A. KazdaA. Kazda

Graph of acidGraph of acid--base regulationbase regulationGraph of acidGraph of acid--base regulationbase regulation

Graf acidobazické regulace (M. Engliš, Prakt. lék. 1972)Graf acidobazické regulace (M. Engliš, Prakt. lék. 1972)

buffersbuffers acid acid basebase % relative% relative present in present in

hydrogenhydrogen--carboniccarbonic HH22COCO33 HCOHCO--33 5151 plasmaplasma

Buffer system in bloodBuffer system in blood

hydrogenhydrogen--carboniccarbonic HH22COCO33 HCOHCO 33 5151 plasmaplasma

hemoglobinhemoglobin oxyhemoglobinoxyhemoglobin deoxyhemoglobindeoxyhemoglobin 3535 erytrocyteserytrocytes

phosphatesphosphates HH22POPO--44 HPOHPO22--

44 77erytrocyteserytrocytes

(plasma)(plasma)

proteinsproteins --COOHCOOH --COOCOO-- 77plasmaplasma

(erytrocytes)(erytrocytes)

HendersonHenderson--HasselbachHasselbach''s equation:s equation:[base][base]

pH = pK + log pH = pK + log

[acid][acid]

HendersonHenderson--HasselbachHasselbach''s equations equation::

[HCO[HCO--33]]

pH = pK + log pH = pK + log

[H[H22COCO33]][H[H22COCO33]]

Carbonic acid concentration can be expressed as a function of pCOCarbonic acid concentration can be expressed as a function of pCO22

[HCO[HCO--33]]

pH = pK + log pH = pK + log

αα . pCO. pCO22

αα = coeficient of solubility of CO= coeficient of solubility of CO22, 0,0306 mol, 0,0306 mol--1111--11torrtorr--11, tj. 0,2295 mol, tj. 0,2295 mol--1111--11kPakPa--11

pK = approximately 6,1 pK = approximately 6,1

tissues COtissues CO22 COCO22 lunglung

COCO22 + H+ H22OO (800)(800)

↕↕

HH22COCO33 (1)(1)

↕↕

HH++ + HCO+ HCO--33 (0,03)(0,03)

Interaction reactionInteraction reaction

HCOHCO--33 HH22COCO33

HH++HH++

Buf HBufBuf HBuf

Retention of CORetention of CO22

HCOHCO--33 HH22COCO33 ← CO← CO22 + H+ H22OO

HH++

Buf HBufBuf HBuf

METABOLIC ACID-BASE DISTURBANCES AND THEIR CLINICAL REASONS

AFTER STEWART

Diagnosis Clinical cause

dilutional acidosis

concentrational alkalosis

hyperchloremic acidosis

every cause of hyponatremia

every cause of hypernatremia

infusions rich in chloridediarrheatubular dysfunction during acute or

hypochloremic alkalosis

acidosis from elevation of UA

hyperphosphatemic acidosis

hypoalbuminemic alkalosis

tubular dysfunction during acute orchronic renal failurecompensation of chronic RAL

loss of gastric juicediureticscompensation of chronic RAC

uremia, ketoacidosis, lacticacidosis, intoxications (salicilates,methanol, ethanol)

every cause of hyperphosphatemia(renal failure)

hepatic insufficiency, malnutrition,

nephrotic sd, burns

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