Electrolytes and Body Water ppt

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102 Terms
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what percentage of our mass is water?
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)
- 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
- weight to volume relationship in mOsmole/L - inaccurate if hyperlipidemia/hyperproteinemia is present
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)
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
- reduces venous pressure - increases vascular permeability - promotes natriuresis and diuresis
- similar to ANP - used to measure stuff in ppl with congestive heart failure (chf)
- 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
- 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
- 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?
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
- 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)
- 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?
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
- 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
potentiometric slides (ortho vitros)
- indicator/reference ISEs incorporated on slide - pt sample and reference fluid are simultaneously metered into drop holes - potential difference measured by electrometer
sweat test - chloride
- screening test for newborns and pediatric for CF - apply pilocarpine nitrate to sweat gland - sweat collected on gauze and Cl is measured by direct ISE