¼±Åà - È­»ìǥŰ/¿£ÅÍŰ ´Ý±â - ESC

 

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¸ÃæÇϸ鼭 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 À־ 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 À־

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¸¦ ¾ÇÈ­½Ãų¼ö 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¶§