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
What are the diagnostic criteria for SIADH? (Hint: think osmolality)
- Excluded other causes of hypoNa
- Concurrent plasma hypo-osmolality (hypoNa) + inappropriately HIGH urine osmolality. Urine [Na+] >20mEq/L. As natriuresis occurs despite hypoNa
- Adequate renal and adrenal function
- Absent hypovolemia, ascites, or edema
- Correction of hyponatremia with fluid restriction.
In a hypoNa animal, how does urine osmolality and/or urine [Na+] help to differentiate cause?
HypoNa + uOsm >100mOsm/L - indicates impaired H2O excretion. (natriuresis occurs despite hypoNa to reduce circulating vol from H2O retention)
HypoNa + uOsm <100mOsm/L - usually primary PD (normal renal urine diluting ability), low solute intake (rare)
Urine [Na] < 20mEq/L suggests hypovolemia. So >20mEq/L expected for SIADH, diuretics, hypoaldos, renal failure (body is not in Na retaining state).
List 5 characteristics of hyperglycemic hyperosmolar syndrome (HHS)?
- BG >540- 600mg/dL; 30-34mmol/L
- Serum osmolality >325-350mOsm/Kg
- Profound dehydration, with progressive CNS depression
- +/- mild acidosis, but usually blood pH >7.3 & [HCO3-] >15mEq/L
- Variable ketosis
What are the main roles of the endothelial glycocalyx?
Forms a layer over the luminal surface of endothelial cells. Maintains the vascular permeability barrier.
- Shield vascular walls from direct exposure to blood flow
- Mediate shear stress–dependent NO (NO) production
- Promotes retention of vascular protective enzymes
- Preserves IV concentration of coagulation inhibition factors
- Immunomodulatory - prevents leukocyte adhesion & binding of chemokines,
cytokines & GFs to the endothelium
What are the tissue safety factors preventing interstitial oedema in health?
What pathological changes occur with oedema formation?
- ISF hydrostatic P is slightly negative (-3mmHg) - holds tissues together (suction like effect)
- IS has low compliance - small changes in ISF volume significantly increases ISF HP significantly (prevents further fluid entry into IS)
- Lymphatic flow increases 10-50x when capillary P increases/fluid accumulates in tissues > carries away large amounts of fluid & proteins > prevents ISF P from rising into the positive range
- Lymphatics carry away protein in the ISF > decreases ISF colloid osmotic pressure & thus prevent further accumulation of ISF.
Increased capillary hydrostatic P, lymphatic obstruction etc.
> fluid enters ISF > when ISF pressure rises >0mmHg, tissue compliance increases markedly so allows large amts of ISF to accumulate with only small increase in pressure
What life-threatening complication may occur if hypertonic saline is administered too rapidly?
Vagally mediated bradycardia, CPA
What are the 2 types of lactic acidosis?
Type A: tissue hypoxia (hypoperfusion 2’ to decreased effective circulating volume)
Type B: not related to tissue hypoxia or hypoperfusion.
Fundamental problem is the inability of mitochondria to process the amount of pyruvate it is presented with.
Which 3 synthetic colloids are commonly used in vet med?
How do molar ratio (degrees of substitution), C2:C6 ratio & molecular weight affect efficacy of synthetic colloids?
Hetastarch (450kDa) > pentastarch (260kDa) > tetrastarch (130kDa)
Higher C2:C6 ratio –> slower degradation by amylase, more soluble product.
Higher MW & higher molar ratio > prolonged volume effect (stays longer in IV space), but associated with more SE.
What are the complications of colloid therapy?
- Fluid overload esp if concurrent dz with increased vascular permeability (smaller colloid particles alb etc. extravasate through leaky vessels into interstitium > lower plasma COP > oedema/third spacing) delayed protein clearance in lungs.
- Nausea, hypotension with rapid infusion (cats)
**3. Anaphylaxis & allergic reactions - ARF**
- Impaired hemostatic disturbances (platelet dysfunction - decr integrin αIIbβ3 expression > decr fibrinogen binding; decr FVIII & vWF - accelerated elimination, interference with fibrin clot stablisation)
- Contributes to hyperchloridemic metabolic acidosis if suspended in 0.9% saline
What factors stimulate vs inhibit PO4 tubular reabsorption?
Stimulate - GH, IGF-1, insulin, thyroid hormone
Inhibit - PTH, FGF-23 (direct effect on Na-P co transporter), incr serum P
(NB: insulin, dextrose, bicarbonate increases PO4 intracellular uptake)
Where are vitamin D receptors predominantly located in the kidneys?
Where is Ca & Mg predominantly reabsorbed in the kidneys?
VDRs most abundant in DTs (less in PTs & glomerular podocytes)
Ca: PCT , Mg: LOH 65%
What electrolyte derangements may occur with hyperthyroidism?
Hyperphos, hypoMg
