Fluid | Electrolytes | Acid-Base Flashcards
Metabolic consequences of persistent hyperCa?
Soft-tissue mineralization
Renal failure
DDx for hyperCa in dogs & most common cause?
Malignancy (LSA, AGASACA) most common
DDx hypoA, primary hyperPTH, hypervit D, osteolysis, granulomatous disease, (iatrogenic, spurious)
What are the general principles of the strong ion approach (SIA)? List independent & dependent variables with this approach.
List advantages over using SIA over traditional methods to assess acid-base status.
Principles:
- Electroneutrality must be maintained.
- AB status is primarily determined by the lungs (which alter pCO2) & kidneys (which alter strong ions).
Independent variables (altered by processes outside the body):
- pCO2: altered by alveolar ventilation.
- Strong ions: fully dissociated at normal pH, exert no buffering effect. Na+, Cl– most abundant (affected by renal excretion & absorption). Also Ca2+, Mg2+, organic acids (e.g. β-HB, lactate).
- Non-volatile weak acids (or Atot): not fully dissociated at physiologic pH. E.g. proteins, phosphate.
Adv:
- More physiologic cf traditional method of assessing AB status. - Optimal method for determining the best treatment for AB abnormalities.
Define strong ion difference (SID).
What does a high vs low SID indicate?
SID = difference between negatively & positively charged strong ions. Represents influence of strong ions on pH & HCO3–; also expressed as BE.
Represented by equation:
SID (inorganic) = Na+ + H+ = Cl– + OH–
OR
SID (inorganic) = Na+ – Cl–corr = OH– – H+.
High SID - alkalosis (increased OH– or decreased H+). Due to loss of Cl– (metabolic alkalosis) or gain of Na+ (contraction alkalosis).
Low SID - acidosis (decreased OH– or increased H+). Due to gain of Cl– (hyperchloremic metabolic acidosis) or a loss of Na+
The influence of strong ions on pH & HCO3– is expressed as the strong ion difference (SID) and BE.
Characteristic electrolyte & AB changes seen with pyloric outflow obstruction?
Other differentials for such changes?
Hypochloremic metabolic alkalosis.
Pyloric outflow obstruction (foreign body, tumor, pyloric hypertrophy)
Gastric stasis, upper intestinal obstruction, duodenal stasis, pancreatitis, removal of large volumes of gastric contents by nasogastric suctioning.
Consequences of phosphorus deficiency? (Name 3)
Hemolytic anemia
Decreased mobility
Metabolic acidosis
What is a respiratory condition that can trigger SIADH?
Aspiration pneumonia
Major complication associated with HCO3 administration? Mechanism?
Worsening acidosis.
Based on equation: HCO3 + H+ <–> H2CO3 <–> CO2 + H2O
HCO3- admin –> equation shifts R –> more CO2 produced. If patient cannot increase RR & effort to remove CO2 excess –> excess CO2 diffuses into CNS (very soluble) –> equation shifts back to L –> parodoxical CNS acidosis + increase serum H+ –> decreases blood pH (reflex respiratory acidosis).
Also excess HCO3- created –> renal excretion –> possible metabolic alkalosis (esp if renal dysfunction)
HypoCl - causes?
Pseudo - marked elevated TP & lipemia, measurement of halides (Br, I, fluoride)
Steroids (HAC or drugs) - mild
Thiazides, loop diuretics (Cl- renal loss disproprionate to Na+)
GI losses (V+) or upper GI obstruction/stasis (also hypoNa)
Chronic respiratory acidosis
Fluid administration with high Na+
Hyperchloremia - causes?
GI losses of Na > Cl + concurrent HCO3- loss (D+, sequestration of intestinal contents - remember bile, pancreatic & duodenal secretions are rich in HCO3-)
Hypoalb (hyperCl likely occurs in response to mild alkalosis 2’ to this)
Renal Cl- retention (causes involving decreased H+ secretion & HCO3- reabsorption):
- Early CKD
- RTA (both proximal + distal) - primary (congenital) vs acquired (hypoA, renal tubular dz)
- Spironolactone tx (similar to hypoA - effects of aldosterone)
- Chronic respiratory alkalosis
- Ketoacidosis (usually during DKA recovery phase - excretion of ketoacid anions as Na+ & K+ salts, Cl- retained in place of them)
High anion gap metabolic acidosis - causes?
‘LUKE, E includes other toxins’
1. Increased phosphorus (renal failure)
2. Toxicities - ethylene glycol, salicylate (aspirin), metaldehyde
3. Organic acidosis - lactic acidosis, renal failure, DKA, uremia
NaHCO3- administration
- Indications
- Adverse effects
- Indications
- HCO3-losing diseases (RTA, D+ - uncommon)
- Severe metabolic acidosis i.e. pH <7.15 & HCO3- <12mEq/L (e.g. uremic AKI, NOT DKA or lactic acidosis).
- Refractory hyperK.
- Contrast-induced nephropathy (some evidence that prevents?) - AE
- Hypervolemia, hyperNa (hypertonic solution > volume expansion), hypotension (if rapid admin undiluted)
- Ionized hypoCa (pH changes > iCa binds to albumin)
- HypoK (K+ translocates into cells due to binding of iCa-alb)
- Respiratory acidosis (increased CO2 production; can occur if unable to increase ventilation appropriately)
- Paradoxical intracellular/CNS acidosis (CO2 pdtn)
- Phlebitis/thrombosis if peripheral v. admin (shouldn’t give >600mOsm/L solution but undiluted = 2000mOsm/L)
NaHCO3 supplementation - equation?
0.6 x BW(kg) x (desired [HCO3-] - measured [HCO3-]) = ____mmol/L
What is osmolal gap (OG)? What is normal in dogs, and what are causes of an elevated OG?
Difference between measured - calculated osmolality (measured usually slightly higher as includes additional osmoles in plasma other than Na, urea & glucose).
Normal </= 10mOsm/kg.
Elevated due to:
- Exogenous solutes in the plasma (e.g. ethylene glycol)
- Reduced fraction of plasma water 2’ to high plasma triglycerides or proteins (e.g. myeloma proteins)
Equation to calculate plasma osmolality?
Plasma osmolality = 2 [Na+] (mEq/L) + ([Glucose] (mg/dl)/18) + ([BUN] (mg/dl)/2.8)
*[Na+] is in mmol/L
Glucose & urea = ineffective osmoles, so contribute to osmolality but not tonicity
