Na+ Chap 50 Flashcards
Patients with hypernatremia or hyponatremia that require intravascular volume expansion should be treated with intravenous fluids that contain:
similar sodium concentration as the patient’s plasma
in critically ill people even sodium concentration changes within the reference interval have been associated with:
increased mortality risk
mmol/L to mEq/L
1 mmol Ca++ to mEq
x valence
1mmol Ca++ = 2 mEq Ca++
what % TBW is intravascular
8.3%
83 m/1000ml (25% of 333 ml) will be distributed to the intravascular compartment
Osmolality
Osmolarity
concentration of osmoles in a mass of solvent
mOsm/kg - measured using an osmometer
concentration of osmoles in a volume of solvent
mOsm/L of water
Calculation of Serum Osmolality
divided by 2.8 and 18 why:
= 2[Na] + [BUN/2.8] + [Gluc./18]
convert them from mg/dl to mmol/L
Regulation of Plasma Osmolality
snsed:
regulation 2 mech.:
hypothalamic osmoreceptors
2 to 3 mOsm/kg
ADH (secreted post. pituit.) and thirst
describe pathway of hypothalmic osmoreceptor sensing increased osmolality:
barorecept:
hypothalamus osmoreceptors shrink - send impulses to posterior pituitary - ADH release
low effective circulating volume - decreased firing baroreceptor cells in the aortic arch and carotid bodies - neural impulses to the pituitary gland that stimulate ADH release
V2 and ADH depends on:
.:. doesn’t work in:
hyperosmolar renal medulla down their osmotic gradient
medullary wash out
diuretic therapy
explain hypoNa and hypoOsm. in CHF
maintenance ECV prioritized over maintenance of normal plasma osmolality
increased thirst and ADH release regardless of their osmolality = increased free water intake (from drinking) and water retention
why is hydration misnomer:
difference bw. total body Na and H2O:Na ratio:
Total body sodium content refers to the total number of sodium molecules in the body, regardless of the ratio of sodium to water.
Na content determines the hydration status of the animal. hydration is a misnomer, because findings such as skin tenting determined by both the sodium content and the H2O:Na ratio in interstitial space
doesn’t accurately reflect TBNa
can patients be hypernatremic an overhydrated?
THM total body sodium reflect hydration NOT plasma Na
sodium/water ratio is independent of the total body sodium
patients may be normally hydrated, dehydrated, or overhydrated (normal, decreased, or increased total body sodium content) and have a normal plasma sodium concentration, hypernatremia, or hyponatremia.
ddx for free water deficit (5):
- V/D
- DI
- toxic - charcoal, salt tox.
- mannitol
- water deprivation
syndrome of hypodipsic hypernatremia has been reported in Miniature Schnauzers
All cells that have Na+/K+-ATPase pumps ___ as a result of hypernatremia
shrink
Physiologic Adaptation to Hypernatremia
minutes - hrs.:
hyperosmolal state, as neuronal water is lost to the hypernatremic circulation, lowered interstitial hydraulic pressure draws fluid from the cerebrospinal fluid (CSF) into the brain interstitium
(CSF hydraulic shift into brain cells)
as plasma osmolality rises, sodium and chloride also appear to move rapidly from the CSF into cerebral tissue
(e- shifts into brain cells)
Physiologic Adaptation to Hypernatremia
hrs. - days (complete 2-7d):
idiogenic osmoles:
glutamate
glutamine
inositol
Treatment of the Normovolemic, Hypernatremic Patient:
should be treated, even if no CS
cases of ongoing free water loss:
Free water loss = 0.6 x kg x (currNa - normNa/normNa)
inadequate but safe starting point
Why is free water replacement alone will not correct clinical dehydration or hypovolemia
because free water replacement = Total Body Sodium Content NOT Plasma Sodium Concentration
complication of therapy for hypernatremia:
Next 3 steps:
Treatment:
CS of cerebral edema: obtundation, head pressing, coma, seizures
- immediately stop the administration of any fluid that has a lower sodium concentration than the patient
- disallow drinking
- measure
mannitol at 0.5 to 1 g/kg
or consider a dose of 7.2% sodium chloride
Hyponatremia ddx (5):
Decreased effective circulating volume =
free water retention
Decreased ECV common cause of hyponatremia which causes ADH release
- congestive heart failure
- excessive gastrointestinal losses
- excessive urinary losses
- body cavity effusions
- edematous states
- Addisons
- Diuretics
- SIADH
- GI parasites
- polydipsia
CHF hydration status vs
GI loss hypoNa
patient has increased total body sodium (is “overhydrated”) bc activation of RAAS
-yet is hyponatremic because of increased water retention in excess of sodium retention
excessive salt and water losses from the GI or urinary tract, the patient is total body sodium depleted (is “dehydrated”) and is hyponatremic as a result of compensatory water drinking and retention to maintain effective circulating volume
HypoNa and Addisons
decreased sodium retention (caused by hypoaldosteronism) + increased water drinking and retention in ADH defense of ECV
atypical - low circulating cortisol concentration leads to increased ADH release and resultant water retention regardless of intravascular volume status
HypoNa and diuretics
Thiazide
loop diuretics
- via induction of hypovolemia, hypokalemia that causes an intracellular shift of sodium in exchange for potassium
- and the inability to dilute urine
Renal failure can cause hyponatremia by similar mechanisms
HypoNa and SIADH
Syndrome of inappropriate ADH secretion (SIADH) causes hyponatremia via:
- water retention in response to improperly high circulating concentrations of ADH
- will be euvolemic/hypervolemic
C/S at what level:
ATPase cells:
<120 mEq/L obtundation, head pressing, seizures, com
all cells that have Na+/K+-ATPase pumps swell
Physiologic Adaptation to Hyponatremia
- Interstitial and intracellular CNS edema increases intracranial tissue hydrostatic pressure - enhances fluid movement into the cerebrospinal fluid - flows out of the cranium through subarachnoid space, central canal into venous circulation
- swollen neurons also expel solutes such as sodium, potassium, and organic osmolytes
- organic osmolytes requires hours to days
Tx
[Na+]p ≥ 130 mEq/) and usually self-corre
Tx of symptomatic hyponatremia
best management approach is controversial
why furosemide too
amount increase
mannitol with furosemide (0.5 to 1 mg/kg IV) to ensure that electrolyte-free water is excreted along with the mannitol.
Fluid loss should be replaced with standard replacement intravenous fluids, unless the patient is overhydrated and the fluid loss desired
no more than 10 mEq/L 24 hours
no more than 18 mEq/L 48 hours of treatmen
never to exceed the low RI
limit of 10 mEq/L during the first day of treatment is more important than the rate over specific period w.in that day
alternate approach to tx
hypertonic saline
human medicine recommendation is to raise by 10% to 15% in the first day of treatment
rate of correction may be as high as 2 mEq/L/hr initially
no more than 15 mEq/L in the first 24 hours
sodium deficit calculated to target plasma sodium concentration of no more than 10% to 15% higher
infused to raise plasma sodium no faster than 2 mEq/L/
major complication of treatment for hyponatremia is:
manifest:
Myelinolysis lesions in dogs are commonly seen in
myelinolysis
many days after intervention
thalamus, rather than the pons as in humans
Volume Expansion in the Hypovolemic, Hyponatremic, or Hypernatremic Patient
23.4% NaCl to the bag- product contains ____ NaCl/ml solution
should be resuscitated with a fluid that has a sodium concentration that matches that of the patient (±6 mEq/L)
4mEqNaCL/ml
100 mg/dl increase in blood glucose, sodium concentration drops
by approximately 1.6 mEq/L
