Physiology Clinical Correlations Flashcards
most forms of persistent, true hyponatremia are associated with…
*elevated ADH (whether appropriate or inappropriate) → fluid retention & persistence of hyponatremia
*note - true hyponatremia is always hypo-osmolar
appropriate ADH elevation
ADH can be elevated due to:
1. true reductions in arterial blood volume (true volume depletion)
OR
2. sensed reductions in arterial blood volume (ineffective circulation)
inappropriate ADH elevation
*SIADH (Syndrome of Inappropriate ADH Secretion)
causes of normal-suppressed ADH
- primary polydipsia
- low solute intake: “tea-toast syndrome” or Beer Potomania (alcoholics or drink a lot of beer)
symptoms of hyponatremia
*“asymptomatic”: subtle mentation changes, gait instability, falls, fractures
*mild to moderate: headache, lethargy/fatigue, nausea/vomiting, dizziness, gait disturbances, confusion, forgetfulness
*severe: seizures, obtundation, coma, respiratory arrest, brainstem herniation, death
acute hyponatremia
*acute: drop in Na+ in less than 48hrs → MEDICAL EMERGENCY
*sudden/acute drop in Na+ can overwhelm the capacity of the brain to regulate cell volume → CEREBRAL EDEMA
chronic hyponatremia
*drop in Na+ in more than 48hrs
*less symptomatic due to cerebral adaptations
effects of hyponatremia on the brain
*immediate effect of sudden hyponatremia: CEREBRAL EDEMA & immediate increased hydraulic pressures
*rapid adaptation: loss of solutes (Na+, K+, Cl-)
*RAPID CORRECTION OF HYPOTONIC STATE → OSMOTIC DEMYELINATION
cerebral edema vs. osmotic demyelination
*cerebral edema occurs due to rapid development of hyponatremia (either rapid correction of hypernatremia or other cause of low Na+)
*osmotic demyelination occurs due to rapid CORRECTION of hyponatremia
clinical approach to hyponatremia
- assess osmolality (is this a true hyponatremia?)
- assess urine osmolarity (is the ADH level normal? kidneys SHOULD be getting rid of free water → low urine osmolality)
- assess volume status
- assess urine Na+ (is the urine concentrated?)
approach to hyponatremia: step 1 - assess serum osmolality
- hypotonic (serum Osm is low, < 275) → true hyponatremia
- isotonic → pseudohyponatremia (increased lipids or increased paraproteins make it LOOK like the sodium is low but it is not)
- hypertonic → translocation hyponatremia (due to hyperglycemia, osmotic agents, contrast)
sodium correction for hyperglycemia
*for every 100 increase in blood glucose (above 100), there is a decrease in Na+ by a factor of 1.6 or 2.4
*if blood glucose < 400, decrease in sodium by factor of 1.6
*if blood glucose > 400, decrease in sodium by factor of 2.4
example of sodium correction for hyperglycemia: Na+ 125, glucose 733, serum Osm 300
*for every 100 increase in blood glucose (above 100), there is a decrease in Na+ by a factor of 1.6 (if BG < 400) or 2.4 (if BG > 400)
step 1: BG > 400, so we use factor of 2.4 for correction
step 2: glucose is 633 mg/dL higher than normal (100) → 6.33 increases of 100mg/dL above 100
step 3: correct sodium by a factor of 2.4: 6.33 x 2.4 = 15.2 → measured sodium is 15.2 mEq/L less than actual sodium level
step 4: corrected sodium level = 125 + 15.2 → 140 mEq/L
approach to hyponatremia: step 2 - assess urine osmolality
*if the patient has a true hypotonic hyponatremia (Sosm < 280), assess urine osmolarity
*urine Osm < 100: suggests normal-suppressed ADH → free water excretion
-can be primary polydipsia or low solute intake
*urine Osm > 100: suggests ADH is present (whether appropriate or inappropriate) → less free water excretion
approach to hyponatremia: step 3 - assess ECF volume
*hypovolemic (orthostatics, low JVP, skin turgor, mucous membranes)
*euvolemic
*hypervolemic (swelling, SOB, orthopnea, etc)
