Sodium Disorders Flashcards
isotonic solutions
0.9% normal saline
lactated ringer
stays in ECF/vasculature
hypotonic solutions
D5W
D5W + 0.45NS
D5W + 0.9 NS
hypotonic - goes into ALL spaces (essentially giving water)
normal fluid balance water movement
moves freely between intracellular space and intravascular space
responds to hydrostatic pressure
allows for osmotic equilibrium
normal fluid balance sodium movement
confined to extracellular space
kidney fluid balance
detect any hypo perfusion as _____
volume depletion
even if nonexistent
transfer water b/t vascular and interstitial compartments is governed by
osmotic balance
hydrostatic balance
major extracellular cation and anion
cat: Na
an: Cl, HCO3
major intracellular cation and anion
cat: K
an: protein
response to decreased ECF
- ADH release
- Decreases ANP
- Renin Release
- Stimulation of thirst
two systems that respond to decreased ECF
+ time
hemodynamically (immediate) via vasoconstriction (raises BP and HR)
renal (12-24hrs) via ADH release and RAAS activation
ADH
from posterior pituitary
closes aquaporin channels
decreased FREE water excretion
no effect on Na
ANP
decreased urinary sodium loss
released by atrial stretch receptors
aldosterone
RAAS activation stimulates release
decreasing sodium and water
effective hemostasis dependent on
functioning kidneys and afferent sensors
afferent sensors
found in: atria, pulmonary vasculature, carotid sinus, aortic arch, juxtaglomerular apparatus
responds to ECV
ECV
fullness and tension in arterial tree
should be = to ECF if no third spacing present
disorders of ECV
disorders of decreased CO or arterial HoTN
HFrEF (decreased pump and strength) Liver failure (third spacing, decreased liver protein production) Renal failure (third spacing, increased liver protein excretion)
body’s response to this is maladaptive
hypovolemia etiologies
renal water loss (nephrogenic DI)
extra renal loss of water (increase RR, sweating, v/d)
marker of hypovolemia
decreased urine output
HoTN
hypovolemia treatment
fluid replacement is mainstay of tx
0.9% NS or colloid (LR) bc fluids stay in ECF
hypervolemia
intake exceeds excretion, fluid shifts from intravascular to interstitial space due to high capillary hydrostatic pressure (third space)
primary or secondary
retention of Na, water
tx: volume restriction, diuretic
primary hypervolemia
increased ECV, caused by:
Oliguria 2/2 AKI, GN
severe CKD
Primary hyperaldosteronism
Cushings
secondary hypervolemia
decreased ECV
occurs in response to decreased ECV
found in CHF or cirrhosis
decreased perfusion = hold onto water
hypervolemia treatment
diuretics - block Na reabsorption at some point in kidney
TZDs can cause hyponatremia (bc works on last stop in tubule)
may need to use a combo to deal with electrolyte disturbances
site of action on tubule:
acetazolamide
proximal convoluted tubule
can cause metabolic acidosis (inhibits HCO3)
weak diuretic
site of action on tubule:
TZD
distal convoluted tubule
site of action on tubule:
spironolacton
aldosterone antagonists
collecting tubule
range of osmolarity
275-295
T or F
changes in osmolarity cause changes in both ECF and ICF
True!
changes in extracellular osmolality cause changes in intracellular volume
calculating osmolality
gives idea of concentration of a toxin (osmolar gap)
uses serum electrolytes
Receptors at work to regulate osmolality
- osmoreceptors
2. baroreceptors
osmoreceptors
located in third ventricle of brain
monitor osmolality of blood in internal cards
when serum osmolality rises, osmoreceptors … (2)
stimulation thirst
stimulate ADH release from posterior pituitary
baroreceptors
atrial and venous circulation sense decrease in ECF
ADH release is stimulated by
10% decrease in ECF
regardless of serum osmolality
once volume is replaced or osmolality is restored, ADH and thirst are suppressed
hyponatremia
low SERUM sodium concentration (<135)
can be found in normal, low, or high total body sodium content OR low, normal, high, serum osmolality
typically a water issue
primary symptoms of hyponatremia
neurological bc
decreased plasma sodium = movement of water into cells
THEREFORE:
swelling of neurons = decreased function
s/s 125-130 Na level
nausea malaise
s/s 115-125 Na level
HA, lethargy worsening confusion
s/s <115 Na level
worsening LOC to eventual obtundaiton
seizures
respiratory arrest
what influences progression of symptoms
speed of sodium loss/progression
sodium level
CNS adaptation to chronic hyponatremia
cerebral cell edema forces ECF out of brain and into CSF
neuron begins to extrude osmolytes not essential for function (this decreases swelling in neuron)
reuptake of osmolytes will occur if
worst complication of hyponatremia
cerebral herniation
rapid loss of Na causes swelling that literally pushes the brain out of the skull
MC patients who get cerebral herniation
- women and children with acute post-op hyponatremia
- hyper acute hyponatremia caused by massive water ingestion (psychosis, marathon running, ecstasy)
- hyponatremic pts with intracranial pathology
s/s of chronic hyponatremia
gradually developing = asymptomatic (even if severely slow)
if they DO develop - non-specific (gait disturbance, forgetfulness, dizziness, weakness, malaise, muscle cramps)
diagnostic approach to hyponatremia
typically due to a water imbalance, not sodium issue
- historical information: body weight change, fluid intake, UO, thirst
- serum electrolytes and osmolality and urine sodium
- determine if hyper, hypo, or isotonic
- IF hyponatremic and hypotonic = asses volume status
hypertonic hyponatremia
+ tx
INCREASED serum osmolality and DECREASED Na
dilution hyponatremia
tx: get rid of underlying solute, use math formulas to determine if due to solute or true Na loss
hypertonic hyponatremia path
osmotically active solute (i.e. glucose) causes FREE WATER to leave intracellular compartment toward ECF
increased water then dilutes concentration of Na = hyponatremia
isotonic hyponatremia
NORMAL osmolality, LOW Na
may be pseudo-, due to absorption of large quantities of isosmolar solution in OR procedures
tx: 0.9% NS
causes of pseudohyponatremia
- hyperlipidemia (TGs)
- hyperproteinemia causes laboratory error
leads to a false lab report of isotonic hyponatremia
procedures that cause isotonic hyponatremia
non-conducting solution used in electrocautery in OR
TURP/Bladder Sx
Hysteroscopy
Laprascopy
absorption of large quantities cause dilution
hypotonic hyponatremia types
must asses volume status via BP and urine output, check lungs for crackers, JVD
hypovolemic hypotonic hyponatremia
hypervolemic hypotonic hyponatremia
euvolemic hypotonic hyponatremia
hypotonic hyponatremia
DECREASED osmolality, DECREASED Na
can be due to excessive consumption of free water or improper retention of free water in kidney
hypovolemic hypotonic hyponatremia
Labs, patho, tx
LOW serum Na, reduced total body sodium, DECREASED ECF
low ECV which causes baroreceptors to stimulated ADH, thirst
increased free water intake and free water retention despite low osmolality
volume replacement: 0.9% NS
hypovolemic hypotonic hyponatremia occurs due to
- GI loss of salt (emesis, diarrhea, dehydration) LOW urine Na levels
- Na loss via medications (diuretics, ACE) HIGH urine Na levels
- sodium loss due to disease (adrenal insufficiency, cerebral salt wasting) HIGH urine Na levels
hypervolemic hypotonic hyponatremia
HIGH ECF (low ECV), LOW osmolality, LOW Na
occurs with severe HF, advance Liver or kidney dz, cirrhosis, nephrotic syndrome
low ECV sensed by baroreceptors and ADH is released, prompting free water and sodium retention (to fix ECV)
hypervolemic hypotonic hyponatremia tx
improve underlying condition
fluid restriction (1L or less) - volume control
loop diuretics (may worsen hyponatremia) - comume control (CAN’T INCREASE FREE WATER)
euvolemic hypotonic hyponatremia
labs and causes (9)
normal ECF/volume, LOW osmolality, LOW Na
- hyponatremia following IV therapy
- SIADH
- psychogenic polydipsia
- hypothyroidism
- beer potomania
- exercise associated hyponatremia
- adrenal insufficiency
- HIV
- Ecstasy
hyponatremia following IV therapy
euvolemic hypotonic hyponatremia
exacerbated by inappropriate ADH secretion due to pain
HYPERtonic urine
SIADH euvolemic hypotonic hyponatremia
ADH secreted without physiological stimulus
inappropriately hypertonic urine and free water retention (hold on to too much H2O, so excretion is highly concentrated with Na)
mc due to pain, malignancy, reset osmostat
psychogenic polydipsia
euvolemic hypotonic hyponatremia
large amounts of free water are ingested due to anti-cholinergic meds or intentionally
beer potomania
excessive amounts of beer (low Na, K, protein) consumed = just enough carbohydrate to suppress protein breakdown
also a “tea and toast” diet
can’t excrete excessive free water bc low solute intake limits ability to make enough urine
exercise associated hyponatremia
euvolemic hypotonic hyponatremia
large volumes of low solute fluid over long endurance event WITH inappropriately elevated ADH levels (intense exercise, n/v, NSAID)
hypernatremia is more common
making the diagnosis of euvolemic hypotonic hyponatremia
evaluation of urine sodium levels and urine osmolality
differentiates between SIADH and psychogenic polydipsia/beer potomania
urine osmolality and urine sodium are ____ in SIADH
inappropriately concentrated (increased Na, increased osmolality)
hold onto water so that you release lots of solute with limited water
urine osmolality and urine sodium are ____ in psychogenic polydipsia/beer potomania
LOW
attempting to get rid of water, maximally diluted urine
distinguishing SIADH and reduced ECV
both have concentrated urine osmolality
reduced ECV: LOW urine sodium and HIGH BUN and uric acid (hypovolemia, no fluid to dilute0
SIADH: urine sodium is normal to elevated, BUN/uric acid LOW (free H2o stays in vascular space to dilute)
risk stratification in hyponatremia
hyperacute (few hours, h2o intoxication)
acute (24 hrs)
subacute (24-48 hrs)
chronic (>48, duration unknown)
mild-moderate symptoms hyponatremia
HA, n/v, gait changes, fatigue confusion
NOT associated with herniation
121-135
severe symptoms of hyponatremia
<120
seizures, obtundation, coma, respiratory arrest
immediate sodium correction in hyponatremia if
- severe symptoms
- acute hyponatremia w/symptoms (even mild)
- hyperactive hyponatremia, even if asymptomatic
GOAL: raise serum Na by 4-6/hr w/hypertonic saline
strategies for patient with normal sodium at baseline but now hyponatremia (6)
- treat underlying dz
- fluid restriction (<1L/day)
- oral salt tablets (1gm Nacl/tab)
- administration of 0.9 NS
- Vasopression receptor antagonist
- demeclocycline or lithium
sodium correction goal
0.5 meq/L/hr
** shoot for 9 (10 realistic) in first 24 hrs ***
if >/= 12 start worrying
4-6 over several hours
vasopressin receptor antagonists used (2)
Tolvaptan (Samsca)
Conivaptan (Vaprisol)
hospitalized, pos <125 Na
conivaptan
selective V1A and V2 receptor agonists
increased urine water excretion, activation of vasoconstriction
CANT be used in HF, liver, renal dz
tolvaptan (Samsca)
selective V2 receptor agonists
urine water excretion (free water loss w/o Na loss)
can be used in euvolemic and hypervolemic
no CI but $$$$
if urgent partial correction of sodium is needed
100 cc bolus of 3% hypertonic solution can be given over 10 min then raise up over next few ours
two more may be given but levels must be measured hourly
TOC of euvolemic hypotonic hyponatremia
free water restriction
oral salt tablets CAN be used bc likely will not listen
TOC for hypervolemic hypotonic hyponatremia
sodium and fluid restriction + loop diuretics
correct underlying cause
consider captain agent
hypovolemic hypotonic hyponatremia TOC
isotonic 0.9% NS to replace volume
this will turn off ADH secretion = more rapid correction of hyponatremia than desired
too rapid correction of fluid may cause
hyponatremia develops
cells of brain respond by extruding osmolytes = osmotic demyelination syndrome
why don’t we give everyone NS?
euvolemic SIADH will excrete all the sodium they give bc of normal aldosterone and ANP response and water will be retained
this lowers concentration of sodium and worsens hyponatremia
osmotic demyelination syndrome
2-6 days following sodium correction
irreversible
dysarthria, dysphagia, parapheresis, behavioral disturbance, coma, seizures
common in pre-menopausal women
prevention by monitoring sodium
hypernatremia causes
due to excess water loss rather than sodium gain
- high insensible loss
- osmotic diuresis
- diabetes insipidus
hypernatremia s/s
dehydration
delerium
hyperthermia
coma
dehydration symptoms in hypernatremia
decreased skin turgor
dry mucous membranes
decreased urine output
tx of hypernatremia
gradual correction over 48hrs
0.5 mEq/L/hr no more than 9-10 /day
monitor closely bc math is only an estimate
hypovolemic hypernatremia
euvolemic hypernatremia
hypo: 0.9% NS first to expand intravascular volume
eu: D5W or .45 NS
corrected too rapidly and seizures and cerebral edema will result
SIADH
ASH screened without appropriate stimulus
following volume expansion, body will have inappropriately hypertonic urine
etiologies of SIADH (7)
- paraneoplastic syndrome
- reset osmostat
- major sx/cardiac cath
- medications
- pulmonary disease
- transphenoid pituitary sx
- other
reset osmostat
osmotic threshold for ADH secretion is slower
secreted at normal osmolalities causing water retention
meds that INCREASE SDH production
antidepressants
carbamezepine
ecstasy
meds that potentiate ADH
carbamezepine
NSAIDS
amiodarone
cerebral salt wasting
depletion due to loss of sodium in urine
occurs following CNS event
volume depletion (HoTN)
isotonic saline TOC
