Fluid & electrolyte disturbances
1. Sodium & water
1) composition of body fluid
water M=60%, F=50%
+- ICF: 55-75%(2/3)
+- ECF: 25-45%(1/3) +- intravascular(plasma water)(1/4)
+- extravascular(interstitial)(3/4)
* major ECF particles: Na+, Cl-, HCO3-
major ICF particles : K+, organic phosphate esters(ATP, creatine phosphate,
phospholipids)
¨ç effective osmolality(or tonicity)
ECF or ICF¿¡ ±¹ÇÑµÈ solute°¡ ±× ±¸È¹ÀÇ effective osmolality(or tonicity)¸¦ °áÁ¤ÇÑ´Ù.
Na+´Â ÁÖ·Î extracellular compartment¿¡ ±¹Çѵǰí K+´Â ÁÖ·Î ICF¿¡ ±¹ÇѵȴÙ.
±×·¯¹Ç·Î intracellular particlesÀÇ ¼ö´Â ºñ±³Àû ÀÏÁ¤Çϸç ICF osmolality°¡ º¯ÇÏ´Â °ÍÀº
ICF water content°¡ º¯Çϱ⠶§¹®ÀÌ´Ù.
¨è osmotic adaptation
Ư¼ö»óȲ¿¡¼ brain cellÀº large water shift¸¦ ¹æÁöÇϱâ À§ÇÏ¿© intracellular solute ¼ö¸¦
Á¶ÀýÇÒ¼ö ÀÖ´Ù. ÀÌ °úÁ¤À» "osmotic adaptation"À̶ó Çϴµ¥ ÀÌ´Â cell volumeÀ» À¯ÁöÇϴµ¥
Áß¿äÇϸç chronic hyponatremia & hypernatremia¿¡¼ ÀϾÙ.
óÀ½¿¡´Â K+ & Na+ÀÇ transcellular shift°¡ ÀϾ°í ±×ÈÄ¿¡´Â inositol, betaine, and
glutamine°ú °°Àº organic solutes(=osmolytes)ÀÇ ÇÕ¼º, À¯ÀÔ, À¯ÃâÀÌ µÚµû¸¥´Ù.
chronic hyponatremia¶§ brain cellÀº solute loss°¡ ÀϾ cell volumeÀ» À¯ÁöÇϰí,
neurologic sxÀ» °¨¼Ò½ÃŲ´Ù. chronic hypernatremia¶§´Â ¹Ý´ëÇö»óÀÌ ÀϾÙ.
¨é ineffective osmoles
urea¿Í °°Àº solutes´Â cell membraneÀ» ÅëÇÑ water shift¿¡ ±â¿©ÇÏÁö ¾Ê´Âµ¥ ÀÌ·¯ÇÑ
solutes¸¦ ineffective osmolesÀ̶ó ÇÑ´Ù.
fluid movement´Â capillary wallÀ» ÅëÇÏ¿© ÀÌ·ç¾îÁö¸ç Starling forces(capillary hydraulic
pressure & colloid osmotic pressure)¿¡ ÀÇÇØ °áÁ¤µÈ´Ù.
plasma -> extravascular space: hydraulic pressure & oncotic pressure
extravascular -> intravascular space: lymphatic flow¸¦ ÅëÇØ À¯ÀÔ
2) water balance
normal plasma osmolality: 275-290 mosmol/kg
1-2%ÀÇ º¯Èµµ °¨ÁöÇÒ¼ö ÀÖ´Â ±âÀüÀÌ ÀÖ¾î ÀÌ·¯ÇÑ Á¼Àº ¹üÀ§°¡ À¯ÁöµÈ´Ù.
ÀÏÁ¤»óŸ¦ À¯ÁöÇϱâ À§ÇØ water intake´Â water excretion°ú °°¾Æ¾ß ÇÑ´Ù.
ÀÌ·¯ÇÑ water homeostasisÀÇ Àå¾Ö´Â hyponatremia or hypernatremia¸¦ ÃÊ·¡ÇÑ´Ù.
Á¤»óÀûÀ¸·Î ÇÏ·ç 600 mosmÀÌ ¹è¼³µÇ¾î¾ß Çϴµ¥ maximum urine osmolality´Â 1200
mosm/kg±îÁö °¡´ÉÇϹǷΠneutral solute balance¸¦ À¯ÁöÇϱâ À§ÇÑ ÃÖ¼ÒÇÑÀÇ urine output
ÀÌ 500 ml/d´Â µÇ¾î¾ß ÇÑ´Ù.
¨ç water intake
¹°À» ¸¶½Ã°Ô ÇÏ´Â ÀÏÂ÷Àû ÀÚ±ØÀº "°¥Áõ, thirst"ÀÌ´Ù.
ÀÌ´Â i) effective osmolalityÀÇ Áõ°¡³ª
ii) ECF volume or BPÀÇ °¨¼Ò¿¡ ÀÇÇØ À¯¹ßµÈ´Ù.
* osmoreceptors
anterolateral hypothalamus¿¡ ÀÖÀ¸¸ç tonicityÀÇ Áõ°¡¿¡ ÀÇÇØ ÀڱصȴÙ.
urea & glucose¿Í °°Àº ineffective osmolesÀº thirstÀڱؿ¡ ¿µÇâÀ» ³¢Ä¡Áö ¾Ê´Â´Ù.
°¥ÁõÀ» ´À³¢´Â Æò±Õ osmotic threshold´Â 295 mosm/kgÀÌ¸ç °³Àθ¶´Ù Â÷À̰¡ ÀÖ´Ù.
Á¤»óÀûÀΠȯ°æ¿¡¼´Â daily water intake°¡ »ý¸®Àû ¿ä±¸·®º¸´Ù ¸¹´Ù.
¨è water excretion
water ingestion°ú´Â ¹Ý´ë·Î water excretionÀº physical factor¿¡ ÀÇÇØ öÀúÈ÷ Á¶ÀýµÈ´Ù.
renal water excretionÀÇ 1Â÷Àû °áÁ¤ÀÎÀÚ´Â AVPÀÌ´Ù.
AVP -> collecting ductÀÇ principle cellÀÇ posterolateral membrane¿¡ ÀÖ´Â
V2 receptor¿¡ °áÇÕ
-> adenylate cyclase activation
-> water channelÀÌ luminal membraneÀ¸·Î °áÇÕÇÏ¿© activation
(water channelÀº aquaporin-2 gene¿¡ ÀÇÇØ encode)
i) hypertonicity: AVP secretionÀÇ major stimulus
major ECF solutes´Â Na+ saltÀ̹ǷΠeffective osmolality´Â ÀÏÂ÷ÀûÀ¸·Î plasma Na+
concentration¿¡ ÀÇÇØ °áÁ¤µÈ´Ù. tonicityÀÇ Áõ°¡¿Í °¨¼Ò´Â °¢°¢ hypothalamic
osmoreceptorÀÇ cell volumeÀÌ Áõ°¡ ȤÀº °¨¼Ò¸¦ ÀÏÀ¸ÄÑ AVP secretionÀÇ Áõ°¡ ȤÀº
¾ïÁ¦½ÃŲ´Ù.
AVP releaseÀÇ osmotic threshold´Â 280-290 mosm/kgÀ̸ç ÀÌ systemÀº plasma
osmolality°¡ 1-2%¸¸ º¯Çصµ AVP release°¡ º¯ÇÒ¸¸Å ¹Î°¨ÇÏ´Ù.
ii) nonosmotic factor
AVP secretionÀ» Á¶ÀýÇÏ´Â nonosmotic factor´Â effective circulating(arterial) volume,
nausea, pain, stress, hypoglycemia, pregnancy & numerous drug µîÀÌ´Ù.
ÀÌ·¯ÇÑ hemodynamic response´Â carotid sinus¿¡ ÀÖ´Â baroreceptor¿¡ ÀÇÇØ Á¶ÀýµÈ´Ù.
baroreceptorÀÇ ¹Î°¨µµ´Â osmoreceptorº¸´Ù ÈξÀ ³·´Ù.
Ç÷¾ÐÀÌ °¨¼ÒÇÒ Á¤µµ·Î blood volumeÀÌ °¨¼ÒÇϸé AVP release°¡ ÀڱصÇÁö¸¸ volumeÀÌ
¾à°£ º¯ÇÏ´Â Á¤µµ·Î´Â ¿µÇâÀÌ °ÅÀÇ ¾ø´Ù.
homeostasis & normal plasma Na+ ³óµµ¸¦ À¯ÁöÇϱâ À§ÇØ solute-free water ingestion
ÇÏ¸é °á±¹ °°Àº ¾ç¸¸ÅÀÇ electrolyte-free water loss¸¦ ÀÏÀ¸ÄÑ¾ß ÇÑ´Ù. kidney°¡ À̿Ͱ°Àº
water load¸¦ excretionÇϴµ¥´Â ¼¼ ´Ü°è°¡ ÀÖ´Ù.
i) nephronÀÇ diluting site·Î water(and electrolyte)ÀÇ filtration & delivery
ii) active reabsorption of Na+ & Cl- without water
in the thick ascending limb of the loop of Henle
iii) maintenance of a dilute urine
3) sodium balance
¼¼Æ÷¸·ÀÇ Na+, K+-ATPase pump¿¡ ÀÇÇØ cell¹ÛÀ¸·Î pumpµÇ¾î ´ëºÎºÐÀÇ Na+(85-90%)´Â
extracellular¿¡ Á¸ÀçÇϸç, ECF volumeÀº total body Na+ contentÀÇ ¿µÇâÀ» ¹Þ´Â´Ù.
osmoregulationÀå¾Ö¿Í volume regulationÀå¾Ö¸¦ ±¸º°ÇÏ´Â °ÍÀÌ Áß¿äÇѵ¥, ¿Ö³ÄÇϸé water
& sodium balance°¡ °¢°¢ µ¶¸³ÀûÀ¸·Î Á¶ÀýµÇ±â ¶§¹®ÀÌ´Ù.
¨ç sodium intake
¼¾çÀÎÀº ÇÏ·ç ´ë·« 150 mmolÀÇ NaClÀ» ¼·ÃëÇÑ´Ù.
Á¤»óÀûÀ¸·Î ±âº» Çʿ䷮º¸´Ù´Â ¸¹Àº ¾çÀÌ´Ù.
dietary Na+ intake´Â ECF volumeÀ» expansion½ÃÄÑ ranal Na+ excretionÀ» Áõ°¡½Ã۰í
°á±¹Àº ¾ÈÁ¤»óÅÂÀÇ Na+ balance¸¦ À¯ÁöÇÏ°Ô µÈ´Ù.
¨è sodium excretion
Na+ excretionÁ¶ÀýÀº multifactorialÀ̸ç Na+ balance¸¦ Á¶ÀýÇÏ´Â ÁÖ °áÁ¤ÀÎÀÚ´Â
Na+ excretionÀÌ´Ù.
effective circulating volumeÀÌ º¯Çϸé GFRµµ µû¶ó¼ º¯ÇÏ°Ô µÈ´Ù.
±×·¯³ª tubule Na+ reabsorptionÀº GFR°ú´Â ´Þ¸® Na+ excretionÀ» Á¶ÀýÇÏ´Â ÁÖ Á¶Àý±âÀü
ÀÌ´Ù.
´ë·« ¿©°úµÈ Na+ÀÇ 2/3°¡ proximal convoluted tubule¿¡¼ ÀçÈí¼öµÇÁö¸¸ ÀÌ °úÁ¤Àº
electroneutral & isoosmoticÇÏ´Ù. ³ª¸ÓÁö ÀçÈí¼ö(25-30%)´Â loop of HenleÀÇ thick
ascending limb¿¡¼ apical Na+, K+-2Cl- cotransporter¸¦ ÅëÇÏ¿© ÀϾÙ. ÀÌ °úÁ¤Àº
active processÀÌ¸ç ¿ª½Ã electroneutralÀÌ´Ù.
distal convoluted tubule¿¡¼µµ Na+ÀçÈí¼ö°¡ ÀϾ´Âµ¥(5%) ÀÌ´Â thiazide-sensitive
Na+-Cl- cotransporter¿¡ ÀÇÇØ ÀϾÙ.
2. Hypovolemia
1) ¿øÀÎ : renal or extrarenal(Tab 49-1)
¨ç renal
i) diuretics : Na+ ÀçÈí¼ö¸¦ Â÷´ÜÇÏ¿© urinary Na+ excretion¡è
ii) glucose(=uncontrolled DM), urea(high-protein hyperalimentation), mannitol
-> osmotic diuresisÀ¯¹ß
iii) ATNÀÇ diuretic phase: Na+ & water loss
iv) CRF¶§ renal salt & water excretionÁ¶Àý´É »ó½Ç(salt-wasting nephropathy)
v) mineralocorticoid deficiency(hypoaldosteronism) -> salt-wasting
vi) DI: massive renal water excretion
¨è extrarenal
i) GI fluid loss: GIT·Î´Â ´ë·« 9LÀÇ fluid°¡ À¯ÀԵǴµ¥(2L=ingestion, 7L=secretion)
ÀÌÁß 98%´Â ÀçÈí¼öµÇ°í 100-200 mL/d¸¸ fecal fluid loss
ii) skin, respiratory tractÀ» ÅëÇÑ insensible loss(500 ml/d)
fever, prolonged heat exposure, or exercise¶§ ¼Õ½Ç Áõ°¡
Á¤»ó ¶¡ÀÇ Na+ ³óµµ = 20-50 mmol/L
½ÉÇÏ°Ô ¶¡À» È긱¶© aldosteroneÀÇ ¿µÇâÀ¸·Î hypotonic
iii) fluid sequestration in a third space
2) º´Å»ý¸®
plasma volume °¨¼Ò ¹× hypotension
-> venous return¡é(=preload¡é), C.O¡é
-> baroreceptorÀÚ±Ø
-> sympathetic nervous system, renin-angiotensin system activation
cardiovascular response¿Í´Â ¹Ý´ë·Î renal response´Â ECF volumeÀ» ȸº¹Çϴµ¥ ÀÖ´Ù.
: GFR¡é, filtered load of Na+¡é
tubular reabsorption of Na+¡è(°¡Àå Áß¿ä)
+- sympathetic tone¡è => proximal tubule Na+ reabsorption¡è, GFR¡é
| afferent arteriolar vasoconstriction
+- angiotensin II¡è, oncotic pressure¡è, hydraulic pressure¡é
=> proximal convoluted tubule¿¡¼ Na+ reabsorption¡è
3) ÀÓ»óƯ¡
careful history(vomiting, diarrhea, polyuria, diaphoresis)¸¦ ÅëÇÏ¿© »óŸ¦ ´ë·« ¾Ë¼ö ÀÖ´Ù.
´ëºÎºÐÀÇ Áõ»óÀº ºñƯÀÌÀûÀÌ´Ù.
skin turgor°¨¼Ò ¹× dry oral mucous membraneÀº interstitial fluid°¨¼Ò¸¦ Àß ¹Ý¿µÇÏÁö
¸øÇÑ´Ù.
4) Lab
BUN/Cre = 10:1(Á¤»ó)
prerenal azotemia > 20:1
±× ¿Ü BUNÀÌ Áõ°¡µÇ´Â »óȲ(=urea production¡è)
i) hyperalimentation(high-protein)
ii) glucocorticoid tx
iii) GI hemorrhage
¨ç hypokalemiaµ¿¹Ý: renal or GI K+ loss¡è
¨è hyperkalemia : renal failure, adrenal insufficiency, metabolic acidosis Áß ÀϺÎÇüÅÂ
¨é metabolic alkalosis: diuretic-induced hypovolemia, vomiting or NG suction
¨ê metabolic acidosis : renal failure, tubulointerstitial disease, adrenal insufficinecy,
diarrhea, ketoacidosis, lactic acidosis
albumin°ú erythrocyte´Â intravascular compartment¿¡ ±¹ÇѵǾî ÀÖÀ¸¹Ç·Î ECF volume
contractionÀÌ ÀÖÀ¸¸é HctÀÇ »ó½Â(hemoconcentration) ¹× plasma albumin concentration
ÀÇ »ó½ÂÀÌ »ý±ä´Ù.
hypovolemia¿¡ ´ëÇÑ ÀûÀýÇÑ ¹ÝÀÀÀº renal Na+ & water reabsorptionÀ̹ǷΠurine Na+
³óµµ´Â ATN°ú °°Àº ÀçÈí¼öÀå¾Ö¸¦ Á¦¿ÜÇϰí´Â <20 mmol/LÀÌ´Ù.
cf. ´Ù¸¥ ¿¹¿Ü: hypovolemia due to vomiting
-> metabolic alkalosis, filtered HCO3-¡è
-> proximal Na+ reabsorptionÀå¾Ö¸¦ ÃÊ·¡
urine Cl- <20 mmol/L
5) Ä¡·á: normovolemia ȸº¹ÀÌ ¸ñÇ¥
i) normonatremic & mildly hyponatremia : isotonic saline
ii) severe hyponatremia: hypertonic saline
iii) hypernatremia: hypotonic solution(half saline or 5% D/W)
iv) significant hemorrhage, anemia or intravascular volume depletion
: blood transfusion or colloid-containing solutions(albumin, dextran)
3. Hyponatremia
1) ¿øÀÎ Tab 49-2
¨ç pseudohyponatremia
plasma Na+ concentration <135 mmol/LÀÏ ¶§ hypotonic state¸¦ ÀǹÌÇÑ´Ù.
±×·¯³ª hyponatremia¶§µµ plasma osmolality´Â Á¤»ó ³»Áö´Â Áõ°¡µÇ¾î ÀÖÀ»¼ö Àִµ¥
À̶§¸¦ pseudohyponatremia¶ó ÇÑ´Ù.
plasma´Â 93%ÀÇ ¹°°ú 7%ÀÇ plasma protein & lipids·Î ÀÌ·ç¾îÁ® ÀÖ´Ù. Na+ ionsÀº ¹°¿¡
³ì¾ÆÀÖÀ¸¹Ç·Î nonaqueous phase°¡ Áõ°¡ÇÔ¿¡ µû¶ó plasma liter´ç Na+³óµµ´Â ³·¾ÆÁö°Ô
µÈ´Ù.
½ÇÁ¦ plasma osmolality ¹× Na+³óµµ´Â Á¤»óÀÌ´Ù. ÀÌ·± ÇüÅÂÀÇ hyponatremia´Â ÀÓ»óÀûÀ¸·Î
°ÅÀÇ Àǹ̰¡ ¾øÀ¸¸ç ´Ù¸¸ hyperproteinemia or hyperlipidemiaÀÇ ¿øÀθ¸ È®ÀÎÇÏ¸é µÈ´Ù.
¨è dilutional hyponatremia
TURB or TURPÈÄ¿¡ isoosmotic hyponatremia°¡ »ý±æ¼ö Àִµ¥ ¼ö¼úÁß »ç¿ëÇÏ´Â
isoosmotic(mannitol) or hypoosmotic(sorbital or glycine) bladder irrigation solutionÀÌ
Èí¼öµÇ¾î dilutional
hyponatremia¸¦ ÃÊ·¡ÇÏ°Ô µÈ´Ù.
¨é hypertonic hyponatremia
hyperglycemia or mannitolÅõ¿©ÈÄ¿¡ ¹ß»ýÇÑ´Ù.
poorly controlled DMÀÇ °æ¿ì myosite¿¡¼ impermeable glucose°¡ ³ª¿À°Ô µÇ´Âµ¥ ÀÌ
glucose´Â effective osmole·Î muscle·ÎºÎÅÍ ¼öºÐÀ» ²ø¾îµé¿© ±× °á°ú hyponatremia¸¦
ÃÊ·¡ÇÑ´Ù.
Ç÷´çÀÌ 100 mg/dL»ó½ÂÇÒ¶§¸¶´Ù plasma Na+³óµµ´Â 1.4 mmol/L¶³¾îÁø´Ù.
* ´ëºÎºÐÀÇ hyponatremia´Â plasma osmolality°¡ ³·´Ù(hypoosmolal hyponatremia).
ÀϹÝÀûÀ¸·Î hypotonic hyponatremia´Â primary water gain(and secondary Na+ loss) ȤÀº
primary Na+ loss(and secondary water gain)À¸·Î »ý±ä´Ù.
ECF volume contractionÀº thirst & AVP ºÐºñ¸¦ ÀÚ±ØÇÑ´Ù.
¹°À» ¸¹ÀÌ ¸¶½ÃÁö¸¸ renal excretionÀÇ Àå¾Ö°¡ ÀÖ´Ù¸é hyponatremia°¡ ÃÊ·¡µÈ´Ù.
¨ê diuretic-induced hyponatremia => renal Na+ loss
diuretic-induced hyponatremia´Â °ÅÀÇ Ç×»ó thiazide diuretics ¶§¹®ÀÌ´Ù.
loop diuretics´Â medullary interstitiumÀÇ tonicity¸¦ °¨¼Ò½Ã۰í maximal urinary
concentrating capacity¿¡ Àå¾Ö¸¦ ÁØ´Ù. ±× °á°ú water retention½ÃŰ´Â AVPÀÇ ÀÛ¿ëÀÌ
Á¦ÇѵȴÙ.
ÀÌ¿Í ¹Ý´ë·Î thiazide diuretics´Â Na+, K+ depletion & AVP-mediated water retentionÀ»
ÀÏÀ¸Å²´Ù.
¨ë large K+ deficit°¡ ÀÖ´Â °æ¿ì¿¡ transcellular ion exchange(K+ exit & Na+ enter cells)°¡
hyponatremia¸¦ ÀÏÀ¸Å²´Ù.
¨ì hyponatremia°¡ "desalination, Å»¿°"À̶ó´Â °úÁ¤¿¡ ÀÇÇØ¼ »ý±â±âµµ ÇÑ´Ù.
À̰ÍÀº urine tonicity°¡ IV fluid tonicityº¸´Ù Ŭ ¶§ »ý±â´Âµ¥ acute postoperative
hyponatremia & cerebral salt wasting after neurosurgery·Î »ý±ä´Ù.
¨í ECF volumeÀÌ expansionµÈ »óȲ¿¡¼µµ hyponatremia°¡ »ý±â´Âµ¥ À̶§´Â ÈçÈ÷ edema
°¡ µ¿¹ÝµÇ¾î ÀÖ´Ù. ¿¹> congestive heart failure, hepatic cirrhosis, nephrotic syndrome
ÀÌ ÁúȯµéÀÇ °øÅëÁ¡Àº effective circulating arterial volumeÀÌ °¨¼ÒÇÏ¿© thirst ¹× AVP level
ÀÌ Áõ°¡ÇÑ´Ù´Â °ÍÀÌ´Ù.
±× ¿Ü solute-free water excretion¿¡ Àå¾Ö¸¦ ÃÊ·¡ÇÏ´Â ÀÎÀڷδ GFRÀÇ °¨¼Ò, diluting site
·ÎÀÇ ultrafiltrate delivery°¨¼Ò(d/t proximal fractional reabsroption of Na+ & water Áõ°¡),
diuretic therapy¸¦ µé¼ö ÀÖ´Ù. hyponatremiaÁ¤µµ´Â underlying conditionÀÇ severity¿Í ºñ·Ê
Çϸç Áß¿äÇÑ ¿¹ÈÄÀÎÀÚ°¡ µÈ´Ù.
¨î SIADH
ECF volume contraction, effective circulating arterial volume°¨¼Ò ȤÀº renal
insufficiency°¡ ¾ø´Â »óÅ¿¡¼ÀÇ hyponatremia´Â ÈçÈ÷ AVP secretionÀÌ Áõ°¡Çϱâ
¶§¹®À̸ç water excretion¿¡ Àå¾Ö°¡ ÀÖ´Ù.
high level of AVP´Üµ¶À¸·Î´Â hyponatremia¸¦ ÀÏÀ¸Å°±â ºÒÃæºÐÇϹǷΠwater ingestion
or administrationÀÌ ¶ÇÇÑ ¿ä±¸µÈ´Ù. ÈçÈ÷ SIADH¶ó°í ºÎ¸£´Â ÀÌ·¯ÇÑ Àå¾Ö´Â
normovolemic hyponatremia¸¦ ÀÏÀ¸Å°´Â °¡Àå ÈçÇÑ ¿øÀÎÀ̸ç posterior pituitary or
ectopic source¿¡¼ AVP°¡ nonphysiologic releaseµÇ±â ¶§¹®¿¡ »ý±ä´Ù.
renal free water excretionÀÇ Àå¾Ö´Â ÀÖÁö¸¸ Na+ balance Á¶Àý¿¡´Â ¿µÇâÀÌ ¾ø´Ù.
SIADHÀÇ °¡Àå ÈçÇÑ ¿øÀÎÀº neuropsychiatric and pulmonary disease, malignant tumors,
major surgery(postoperative pain), and pharmacologic agent µîÀÌ´Ù.
severe pain & nauseaµµ AVP secretionÀÇ »ý¸®Àû ÀÚ±ØÀÎÀÚÀÌ´Ù. ´Ù¾çÇÑ CNS disorder°¡
SIADH¿Í °ü·ÃÀִµ¥ ¿©±â¿¡´Â meningitis, encephalitis, hemorrhage, stroke, psychosis,
primary and metastaitc tumor, acute porphyria µîÀÌ ÀÖ´Ù.
pneumonia, empyema, tuberculosis, and acute respiratory failureµµ SIADH¿¡ ÀÇÇØ 2Â÷
ÀûÀ¸·Î hyponatremia°¡ »ý±æ¼ö ÀÖ´Ù.
hypoxemia, hypercarbia, and positive-pressure ventilationµµ AVP releaseÀÇ
nonosmotic stimuliÀÌ´Ù. ´Ù¾çÇÑ Á¾¾ç(oat cell carcinoma of the lung)ÀÌ ectopic AVP
secretionÀ» ÀÏÀ¸Å²´Ù.
¸¹Àº ¾àÁ¦°¡ AVP release¸¦ ÀÚ±ØÇϰųª ±× ÀÛ¿ëÀ» °ÈÇÑ´Ù.
SIADH¸¦ ºÐ·ùÇϱâ À§ÇØ AVP secretion patternÀ» 4°¡Áö subtypesÀ¸·Î ±¸ºÐÇÑ´Ù.
i) erratic autonomous AVP secretion(ectopic production)
ii) normal regulation of AVP release around a lower osmolality set point
or reset osmostat(cachexia, malnutriton)
iii) normal AVP response to hypertonicity with failure to suppress completely
at low osmolality(incomplete pituitary stalk section)
iv) normal AVP secretion with increased sensitivity to its actions or secretion of some
other antidiuretic factor(rare)
¨ï adrenal insufficiency
hormonal excess or deficiency´Â hyponatremia¸¦ ÀÏÀ¸Å³¼ö ÀÖ´Ù. adrenal insufficiency
& hypothyroidism¿¡¼µµ hyponatremia¸¦ º¸Àϼö Àִµ¥ SIADH¿Í È¥µ¿Çؼ´Â ¾ÈµÈ´Ù.
adrenal insufficiency¿¡¼ mineralocorticoid°¡ °¨¼ÒÇϸé hyponatremia¸¦ ÀÏÀ¸Å³ ¼ö
ÀÖÁö¸¸ cortisol deficiency´Â Á÷,°£Á¢ÀûÀ¸·Î AVP hypersecretionÀ» ÀÏÀ¸Å²´Ù.
+- indirectly: cortisol deficiency -> volume depletion -> AVP hypersecretion
+- directly: cortisol deficiency -> CRF ºÐºñ¿Í ÇÔ²² AVPºÐºñ
¨ð hypothyroidism
hypothyroidismÀÌ hyponatremia¸¦ ÀÏÀ¸Å°´Â ±âÀüÀº C.O ¹× GFRÀÌ °¨¼ÒµÇ°í
hemodynatic stimuli¿¡ ¹ÝÀÀÇÏ¿© AVP secretionÀÌ Áõ°¡µÇ±â ¶§¹®ÀÌ´Ù.
¨ñ primary polydipsia
kidney°¡ dietary water load¸¦ excretionÇÏÁö ¸øÇÑ´Ù¸é AVP ¹× renal failure°¡ ¾ø´Â
»óȲ¿¡¼µµ hyponatremia°¡ »ý±æ¼ö ÀÖ´Ù. psychogenic or primary polydipsia,
compulsive water consumptionÀÌ Á¤»óÀûÀÎ renal excretory capacity¸¦ ³Ñ¾î¼³ ¶§ ¹ß»ý
ÇÒ¼ö ÀÖ´Ù(>12L/d).
ÀÌ·¯ÇÑ È¯ÀÚµéÀº ÈçÈ÷ psychiatric illness°¡ ÀÖ°í phenothiazine°ú °°Àº medicationÀ» Çϰí
ÀÖ¾î dry mouth¿¡ ÀÇÇØ °¥ÁõÀÌ Áõ°¡ÇÑ´Ù.
¨ò osmotic diuresis
Á¤»óÀûÀ¸·Î À½½ÄÀ» ÅëÇØ ÇÏ·ç 600 mosm/dÀÌ »ý¼ºµÇ¸ç minimal urine osmolality´Â 50
mosm/kgÀÌ´Ù. ±×·¯¹Ç·Î ÃÖ´ë ÇÏ·ç urine outputÀº 12L°¡ µÈ´Ù. solute excretion rate°¡
¡750 mosm/d
ÀÌ»óÀ̸é Á¤ÀÇ»ó osmotic diuresis¶ó ÇÑ´Ù.
low-protein diet´Â 250 mosmol/d ¹Ì¸¸ÀÌÁö¸¸ minimum urine tonicity¸¦ 50 mosmol/kg·Î
Çϱâ À§ÇÑ maximal urine outputÀº 5L/d°¡ µÇ¾î¾ß ÇÑ´Ù.
¨ó beer potomania
beer drinker´Â ÀüÇüÀûÀ¸·Î dietary protein & electrolyte intake°¡ poorÇϰí renal excretory
capacity¸¦ ÃʰúÇÏ´Â ¸¹Àº ¾çÀÇ ¸ÆÁÖ¸¦ ¼·ÃëÇÏ¿© hyponatremia¸¦ ÀÏÀ¸Å°´Âµ¥ ÀÌ·¯ÇÑ Çö»ó
À» "beer potomania"¶ó ÇÑ´Ù.
2) ÀÓ»óƯ¡
osmotic water shift°¡ ÀϾ ICF volumeÀÌ Áõ°¡ÇÏ¿© brain cell swelling or cerebral
edema°¡ »ý±æ¼ö ÀÖ´Ù. ±×·¯¹Ç·Î ÀÌ·± Áõ»óÀº ÀÏÂ÷ÀûÀ¸·Î´Â ½Å°æ°úÀûÀÌ¸ç ½ÉÇÑÁ¤µµ´Â
plasma Na+ ³óµµÀÇ °¨¼Ò¼Óµµ¿¡ ´Þ·ÁÀÖ´Ù. ¹«Áõ»óÀϼöµµ ÀÖ°í nausea, malaise¸¦ È£¼ÒÇÒ
¼öµµ ÀÖ´Ù. plasma Na+ concentrationÀÌ ³·¾ÆÁü¿¡ µû¶ó Áõ»óÀÌ Á¡Â÷ ÁøÇàÇÏ¿© headache,
lethargy, confusion, and obtundationÀÌ »ý±ä´Ù. plasma Na+ ³óµµ°¡ 120 mmol/LÀÌÇÏ·Î
±Þ°ÝÈ÷ ¶³¾îÁöÁö ¾Ê´Â´Ù¸é stupor,
seizure, coma´Â Àß ¹ß»ýÇÏÁö ¾Ê´Â´Ù. ¾Õ¿¡¼µµ ¾ð±ÞÇßÁö¸¸ chronic hyponatremia¿¡¼´Â
cell volumeÀ» À¯ÁöÇϱâ À§ÇÑ adaptive mechanismÀÌ ÀÖ´Ù. Na+, K+ lassÀÌÈÄ¿¡ organic
osmolytes°¡ brain cells¿¡¼ transcellular water shifts(ICF-> ECF)¸¦ ÀÏÀ¸Å´À¸·Î½á 2Â÷Àû
À¸·Î brain swellingÀ» °¨¼Ò½ÃŲ´Ù.
3) Áø´Ü
hyponatremia´Â Áúº´ÀÌ ¾Æ´Ï¶ó ´Ù¾çÇÑ ÁúȯµéÀÇ ¹ßÇöÇüÅÂÀÌ´Ù. Á¤È®ÇÑ º´·Â°ú ÁøÂûÀ»
ÅëÇÏ¿© ¿øÀÎÁúȯÀ» ã´Â °ÍÀÌ Áß¿äÇϸç ÁøÂû¿¡´Â ECF volume status¿Í effective
circulating arterial volumeÀÇ Æò°¡°¡ Æ÷ÇԵȴÙ.
* hyponatremiaÀÇ °¨º°Áø´Ü
i) expanded ECF volume & decreased circulating volume
: CHF, hepatic cirrhosis, nephrotic syndrome
ii) near-normal ECF volume & decreased effective circulating arterial volume
: hypothyroidism, adrenal insufficiency
iii) euvolemic : SIADH
* hyponatremia¸¦ °¨º°Áø´ÜÇϱâ À§ÇØ ´ÙÀ½ 4°¡Áö lab findingsÀÌ À¯¿ëÇÏ°Ô »ç¿ëµÈ´Ù.
i) plasma osmolality
ii) urine osmolality
iii) urine Na+ concentration
iv) urine K+ concentration
ECF tonicitity´Â ÀÏÂ÷ÀûÀ¸·Î Na+ ³óµµ¿¡ ÀÇÇØ °áÁ¤µÇ¹Ç·Î hyponatremiaȯÀÚ ´ëºÎºÐÀº
plasma osmolality°¡ °¨¼ÒµÇ¾î ÀÖ´Ù. ¸¸¾à plasma osmolality°¡ °¨¼ÒµÇ¾î ÀÖÁö ¾Ê´Ù¸é
pseudohyponatremia¸¦ ¹èÁ¦ÇØ¾ß ÇÑ´Ù.
Na+°¡ major ECF cationÀ̸ç ÁÖ·Î ECF¿¡ ±¹ÇѵǾî ÀÖÀ¸¹Ç·Î ECF volume contractionÀº
total body Na+ content deficit¸¦ ÀǹÌÇÑ´Ù. ±×·¯¹Ç·Î renal functionÀÌ Á¤»óÀΠȯÀÚ¿¡¼
volume depletionµÇ¸é tubule Na+ reabsorptionÀÌ Áõ°¡µÇ¾î urine Na+ ³óµµ´Â 20 mmol/L
ÀÌÇϰ¡ µÈ´Ù.
hypovolemic hyponatremia¿¡¼ urine Na+ > 20 mmol/LÀ̸é salt-wasting nephropathy,
diuretic therapy, hypoaldosteronism, or occasionally vomitingÀ» ÀǹÌÇÑ´Ù.
SIADH ȯÀÚ´Â ÀüÇüÀûÀ¸·Î normovolemicÀ̸ç normal Na+ balance¸¦ °®´Â´Ù. water
retention¿¡ ÀÇÇØ 2Â÷ÀûÀ¸·Î ´Ù¼Ò volume expansionµÇ¸ç urine Na+ excretion rate´Â
intake¿Í °°´Ù(urine Na+ > 40 mmol/L). Á¤ÀÇ»ó normal renal, adrenal, thyroid function &
normal K+, acid-base balance¸¦ °®´Â´Ù. volume expansion¿¡ ÀÇÇØ uricosuric state°¡
µÇ¹Ç·Î hypouricemia¸¦ µ¿¹ÝÇÑ´Ù.
4) Ä¡·á
* ¸ñÇ¥ i) water intake¸¦ Á¦ÇÑÇϰí water loss¸¦ ÃËÁøÇÏ¿© plasma Na+ ³óµµ¸¦ Áõ°¡½Ã۰í
ii) underlying disorder¸¦ ±³Á¤ÇÏ´Â °ÍÀÌ´Ù.
¨ç asymptomatic hyponatremia associated ECF volume contraction: isotonic saline
Åõ¿©ÇÑ NaClÀÌ plasma Na+³óµµ¿¡ ¹ÌÄ¡´Â ¿µÇâÀº ¹Ì¹ÌÇÏÁö¸¸ euvolemia¸¦ ȸº¹ÇÔÀ¸·Î½á
AVP release¸¦ ÀÚ±ØÇÏ´Â ¿ä¼Ò¸¦ ¾ø¾Ø´Ù.
¨è hyponatremia associated with edematous state
underlying disease severity¸¦ ¹Ý¿µÇϸç ÈçÈ÷ ¹«Áõ»óÀÌ´Ù.
Ä¡·á´Â Na+, water restrictionÇϰí, hypokalemia¸¦ ±³Á¤Çϸç, Na+°¡ °úµµÇÑ »óÅ¿¡¼ÀÇ
water loss¸¦ ÃËÁø½ÃŰ´Â °ÍÀÌ´Ù.
water loss¸¦ Áõ°¡½Ã۱â À§Çؼ net free water excretionÀ» Áõ°¡½Ã۱â À§ÇØ
urinary Na+ loss¸¦ º¸ÃæÇÏ¸é¼ loop diuretics°¡ ÇÊ¿äÇÒ¼öµµ ÀÖ´Ù.
dietary water restrictionÀº urine outputº¸´Ù Àû¾î¾ß ÇÑ´Ù.
¨é ±³Á¤¼Óµµ
i) ¹«Áõ»óȯÀÚ´Â plasma Na+ ³óµµ¸¦ ½Ã°£´ç 0.5-1 mmol/LÀÌ»ó ¿Ã¸®Áö ¸»¾Æ¾ß Çϸç
ù 24½Ã°£µ¿¾È 10-12 mmol/LÀÌ»ó ¿Ã¸®Áö ¾Êµµ·Ï ÇÑ´Ù.
ii) acute or severe hyponatremia(plasma Na+ < 110-115 mmol/L)·Î altered mental
status and/or seizure°¡ ¹ß»ýÇÒ À§ÇèÀÌ Å¬ ¶§ º¸´Ù »¡¸® ±³Á¤ÇØ¾ß ÇÑ´Ù.
seizure°¡ ¾ø¾îÁú ¶§±îÁö ù 3-4½Ã°£Àº ½Ã°£´ç 1-2 mmol/L±îÁö Áõ°¡½ÃŰ¸ç ±×ÈķδÂ
24½Ã°£µ¿¾È 12 mmol/LÀÌ»ó ¿Ã¸®Áö ¾Ê´Â´Ù.
cf. Na+ Çʿ䷮ °è»ê(70kg, ³²ÀÚ, 105 -> 115 mmol/L·Î ¿Ã¸®°íÀÚ ÇÒ °æ¿ì)
= (115-105) ¡¿ 70kg ¡¿ 0.6 = 420 mmol
¨ê ºÎÀÛ¿ë: osmotic demyelination syndrome
hyponatremia¸¦ ³Ê¹« »¡¸® ±³Á¤Çϸé osmotic demyelination syndrome(ODS)°¡ ¹ß»ýÇÒ
À§ÇèÀÌ ÀÖ´Ù. À̰ÍÀº flaccid paralysis, dysarthria, dysphagia¸¦ Ư¡À¸·Î ÇÏ´Â ½Å°æÇÐÀû
ÁúȯÀ̸ç ÀÓ»óÀûÀ¸·Î ½±°Ô ÀǽÉÇÒ¼ö ÀÖ°í ÀûÀýÇÑ neuroimaging study·Î È®ÀÎÇÒ¼ö ÀÖ´Ù.
Ưº°ÇÑ Ä¡·á´Â ¾øÀ¸¸ç morbidity & mortality°¡ ³ô´Ù. chronic hyponatremiaȯÀÚ´Â
adaptive mechanism¿¡ ÀÇÇØ brain cell volumeÀÌ °ÅÀÇ Á¤»óÀ¸·Î À¯ÁöµÇ°í Àֱ⠶§¹®¿¡
hypertonic salineÀ» Åõ¿©ÇÏ¸é °©ÀÚ±â brain cellÀÇ ¼öÃàÀ» ÃÊ·¡ÇÏ¿© ODS°¡ »ý±â±â ½±´Ù.
* ±×¿Ü ODS°¡ Àß»ý±â´Â À§ÇèÀÎÀÚ
i) prior cerebral anoxic injury
ii) hypokalemia
iii) malnutrition, ƯÈ÷ aldoholism¿¡ ÀÇÇØ 2Â÷ÀûÀ¸·Î ¹ß»ýÇÑ malnutrition
4. Hypernatremia >145 mmol/L
1) ¿øÀÎ
hypernatremia = a state of hyperosmolality
ICF particlesÀº °íÁ¤µÇ¾î ÀÖ¾î¼ hypernatremia¶§ osmotic equilibriumÀÇ À¯Áö¸¦ À§Çؼ
ICF volumeÀº contractionµÈ´Ù.
¿øÀÎÀº primary Na+ gain or water deficit·Î ´ëº°ÇÒ ¼ö°¡ ÀÖÀ¸³ª ½ÇÁ¦·Î ´ëºÎºÐÀº
water loss¿¡ ÀÇÇØ ¹ß»ýÇÑ´Ù.
ICF:ECF »çÀÌÀÇ ¹°ÀÇ ºÐÆ÷°¡ 2:1À̹ǷΠsolute-free water loss°¡ ÀÖÀ» ¶§ ICF¿¡¼ 2¹è´õ
¼Ò½ÇµÈ´Ù.
¿¹> i) free water 1L ¼Ò½Ç½Ã ICF volume = 667 ml°¨¼Ò
ECF volume = 333 ml°¨¼Ò
ii) isotonic fluid 1L¼Ò½Ç½Ã ECF voluem¸¸ 1L °¨¼Ò
iii) half isotonic fluid 1L(=water 500 ml + isotonic 500 ml) ¼Ò½Ç½Ã
ICF = 500¡¿2/3 = 333 ml
ECF = 500 ¡¿1/3 + 500 = 667 ml
thirst mechanismÀÌ Á¤»óÀûÀ¸·Î ÀÛµ¿ÇÑ´Ù¸é hyperosmolality Á¤µµ´Â ¹Ì¹ÌÇÏ´Ù.
- thirst mx¿¡ ÀÌ»óÀÌ Àְųª ¹°À» ½±°Ô ¸¶½Ç¼ö ¾ø´Â °æ¿ì¿¡ hypernatremia°¡ ¹ß»ýÇÑ´Ù.
: infant, physically handicapped, impaired metal status, postop state, ICU pt
µå¹°°Ô primary hypodipsia
hypodipsic hypernatremia = essential hypernatremia
- free water source: renal or extrarenal
¨ç nonrenal loss : skin & respiratory tract¿¡¼ÀÇ ¼Ò½Ç(=insensible loss), GIT loss
fever, exercise, heat exposure, severe burn, mechanically ventilated pt¿¡¼´Â
insensible loss°¡ Áõ°¡ÇÑ´Ù.
½ÉÇÑ ¹ßÇÑ¿¡´Â Na+ ³óµµ°¡ ³·À¸¹Ç·Î solute-free water loss°¡ ´õ¿í Áõ°¡ÇÑ´Ù.
diarrhea´Â hypernatremiaÀÇ °¡Àå ÈçÇÑ GI sourceÀÌ´Ù.
osmotic diarrhea(lactulose, sorbitol or malabsorption of carbohydrate) & viral
gastroenteritis·Î ÀÎÇØ °úµµÇÑ Na+, K+ loss°¡ ÀϾÙ.
¹Ý´ë·Î secretory diarrhea(¿¹, cholera, carcinoid, VIPoma)´Â plasma osmolality¿Í À¯»ç
ÇÑ fecal osmolality(Na+ & K+ ³óµµÀÇ ÇÕÀÇ 2¹è)°¡ ÀÖÀ¸¸ç ECF volume contraction &
normal plasma Na+ ³óµµ or hyponatremia¸¦ º¸ÀδÙ.
¨è renal water loss: most common cause of hypernatremia
drug-induced or osmotic diuresis or DI
i) loop diretics´Â countercurrent mxÀ» ¹æÇØÇÏ¿© isoosmotic, solute diuresis¸¦ ÀÏÀ¸Å°°í
medullary interstitial tonicity¸¦ °¨¼Ò½ÃÄÑ renal concentrating activity¸¦ ¼Õ»ó½ÃŲ´Ù.
tubule lumen³»ÀÇ non-reabsorbed organic solutes´Â ¹°ÀÇ osmotic reabsorptionÀ»
ÀúÇØÇÏ¿© °úµµÇÑ Na+, K+(=osmotic diuresis)¸¦ ÀÏÀ¸Å²´Ù.
ii) osmotic diuresisÀÇ °¡Àå ÈçÇÑ ¿øÀÎÀº poorly controlled DM¿¡¼ hyperglycemia &
glucosuriaÀÌ´Ù. IV mannitol or endogenous urea productionÀÇ Áõ°¡(high-protein diet)
¶ÇÇÑ osmotic diuresis¸¦ ÀÏÀ¸Å³¼ö ÀÖ´Ù.
nonosmotic urinary water loss¿¡ ÀÇÇØ 2Â÷ÀûÀ¸·Î ¹ß»ýÇÏ´Â hypernatremia´Â
i) central or neurogenic DM
ii) nephrogenic DI°¡ ÀÖ´Ù.
iii) CDIÀÇ °¡Àå ÈçÇÑ ¿øÀÎÀº neurophypophysis destructionÀÌ´Ù.
congenital NDI´Â X-linked recessive trait¸¦ º¸À̸ç V2 receptor gene mutationÀ»
º¸ÀδÙ.
aquaporin-2 geneÀº water channel proteinÀ» encodeÇϴµ¥ aquaporin-2 gene
mutationµµ NDI¸¦ ÀÏÀ¸Å³¼ö ÀÖ´Ù.
* sporadic NDIÀÇ ¿øÀÎ
drugs(ƯÈ÷ lithium), hypercalcemia, hypokalemia, medullary hypertonicity¿¡ Àå¾Ö¸¦
ÃÊ·¡ÇÏ´Â »óȲ(¿¹, papillary necrosis or osmotic diuresis)
Àӽſ©¼º¿¡¼ 2nd or 3rd trimester¶§ placenta¿¡¼ °úµµÇÑ vasopressinase°¡ »ý»êµÇ¾î
NDI°¡ »ý±æ¼ö ÀÖ´Ù.
2) ÀÓ»óƯ¡
contracted ICF volume, brain cell volume¡é
subarachnoid or intracerebral hemorrhageÀ§ÇèÀÌ ³ô´Ù.
hypernatremiaÀÇ ÁÖ¿äÁõ»óÀº ½Å°æÇÐÀû Áõ»óÀÌ´Ù.
: altered mental status, weakness, neuromuscular irritability, focal neurologic deficits
occasionally coma or seizures
polyuria or thirst
plasma Na+>180 mmol/LÀÏ ¶§ »ç¸Á·üÀÌ ¾ÆÁÖ ³ô´Ù.
ÀÓ»ó¹ßÇöÀÇ ½ÉÇÑ Á¤µµ´Â hyponatremiaó·³ Na+ Áõ°¡¼Óµµ¿¡ ´Þ·ÁÀÖÀ¸¸ç chronic
hypernatremia´Â adaptive mechanismÀ¸·Î Áõ»óÀÌ Àû´Ù.
3) Áø´Ü
Hx: thirst À¯¹«, diaphoresis, diarrhea, polyurea, ECF volume contraction, ÃÖ±Ù
medication¿©ºÎ
P/E: mental status Æò°¡ ¹× neurologic assessment
hyperosmolalityÆò°¡¿¡ ÀÖ¾î urine volume & osmolalityÃøÁ¤ÀÌ ÇʼöÀûÀÌ´Ù.
urine osmolality > 800 mosm/kg±îÁö ÃÖ´ë·Î ³óÃà½Ã۱â À§Çؼ urine volume 500 ml/d
±îÁö °¡´ÉÇÏ´Ù.
4) Ä¡·á
underlying cause¸¦ Ä¡·áÇÏ¿© ongoing water loss¸¦ ÁߴܽÃ۰í water deficit¸¦ ±³Á¤ÇÑ´Ù.
* water deficit
= (Na+-140)/140 ¡¿ B.W ¡¿ 0.5(³²ÀÚ), 0.4(¿©ÀÚ)
¿¹> 50 kg ¿©¼º, plasma Na+ 160 mmol/L
water deficit = (160-140)/140 ¡¿ 50 ¡¿ 0.4 = 2.9L
hyponatremiaó·³ hypernatremia¿¡¼µµ ºü¸£°Ô ±³Á¤Çϸé À§ÇèÇѵ¥ brain cell swellingÀÌ
ÀϾ seizure or permanent neurologic damage°¡ »ý±æ¼ö ÀÖ´Ù.
±×·¯¹Ç·Î water deficitÀº ÃÖ¼Ò 48-72½Ã°£ ÀÌ»ó¿¡ °ÉÃÄ ÃµÃµÈ÷ ±³Á¤ÇØ¾ß ÇÑ´Ù.
water replacement ¼Óµµ¸¦ °è»êÇÒ ¶§ ongoning loss¸¦ °è»ê¿¡ ³Ö¾î¾ß Çϸç plasma Na+
³óµµ´Â 0.5 mmol/L/hr¼Óµµ·Î ³·Ãß°í 24½Ã°£µ¿¾È 12 mmol/L¸¦ ³ÑÁö ¾Êµµ·Ï ÇÑ´Ù.
°¡Àå ¾ÈÀüÇÑ ¹æ¹ýÀº °æ±¸ ȤÀº NG tube·Î Åõ¿©ÇÏ´Â °ÍÀÌ¸ç ±× ´ÙÀ½À¸·Î 5% D/W or half
salineÀ¸·Î IVÇÏ´Â °ÍÀÌ´Ù.
CDI¿¡´Â desmopressin(intranasal)À» Åõ¿©ÇÑ´Ù. ´Ù¸¥ optionÀ¸·Î´Â low-salt diet +
low-dose thiazide°¡ ÀÖ´Ù.
partial CDI¿¡¼ AVP secretionÀ» Áõ°¡½ÃŰ°Å³ª kidney¿¡¼ÀÇ ÀÛ¿ëÀ» °ÈÇϱâ À§ÇÑ ¾à¹°À»
»ç¿ëÇÒ¼ö ÀÖ´Ù.
: chlorpropamide, clofibrate, carbamazepine, NSAIDs
NDI : ¿øÀÎÀ» Á¦°ÅÇϰí low-salt diet + thiazide
NSAIDs´Â renal prostaglandinÇÕ¼ºÀ» ¹æÇØÇÏ¿© AVP ÀÛ¿ëÀ» °ÈÇÏ¿© urine osmolality¸¦
Áõ°¡½Ã۰í, urine volumeÀ» °¨¼Ò½Ãų¼ö ÀÖ´Ù.
amilorideµµ lithiumÀÌ ÇÊ¿äÇÑ NDI Ä¡·á¿¡ À¯¿ëÇÏ´Ù.
5. Potassium
1) Potassium balance normal 3.5 - 5.0 mmol/L
cell³» 150 mmol/L
ECF: 30-70 mmol(<2% of total)
total: 2500-4500 mmol
ICF: ECF = 38 : 1
basolateral Na+,K+-ATPase pump¿¡¼ K+À» ¼¼Æ÷¾ÈÀ¸·Î, Na+À» ¼¼Æ÷¹ÛÀ¸·Î actively
transport(2:3ÀÇ ºñÀ²·Î)
K+ÀÇ passive outward diffusionÀÌ resting membrane potentialÀ» »ý¼ºÇÏ´Â °¡Àå Áß¿äÇÑ
ÀÎÀÚÀÌ´Ù. electrogenic Na+,K+-ATPase pump´Â intracellular Na+³óµµÀÇ Áõ°¡·Î ÀڱصǸç
digoxin toxicity or heart failure or renal failure°°Àº chronic illness¶§´Â ¾ïÁ¦µÈ´Ù.
K+ÀÇ ºÐÆ÷´Â ´Ù¸¥ ÀÎÀÚµéÀÇ ¿µÇâµµ ¹Þ´Â´Ù.
: hormones, acid-base balances, osmolality, and cell turnover
i) insulin: Na+,K+-ATPase activity¸¦ °£Á¢ÀûÀ» Áõ°¡½ÃÄÑ K+À» muscle & liver cell³»·Î shift
½ÃŲ´Ù.
¹Ý´ë·Î insulin deficiency¶§´Â ICF -> ECF·Î K+ shift
ii) ¥â2 agonist: insulin secretion & Na+,K+-ATPase pump stimulation
-> cell³»·Î K+ uptakeÁõ°¡
iii) ¥á agonist: ¥â2 agonist¿Í ¹Ý´ëÀÛ¿ë
iv) aldosterone: K+ excretionÁõ°¡
v) metabolic acidosis
electroneutrality¸¦ À¯ÁöÇϱâ À§ÇØ H+ ionÀº intracellular K+°ú exchange
vi) hyperosmolar state¿¡¼ solvent drag¿¡ ÀÇÇØ ¹°°ú ÇÔ²² cell¹ÛÀ¸·Î K+ diffusion
vii) tissue destruction or breakdown -> intracellular K+ release
viii) moderate to severe exercise
K+ release from muscle -> glycogenolysis & local vasodilatation, ÀϽÃÀû
¼¾çÀÎÀÇ Æò±Õ K+ ¼·Ãë·® : 40-120 mmol/d(´ë·« 1 mmol/kg/d)
90%´Â GIT·Î Èí¼ö
ÆòÇü»óŸ¦ À¯ÁöÇϱâ À§Çؼ´Â K+ ingestion & excretionÀÇ ÀÏÄ¡°¡ ÇÊ¿äÇÏ´Ù.
óÀ½¿£ extrarenal adaptive MxÀÌ ÀÛµ¿ÇÏ°í ±×ÈÄ¿£ urinary excretionÀÌ ÀϾÙ.
óÀ½¿¡ Èí¼öµÈ K+Àº insulin release & basal catecholamine level¿¡ ÀÇÇØ cell³»·Î À¯ÀÔ
µÇÁö¸¸ °ú´ÙÇÑ K+Àº urineÀ¸·Î excretionµÈ´Ù.
2) Potassium excretion
filtered load of K+ = GFR ¡¿ plasma K+ = 180 L/d ¡¿ 4 mmol/L = 720 mmol/d
720 mmolÀ̶õ ¾çÀº ECFº¸´Ù 10-20¹è ´õ ¸¹´Ù.
90%´Â proximal convoluted tubule & loop of Henle¿¡¼ ÀçÈí¼öµÈ´Ù.
proximal¿¡¼´Â Na+, water¿Í ÇÔ²² passively reabsorptionµÈ´Ù.
¹Ý¸é luminal Na+,K+-2Cl- cotransporter´Â thick ascending limb of the loop of Henle¿¡¼
K+ uptake¸¦ Á¶ÀýÇÑ´Ù.
K+ secretionÀº aldosterone°ú hyperkalemiaÀÇ 2°¡Áö »ý¸®Àû Àڱؿ¡ ÀÇÇØ Á¶ÀýµÈ´Ù.
i) aldosterone : zona glomerulosa¿¡¼ »ý»êµÇ¾î principle cell¿¡ ÀÛ¿ëÇÏ¿©
Na+,K+-ATPase¸¦ ÀÚ±ØÇÏ¿© luminal K+ channelÀ» Áõ°¡½ÃŲ´Ù.
ii) hyperkalemia: aldosterone°ú ¹«°üÇÏ°Ô K+ secretion¿¡ Á÷Á¢ ¿µÇâÀ» ÁØ´Ù.
6. Hypokalemia < 3.5 mmol/L
1) ¿øÀÎ Tab 49-3
net intake¡é, shift into cells, net loss¡è
¨ç redistribution into cells
metabolic alkalosis, insulin, ¥â2 agonist, ¥á-blocker
anabolic state: vit B12, GM-CSF, TPN
pseudohypokalemia, hypothermia, hypokalemic periodic paralysis, barium toxicity
massive transfusion: Ç÷¾×ÀúÀå Áß¿¡ K+ÀÇ Àý¹ÝÀº ¼Ò½ÇµÈ´Ù.
¨è nonrenal loss of K+
excessive sweating
profuse diarrhea(ÈçÈ÷ secretory): villous adenoma, VIPoma, laxative abuse
-> volume contraction -> aldosteroneºÐºñ¡è -> hypokalemia °¡¼ÓÈ
¨é renal loss of K+
i) primary hyperaldosteronism: adrenal adenoma(Conn's syndrome) or carcinoma
or adrenocortical hyperplasia
ii) GRH(glucocorticoid-remidiable hyperaldosteronism)
iii) 11¥â-hydroxylase deficiency
iv) renin-secreting tumor
v) other tumor: RCC, ovarian ca, Wilms' tumor
vi) Liddle's syndrome
vii) Bartter's syndrome
viii) carbonic anhydrase inhibitors, loop diuretics, thiazides
2) ÀÓ»óƯ¡
3 mmol/LÀÌÇϱ⠵DZâÀü¿¡´Â Áõ»óÀÌ µå¹°´Ù.
fatigue, myalgia, muscular weakness, profound K+ depletion½Ã rhabdomyolysisÀ§ÇèÀÌ
Áõ°¡
paralytic ileus
* ECG changes
delayed ventricular repolarization: K+ ³óµµ¿Í ºñ·ÊÇÏÁö ¾ÊÀ½
T flattening or inversion
prominent U, ST depression, prolonged QU interval
½ÉÇϸé PR prolongation
ventricular arrhythmia risk¡è(ƯÈ÷ myocardial ischemia or LVHȯÀÚ¿¡¼)
3) Áø´Ü
K+ depletion¶§ÀÇ ÀûÀýÇÑ ¹ÝÀÀÀº urine K+ excretionÀ» 15 mmol/dÀÌÇÏ·Î ÁÙÀÌ´Â °ÍÀÌ´Ù.
net K+ secretionÀÇ driving force¸¦ Æò°¡ÇÏ´Â ºü¸£°í °£ÆíÇÑ ¹æ¹ýÀ¸·Î TTKG°¡ ÀÖ´Ù.
* TTKG(transtubular potassium concentration gradient) = (U/P)K/(U/P)osm
ÀÌ´Â lumen°ú plasmaÀÇ K+ ³óµµÀÇ ºñ¸¦ ÀǹÌÇÏ¸ç ±× ÃøÁ¤¿¡´Â ´ÙÀ½°ú °°Àº ¼¼°¡Áö
°¡Á¤À» ÀüÁ¦·Î ÇÑ´Ù.
i) medullary collecting duct¿¡¼´Â solute ÀçÈí¼ö°¡ ¾ø´Ù.
ii) MCD¿¡¼ K+Àº ºÐºñµµ ÀçÈí¼öµµ µÇÁö ¾Ê´Â´Ù.
iii) terminal CCD¿¡¼ fluid osmolality´Â ¾Ë°í ÀÖ´Ù.
TTKG >4ÀÏ ¶§ distal K+ secretion Áõ°¡¿¡ ÀÇÇÑ renal K+ loss¸¦ ÀǹÌÇÑ´Ù.
* Approach Fig 49-3
urine K+ >15mmol/dÀ̸é TTKGÃøÁ¤
TTKG >4 => metabolic acidosis¸é RTA or DKA, amphotericin B
metabolic alkalosis¸é
mineralocorticoid excess or Liddle's syndrome(hyertension À¯)
Bartter's syndrome, hypomagenesemia, diuretics(hypertension ¹«)
TTKG <2 => Na+ wasting nephropathy, osmotic diuresis
4) Ä¡·á * ¸ñÇ¥: K+ deficit ±³Á¤ ¹× ongoing loss¸¦ ÃÖ¼ÒÈ
transcellular shift·Î ÀÎÇÑ hypokalemia¿¡¼ periodic paralysis¸¦ Á¦¿ÜÇϰí´Â IV
supplementationÀÌ ÇÊ¿äÇÑ °æ¿ì´Â µå¹°´Ù. ¿ÀÈ÷·Á rebound hyperkalemai¹ß»ý °¡´É
ÀϹÝÀûÀ¸·Î oral route·Î Ä¡·áÇÏ´Â °ÍÀÌ ¾ÈÀüÇϸç K+ depletionÁ¤µµ¿Í plasma K+³óµµ´Â Àß
ºñ·ÊÇÏÁö ¾Ê´Â´Ù.
plasma K+ 1mmol/L °¨¼ÒÇÒ¶§(4 -> 3 mmol/L) total K+ deficit´Â 200-400 mmol deficit°¡
ÀÖ°í 3 mmol/LÀÌÇÏÀ϶§´Â ±³Á¤À» À§Çؼ 600 mmolÀÌ»ó ÇÊ¿äÇÏ´Ù.
KClÀÌ ÀϹÝÀûÀ¸·Î choice
potassium bicarbonate or citrate´Â HCO3-·Î ´ë»çµÇ¾î alkalinizeµÇ´Â °æÇâÀÌ ÀÖ¾î¼
chronic diarrhea or RTA°¡ µ¿¹ÝµÈ hypokalemia¶§ ´õ ÁÁ´Ù.
severe hypokalemia¶© IV°¡ ÇÊ¿äÇѵ¥ IV¶§ÀÇ ¿øÄ¢Àº
ÃÖ´ë³óµµ´Â peripheral lineÀ¸·Î´Â 40 mmol/L, central lineÀ¸·Î´Â 60 mmol/L
infusion rate ¡Â 20 mmol/L(paralysis, malignant ventricular arrhythmia¸¦ Á¦¿ÜÇϰí´Â)
ÀÌ»óÀûÀ¸·Î´Â normal saline¿¡ KClÀ» mixÇÏ¿© ÁÖ´Â °ÍÀÌ ÁÁ´Ù.
dextrose solution¿¡ mixÇϸé óÀ½¿¡ hypokalemia¸¦ ¾ÇȽÃų¼ö Àֱ⠶§¹®ÀÌ´Ù.
7. Hyperkalemia >5 mmol/L
1) ¿øÀÎ
¨ç iatrogenic hyperkalemia: renal insufficiencyȯÀÚ¿¡¼ °ú´ÙÇÑ replacement¸¦ ÇßÀ»¶§
¨è pseudohyperkalemia: ³Ê¹« ¿À·¡ touniquetÀ» ¹Àº »óÅ¿¡¼ äÇ÷Çϰųª ÁÖ¸ÔÀ» ¹Ýº¹
ÇÏ¿© ¼¼°Ô ÁåÈÄ Ã¤Ç÷ÇÒ ¶§, hemolysis & marked leukocytosis, thrombocytosis
¨é intravascular hemolysis, tumor lysis syndrome, rhabdomyolysis -> tissue destruction
¨ê metabolic acidosis
¨ë insulin deficiency & hypertonicity(hyperglycemia)
¨ì ¥â-blocker
¨í hyperkalemic periodic paralysis: rare autosomal domiant disorder
¨î severe digitalis toxicity : Na+,K+-ATPase pump inhibition
¨ï depolarizing muscle relaxant: succinylcholine
¨ð chronic hyperkalemiaÁß hypoaldosteronism : primary, secondary, aldosterone
resistance
¨ñ drugs: NSAIDs-reninºÐºñ ¾ïÁ¦, vasodilatory renal PGÇÕ¼º ¾ïÁ¦, ACE inhibitor,
K+ sparing diuretics,
trimethoprim & pentamidine(HIV¿¡¼ pneumocystic carini pneumoniaÄ¡·á¾àÁ¦)
¨ò Cl- shunt(electroneutral Na+ reabsorption)
Gorden's syndrome: hyperkalemia + metabolic acidosis + normal GFR
volume expansion, renin & aldosterone¾ïÁ¦
type 4 RTA
cyclosporine nephrotoxicity
2) ÀÓ»óƯ¡
most serious effect = cardiac toxicity
plasma K+ ³óµµ¿Í Àß ºñ·ÊÇÏÁø ¾Ê´Â´Ù.
* ECG changes
óÀ½¿£ T amplitude¡è, T peak
½ÉÇϸé PR prolongation, QRS duration¡è, AV conduction delay, P wave ¼Ò½Ç
-> Á¡Â÷ QRS widening
-> T wave sinus pattern -> VF or asystole
3) Áø´Ü & approach Fig 49-4
¸ÕÀú pseudohyperkalemia, transcellular shift, oliguric renal failure, drug(NSAIDs, ACEIµî)
¹èÁ¦
TTKG <5 À̸é K+ secretionÀÇ driving force °¨¼ÒÀǹÌ
=> hypoaldosteronism°ú aldosterone resistance°¨º°À§ÇØ 9¥á-fludrocortisoneÅõ¿©ÇÑÈÄ
´Ù½Ã TTKGÃøÁ¤
response°¡ ÀÖÀ¸¸é(TTKG ¡Ã10) => hypoaldosteronism
response°¡ ¾øÀ¸¸é(TTKG <10) => resistanceµî ÀǹÌ
3) Ä¡·á
7.5¸¦ ³Ñ±âÀü¿¡´Â fatal hyperkalemia°¡ µå¹°´Ù.
¨ç Ca gluconate 10 ml IV over 2-3 min
¨è glucose(25-50g = 20% D/W 100cc ¡¿ 2) + insulin(10-20U)
15-30ºÐ³» K+ 0.5-1 mmol/L°¨¼Ò
¨é NaHCO3 3Amp/L IV
¨ê ¥â-agonist
¨ë diuretics: thiazide
¨ì cation-exchange resin: 1g´ç Na+ 2-3 mmol, K+ 1 mmol°áÇÕ
°æ±¸·Î 25-50gÀ» 20% sorbitol 100cc¿¡ mixÇÏ¿© Åõ¿©ÇÑ´Ù.
1-2½Ã°£³» 0.5-1.0 mmol/L¸¦ ³·Ã߸ç 4-6½Ã°£ Áö¼ÓµÈ´Ù.
postopȯÀÚ, ƯÈ÷ renal transplantatoinȯÀÚ¿¡¼ sorbitol enema´Â ÇÇÇØ¾ß Çϴµ¥
sorbitol-induced colonic necrosisºóµµ°¡ Áõ°¡Çϱ⠶§¹®ÀÌ´Ù.
¨í hemodialysis: conservative tx¿¡ ¹ÝÀÀÀÌ ¾ø´Â severe life-threatening hyperkalemia¶§