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ACID BASEDISORDERS
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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.
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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
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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.
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Regulation of pH
Respiratory regulationRenal regulation
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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).
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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
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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
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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.
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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
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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)
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Acid base disorders
Respiratory acidosisMetabolic acidosisRespiratory alkalosisMetabolic alkalosis
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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.
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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)
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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.
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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
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Metabolic alkalosis
Exogenous base intakeHCO3 containing IV fluid therapyMassive blood transfusion (sodium citrate
overload)Antacids in case of peptic ulcer or hyperacidity
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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)
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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.
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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
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Respiratory acidosis
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)
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Compensatory mechanisms
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) .
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Respiratory alkalosis
CausesIncrease rate and depth of respiration excessive elimination of co2
Non pulmonary stimulation of respiratory centreAnxiety
Febrile statesSepticemiaHypoxiaHyperthyroidism
Pulmonary disorders
PneumoniaAsthmaCCFPulmonary emboli
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Respiratory alkalosis
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)
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Compensatory mechanisms
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) .
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Assessment of acid basestatus
Check pH
Low (<7.35) High (>7.45)
Acidaemia
Alkalaemia
LowHCO3
HighPCO2
Metabolicacidosis
Respiratory acidosis
HighHCO3
LowPCO2
Metabolicalkalosis
Respiratory alkalosis