Electrolytes Flashcards
water in =
water out- bowel movement, respiration (humidified air in ventilator), urine
-water in- IV, drinking, food
water distribution
-intracellular- 66%
-interstitial- 25%
-intravascular- 9%
electrolytes and water
-main extracellular- Na
-main intracellular- K
-Since Na+ is largely restricted to extracellular compartment
-total body Na+ content is a reflection of ECF volume
-Likewise, K+ and its attendant anions are predominantly limited to the ICF and are necessary for normal cell function
-Therefore, the number of intracellular particles is relatively constant, and a change in ICF osmolality is usually due to a change in ICF water content
-However, in certain situations, brain cells can vary the number of intracellular solutes in order to defend against large water shifts
-This process of osmotic adaptation is important in the defense of cell volume and occurs in chronic hyponatremia and hypernatremia
-This response is mediated initially by transcellular shifts of K+ and Na+, followed by synthesis, import, or export of organic solutes (so-called osmolytes) such as inositol, betaine, and glutamine.
normal values
-plasma osmolality- 275-290 (cations and anion)
-Na- 135-145 (about half of osmolality)
-Na and H2O balance are typically linked
-Loss of Na -> loss of H2O
-Half of plasma osmolality is due to [Na+]
normal plasma osmolality: excretion and intake
-EXCRETION:
-Osmoreceptors (in brain) are stimulated by a rise in tonicity and increase secretion of AVP
-Osmotic threshold for AVP release is 280–290 mosmol/kg
-AVP stimulates collecting duct -> bring water back into body -> dilute down
-Principal determinant of renal water excretion is AVP to V2 receptors on the basolateral membrane of principal cells in the collecting duct leads to the insertion of water channels into the luminal membrane
-INTAKE:
-Osmoreceptors, located in the anterolateral hypothalamus, are stimulated by a rise in tonicity.
-Threshold for thirst is approximately 295 mosmol/kg
-295- your already hyperosmolar
general difference in osmolarity vs tonicity
-OSMOLARITY:
-finding in particular solution
-no relation to membrane permeability needed
-what you measure in a test tube/blood draw
-TONICITY!:
-THE EFFECTIVE OSMOLARITY *
-is in relation to the membrane and permeability
-better bc it is whats going on in body
renal causes of hypovolemia
-Diuretics
-Osmotic diuresis
-Hypoaldosterone state
-Salt-wasting
-Diabetes insipidus*
extra-renal causes of hypvolemia
-GI loss
-skin
-respiratory
-hemorrhage- if you measure hmg, bun, cr right after hemorrhage it might look normal
-after giving IV fluid it may show low -> in relation to the fluid
hypovolemia: when the ECF is normal or expanded
-third spacing
-hypovolemic but the fluid is still in the body
-decreased CO
-redistributional: hypoalbuminemia and capillary leakage
-sepsis
diagnosis
-full history and physical
-pt most likely won’t say they are volume depleted, but will present with manifestations of hypovolemia or related electrolyte abnormalities.
-dry mouth, AMS, headache, light headed
-labs:
-BUN:creatinine ratio
-Normal 10:1
-Pre-renal azotemia ≥20:1 -> (GI conditions/bleeding may cause elevated ratio)
-Urinary Sodium concentration- <20 mmol/L
-Urine Osm- >450 mosmol/kg
-Specific Gravity- 1.015
treatment
-Based on severity
-May be able to oral rehydrate if mild
-IV fluids:
-Will be based on:
-Electrolyte abnormality
-Cause of hypovolemia
types of IV fluids
-normal saline:
-ECF replacement
-mostly distributed to interstitial
-too much -> third space
-FFP:
-colloid
-primarily stays intravascular
-D5W:
-maintenance fluid
-distributed through all fluid compartments (ECF, ICF, intravascular)
-can add dextrose
-others
hyponatremia
-plasma Na level < 135
-typically assoc with hypovolemia
-asymptomatic -> nausea + malaise -> headache, lethargy, confusion -> stupor, seizure, coma
-dependent on:
-plasma level of Na
-RATE OF DECREASE
-135 to 110 slowly -> asymptomatic
-135 to 110 over a few hours -> symptomatic
IMPORTANT IMAGE
-normal brain
-hypotonic state -> less Na
-there will be more salt in the brain than in the plasma
-water shifts into the brain -> compresses brain
-RAPID ADAPTATION - via active transport pushes Na, K, Cl out
-goes back to normal -> the body can only do active transport so much…
-SLOW ADAPTATION
-loss of organic osmoltyes (proteins) -> this also takes energy
-RAPID CORRECT OF HYPOTONIC STATE
-OSMOTIC DEMYELINATION
tx- slow correction of hypotonic state
labs needed to complete hyponatremia dx
-42 y/o female presents to an ER with confusion and headache. She is found to have a plasma sodium level of 126 on initial labs.
-What other tests would help make the diagnosis?
-Plasma osmolality- is it just sodium thats low?
-Urine osmolality- albumin, Na, dilute
-Urine Sodium concentration
-Urine Potassium concentration
hyponatremia with high plasma osmolality
-hyperglycemia- water follow glucose and Na will leave to balance out the glucose
-mannitol- increased intracranial pressure -> fluid follows mannitol outside the brain (mannitol cant pass BBB)
hyponatremia with plasma osmolality normal
-hyperproteinemia- multiple myeloma produces proteins
-hyperlipidemia- severe
-s/p bladder irrigation- glycine (doesnt conduct electricity)
hyponatremia with low plasma osmolality
-first look at urine osmolality…
-urine osmolality <100:
-primary polydipsia
-reset osmostat
-urine osmolality >100:
-evaluate for extracellular fluid compartment volume status
-INCREASED (swelling): CHF, cirrhosis, nephrotic syndrome, renal insufficiency
-NORMAL: SIADH, hypothyroidism, adrenal insufficiency
-DECREASED:
-urine Na <10: extra renal loss, remote vomiting (body is compensating), remote diuretic use
-urine Na > 10: sodium salt wasting nephropathy, hypoaldosteronism, diuretic use, vomiting
treatment
-end point goals:
-increase plasma sodium to normal
-correct underlying disorder -> disorder may be multifactorial
-correct other electrolyte abnormalities
-tx is dependent on underlying cause (make precise dx prior to tx)
-volume overload -> fluid restriction
-loop diuretic
-salt restriction
-Normal saline via IV
-hormone replacement
-potassium replacement
rate of correction
-KEY point in tx is the rate
-asymptomatic pt:
-0.5-1.0 per hour
-do not correct > 10-12 for 1st 24 hr
-emergency symptoms (coma, seizure):
-use hypertonic saline and increase 1-2 for 3-4 hours or until symptoms improve
-follow asymptomatic correct rate
-do not correct > 10-12 for 1st 24 hr
-IF YOU GO TOO FAST -> osmotic demyelination
amount of sodium needed
-(target Pna - current Pna) x weight x 0.6
-weight in kilos
-assuming average body mass
-knowing that normal saline fluid has 150mmol/L Na+…
-you can estimate the amount needed to replace and at an approx rate
-remember in clinical setting this pt will have frequent monitoring (even up to hourly)
hypernatremia
-plasma sodium concentration > 145
-hypernatremia is manifestation of ds or disorder in fluid maintenance
-causes:
-primary Na gain
-water deficit
-assoc electrolyte abnormalities
-intracellular water 2/3
-extracellular water 1/3
-thirst/polyuria -> AMS -> weakness -> neurologic deficit -> seizure -> coma
-similar to hyponatremic -> cant tell off of presentation
-severity of symptoms due to rate of change and severity of hypernatremia
-brain has mechanism to protect ICF volume
where is water loss occurring in hypernatremia
-RENAL:
-osmotic diuresis - mannitol, urea, glucose
-impaired water reabsorption due to organic solutes in tubular lumen
-water loss surpasses concentrating ability
-drug induced- loop diuretics -> isoosmotic diuresis
-lab findings should support impaired concentrating ability of nephrons
-diabetes insipidus- nephrogenic or central
-EXTRARENAL:
-skin
-respiratory
-GI- loss or poor intake
what is expected response to body hypernatremia
-Maximally concentrated urine with a minimal volume
-500 mL/day
-Urine osm >800 mosmol/kg
-Thirst mechanism should maintain adequate intake of free water to replace lost water
hypernatremia treatment
-Identify the underlying cause and attempt to correct it
-Correct the water deficit- oral preferred (bc its slower)
-Remember slow and steady concept in hyponatremia correct? It applies here too!
-Correct water deficit over 48-72 hours
-exception- if you know someone is healthier prior to electrolyte change (marathon runner) -> you can correct a little faster
-Plasma sodium decrease should be limited to 0.5mmol/L per hour or 12mmol/L per 24 hours
calculating water deficit
-water deficit = (plasma sodium concentration - 140) / 140) x (weight in kg x 60%)
-50% in females and elderly
-enteral replacement is ideal but not always possible
-IV fluid then may be needed
estimating rate of IV fluids
-expected change in plasma sodium per liter of fluid administered = infusate Na - Serum Na / weight in kg x 0.6-1
-use the above equation to evaluate how different IV fluids will affect the Plasma Na
-This will help determine the rate of infusion
-Frequent laboratory monitoring is still needed -> 1 hour after tx blood labs, every 2-3 hours until stability
diabetes insipidus: how to tell apart NDI vs CDI
-fluid restrict the pt
-administer desmopressin (ADH)
-Uosm increase by 50% -> CDI
-Uosm unchanged -> NDI
nephrogenic diabetes insipidus
-“Resistance to AVP secretion”
-Inherited form:
-X-linked recessive with V2 receptor gene
-Autosomal Aquaporin-2 gene mutation
-Acquired:
-Medications, including Lithium!
-Hypercalcemia
-Hypokalemia
-Pregnancy state in 2nd-3rd trimesters!
-tx
-Treat underlying cause
-Low salt diet with low dose thiazide-diuretic
-NSAIDs role
-Amiloride for patients taking Lithium
central diabetes insipidus
-“Impairment of AVP secretion”
-MC cause: destruction of pituitary -> tumor, head injury, pregnancy!
-May be idiopathic or hereditary
-Primary polydipsia, often associated with psychiatric disorders or iatrogenic
-tx:
-Treat with intranasal desmopressin
-Low Salt diet with low dose thiazide-diuretic
-May attempt use of medications that stimulate AVP secretion
