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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־´Â 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» ¾ÇÈ­½ÃŰ¹Ç·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¸¦ ¾ÇÈ­½Ãų¼ö

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¸¦ ¾ÇÈ­½Ãų¼ö 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¿© ¾ÇÈ­µÉ¼ö 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 urineÀ̸鼭 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¤»óÈ­½Ã۸é 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.