Acid Base Disorders 11-3-11

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ACID BASEDISORDERS



Definitions

Acids are chemical substances that candonate protons (H ions) in solution.Bases are substances that accept protons.

pH of solution is defined as negative logarithmof the hydrogen ion activity.

pH= -log HDecrease of one pH unit represents ten foldincrease in H ion activity.



Buffer is a substance (usually a weak acid and itsbase) that is able to release or take up H ions tominimize any changes in H ion concentration.

Buffers minimize changes in pH but do notremove acid from bodyH+ + HCO 3

- H2CO 3 ECF Buffer: HCO 3 is the most important buffer in

the ECF. HCO 3 buffers H+

to generate water andCo 2 that is excreted by alveolar ventilation.HCO 3

- + H + H2O + CO 2



ICF Buffer: theses comprise variousintracellular proteins (imidazole group orhistidine),

hemoglobin in erythrocytes (H + + Hb - ),HCO 3

- andPhosphates (HPO 4

-2 + H + H2PO 4- )

Majority of H + is buffered initially bybicarbonate in the extracellular fluid. Otherbuffers are recruited as acid load increases.



Regulation of pH

Respiratory regulationRenal regulation



Respiratory regulation

Decrease plasma pH (increase H ion)stimulation of chemoreceptor's and respiratorycentre hyperventilation occurs

plasma pCo 2 decreases decreaseH2CO3 (Ph normalizes).H+ + HCO 3

- H2CO 3 H2O + CO 2

Increase plasma pH (decrease H ion)depression of respiratory centrehypoventilation occur plasmapCo 2 increases (pH normalizes).



Renal regulation

Renal excretion of acid and conservation ofHCO 3 occur through several mechanismsincluding

The Na-H exchangeProduction of ammonia and excretion of NH 4

+

Recovery of HCO 3



Na-H exchange

In renal tubules Na-H exchangers extrude Hion into tubular fluid in exchange for Na ions.Na-H exchange is

Enhanced in case of acidosisInhibited in alkalotic states



Renal production of ammoniaand excretion of ammonium ions

Glutamine and other amino acids convert intoammonia.Ammonia (NH 3) is a gas and diffuses readilyacross cell membrane into tubular lumen.In case of acidosis (increase H ions)

NH3 + H + NH4+

NH4+ formed can not easily cross back throughcell membrane of tubular lumen and thusexcreted through urine.



Excretion of H + as H 2PO 4(Phosphate buffer)

In case of acidosis (Excess H + )Increase Na-H exchange increase H intotubular lumen H + HPO 4

-2 H2PO 4-

excretion thru urine



Recovery of filtered HCO 3

Glomerular filtrate has the same concentrationof HCO 3 as does plasma.In case of acidosis (excess H ion):

Increase Na-H exchange increase H intotubular lumen H + + HCO 3-

H2CO 3 CO 2 + H 2O.CO 2 diffuses into the proximal tubular cells

CO 2 + H 2O H 2CO 3 H + HCO 3H+ ions excreted in urine buffered by phosphateand ammonia while HCO 3 enters in circulation (pH normalizes)



Acid base disorders

Respiratory acidosisMetabolic acidosisRespiratory alkalosisMetabolic alkalosis



Metabolic acidosis

CausesProduction of organic acids that exceeds the rateof elimination (production of acetoacetic acid and

beta hydroxy butyric acid in diabetic acidosis and of lactic acid in lactic acidosis ).Reduced excretion of acids H ion ( occurs in renalfailure and some renal tubular acidosis).

Excessive loss of HCO3Excessive loss of duodenal fluid ( as in diarrhea).Pancreatic, intestinal and biliary fistulae or drainage.



Metabolic acidosis

When any of this condition existRatio of HCO3/CO2 decreases because ofprimary decrease in HCO3

Resulting pH will be droppedMeasured by

Low pH

Low HCO3Low PCO2 (Compensatory phenomena)



Compensatory mechanisms formetabolic acidosis

Respiratory mechanism:Decrease pH stimulation of respiratory centre

hyperventilation(kussmaul respiration)

Decrease PCO 2 decrease H 2CO 3 (pHnormalizes) .

Renal mechanism:Increase Na-H exchange rate increase

ammonia formation increase H lossIncrease HCO3 re-absorption.



Metabolic alkalosis

CausesLoss of acid (H ion)

Vomiting , pyloric or upper doudenal obstruction: loss

of HClRenal loss of H ion : Excess aldosteroneincrease Na H exchange in kidney Na retention,H excretion

Cushing’s syndrome: excess corticosteroid have somemineralocorticoid effects

Retention of baseUse of diuretics : increase loss of water in ECS whichis poor in bicarbonate increase preservation ofHCO3



Metabolic alkalosis

Exogenous base intakeHCO3 containing IV fluid therapyMassive blood transfusion (sodium citrate

overload)Antacids in case of peptic ulcer or hyperacidity



Metabolic alkalosis

When any of this condition existRatio of HCO3/CO2 increases because ofprimary excess in HCO3

Resulting pH will be increasedMeasured by

High pH

High HCO3High PCO2 (Compensatory phenomena)



Compensatory mechanisms

Respiratory mechanism:Increase pH depression of respiratorycentre

hypoventilation increase PCO2Increase H2CO3 (pH normalizes) .

Renal mechanism:Decrease Na-H exchange rate decreaseammonia formation decrease H lossdecrease HCO3 reclamation.



Respiratory acidosis

CausesDirect depression of respiratory centre

Drugs: narcotics, barbituratesCNS trauma, tumor and degenerative disordersCNS infections: encephalitis, meningitisCVA: Intracranial hemorrhage

Conditions affect respiratory apparatusCOPDPulmonary fibrosisARDSChest wall disease and deformities




When any of this condition existRatio of HCO3/CO2 decreases because ofprimary excess in CO2

Resulting pH will be decreasedMeasured by

Decrease pH

High PCO2High HCO3 (Compensatory phenomena)




Buffer system:By hemoglobin and protein buffer system

Renal mechanism:

Increase Na-H exchange rate increaseammonia formation increase H lossIncrease HCO3 re-absorption.

Respiratory mechanism:Decrease pH stimulation of respiratory centre

hyperventilation(kussmaul respiration)Decrease PCO2 decrease H2CO3 (pHnormalizes) .



Respiratory alkalosis

CausesIncrease rate and depth of respiration excessive elimination of co2

Non pulmonary stimulation of respiratory centreAnxiety

Febrile statesSepticemiaHypoxiaHyperthyroidism

Pulmonary disorders

PneumoniaAsthmaCCFPulmonary emboli




When any of this condition existRatio of HCO3/CO2 increases because ofexcessive elimination of CO2

Resulting pH will be increasedMeasured by

High pH

Low PCO2Low HCO3 (Compensatory phenomena)




Buffer system:Erythrocytes and tissue buffers

Renal mechanism:

Decrease Na-H exchange rate decreaseammonia formation decrease H lossdecrease HCO3 reclamation.

Respiratory mechanism:Increase pH depression of respiratorycentre

hypoventilation increase PCO2Increase H2CO3 (pH normalizes) .



Assessment of acid basestatus

Check pH

Low (<7.35) High (>7.45)

Acidaemia

Alkalaemia

LowHCO3

HighPCO2

Metabolicacidosis


HighHCO3

LowPCO2

Metabolicalkalosis


Acid Base Disorders 11-3-11

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