what percentage of our mass is water?
60%
what are the three places water can be?
ICF: all water within cell membranes
ECF: intravascular and interstitial
transcellular water (CSF and vitreous)
what determines water distribution?
solutes (electrolytes) exert a pressure against water (osmotic pressure)
osmolality
measure of dissolved particles in a soln
what affects water metabolism?
activity levels
environmental conditions (humid/dry)
disease
water balance
oral (1/2-2/3)
kidney (excretion and conservation)
skin, lungs, GI = loss of water
plasma water
water phase with ions only (no proteins)
ions and chemical activity are normal (not affected by hyperproteinemia/hyperlipidemia)
electrolyte exclusion effect
exclusion of electrolytes from the fraction of the total plasma volume that is occupied by solids which leads to underestimation of electrolytes
which has the highest conc of cation and anion inside the cell?
potassium and phosphate
which has highest conc of cation and anion in interstitial and plasma?
sodium and chloride
difference between plasma and interstitial solutes
practically no protein in interstitial fluid
balance of water due to...?
hydrostatic pressure from heart drives water into tissues
plasma proteins draw water into circulation from intracellular spaces
so low protein in vessels means most water will remain in tissues
what can cause permeability b/w ISF and plasma to increase?
some disease states like bacterial sepsis leading to leakage of alb, reduced plasma volume (shock) and hypotension
osmotic pressure def
hydrostatic pressure that develops and is maintained when 2 solns of different concentrations exist on opposite sides of a semipermeable membrane
number of solid particles/unit volume or weight of soln
force that moves water from dilute solns to conc solns
osmolarity
weight to volume relationship in mOsmole/L
inaccurate if hyperlipidemia/hyperproteinemia is present
osmolality
a weight to weight relationship in mOsmole/kg
colligative properties
related to number of total particles in soln and properties of those particles
includes BP, vapor pressure, osmotic pressure, FP
uses of osmolality
determines if serum water content deviates from normal
detects the presence of foreign lmw subs in blood
use of urine/serum ratios to determine concentrating ability of kidney
assess electrolytes and acid base disturbances
serum osmolality equation
(Na)(1.86) + (BUN)/(2.8) + (glucose)/(18)
(Na)(2) + (BUN)/(3) + (glucose)/(20)
osmolal gap
should be less than 10 mOsm/kg (6-10)
causes of increased difference in osmolal gap
attributed to other osmotically active cmpds other than sodium, glucose, urea
diabetic acidosis (ketones)
ethylene glycol poisoning
alcohol consumption (ethanol, methanol)
inc lipids inc proteins dec %water
what is the specimen to measure osmolality?
serum or random urine (cf if turbid)
plasma not recommended because it contains osmotically active ions (anticoag)
osmometer
finds freezing point depression by supercooling sample and then begin warming under constant value
what 3 mechanisms regulate water balance?
AVP, RAAS, thirst center
what is AVP also known as?
ADH (antidiuretic hormone)
thirst center
inc in plasma osmolality (stimulates osmoreceptors in hypothalamus)
dec in intravascular volume
angiotensin II acts upon neurons in hypothalamus to produce sense of thirst
controls the balance of free water and output (without solute) by the kidney and free water intake
arginine vasopressin hormone (AVP)
stimulated by inc plasma osmolality and dec plasma volume
produced in posterior pituitary
increases water absorption in kidney (collecting ducts)
renin angiotensin aldosterone system (RAAS)
dec blood volume, BP, ECF
results in secretion of renin in kidney
renin activates plasma angiotensinogen to angiotensin I
angiotensin I(in lung) becomes angiotensin II (vasoconstrictor) via ACE
aldosterone (adrenal cortex) increases Na absorption and H and K excretion
ACE inhibitors
interfere with RAAS by stimulating dilation of vessels via blocking production of angiotensin II
leads to inc sodium and urine excreted, inc venous capacity, dec cardiac output
natriuretic peptides
released in response to intravascular volume expansion (reduces BP and plasma volume)
produced in heart and released when heart feels a volume expansion, pressure overload
ANP
reduces venous pressure
increases vascular permeability
promotes natriuresis and diuresis
BNP
similar to ANP
used to measure stuff in ppl with congestive heart failure (chf)
CNP
function not understood
potent vasodilator, no natriuretic effects
clinical significance - osmolality
water load, diabetes insipidus, SIADH, water deficit
water load
xs water intake (polydipsia)
dec osmol
no response from AVP (lose large volumes of water and it causes hyperosmolality and hyponatremia only in ppl with impaired renal excretion
diabetes insipidus
urine osmol dec
SIADH
increase in AVP leading to in urine osm
secondary in asthma, pneumothorax, bacterial/viral pneumonia, copd, right side heart failure
water deficit
inc in plasma osmol
triggers AVP and thirst mechanism
not usually a concern unless pt is infant, unconscious, elderly, or dec mental status
electrolyes
important substances influencing distribution and retention of water
sum all all charges must equal zero between ECF/ICF
anion gap
difference between cations and anions
can include or exclude potassium
range w: 10-22
range w/o: 6-18
what are the measured electrolytes in the laboratory?
na, k, cl, hco3
clinical significance of anion gap
differential diagnosis of metabolic acidosis
QC indicator
what could a dec AG mean as a QC indicator?
lab error (overestimation of cl or underestimation of na)
MM: myeloma proteins act as cations
what is an increase in the anion gap usually caused by?
usually by unmeasured anions (cations have little effect)
inc organic acids
chronic renal disease
diabetes mellitus-ketoacidosis
salicylate, methanol, ethylene glycol poisoning
sodium functions
maintain osmotic pressure and water distribution
acid base balance exchange for hydrogen in renal tubes
responsible for 1/2 osmotic strength of plasma
kidney control of sodium
major route of excretion (glomerulus)
80-90% reabsorbed in the proximal tubule
hormonal control of sodium
ADH lessens the filtration of na and GFR
aldosterone: inc na reabsorption in distal tubule and collecting duct
hypernatremia symptoms/causes
neurological (ataxia, irritability, fever, confusion, coma)
hypovolemia: xssive water loss/failure to replenish lost water
hypervolemia: inc in sodium intake
hypovolemia - xs water loss causes
diabetes insipidus (no ADH or no response to ADH)
renal disease (damaged glomerulus = dec na excretion)
nephrotic syndrome (loss of proteins in urine = low osmotic pressure so fluid shifts to interstitial space)
sweating, diarrhea
hypovolemia - dec water intake
seen in older persons, infants, and those with mental impairment
most ppl can respond to thirst mechanism so this rarely occurs
extrarenal water loss
urine osm >700
Na >20
GI/skin loss
renal water loss
urine osm low to normal
urine Na high
thiazides w/o water replacement
hypervolemia - inc Na/retention
hospitalized pts get hypertonic saline/bicarb
hyperaldosteronism: inc Na absorption and potassium excretion, more water retained
cushing's syndrome
chf: retention and more reabsorbed
liver disease: venous pressure in and forces fluid into peritoneal space (lowering plasma volume)
pregnancy (unknown interruption b/w sodium and body water)
osmotic diuresis
inc urination from large molecules in the kidneys that draw water from the bloodstream into the urine
urine osm 300-700
hyponatremia symptoms
120 = malaise, nausea
110-120 = generalized weakness, mental confusion
90-105 = mental impairment, seizures, coma, death
what is the most common electrolyte disorder in hospitalized/non hospitalized pts?
hyponatremia
hyposomotic causes of hyponatremia
inc na los (depletional)
inc water retention (dilutional)
water imbalance
hyposomotic - inc Na loss
hypoaldosteronism (na excreted)
diuretics (thiazides): lose na
ketonuria: na loss with ketones
renal disorder (salt wasting nephropathy )
prolonged vomiting, diarrhea
burns
determining cause of Na loss
urine na <10 = extrarenal (GI/skin)
urine na >20 = renal (osmotic diuresis, thiazides, adrenal insuff, metabolic alkalosis)
hyposomotic - inc water retention aka dilutional hyponatremia
acute/chronic renal failure
nephrotic syndrome
hepatic cirrhosis
chf
detected by weight gain/edema
hyposmotic - water imbalance
normal volume but nacl deficit
SIADH
defect in AVP prod
hypothyroidism
adrenal insufficiency
SIADH
inc ADH release causes water to be retained
urine osm > plasma osm by 100
defect in AVP production causes
pulmonary disease
malignancies
trauma
infection
hyperosmotic hyponatremia
inc amts of other solutes
caused by severe hyperglycemia
causes shift of ECF or ICF shift of Na
isosmotic hyponatremia
pseudohyponatremia (hyperlipidemia/hyperproteinemia - MM)
detected by osm (urine > plasma)
pseudohyponatremia
analytical error giving a false low sodium
glucose, plasma osm and urea are normal
potassium functions
influences excitability of muscle
influences osmotic pressure inside cell
involved in cellular metabolism
kidney control of potassium
major route of excretion (glomerulus)
almost completely reabsorbed in proximal tubule
hormonal control of potassium
aldosterone: secretion of K in distal tubule and collecting duct
hyperkalemia causes
decreased renal excretion (inc retention)
inc K intake
redistribution or cellular shift
artifactual
hyperkalemia symptoms
mental confusion, weakness, tingling, flaccid paralysis in limbs, weakness of the respiratory muscles, bradycardia
7 potassium
vascular collapse and cardiac arrest (check for hemolysis before notifying floor)
10 potassium
incompatible with life
hyperkalemia - dec renal excretion
acute/chronic renal failure (most common)
hypoaldosteronism (ace inhibs block aldo)
addison's disease
diuretics (potassium sparing)
hyperkalemia - inc intake
oral or IV replacement therapy
hyperkalemia - redistribution (cellular shift)
acidosis: K shifts to ECF as H shift to ICF
muscle/cellular injury
hemolysis
drugs: digoxin, beta blockers, nsaids, spironolactone, cyclosporine, heparin therapy
hyperkalemia - artifactual
sample hemolysis
thrombocytosis/leukocytosis
prolonged tourniquet/xssive fist clenching
hypokalemia causes
GI loss
renal loss
cellular shift
dec intake
hypokalemia - GI loss
diarrhea
intestinal tumor
malabsorption
chemo/radiation therapy
large doses of laxative
hypokalemia - renal loss
nephritis, RTA
hyperaldosteronism (K excretion)
cushings syndrome (high cortisol = dec in potassium)
hypomagnesemia (promotes K excretion)
acute leukemia
hypokalemia - cellular shift
alkalosis (K shifts to ICF as H shifts to ECF)
insulin therapy
chloride functions
osmotic pressure regulation
production of HCl in gastric
which cation does chloride follow?
sodium unless there is an acid base disturbance
kidney control of chloride
major route of excretion (glomerulus)
97% reabsorbed by tubules
hyperchloremia causes
renal tubular acidosis (kidney unable to make bicarb)
metabolic acidosis (severe diarrhea)
prolonged vomiting - loss of nahco3
dehydration
xssive reabsorption from GI tract
hypochloremia causes
loss of gastric juice (vomiting or pyloric obstruction)
inc urinary excretion (diuretics or chronic pyelonephritis - salt losing)
metabolic alkalosis (inc bicarb = chloride shift)
specimen collection for measuring electrolytes
plasma or serum
heparinized whole blood or arterial/venous specimens from ABG
serum for K can be elevated from clotting process
interferences for sodium
high lvl of macromoles (proteins/lipids) will give falsely dec results in indirect methods
hemolysis = dilutional effect
potassium interferences
tourniquet in place too long
hemolysis
leukocytosis/thrombocytosis will falsely inc
chloride interferences
inc with prolonged exposure bc CO2 lost so Cl moves to serum
once separated from the cells, the Cl is stable
test methodologies
atomic absorption
flame photometry
amperometry
ISE (direct and indirect)
what does flame photometry measure?
Na and K
what does amperometry measure?
Cl
direct ISE
measures free ion activity in plasma water and does not take into account total volume so other solids do not interfere
no dilution
blood gas analyzers, POCT, single use instruments
indirect ISE
based on sample dilution and based on total volume so solids are included and protein/lipids will interfere
measures total ion concentration
adv: large sample volume to adequately cover membrane surface
more common in lab instruments
ion selective membranes
potential produced is proportional to the log of ionic activity or conc
errors of ISE
lack of analytical sensitivity
repeated protein coating of membrane
contam of the membrane or salt bridge
ISEs
used for Na, K, Cl, K
uses direct measurement of electrical potential due to acitivity of ion
Ag/AgCl: internal reference
sodium ISE
glass membrane permeable to only Na
potassium ISE
liquid ion exchange membrane with valinomycin