acid base balance3

7/28/2019 Acid Base Balance3

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Acid-Base Balance


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acid-base balance- general -

acid any molecule that dissociates in solution to release a

hydrogen iron (H+) or proton

base any molecule capable of accepting a hydrogen iron

or proton


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acid-base balancebuffer system - general -

buffer : any substance that can reversiblybind hydrogen irons

Buffer + H+ HBuffer


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acid-base balancebuffer system - general -

three (3) primary systems regulating H+concentration in body fluids

1) chemical acid-base buffer systems of bodyfluids.

2) respiratory center (regulating removal ofCO2)

3) kidneys (excreting acid and alkaline urine)

buffer : any substance that can reversiby

bind hydrogen irons

Buffer + H+ HBuffer


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acid-base balancebuffer system -

1) acid-base buffer systems

a. bicarbonate buffer

HCO3- + H+ H2CO3 CO2 + H2O

H+ + HCO3- H2CO3 CO2 + H2O

excess CO2 will stimulate respiration

elimination of CO2


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acid-base balance- bicarbonate buffer -

H+ = K xCO2

HCO3-

most clinical labs measure blood CO2 tension (Pco2)amount of CO2 in blood is a linear function of Pco2

CO2 = (0.03) x Pco2

H+ = K xHCO3

-

(0.03 )x Pco2


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pH = - log H+

pH = pK -HCO3

-(0.03 )x Pco2log

pH = pK + HCO3-

(0.03 )x Pco2log

metabolic factor

respiratory factor


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pH = pK +HCO3

-

(0.03 )x Pco2log

Pco2 35 45 mmHg

HCO3- 20 - 26 mEq/L

increase in bicarbonate pH

increase in Pco2 pH


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1) acid-base buffer systems

b. phosphate buffer

playing a major role in buffering renal tubularfluid and intracellular fluids

HCl + Na2HPO4 NaH2PO4 + NaCl

NaCl + Na2H2PO4 Na2HPO4 + H2O


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1) acid-base buffer systemsc. proteins

d. - buffer systems within the cells helpto prevent changes in pH of extracellularfluids

e. - may take several hours to become

maximally effective

f. hemoglobin H+ + Hb HHb


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2) respiratory regulation of acid-basebalance- increased hydrogen ion concetration (pH)

stimulates alveolar ventilation

- pulmonary expiration of CO2

balancesmetabolic formation of CO2

- increasing alveolar ventilationdecreases extracellular fluid H+ and pH

[H+] alveolar ventilation

(-) Pco2


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3) renal regulation of pH

body normally consumes more acid-producing foods than base-producing foods

kidney tubules secrete (a) hydrogen, (b)ammonium, and (c) phosphate ions into urine

when a hydrogen ion is secreted into tubular

urine, a sodium ion is simultaneouslyreabsorbed


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H+-sodium exchange

1) rids excess H+ into urine

2) conserves sodium

3) preserves ionic equivalence

4) generates sodium bicarbonate for furtherbuffering


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renal correction

acidosis (1) increased excretion of H+(2) addition of HCO3

- to extracellular

fluid

alkalosis (1) decreased tubular secretion of H+

(2) increased excretion of HCO3-


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clinical causes of acid-base disorders

1. respiratory acidosis [pH, Pco2]

due to: decreased CO2 removal from lungs

causes: a. damage to respiratory centersb. airway obstructionc. pneumonia, chronic bronchitisd. decreased pulmonary membrane

surface area

e. pulmonary edema compensatory mechanism:

(1) body fluid buffers(2) kidneys

pH 7.34, Pco2 60mmHg, [HCO3- 31mEq/L]


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2. respiratory alkalosis [pH, Pco2]

due to: increased loss of CO2 from lungs

causes: a. hyperventilation(i) emotional disturbances(ii) drug overdose

(iii) high altitude (low Po2)

compensatory mechanism:(1) body fluid buffers(2) kidneys

pH 7.50, Pco2 29mmHg, [HCO3- 22mEq/L]


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3. metabolic acidosis [pH, HCO3-]

due to: (1) failure of kidneys to excretemetabolic acids

(2) metabolic production of acids(3) addition of acids to body

(4) loss of bases

causes: (1) renal tubular acidosis

(i) Addisons disease(ii) Fanconis syndrome

(2) chronic renal failure(3) diabetes mellitus

pH 7.20, [Pco2 21mmHg], HCO3- 8mEq/L


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3. metabolic acidosis[pH, HCO3]

causes: (4) acid ingestion(i) aspirin(ii) methanol formic acid

(5) diarrhea(6) vomiting from deeper GI tract

(7) malnutrition(8) starvation

compensatory mechanism:(1) lungs

(2) kidneys



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4. metabolic alkalosis [pH, HCO3-

] due to: (1) excess loss of acid

(2) uptake of alkaline substances causes: (1) diuretics H+ secretion

HCO3-

reabsorption (2) excess aldosterone sodium

reabsorption H+ secretion(3) vomiting of gastric contents(4) ingestion of alkaline drugs (e.g.

antacids)

compensatory mechanism:1 lun s



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systemic effect of alkalosis

alkalosis

overexcitability of central andperipheral nervous system

1) muscle tetany

2) convulsion

3) respiratory arrest death


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clinical measurements and analysis ofacid-base disorders

Step 1: examine pH acidosis (pH 7.4)

Step 2: check Pco2 (nl: 40 mmHg)

HCO3- (nl: 24 mEq/L)

pH Pco2 HCO3-

respiratory acidosis ()

metabolic acidosis ()

respiratory alkalosis ()

metabolic alkalosis ()


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Anion-Gap

total concentration of anions and cations inplasma must be equal to maintain electricalneutrality

but, only certain cation (Na+) and anions (Cl-,HCO3

-) are routinely measured in clinicallaboratory


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Anion-Gap

anion gap : difference between unmeasuredanions and unmeasured cations

Na+

unmeasuredcations

unmeasured

anions

Cl- HCO3-


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Anion-Gap

anion gap = [Na+] {[HCO3

-] + [Cl-]}

= 144 - { 24 + 108}

= 10 mEq/L

Na+

unmeasured

cations

unmeasured

anions

Cl- HCO3-


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Anion-Gap

if unmeasured anions relative amount of Cl- &

HCO3-

anion gap

if unmeasured cation relative amount of Na+

Na+

unmeasured

cations

unmeasured

anions

Cl- HCO3-

albumin, phosphate, sulfate,other organic anions

calcium, magnesium, potassium


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clinical use of anion-gap

Inmetabolic acidosis (low HCO3-)

if plasma Na+ is unchanged,

concentration of anions (Cl- or unmeasured anion)

must increase to maintain electroneutrality(1) if Cl- remains unchanged:

there must be increased unmeasured anion(= anion gap)

a. diabetes mellitus (ketoacidosis)

b. lactic acidosis

c. chronic renal failure

d. aspirin (acetylsalicylic acid)

e. methanol

f. ethylene glycol


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clinical use of anion-gap

(2) if Cl- increases in proportion to the fall of HCO3-:

(normal anion gap)

(hyperchloremic metabolic acidosis)

a. diarrhea

b. renal tubular acidosis

acid base balance3

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