Acidosis & Alkalosis
1. Normal acid-base homeostasis
normal pH : 7.35 - 7.45
PaCO2 control: CNS & respiratory system
HCO3- control: kidney¿¡¼ acid & alkali excretion & retentionÁ¶Àý¿¡ ÀÇÇØ
* Henderson-Hasselbach equation
pH ¡ð HCO3-/PaCO2 (HCO3-°¡ Áõ°¡Çϸé PaCO2µµ Áõ°¡ÇÑ´Ù)
steady-state¿¡¼ PaCO2 = 40 mmHg
- PaCO2ÀÇ 1Â÷Àû °áÁ¤ÀÎÀÚ´Â neural respiratory factors(CO2 production rate°¡ ¾Æ´Ô)
¿¹> hypoventilation -> hypercapnia
PaCO2°¡ 1Â÷ÀûÀ¸·Î º¯Çϸé respiratory acidosis or alkalosis°¡ À¯¹ßµÇ°í cellular buffering
& renal adaptationÀÌ ÀϾÙ.
- ¹Ý´ë·Î plasma [HCO3-]°¡ ÀÏÂ÷ÀûÀ¸·Î º¯Çϸé ventilation¿¡ ÀÇÇÑ compensatory change
°¡ ÀϾ blood pHº¯È¸¦ ÃÖ¼ÒÈÇÑ´Ù. ÀÌ·¯ÇÑ º¯È¸¦ secondary or compensatory
change¶ó ÇÑ´Ù.
- kidney°¡ plasma [HCO3-]¸¦ Á¶ÀýÇÏ´Â µ¥´Â 3°¡Áö ÁÖ¿ä°úÁ¤ÀÌ ÀÖ´Ù.
i) "reabsorption" of filtered HCO3-
ii) titrable acid formation
iii) urine¿¡¼ NH4+ excretion
- kidney´Â ÇÏ·ç ´ë·« 4000 mmolÀÇ [HCO3-]¸¦ ¿©°úÇϹǷΠHCO3-ÀÇ ÀçÈí¼ö¸¦ À§Çؼ´Â
renal tubule¿¡¼ 4000 mmolÀÇ H+ secretionÀÌ ÇÊ¿äÇÏ´Ù.
HCO3-Áß 80-90%´Â proximal tubule¿¡¼ ÀçÈí¼öµÇ°í ³ª¸ÓÁö´Â distal nephron¿¡¼ ÀçÈí¼ö
µÈ´Ù.
- renal functionÀÌ Á¤»óÀÏ ¶§ metabolic acidosis°¡ µÇ¸é NH4+ production & excretionÀÌ
Áõ°¡µÇ°í CRF, hyperkalemia & RTA¿Í °°Àº »óȲ¿¡¼´Â NH4+ production & excretionÀÌ
°¨¼ÒµÈ´Ù.
2. Acid-base disturbanceÀÇ Áø´Ü
1) simple acid-base disorders
primary PaCO2 changes -> secondary [HCO3-] change
primary metabolic disturbance -> compensatory repiratory responseÀ¯¹ß
* physiologic compensation(Tab 50-1)
¿¹> endogenous acid¡è(metabolic acidosis)
-> medullary chemoreceptor ÀÚ±Ø
-> hyperventilation
-> [HCO3-] to PaCO2 ratio Á¤»óÈ
¡Å pH´Â Á¤»ó±îÁö´Â ¾Æ´Ï´õ¶óµµ Á¤»óÂÊÀ¸·Î À̵¿
* Tab 50-1
metabolic acidosis¿¡¼ PaCO2 = 1.5 ¡¿HCO3- + 8
or ¡é 1.25 per¡émmol/L HCO3-
or HCO3- + 15
¸¸¾à [HCO3-]°¡ 12 mmol/L¶ó¸é PaCO2 = 1.5 ¡¿ 12 + 8 = 26 mmHg(24-28)
PaCO2 > 28 mmHgÀ̸é respiratory acidosis
PaCO2 < 24 mmHgÀ̸é respiratory alkalosis°¡ °øÁ¸ÇÔÀ» ÀǹÌ
* Fig 50-1 acid-base normogram - 90%ÀÇ confidence limit
2) mixed acid-base disorders
2°¡Áö ÀÌ»óÀÇ Àå¾Ö°¡ µ¶¸³ÀûÀ¸·Î Á¸Àç
¿¹> i) DKA(metabolic acidosis)ȯÀÚ°¡ respiratory acidosis or alkalosis°¡ ÇÔ²² Á¸Àç
ii) underlying pulmonary diseaseȯÀÚ°¡ metabolic acidosis¿¡ ´ëÇØ ÀûÀýÇÑ ¹ÝÀÀÀ»
¸øÇÒ ¶§
iii) metabolic acidosis¿Í metabolic alkalosis°¡ °øÁ¸ÇÒ ¶§. À̶§´Â pH°¡ Á¤»óÀϼö ÀÖ´Ù.
iv) pH°¡ Á¤»óÀÏ ¶§ AGÀÌ Áõ°¡µÇ¾î ÀÖÀ¸¸é metabolic acidosis°¡ Á¸ÀçÇÔÀ» ÀǹÌÇÑ´Ù.
v) DKAȯÀÚ°¡ renal dysfunctionÀÌ ÀÖÀ¸¸é µÑ´Ù metabolic acidosis¸¦ ÃÊ·¡ÇÑ´Ù.
vi) drugÀÇ °æ¿ì¿¡µµ mixed disturbances¸¦ ÃÊ·¡ÇÒ¼ö ÀÖ´Ù.
: metabolic acidosis + respiratory acidosis or respiratory alkalosis°¢°¢
¼¼°¡Áö ÀÌ»óÀÇ acid-base disturbance°¡ Á¸ÀçÇÒ¼öµµ ÀÖ´Ù.
3) Áø´Ü
ȯÀÚ¿¡°Ô history takingÇÒ¶§ °¡Àå ÈçÇÑ ¿øÀÎÀ» ¿°µÎ¿¡ µÎ¾î¾ß ÇÑ´Ù.
¿¹¸¦ µé¸é, CRF -> metabolic acidosis
chronic vomiting -> metabolic alkalosis
pneumonia, sepsis, or cardiac failure -> respiratory alkalosis
COPD, sedative drug overdose -> respiratory acidosis
drug historyµµ Áß¿äÇѵ¥ loop or thiazide diuretics¿Í °°Àº °ÍµéÀº metabolic alkalosis¸¦
ÀÏÀ¸Å°°í, carbonic anhydrase inhibitorÀÎ acetazolamide´Â metabolic acidosis¸¦
ÀÏÀ¸Å²´Ù.
Ä¡·áÀü¿¡ electrolyte »óŸ¦ °í·ÁÇØ¾ß Çϴµ¥ metabolic acidosis´Â hyperkalemia¸¦
ÀÏÀ¸Å²´Ù.
cf. pH 0.1ÀÌ °¨¼ÒÇϸé K+´Â 0.6 mmol/LÁõ°¡
Ç×»ó ÀÌ·¯ÇÑ °ü°è°¡ ¼º¸³ÇÏ´Â °ÍÀº ¾Æ´Ï´Ù.
DKA, lactic acidosis, diarrhea, RTAµîÀº underling K+ wasting ¶§¹®¿¡ K+ depletionÀÌ
µ¿¹ÝµÈ´Ù.
* Anion gap = Na+ - (Cl- + HCO3-) normal 10-12 mmol/L
unmeasured anions: anionic proteins, phosphate, sulfate, organic anions
acid anions: acetoacetate, lactate
AG¡è: ´ëºÎºÐ unmeasured anionÀÇ Áõ°¡¶§¹®, ÀϺδ unmeasured cation(Ca, Mg, K+)
°¨¼Ò¶§¹®
AG¡é d/t i) unmeasured cation¡è
ii) abnormal cation(lithium intoxication)¡è
or cationic immunoglobulin¡è(plasma cell dyscrasia)
iii) major plasma anion albumin concentration¡é(nephrotic syndrome)
iv) acidosis¿¡ ÀÇÇØ albuminÀÇ effective anion charge¡é
v) hyperviscosity & severe hyperlipidemia(-> NaCl³óµµÀÇ underestimation)
serum albuminÀÌ Á¤»óÀÏ ¶§ high AGÀº non-chloride-containing acid¿¡ ±âÀÎÇϴµ¥
¿©±â¿¡´Â inorganic(phosphate, sulfate), organic(ketoacid, lactate, uremic organic
anions),
exogenous(salicylate or ingested toxin with organic acid production),
unidentified anionsÀÌ Æ÷ÇԵȴÙ.
[HCO3-], PaCO2, pH°¡ Á¤»óÀ̶ó°í ÇØ¼ acid-base disturbance°¡ ¾ø´Â °ÍÀº ¾Æ´Ï´Ù.
¿¹¸¦ µé¾î, alcoholics with vomiting¶§
pH = 7.55, PaCO2 = 48 mmHg, HCO3- = 40 mmol/L, Na =135, Cl = 80, K+ = 2.8
ÀÌ·¯ÇÑ metabolic alkalosis»óÅ¿¡¼ alcoholic ketoacidosis°¡ °ãÄ¡¸é
pH = 7.40, [HCO3-] = 25 mmol, PaCO2 = 40 mmHgÀϼö ÀÖ´Ù. ºñ·Ï blood gas°¡
Á¤»óÀÌ´õ¶óµµ AG = 30 mmol/L·Î Áõ°¡Çϸç ÀÌ´Â metabolic alkalosis + metabolic
acidosis°¡ ÇÔ²² ÀÖÀ½À» ÀǹÌÇÑ´Ù.
3. Metabolic acidosis
- ¹ß»ý±âÀü
i) endogenous acid production(lactate & ketoacid µî)ÀÌ Áõ°¡Çϰųª
ii) bicarbonate loss(¿¹, diarrhea) ȤÀº
iii) endogenous acid accumulation(¿¹, renal failure)µÉ ¶§ ¹ß»ýÇÑ´Ù.
- metabolic acidosis°¡ µÇ¸é respiratory, cardiac, and nervous system¿¡ ½É°¢ÇÑ ¿µÇâÀ»
³¢Ä¡°Ô µÈ´Ù.
i) ventilationÀÌ Áõ°¡ÇÏ¿© Kussmaul respirationÀ» À¯¹ßÇϱ⵵ Çϰí
ii) intrinsic cardiac contractility´Â °¨¼ÒÇÏÁö¸¸ inotropic functionÀº catecholamine release
·Î ÀÎÇÏ¿© Á¤»óÀÌ´Ù.
peripheral vasodilatation & central vasoconstriction µÑ´Ù Á¸ÀçÇϴµ¥ central &
pulmonary
vascular compliance°¡ °¨¼ÒÇÏ¿© ¾à°£¸¸ volume overloadµÇ¾îµµ pulmonary edema°¡
»ý±â±â ½±´Ù.
iii) CNS function¿ª½Ã ÀúÇϵǾî headache, lethargy, stupor, ÀϺο¡¼´Â coma°¡ ÀϾ±â
µµ ÇÑ´Ù.
iv) glucose intolerance¶ÇÇÑ ÀϾÙ.
- metabolic acidosisÀÇ major 2 category(Tab 50-2 & Tab 50-3)
i) high AG
ii) normal AG, or hyperchloremic acidosis
- Ä¡·á
no "potential HCO3-" patient¸¦ Á¦¿ÜÇϰí´Â severe acidemia¶§ alkali »ç¿ëÀº º¸·ùÇÏ¿©¾ß
ÇÑ´Ù.
cf. potential [HCO3-] = AG = patient's AG -10
plasma acid anionÀÌ metabolizableÀÎÁö nonmetabolizableÀÎÁö¸¦ °áÁ¤ÇØ¾ß ÇÑ´Ù.
cf. metabolizable anion : ¥â-hydroxybutyrate, acetoacetate, and lactate
nonmetabolizable anion: CRF¶§ ÃàÀûµÇ´Â anion, toxin ingestionÈÄÀÇ anion
nonmetabolizable anion¿¡ ÀÇÇÑ metabolic acidosis¿¡¼ [HCO3-] deficit¸¦ ȸº¹Çϱâ
À§Çؼ´Â ½Å±â´ÉÀÇ È¸º¹ÀÌ ÇÊ¿äÇÏ´Ù. °á°úÀûÀ¸·Î normal AG acidosis(hyperchloremic
acidosis), slightly elevated AG(mixed hyperchloremic and AG acidosis), or
nonmetabolizable anion¿¡ ±âÀÎÇÏ´Â
AG ȯÀڵ鿡 À־ alkali therapy°¡ ÇÊ¿äÇϸç plasma [HCO3-]¸¦ 20-22 mmol/L±îÁö
¼¼È÷ ¿Ã¸°´Ù. : orally(NaHCO3 or Shohl's solution) or IV
pure AG acidosisȯÀÚ¿¡¼ alkali»ç¿ëÀº ³í¶õÀÌ ÀÖÀ¸³ª ÀϹÝÀûÀ¸·Î severe
acidosis(pH<7.2)¿¡¼´Â NaHCO3 50-100 mEq¸¦ 30-45ºÐ¿¡ °ÉÃÄ IVÇÏ´Â °ÍÀÌ Á¤´çÇÏ´Ù.
ÁߵÀÇ alkali °ø±ÞÀº ¾ÈÀüÇÏÁö¸¸ plasma electrolyte¸¦ Àß monitorÇØ¾ß ÇÑ´Ù. ¸ñÇ¥´Â
[HCO3-]¸¦ 10 meq/L, pH 7.25±îÁö ¿Ã¸®´Â °ÍÀÌ´Ù.
1) High AG acidosis (Tab 50-2)
* 4 principle causes
(1) lactic acidosis
(2) ketoacidosis
(3) ingested toxin
(4) acute and chronic renal failure
°¨º°Áø´ÜÀ» À§ÇÏ¿© initial screeningÀÌ ÇÊ¿äÇÏ´Ù.
i) drug & toxin ingestionÀÇ º´·ÂûÃë, ABGA¸¦ ÃøÁ¤ÇÏ¿© coexisting repiratory alkalosis
È®ÀÎ(salicylates)
ii) DMÀÖ´ÂÁö È®ÀÎ(DKA)
iii) alcholism evidenceÈ®ÀÎ ¹× ¥â-hydroxybutyrate Áõ°¡È®ÀÎ(alcoholic ketoacidosis)
iv) uremiaÀÖ´ÂÁö BUN, creatinineÈ®ÀÎ(uremic acidosis)
v) urine¿¡ oxalate crystalÈ®ÀÎ(ethylene glycol)
vi) lactate levelÀÌ Áõ°¡ÇÒ¼ö ÀÖ´Â ¸¹Àº ÀÓ»ó»óȲ È®ÀÎ
: hypotension, shock, cardiac failure, leukemia, cancer & drug or toxin ingestion
(1) Lactic acidosis
type A : poor tissue perfusionÀ¸·Î ÀÎÇÏ¿© L-lactateÁõ°¡
circulatory insufficiency(shock, circulatory failure), severe anemia, mitochondrial
enzyme defects, and inhibitors(carbon monoxide, cyanide)
type B : aerobic disorders
malignancy, DM, renal or hepatic failure, severe infections(cholera, malaria),
seizure, AIDS, or drugs/toxins(biguanides, ethanol, methanol, isoniazid, AZT
analogues, and fructose)
severe atherosclerosis¿¡¼ unrecognized bowel ischemia or infarction
cardiac decompensation receiving vasopressors
* Ä¡·á: ¸ÕÀú underlying conditionÀ» ±³Á¤Çϵµ·Ï ÇÏ¿© tissue perfusionÀ» ȸº¹Çϵµ·Ï ÇÑ´Ù.
i) vasoconstrictor´Â tissue perfusionÀ» ¾ÇȽÃŰ¹Ç·Î »ç¿ëÇØ¼´Â ¾ÈµÈ´Ù.
ii) alkali therapy: ÀϹÝÀûÀ¸·Î acute, severe acidemia(pH < 7.1)ÀÏ ¶§ cardiac function ¹×
lactate utilizationÀ» Çâ»ó½Ãų ¸ñÀûÀ¸·Î »ç¿ëÇÒ¼ö ÀÖÀ¸³ª
paradoxically cardiac performance depression ¹× acidosis¸¦ ¾ÇȽÃų¼ö
ÀÖÀ¸¹Ç·Î »ç¿ë¿¡ ÁÖÀǸ¦ ¿äÇϸç arterial pH¸¦ 7.2ÀÌ»ó ¿Ã¸®Áö ¾Êµµ·Ï ÇÑ´Ù.
cf. alkali therapy -> HCO3-°¡ phosphofructokinase¸¦ ÀÚ±ØÇÏ¿© lactate¸¦ »ý»êÀ»
ÃËÁøÇÏ¿© acidosis¸¦ ¾ÇȽÃų¼ö ÀÖ´Ù.
iii) NaHCO3 therapyÀÇ ºÎÀÛ¿ë: fluid overload & hypertension, overshoot alkalosis
(2) Ketoacidosis
¨ç diabetic ketoacidosis
fatty acid metabolismÀÇ Áõ°¡¿Í ketoacids(acetoacetate & ¥â-hydroxybutyrate)ÀÇ ÃàÀû¿¡
ÀÇÇØ »ý±ä´Ù. ÈçÈ÷ IDDAȯÀÚ¿¡¼ insulinÁß´ÜÀ̳ª infection, gastroenteritis, pancreatitis,
or MI¿Í °°Àº intercurrent illness·Î ÀÎÇÏ¿© insulin¿ä±¸·®ÀÌ ÀϽÃÀûÀ¸·Î ±Þ°ÝÈ÷ Áõ°¡ÇÏ¿©
¹ß»ýÇÑ´Ù. ketoacidsÀÇ ÃàÀûÀ¸·Î AGÀÌ Áõ°¡Çϸç hyperglycemia(>300 mg/dL)°¡ ´ëºÎºÐ
µ¿¹ÝµÈ´Ù.
½ÉÇÑ acidemia(pH<7.1)¸¦ Á¦¿ÜÇϰí´Â bicarbonate therapy´Â °ÅÀÇ ÇÊ¿äÄ¡ ¾ÊÀ¸¸ç insulin
ÀÌ ketone »ý¼ºÀ» ¾ïÁ¦ÇÑ´Ù.
¨è alcoholic ketoacidosis
chronic alcoholics°¡ ¼úÀ» °©ÀÚ±â Áß´ÜÇßÀ» ¶§ ketoacidosis°¡ »ý±æ¼ö ÀÖ´Ù. ÈçÈ÷ ÆøÀ½,
vomiting, abdominal pain, starvation, and volume depletion°ú °ü·ÃÀÖ´Ù. Ç÷´çÀº Á¤»ó
³»Áö´Â °¨¼ÒµÇ¸ç acidosis´Â ketones, ƯÈ÷ ¥â-hydroxyutyrateÀÇ Áõ°¡·Î ½ÉÇÒ¼ö ÀÖ´Ù.
nitroprusside ketone reaction(Acetest)Àº acetoacetic acid¸¦ detectÇÒ ¼ö ÀÖÀ¸³ª
¥â-hydroxybutyrate´Â detectÇÒ¼ö ¾øÀ¸¹Ç·Î ketosis & ketouriaÁ¤µµ¸¦ underestimateÇÒ ¼ö
ÀÖ´Ù.
ÀüÇüÀûÀ¸·Î insulin levelÀº ³·À¸¸ç, TG, cortisol, glucagon, and growth hormoneÀº Áõ°¡
ÇÑ´Ù.
<Ä¡·á>
Saline & glucose(5% dextrose in normal saline)¸¦ IVÇÏ¿© extracellular fluid deficits¸¦
º¸ÃæÇÑ´Ù. hypophosphatemia, hypokalemia, and hypomagnesemia°¡ ÀÖÀ»¼ö Àִµ¥
±³Á¤ÇÏ¿©¾ß ÇÑ´Ù. hypophosphatemia´Â ÈçÈ÷ ÀÔ¿øÈÄ 12-24½Ã°£Â° Àß »ý±â´Âµ¥ glucose
Åõ¿©·Î ÀÎÇÏ¿© ¾Çȵɼö ÀÖÀ¸¸ç ½ÉÇϸé rhabdomyolysis¸¦ ÀÏÀ¸Å³¼ö ÀÖ´Ù.
UGI hemorrhage, pancreatitis, and pneumonia°¡ ÇÕº´µÉ¼ö ÀÖ´Ù.
(3) Drug- and Toxin-induced acidosis
¨ç salicylates (-> chap 396, drug poisoningÆí ÂüÁ¶)
¼ºÀο¡¼ÀÇ salicylate intoxicationÀº respiratory alkalosis ȤÀº mixed metabolic
acidosis-respiratory alkalosis, or pure high AG metabolic acidosis¸¦ ÀÏÀ¸Å²´Ù
lactic acidµµ Áõ°¡µÈ´Ù.
excessive insensible fluid loss·Î ÀÎÇÏ¿© severe volume depletion & hypernatremia°¡
»ý±æ¼ö ÀÖ´Ù.
<Ä¡·á>
i) vigorous gastric lavage with isotonic saline(not NaHCO3)
ii) activated charcol
iii) NaHCO3 IV: urine alkalinization(urine pH>7.5)½ÃÄÑ salicylate Á¦°Å¸¦ ÃËÁø
Ä¡·áÁß hypokalemia°¡ »ý±æ¼ö ÀÖÀ¸¸ç À̶§´Â Àû±ØÀûÀ¸·Î Ä¡·áÇØ¾ß ÇÑ´Ù.
iv) acetazolamide : alkaline diuresis°¡ ÀÌ·ç¾îÁöÁö ¾ÊÀ» ¶§ Åõ¿©ÇÒ¼ö ÀÖÁö¸¸ HCO3-°¡
º¸ÃæµÇÁö ¾ÊÀ¸¸é systemic acidosis¸¦ ÀÏÀ¸Å³¼ö ÀÖ´Ù.
v) glucose-containing fluids: hypoglycemiaÀÇ À§ÇèÀÌ ÀÖÀ¸¹Ç·Î Åõ¿©ÇÑ´Ù.
vi) hemodialysis: renal failure°¡ »ý°Ü salicylate clearance°¡ µÇÁö ¾ÊÀ¸¸é bicarbonate
dialysate¸¦ ÀÌ¿ëÇÏ¿© Åõ¼®ÇÑ´Ù.
¨è alcohols
´ëºÎºÐÀÇ »ý¸®Àû »óÅ¿¡¼ Ç÷Áß »ïÅõ¾ÐÀº sodium, urea, glucose·Î Çü¼ºµÈ´Ù.
* calculated plasma osmolality
= 2Na+ + Glu/18 + BUN/2.8
measured osmolality°¡ calculated osmolalityº¸´Ù 15-20 mmol/kgÀÌ»óÀÏ ¶§ ´ÙÀ½ µÑÁß
Çϳª¸¦ »ý°¢ÇÒ¼ö ÀÖ´Ù.
i) pseudohyponatremia : hyperlipidemia or hyperproteinemia
ii) sodium salts, glucose, or ureaÀÌ¿ÜÀÇ osmolytes: mannitol, radiocontrast media,
isopropyl alcohol, ethylene glycol, ethanol, methanol, and acetone
ÀÌ·± »óÅ¿¡¼´Â osmolar gap(calculated osmolality - measured osmolality)
Àº unmeasured solute ³óµµ¿¡ ºñ·ÊÇÑ´Ù.
¨é ethylene glycol(ÈçÈ÷ ºÎµ¿¾×À¸·Î »ç¿ë)
metabolic acidosis & severe damage to the CNS, heart, lung, and kidneys
AG & osmolar gapÀÇ Áõ°¡´Â ethylene glycol°ú ±× metabolitesÀÎ oxalic acid, glycolic
acid, and other organic acids ¶§¹®ÀÌ´Ù.
<Áø´Ü> urine¿¡¼ oxalate crystalÀ» È®ÀÎÇÏ¿© ÇÒ¼ö ÀÖÀ¸¸ç
serum¿¡¼´Â osmolar gapÀÌ Á¸ÀçÇϰí, high-AG acidosis¸¦ º¸ÀδÙ.
<Ä¡·á> ethylene glycol level °á°ú°¡ ³ª¿Ã¶§±îÁö Ä¡·á¸¦ ÁöÃ¼ÇØ¼´Â ¾ÈµÈ´Ù.
i) Áï°¢ saline or osmotic diuresis½ÃŲ´Ù.
ii) thiamine & pyridoxine supplements
iii) fomepizole or ethanol IV
iv) hemodialysis
* fomepizole(4-methyl-pyrazole) : new alcohol dehydrogenase inhibitor
°ªÀÌ ºñ½ÎÁö¸¸ ºÎÀÛ¿ë¾øÀÌ ethylene glycol levelÀ» °¨¼Ò½Ãų¼ö ÀÖ´Ù.
¿©ÀÇÄ¡ ¾ÊÀ¸¸é ´ë½Å ethanolÀ» IVÇÒ¼ö ÀÖ´Ù(Ç÷Áß³óµµ 100 mg/dLÀ¯Áö)
¨ê methanol
metabolic acidosis, and its metabolites formaldehyde and formic acid
-> severe optic nerve & CNS damage¸¦ ÀÏÀ¸Å´
<Ä¡·á> ethylene glycol intoxication°ú À¯»çÇÏ´Ù.
¨ë renal failure
moderate renal failure¿¡¼ hyperchloremic acidosisÀÌ´ø °ÍÀÌ °á±¹Àº advanced renal
failure·Î ÁøÇàÇϸé high-AG acidosis°¡ µÈ´Ù.
renal disease°¡ ÁøÇàÇÒ¼ö·Ï functioning nephronÀÇ ¼ö°¡ net acid production°ú º¸Á¶¸¦
¸ÂÃ߱⿣ ºÒÃæºÐÇØÁø´Ù. ±×·¯¹Ç·Î uremic acidosis´Â NH4+ production & excretionÀÇ
¼Óµµ°¡ °¨¼ÒµÇ´Â °ÍÀÌ Æ¯Â¡Àε¥ ÀÌ´Â ÀÏÂ÷ÀûÀ¸·Î renal mass°¡ °¨¼ÒµÇ±â ¶§¹®ÀÌ´Ù.
[HCO3-]°¡ 15 mmol/LÀÌÇÏ·Î ¶³¾îÁö°Å³ª AGÀÌ 20 mmol/LÀÌ»óÀº µå¹°´Ù.
chronic renal disease¿¡¼ ÃàÀûµÇ´Â »êÀ» ÁßÈÇϱâ À§Çؼ bone¿¡¼ À¯¸®µÇ´Â alkaline
salt°¡ ÀÌ¿ëµÈ´Ù. »êÀÌ »ó´çÈ÷ ÃàÀûµÇ´õ¶óµµ serum [HCO3-]´Â ´õ ÀÌ»ó °¨¼ÒÇÏÁö ¾Ê´Âµ¥
ÀÌ´Â
extracellular compartment ¿ÜÀÇ buffer°¡ °ü¿©ÇÔÀ» ÀǹÌÇÑ´Ù. chronic metabolic acidosis
´Â bone calcium carbonate °¨¼Ò·Î ÀÎÇÏ¿© »ó´ç·®ÀÇ bone mass loss¸¦ ÃÊ·¡ÇÑ´Ù.
<Ä¡·á>
renal failure·Î ÀÎÇÑ uremic acidosis & hyperchloremic acidosis µÑ´Ù [HCO3-]¸¦ 20-24
mmol/L·Î À¯ÁöÇϱâ À§ÇØ alkali therapy°¡ ÇÊ¿äÇÏ´Ù. ´ë·« ¾à°£ÀÇ alkali(1.0-1.5 mmol/kg)
°¡ ÇÊ¿äÇÏ´Ù.
alkali replacement¸¦ Çϸé bone¿¡ ¹ÌÄ¡´Â harmful H+ balance¸¦ ¿¹¹æÇÒ¼ö ÀÖ°í, muscle
catabolismÀ» Áö¿¬½Ãų¼ö ÀÖ´Ù. alkalinizing salts·Î sodium citrate(Shohl's solution) or
NaHCO3 tabletsÀÌ È¿°úÀûÀÌ´Ù.
citrate´Â À§Àå°ü¿¡¼ aluminumÈí¼ö¸¦ Áõ°¡½ÃŰ¹Ç·Î aluminum-containing antacid¿Í ÇÔ²²
»ç¿ëÇØ¼´Â ¾ÈµÈ´Ù. ¡ñ aluminum intoxicationÀ§ÇèÀÌ ÀÖÀ¸¹Ç·Î.
hyperkalemia°¡ ÀÖÀ»¶§´Â furosemide(60-80 mg/d)¸¦ Ãß°¡Çϵµ·Ï ÇÑ´Ù.
2) hyperchloremic metabolic acidosis Tab 50-3
diarrhea¶§ GI·Î alkali lossµÇ°Å³ª RTA¶§ kidney¸¦ ÅëÇÏ¿© alkali loss°¡ ÀÖÀ»¼ö ÀÖ´Ù.
À̶§ [Cl-]¿Í [HCO3-]ÀÇ reciprocal change°¡ »ý°Ü AGÀº Á¤»óÀÌ´Ù. ±×·¯¹Ç·Î pure
hyperchloremic acidosis¿¡¼´Â [Cl-]°¡ Áõ°¡µÇ´Â ¸¸Å [HCO3-]°¡ °¨¼ÒÇÑ´Ù.
ÀÌ·± °ü°è°¡ ¼º¸³µÇÁö ¾Ê´Â´Ù¸é mixed disturbance¸¦ ÀǹÌÇÑ´Ù.
stool¿¡´Â [HCO3-]³óµµ°¡ ³ôÀ¸¹Ç·Î diarrhea¶§´Â volume depletion°ú ÇÔ²² metabolic
acidosis°¡ »ý±ä´Ù. systemic acidosisÀ̹ǷΠurine pH°¡ »ê¼ºÀÌ µÇ¾î¾ß ÇÒ°ÍÀ¸·Î ¿¹»ó
µÇÁö¸¸ ½ÇÁ¦ urine pH´Â 6Á¤µµ µÇ´Âµ¥ ÀÌ´Â metabolic acidosis & hypokalemia°¡ NH4+ÀÇ
renal synthesis & excretionÀ» Áõ°¡½Ã۱⠶§¹®ÀÌ´Ù. À̰ÍÀÌ urine pH¸¦ Áõ°¡½ÃŰ´Â
urinary buffer·Î ÀÛ¿ëÇÑ´Ù.
urine NH4+ excretionÀÌ RTA¿¡¼´Â ³·°í, diarrhea‹š´Â ³ôÀ¸¹Ç·Î À̰ÍÀ¸·Î µÑÀ» ±¸º°ÇÒ ¼ö
ÀÖ´Ù.
* urinary NH4+ levelÀº urine anion gap(UAG)À» °è»êÇÔÀ¸·Î½á ÃøÁ¤ÇÒ¼ö ÀÖ´Ù.
UAG = [Na+ + K+]U - [Cl-]U
[Cl-]U > [Na+ + K+]UÀÏ ¶§ urine ammonium levelÀº Áõ°¡µÇ¸ç ÀÌ´Â extrarenal causeÀÇ
acidosis¸¦ ÀǹÌÇÑ´Ù.
GFRÀÌ 20-50 ml/minÀ϶§´Â hyperchloremic acidosis°¡ »ý±â°í renal disease°¡ ÁøÇàÇÏ¿©
GFRÀÌ 20 ml/min¹Ì¸¸ÀÌ µÇ¸é high AG acidosis°¡ µÈ´Ù.
ÀÌ·± ÇüÅ´ tubulointerstitial disease¿¡¼ ÈçÇϸç advanced glomerular disease¿¡¼´Â
°è¼Ó hyperchloremic metabolic acidosis°¡ Áö¼ÓÇÒ¼ö ÀÖ´Ù.
advanced renal failure¿¡¼ ammoniogenesis´Â functional renal mass °¨¼Ò¿¡ ºñ·ÊÇÏ¿©
°¨¼ÒÇÑ´Ù.
acidosis¿¡ ´ëÇÑ ÀûÀÀ±âÀüÀ¸·Î collecting duct ¹× colon¿¡¼ÀÇ K+ secretionÀÌ Áõ°¡ÇϹǷÎ
chronic renal insufficiency¿¡¼ÀÇ acidosis´Â ÀüÇüÀûÀ¸·Î normokalemicÀÌ´Ù.
Proximal RTA(type 2)´Â Fanconi syndromeÀ¸·Î Ç¥ÇöµÇ´Â generalized proximal tubular
dysfunctionÀ¸·Î °¡Àå ÈçÈ÷ »ý±ä´Ù.
cf. Fanconi syndrome: glycosuria, generalized aminoaciduria, phosphaturia
urine pH < 5.5
classic distal RTA(type 1 RTA)
hypokalemia, hyperchloremic acidosis, low urinary NH4+ excretion(positive UAG,
low urine NH4+, high urine pH(>5.5)
hypocituria, hypercalciuria -> nephrolithiasis, nephrocalcinosis and bone disease°¡
ÈçÇÏ´Ù.
type 4 RTA: hyperkalemia(potassium and acid secretionÀå¾Ö°¡ µ¿¹ÝµÇ¹Ç·Î)
urinary ammonium excretion¡é
¿¹> i) diabetic nephropathy
ii) amyloidosis
iii) tubulointerstitial disease
* hyporeninemic hypoaldosteronism
DMÀÖ´Â ³ëÀÎ, tubulointerstitial disease and renal insufficiency¿¡¼ °¡Àå ÈçÇÏ´Ù.
ȯÀÚ´Â ÈçÈ÷ mild to moderate renal insufficiency & acidosis,
serum [K+] levelÀº ³ô°í(5.2-6.0 mmol/L)
concurrent hypertension, CHF°¡ µ¿¹ÝµÈ´Ù.
NSAIDs, trimethoprim, pentamidine, ACE inhibitors°°Àº ¾àµéÀÌ renal insufficiencyȯÀÚ¿¡¼
hyperkalemia with hyperchloremic metabolic acidosis¸¦ ÀÏÀ¸Å³¼ö ÀÖ´Ù.
4. Metabolic alkalosis
ÈçÈ÷ hypochloremia & hypokalemia¿Í µ¿¹ÝµÈ´Ù.
high [HCO3-] & low [Cl-] ȯÀÚ´Â metabolic alkalosis°¡ ÀÖ´øÁö, ¾Æ´Ï¸é chronic
respiratory acidosis°¡ ÀÖ´Ù.
[HCO3-]°¡ 10 mmol/L°¡ Áõ°¡ÇÔ¿¡ µû¶ó PaCO2´Â 6 mmHg°¡ Áõ°¡ÇÑ´Ù.
¾à°£ ´Ù¸¥ ¹æ¹ýÀº predicted PaCO2´Â ´ë·« [HCO3-] + 15¿Í °°´Ù.
1) º´ÀÎ
net [HCO3-] gain or nonvolatile acid(ÈçÈ÷ vomitingÀ¸·Î ÀÎÇÑ HCl) loss·Î ÀÎÇØ ¹ß»ýÇÑ´Ù.
metabolic alkalosis´Â ´ÙÀ½ µÎ stageÀÇ Àå¾Ö°¡ Àִµ¥ generative stage¿¡¼´Â acid loss·Î
ÀÎÇÏ¿© alkalosis°¡ ¹ß»ýÇϰí maintenance stage¿¡¼´Â volume contraction, low GFR, Cl-
or K+ depletion ¶§¹®¿¡ kidney°¡ HCO3-excretionÀ» ÅëÇÑ º¸»óÀ» ÇÒ¼ö ¾ø¾î¼ alkalosis°¡
¹ß»ýÇÑ´Ù.
´ÙÀ½°ú °°Àº »óȲ¿¡¼ kidney´Â °ú´ÙÇÑ alkali¸¦ excretionÇÏÁö ¾Ê°í retainÇÔÀ¸·Î½á alkalosis
°¡ ¹ß»ýÇÑ´Ù.
i) volume deficiency, chloride deficiency, and K+ deficiency + GFR¡é
=> distal tubule H+ secretion ÃËÁø
ii) autonomous hyperaldosteronism¿¡ ÀÇÇÑ hypokalemia
i)Àº NaCl or KCl·Î ±³Á¤ÇÒ¼ö ÀÖÁö¸¸ ii)´Â salineÅõ¿©·Î ÇØ°áµÇÁö ¾Ê°í pharmacologic or
surgical interventionÀ» ÅëÇØ alkalosis¸¦ ±³Á¤ÇØ¾ß ÇÑ´Ù.
2) °¨º°Áø´Ü Tab 50-4
metabolic alkalosisÀÇ ¿øÀÎÀ» ¹àÈ÷±â À§Çؼ ¸ÕÀú extracellular fluid volume(ECFV) status,
recumbent and upright BP, serum [K+], renin-aldosterone systemÀÇ Æò°¡°¡ ÇÊ¿äÇÏ´Ù.
¿¹¸¦ µé¸é, chronic hypertension & chronic hypokalemia°¡ ÀÖÀ» ¶§ mineralocorticoid
excess ȤÀº °íÇ÷¾ÐȯÀÚ°¡ diuretic therapy¸¦ ¹Þ°í ÀÖ´Â °æ¿ì¸¦ »ý°¢ÇÒ¼ö ÀÖ´Ù.
diuretics¸¦ ¸ÔÁö ¾ÊÀ» ¶§ plasma renin activity°¡ ³·°í, urine [Na+], [Cl-]ÀÌ Á¤»óÀ̶ó¸é
primary mineralocorticoid excess syndromeÀ» ÀǹÌÇÑ´Ù.
normotensive, nonedematous patient¿¡¼ hypokalemia & alkalosis´Â Bartter's syndrome
or Gitelman's syndrome, Mg deficiency, vomiting, exogenous alkali, or diuretic ingestion
¿¡ ÀÇÇØ »ý±æ¼ö ÀÖ´Ù.
urine electrolyteÀÇ ÃøÁ¤(ƯÈ÷ urine [Cl-]) & diuretics¿¡ ´ëÇÑ urine screeningÀÌ ¶ÇÇÑ
µµ¿òÀÌ µÈ´Ù. alkaline urineÀÏ ¶§ [Na+], [K+]°¡ ³ôÁö¸¸ [Cl-]ÀÌ ³·À¸¸é vomiting ¶Ç´Â alkali
ingestion¶§¹®ÀÌ´Ù. acidic urineÀÌ¸é¼ Na, K, ClÀÇ ³óµµ°¡ ³·´Ù¸é prior vomiting,
posthypercapnic state, prior diuretic ingestionÀÇ °¡´É¼ºÀÌ ¸¹´Ù. ¹Ý´ë·Î urine Na, K, Cl
¾î´À°Íµµ °¨¼ÒµÇ¾î ÀÖÁö ¾ÊÀ¸¸é Mg deficiency, Bartter's or Gitelman's syndrome or
current diuretic ingestionÀ» ¸ÕÀú »ý°¢ÇÑ´Ù. Bartter's syndrome°ú Gitelman's syndromeÀº
hypocalcemia & hypomagnesemia·Î °¨º°ÇÒ¼ö ÀÖ´Ù. (Gitelman's syndrome¿¡¼´Â
hypocalcemia & hypomagnesemia°¡ ÀÖÀ½)
* Alkali administration
HCO3- excretionµÇ´Â °Íº¸´Ù ÀçÈí¼öµÇ´Â °ÍÀÌ ´õ ¸¹À» ¶§ alkalosis°¡ »ý±æ¼ö ÀÖ´Ù.
ÀÌ·± °æ¿ì´Â oral or IV HCO3-, acetate loads(parenteral hyperalimentation solutions),
citrate loads(transfusion), or antacids + cation-exchange resins(aluminum hydroxide
and sodium
polystyrene sulfonate)¸¦ Åõ¿©¹Þ´Â °æ¿ì µîÀÌ ÀÖ´Ù.
3) metabolic alkalosis + ECFV contraction, K+ depletion,
and secondary hyperreninemic hyperaldosteronism
(1) GI origin
vomiting or gastric aspirationÀ¸·Î ÀÎÇÑ H+ loss´Â HCO3- retentionÀ» ÃÊ·¡ÇÑ´Ù.
fluid & NaCl loss -> ECFV contraction & renin, aldosterone secretion¡è
-> GFR¡é, renal tubule¿¡¼ HCO3- ÀçÈí¼ö´É Áõ°¡
ECFV contraction & hypochloremia·Î ÀÎÇÏ¿© kidney¿¡¼ Cl-Àº conserveµÈ´Ù.
contracted ECFV with NaCl ¹× K+À» ±³Á¤Çϸé acid-base disorder°¡ ±³Á¤µÈ´Ù.
(2) Renal origin
¨ç diuretics : thiazide, loop diuretics´Â total body bicarbonate content¸¦ º¯È½ÃŰÁö
¾Ê°í ECFVÀ» ±Þ¼ÓÈ÷ °¨¼Ò½ÃŲ´Ù. serum [HCO3-]´Â Áõ°¡µÈ´Ù.
diuretics¸¦ ¸¸¼ºÀûÀ¸·Î Åõ¿©Çϸé distal salt delivery°¡ Áõ°¡ÇÏ¿© alkalosis¸¦ ÀÏÀ¸Å°°í
K+, H+ secretionÀÌ ÀڱصȴÙ.
ECFV contraction, secondary hyperaldosteronism, K+ deficiency ¹× diureticsÀÇ
direct effect¿¡ ÀÇÇÏ¿© alkalosis°¡ Áö¼ÓµÈ´Ù.
isotonic salineÀ¸·Î ECFV deficit¸¦ ±³Á¤Çϸé alkalosis°¡ ±³Á¤µÈ´Ù.
¨è Bartter's syndrome & Gitelman's syndrome -> chap 276
¨é nonreabsorbable anions and Mg deficiency
penicillin or carbenillin°°ÀÌ ÀçÈí¼öµÇÁö ¾Ê´Â anionÀ» ´Ù·® Åõ¿©Çϸé transepithelial
potential difference°¡ Áõ°¡(lumen negative)ÇÏ¿© distal acidification & K+ secretionÀÌ
Áõ°¡µÉ¼ö ÀÖ´Ù.
Mg deficiency´Â renin, aldosterone secretionÀ» ÀÚ±ØÇÔÀ¸·Î½á distal acidificationÀ»
Áõ°¡½ÃÄÑ hypokalemic alkalosis°¡ ÃÊ·¡µÈ´Ù.
¨ê K+ depletion
chronic K+ depletionÀº urinary acid excretionÀ» Áõ°¡½ÃÅ´À¸·Î½á metabolic alkalosis¸¦
ÀÏÀ¸Å²´Ù. NH4+ production & absorptionµÑ´Ù Áõ°¡µÇ°í HCO3- reabsorptionÀÌ ÀÚ±Ø
µÈ´Ù.
K+ deficiency¸¦ ±³Á¤Çϸé alkalosis°¡ ±³Á¤µÈ´Ù.
¨ë lactic acidosis or ketoacidosisÄ¡·áÈÄ
¨ì posthypercapnia
¸¸¼ºÀûÀ¸·Î CO2 retentionµÇ¸é renal HCO3- absorption & new HCO3- »ý»êÀÌ Áõ°¡µÈ´Ù
°©ÀÚ±â PaCO2¸¦ Á¤»óȽÃ۸é Áö¼ÓÀûÀ¸·Î Áõ°¡µÇ¾î ÀÖ´ø [HCO3-] ¶§¹®¿¡ metabolic
alkalosis°¡ ÃÊ·¡µÈ´Ù.
4) metabolic alkalosis + ECFV expansion, hypertension & hyperaldosteronism
mineralocorticoid Åõ¿© ȤÀº °ú´Ù»ý»ê(primary aldosteronism, adrenal cortical enzyme
deficiency)
-> salt retention(-> ECFV expansion, hypertensionÃÊ·¡)
kaliuresis(-> continured K+ depletion with polydipsia, polyuriaÃÊ·¡)
net acid excretionÀÌ Áõ°¡µÇ°í K+ deficiency¿¡ ÀÇÇØ metabolic alkalosisÃÊ·¡
* Liddle's syndrome: collecting duct Na+ channel(ENaC)ÀÇ acitivtyÁõ°¡·Î ÀÎÇÏ¿©
volume expansion¿¡ ÀÇÇÑ hypertensionÀÌ µ¿¹ÝµÇ´Â µå¹® inherited disorder
hypokalemic alkalosis & normal aldosterone level
* Áõ»ó: metabolic alkalosis·Î ÀÎÇÏ¿© CNS & PNS function¿¡ º¯È°¡ »ý±â´Âµ¥ ÀÌ´Â
hypocalcemia¶§ÀÇ Áõ»ó°ú À¯»çÇÏ´Ù.
mental confusion, obtundation, predisposition to seizure, paresthesia, muscular
cramping, tetany, aggrevation of arrhythmia, and hypoxemia in COPD
5. Respiratory acidosis Tab 50-5
chronic respiratory acidosis(24hr)¶§ renal adaptationÀº PaCO2°¡ 10 mmHg°¡ Áõ°¡ÇÔ¿¡
µû¶ó [HCO3-]´Â 4 mmol/L°¡ Áõ°¡ÇÑ´Ù. ±×·¯³ª serum HCO3-´Â 38 mmol/LÀÌ»óÀ¸·Î Áõ°¡
ÇÏÁö´Â ¾Ê´Â´Ù.