrogenic
(physiologic: pregnancy, neonatal)
(pathologic: heart failure, oliguric/anuric renal failure)
(Sodium)
- What promotes sodium retention?
- what promotes excretion?
- angiotensin/aldosterone
- natriuretic peptides
(Hyponatremia)
never get from diet
1-3. what three ways?
plus examples of each
- loss of greater amounts of Na than water
diarrhea, renal dz, sweating, diuretics
- loss of equal amounts and replacement of water
exudative skin lesions, third space loss, GI fluid loss (diarrhea), hemorrhage
- dilution
osmotic forces (hyperglycemia), pathologic gain (oliguric/anuric), pregnancy/neonatal
(Hypernatremia)
- how common is increased intake?
2-3. What are the two causes then?
- rare
- decreased water intake
adipsia, critical care, lack of access (absence of thirst is rare)
- excess loss of water
some diarrhea, panting, renal
(Chloride)
- Large amount in GI fluid, sweat (saliva in LA)
- usually change with Na, but can become independent how?
- analytical cross reactivity with what?
- if acid/base abnormalities
- bromide
(Hypochloremia)
- parallel to sodium
- sequestration/loss of GI fuid
(acid base abnormalities)
- varies how with bicarbonate?
If not what does this mean?
- inversely
that there is a complex/mixed acid/base problem w/ concurrent metabolic acidosis and alkalosis
(Hyperchloremia)
- parallel to what?
- will see with acidosis or alkalosis?
- interefering substances like what?
- acidosis (inverse to bicard)
- KBr
(Potassium)
1-2 serum K managed by what 2 mechanisms?
- interchange btwn intra/extra (traded for H, cell damage/death)
- intake via diet vs renal/GI excretion
(losses as for other analytes but renal emphasis)
(Hypokalemia)
1-3. What three things cause?
- decreased intake (anorexia, only cause with ^losses)
- increased losses (GI, renal, 3rd space, cutaneous)
- intracellular shift (alkalosis, insulin, glucose)
(Hyperkalemia)
1-3. What three things cause?
- iatrogenic excess
- failure of elimination/renal retention
(hypoadrenocorticism, oliguria/anuria)
- extracelluar shift
(hemolysis in LA, massive musc necrosis, metabolic acidosis, insulin def/resistance)
(Electrolyte Patterns)
Give possible causes for each
- all electoryltes increased
- all electrolytes decreased
- low sodium and chloride, high potassium
- free water loss, oversupplementation (calves)
- loss of high electrolyte content fluid, loss of isotonic fluid with water replacement
- hypoadrenocorticism, uroabdomen/oliguric-anuric renal failure
(Bicarbonate)
increased = alkalemia
- due to what?
- loss of acid, often GI or renal
failure to eliminate base
(Bicarbonate)
decreased = acidemia
(with high anion gap)
- due to what?
(with normal anion gap)
- due to what?
- excessive acid generated ketones, lactic acidosis
toxicity: salycyclic acids, ethylene glycol
decreased renal clearance - uremic acidosis
- increased bicarbonate losses (GI, renal)
(anion gap)
- anion gap = ?
- AG is what?
- (Sodium + potassium) - (chloride + bicarbonate)
- difference between major MEASURED cation and anions = approximation of unmeasured anions
(unmeasured = mostly negatively charged plasma proteins)
(Decreased Anion Gap)
1-2. due to what?
- low albumin
- increased cationic proteins from gammopathies (rare)
(Increased Anion Gap)
- due to what?
- increase in unmeasured anions
(lactic acidosis in exercising horses, grain overload, shock, diabetic ketoacidosis, uremic acidosis, intoxication - ethylene glycol)
(Chloride Revisited)
- Usually changes how with what?
- When Cl- changes disproportionall to sodium, evaluate what?
- ^bicarb and dec Cl =
- what if bicarb and Cl change in same direction?
- Na
- acid base status
- alkalosis (opp = acidosis)
- mixed acid base disorder (arterial blood gas needed for full characterization) but if disorder is metabolic you can fix by correcting the underlying cause
