Electrolytes Flashcards
What are the major ECF ions
Na and Cl
What are the major ICF ion
K
how is Hco3 generated
Carbonic anhydrase reactions in the lungs, gastric mucosa, kidney and RBC
TCO2
Total extractable CO2 from serum or plasma by addition of an acid. Most of it (955) bicarb. and HCO2 and TCO2 are essentially equal
What can cause abnormal electrolyte concentrations in plasma or serum
- Increased or decreased intake
- Shift between ECF and ICF
- Increased renal retention
- Increased loss through GI, renal, skin, airway
Hydration is essential to assessment
Mechanisms of dehydration and Na changes
- Loss or sequestration of hypotonic fluid (hypertonic dehydration)
- Loss of isotonic fluid (isotonic dehydration)
- Loss of hypertonic fluids (hypotonic dehydration)
Hypertonic dehydration
-Pure water loss results in hypernatremia
-ICF and ECF share burden but ECF has greater osmolality so water shifts to ECF
Causes of hypertonic dehydration
No access to water with continued insensible loss
(Panting, hyperventilation, fever)
Isotonic dehydration
-Fluids lost have the same amount of electrolytes as blood or serum
-Normonatremia
-ICF osmolality=ECF
-Animal shows other signs of dehydration (skin turgor, hyperalbuminemia, relative erthrocytosis)
Causes of isotonic dehydration
Vomiting and Diarrhea
Hypotonic dehydration
-Fluids with more electrolytes lost compared with blood/serum
-ECF osmolality < ICF fluid shifts into ICF
Hypotonic dehydration causes
Secretory diarrhea
Tonicity
Effective osmolality of a solution
Effective osmole-> do not cross permeable membranes
Ineffective osmoles-> readily cross membranes
Measured osmolality
Uses freezing point (lower if the concentration is raised) and measures effective and ineffective osmoles
Calculated osmolality
2(Na + K) if glucose and UN normal
Typically 300-310 and 10mOsm less than the measured
Osmolar gap
Measured osm- calculated osm
Normally 10mOsm
Increased osmolal gap
Increased number of osmotically active particles in blood not accounted for in equation (Lactate, ketones, alcohols, ethylene glycol, mannitol, oxalic acid, salicylic acid)
What is the mahor determinant of extracelullar tonicity
Na
Plasma Na controlled by
- Regulation of blood volume
- Regulation of plasma osmolality/ tonicity
Serum Na is dependent on what
Ratio of total body Na/tbH2O
Hypernatremia means that increase in Na means tbH2O is normal or there is normal Na but decreased tbH2O or decrease in Na leads to severe decrease in tbH2)
Mechanisms of hypernatremia
-Decreased H2O intake
-Pure H2O loss
-H2O loss> Na loss
-Excess Na intake
-Decreased Na excretion
Hyponatremia mechanisms
-Na loss> H2O loss
-Renal Na wasting
-H2O retention> Na retention (with or without edema)
-Osmotic shifting of H2O to ECF
-Shift of Na down concentration gradient from intravascular to extravascular
Normonatremia
Does not necessarily mean normal tbNa
-Hypervolemic
-Hypovolemic/dehydration
Serum K is dependent on
- Shifting of K in and out of cells
- TbK (from intake and excretion)
If acid base is normal-> K reflects tbK
If not normal A/B-> abnormal tbK
Alkalosis and K
Increased bicarb-> hypokalemia
Inorganic Acidosis and K
Decrease bicarb-> hyperkalemia
Organic acidosis and K
No hyperkalemia because as H enters the cell it is travelling with its anion (lactate) and maintains electroneutrality
Excess K loss and acid base
Leads to alkalosis because K enters the plasma from the cell and H enters the cell
Mechanisms of hyperkalemia
-Shift in exchange for H
-Cellular necrosis
-Pseudohyperkalemia
-Insulin deficiency
-Decreased renal excretion of K
-Increased intake
Pseudohyperkalemia
Marked thrombocytosis and take a serum sample which clots and releases K from platelets and if they have a lot of platelets have a lot of K. to determine but it in a heparinized tube (green top)
Mechanisms of hypokalemia
-ECF-> ICF shift in exchange for H
-Insulin administration
-Decreased K intake
-Increased K excretion
-Increased alimentary K loss
Sodium: Potassium ratio
If it Na decreased , K may be ok
If K is increased , Na may be ok
If Na is decreased, K may be increased
Hypoadrenocorticism and Na: K ration
Increased Na loss and increased K retention
<15
Control of Cl
- Renal resorption and excretion
- Alimentary tract functions
Shifts in Cl
Maintain electroneutrality
-Usually follows Na
-Inverse to HCO3
Interpreting Hyperchloremia
-Concurrent hypernatremia-> same cause
-Normonatremia-> due to decreased HCO3
-Hyperchloremic metabolic acidosis-> Loss of NaHCO3 fluid (diarrhea)
Interpreting hypochloremia
-Concurrent hyponatremia-> same cause
-Normonatremia-> due to increased HCO3 and loss of HCl
-Normonatremia-> decreased HCO3-> must have unmeasured anions present (metabolic acidosis)
Alimentary tract causes of hypochloremia
HCl is not being recycles but still get bicarb is being made. Cl has to leave ECF due to the bicarb and you get Cl loss. Causes metabolic alkalosis
Renal mechanisms for hypochloremia
Occurs with metabolic acidosis. Look at chart
If Na and Cl change in same direction
THink hydration problems
If Na and Cl change in opposite directions
Think acid/base abnormalities
Metabolic alkalosis
Increase in HCO3, usually due to loss of H or compensation for chronic respiratory acidosis
Metabolic acidosis
Decrease of HCO3, usually due to generation of excess H or loss of HCO3. May see with compensation for chronic respiratory alkalosis
Mechanisms for increased HCO3
-Gastric loss of H
-Renal loss of H
-Shift from ECF to ICF in exchange for K (Hypokalemia)
Mechanisms for decreased HCO3
-Increased H from metabolic process and HCO3 gets used up
-Decreased renal H clearance and HCO3 used up
-Alimentary losses
-Renal loss
Lactate production
Product of anaerobic glycolysis during hypoxia in skeletal muscles and can then be used for glyconeogenesis
Types of hyperlactatemia
- Hypoxia
- Metabolic: grain overload
Metabolic hyperlactemia
Grain overload leads to increase formation of L lactate and (D lactate by bacteria) increases lactate absorption by ruminal mucosa and increases plasma lactate
