electrolytes 2 (Na+, K+, Cl-,HCO3-) Flashcards
major cation ECF
Na+ ( 90%)
- maintains water distribution & osmotic pressure
- intake 130-260 mmol NaCl
- body uses 1-2 mmol/day the rest is excreted
ATPase ion Pump
Na+ & K+ move between ICF & ECF by Na+/K+ ATPase ion pump
- 3 Na+ ions move out in exchange for 2 K+ ions as ATP is converted to ADP
- water follows Na+ out of cell which prevents osmotic rupture*
3 processes for regulation of sodium
- intake of H2O in response to thirst
- stimulated/supppressed by plasma osmolality - excretion of H2O
- in response to AVP ( causes water to be reabsorbed) - excretion of Na+
- involves aldosterone, angiotensin ll & atrial natiuretic peptide (ANP)
sodium specimen collection
- serum
- heparinized plasma ( lithium heparin )
- urine ( random or 24hr)
- not significantly affected by hemolysis ( but if grossly hemolyzed Na+ decreased
bc of dilution) - refrigerate or freeze for delayed analysis
methods of analysis - sodium
chemical methods- outdated
flame emission spectrophometry
atomic absorption spectrophotometry (AAS)
ion- selective electrodes (ISEs)
- most common method in clinical labs
Sodium electrode
- a glass ion-exchange membrane is used for Na+ measurement
- Na+ interacts with the tip ( measuring electrode) producing a potential that is dependent on the activity/concentration of Na+
- reference electrode maintains a constant potential
- difference in potential between the reference & measuring electrodes = the activity of Na+
direct vs indirect measurement for ISEs
Direct
- undiluted
- elevated lipid/proteins don’t interfere
- more accurate
Indirect
- diluted
- increased lipids & proteins cause electrolyte exclusion effect
electrolyte exclusion effect
- excess lipids or proteins displace plasma water
- less aqueous phase gets added to the diluent
- causes Pseudohyponatremia***- falsely decreased Na+ concentration
Sodium electrode -sources of error
protein build up on electrode membranes through continuous use
- causes poor selectively & poor reducibility for results
solution
- routine maintenance to remove protein build up
VITROS analyzers slide
use disposable ISE slides
- drop of sample & reference fluid are applied at same time
- dry slide technology
Hyponatremia
Na+ level < 135 mmol/L
caused by
- increased Na+ loss ; hypoaldsosteronism, K+ deficiency, diuretics, ketonuria
- Increased H2O retention; renal failure, nephrotic syndrome, CHF
- water imbalance; excessive water intake, pseudohyponatremia
hypernatremia
Na+ >145mmol/L
caused by
- increased intake or retention; hyperaldosteronism, excess salt ingestion
- excess H2O loss; diabetes insipidus, profuse sweating
- decreased H2O intake; older ppl or infants, mental impairment
Sodium reference ranges
- serum/plasma
- critical
serum/plasma: 135-145 mm/L ( CSF is around the same)
critical <120 or >160 mmol/L
major cation in ICF
potassium (K+)
- dietary requirement : 50-150mmol/day
- small amount used, most excreted by kidneys ( not stored well)
- K+ conc regulates neuromuscular excitability, heart contractions
- too low or too high can lead to cardiac arrest
regulation of potassium
- nearly all K+ is reabsorbed in the proximal tubules of the kidney
- additional K+ is secreted into urine in exchange for Na+
- any excess K+ consumed in the diet is excreted in the urine; can accumulate to toxic levels in renal failure
factors that influence distribution of K+
K+ loss due to Na+, K+ ATPase pump inhibition
- hypoxia, hypomagnesemia, digoxin overdose
Insulin promotes acute entry of K+ into skeletal muscle & liver by increase Na+,K+ATPase activity
Catecholamines like epinephrine ( beta- stimulator) promote entry of K+ into cells
Propanolol ( beta-blocker) impairs entry of K+ into cells
excercise
- K+ released from muscle cells during excercise
- fist pumping during venipuncture can cause falsely high K+ levels
cellular breakdown
- damage to RBCs releases K+ into ECF
Specimen collection - potassium
serum
plasma ( heparin preferred)
don’t use EDTA ( K2 EDTA contains potassium )
urine ( random or 24 hr)
Minimize hemolysis ( hemolysis falsely increases K+ results )
separate plasma/ serum from cells ASAP or may give false increased K+
methods of measurement for Potassium
flame photometry
-older method q
ion-selective electrodes (ISEs)
-most routinely used
Potassium electrode
ion-exchange electrode
solid plastic membrane contianing valinomycin
- an antibiotic that will selectively bind with K+
KCL is the inner electrolyte solution
Can be direct or indirect mode
- difference between the two method is only slight compared to Na+
clinical significance of potassium
increased or decreased concentration of K+ will affect muscle irritability = cardiac arrest
K+ reference ranges
serum
critical
serum : 3.5-5.1 mmol/L
critical: < 2.8 or >6.0
- always check for hemolysis first
Major anion in ECF
Chloride
- major contributor to osmolality ( with Na+ )
Regulation of Chloride
Cl- usually shifts due to changes in Na+ or HCO3-
Cl- in the diet
- absorbed by intestinal tract
- then filtered by glomerulus
- then passively reabsorbed ( with Na+) by proximal tubules
excess Cl- is ecreted in urine & sweat
excessive sweating stimulates aldosterone to act on the sweat glands to conserve Na+ & Cl-
How Chloride maintains Electroneutrality
- Na+ is reabsorbed along with Cl- in proximal tubules
- Na+ reabsorption is limited by amount of Cl- available - Chloride shift ( hamburger phenomenon)
- CO2 from cellular metabolism in tissues moves into the plasma & the red cells
- in RBCs, CO2 form carbonic acid which splits into H+ & HCO3-
- Deoxyhemoglobin (HHb) buffers H+
- HCO3- moves diffuses into plasma
- Cl- dissuses into RBC & electric balance is maintained
Chloride specimen collection
serum/plasma ( separate from cells)
lithium heparin ( best anticoagulant)
urine ( 24hr is best )
CSF ( decreased CL in bacterial meningitis ; glucose also decreased in bacterial meningitis)
Sweat ( screen for cystic fibrosis )
- >60 mmol/L is positive for CF
Chloride methods of analysis
- amperometric -coulometric titration
- mercurimetric titration
- colorimetry
- ion -selective electrode (ISE)
Amperometric - coulometric titration analysis of chloride
• Silver ions are generated coulometrically from a silver electrode
and combine with chloride ions in the patient sample.
• Ag+ + Cl- → AgCl
• When all of the Cl- in the sample has bound to Ag+, the free Ag+
indicates the endpoint.
• The coulometric generator and timer shut off and the amount of
time elapsed is used to calculate the Cl- in the sample.
• An example of this is the Cotlove Chloridometer.
Amperometric - coulometric titration analysis of chloride
• Silver ions are generated coulometrically from a silver electrode
and combine with chloride ions in the patient sample.
• Ag+ + Cl- → AgCl
• When all of the Cl- in the sample has bound to Ag+, the free Ag+
indicates the endpoint.
• The coulometric generator and timer shut off and the amount of
time elapsed is used to calculate the Cl- in the sample.
• An example of this is the Cotlove Chloridometer.
Ion selective electrode for chloride
• Most common method
• Uses an ion-exchange membrane to selectively bind Cl- via a redox
reaction
• Used in clinical chemistry analyzers
Chloride clinical significance
Cl- passively follows Na+ therefore Cl- disorders often have the same causes as Na+ disorders
causes of Hypochloremia
- increased Cl- ( vomiting, diabetic ketoacidosis, aldosterone deficiency,Pyelonephritis)
- high serum HCO3- ( respiratory acidosis, metabolic alkalosis)
causes of hyperchloremia
- increased intake
- excess loss of HCO3- ( renal tubular acidosis, metabolic acidosis, through GI tract)
Chloride references ranges
serum/ plasma 98-107mmol/L
Bicarbonate (HCO3-) or total CO2 (TCO2)
bicarbonate is the 2nd most abundant anion in ECF
total CO2 is comprised of
- dissolved CO2
- carbonic acid ( H2CO3)
- bicarbonate
bicarbonate accounts for 90% of total CO2
Bicarbonate importance in the body
HCO3- is a major component of buffer systems in blood.
• NaHCO3-/H2CO3 (sodium bicarbonate/carbonic acid)
Chloride Shift in the tissues and lungs
• This maintains electroneutrality (pluses = minuses on either side of the cell membrane)
• If HCO3- → into cell
Then out ← Cl-
And vice versa
Regulation of Bicarbonate (HCO3-)
• 85% of HCO3- is reabsorbed by proximal tubules in kidneys;
15% by distal tubules.
• Tubules are only slightly permeable to bicarb, so usually reabsorbed as CO2. - HCO3- combines with H+ to form H2CO3 - H2CO3 dissociates into H2O and CO2 - CO2 diffuses back into ECF
• Excess HCO3- flows into the urine
- In alkalosis:
- Kidneys increase excretion of HCO3- in urine to correct pH
• In acidosis:
• HCO3- is reabsorbed by the proximal and distal tubules to
correct pH.
Bicarbonate Specimen Collection
- Serum and lithium heparin plasma• (arterial and whole blood measurements were discussed last chapter)
- Analyze ASAP
- Keep anaerobic
- i.e. Don’t decap specimen
- Exposure to air causes a loss of CO2 = ↓TCO2
- Can ↓ by 6 mmol/L per hour
TCO2 Methods of Analysis
- ISE Method (pCO2)
- Combination pH electrode
- Silicon rubber membrane which is permeable to CO2 gas
- pH sensitive glass electrode detects a change in pH (↓ pH is measured)
OR
• Gas-sensing electrode
PCO2 (Bicarbonate) pH Glass Electrode
The sample is acidified
first to convert all froms
of CO2 to CO2 gas
↓ in pH measured
i.e. H+ ions that are produced
Gas-Sensing CO2 Electrode
same equation as ISE
The membrane is in contact with a solution that is permeable only to CO2. The change in pH of the HCO3- is detected by a pH electrode. TCO2
TCO2 enzyme method
• Sample is alkalinized to convert all forms of CO2 to HCO3-
Phosphoenolpyruvate + HCO3- ——-> Oxaloacetate + H2PO4-
Oxaloacetate + NADH + H+ ———> Malate + NAD+
The rate of change in absorbance of NADH ~ [HCO3-]
TCO2 /HCO3- - Clinical Significance
Causes of Decreased HCO3- Metabolic acidosis Renal Tubular Failure with Hyperchloremia Compensated Respiratory Alkalosis Severe Diarrhea
Causes of Increased HCO3- Metabolic Alkalosis - Severe vomiting - Excessive intake of alkali Compensated Respiratory Acidosis
CO2 reference ranges
Plasma / serum TCO2 (venous) 23-29 mmol/L
Plasma / serum HCO3- 21-28 mmol/L
Anion Gap
- A number that represents the concentration of unmeasured anions (proteins, phosphates, sulfates and organic acids)
- Not a real Gap in anions and cations
- Created by concentration differences between commonly measured cations (Na+ + K+) and anions (Cl- + HCO3-)
• Useful for:
- Indicating an increase in one or more unmeasured anions in serum (Metabolic Disorders)** if an increased anion gap usually indicates a metabolic disorder
- Quality control for analyzer used to measure electrolytes** should never be a negative number if negative indicates a problem with the analyzer
Anion gap calculation
Calculation: measured cations – measured anions
Na+) - (Cl- + HCO3-) OR
(Na+ + K+ ) - (Cl- + HCO3-
Anion Gap refernece range
Anion Gap (AGap) should be positive
• 7 - 16 mmol/L or
• 10 - 20 mmol/L if K+ included
Abnormal anion gap
Low(rare)
- multiple myeloma
- analyzer error
High • Methanol • Uremia • Diabetic ketoacidosis • Paraldehyde • Iron, inhalants, ibuprofen • Lactic acidosis • Ethylene glycol, ethanol ketoacidosis • Salicylates, starvation ketoacidosis
