DEPARTMENT OFANESTHESIOLOGYJJMMC, DAVANGERE.SEMINAR ON ACID BASE BALANCE AND ABG ANALYSISCHAIR PERSON PRESENTED BYDr.RAVI....
Over view1. Basics concepts2. History ;approaches3. Acid base disorders &regulation4. Treatment5. interpretation
In pure water at 25°C, the [H+] and [OH-] are 1 × 10-7mmol/L.A solution is considered acidic if the concentration ofhydrog...
• pH -the negative logarithm of the hydrogenion concentration• pH for pure water is 7.0• Physiologic pH, for the ECF, is 7...
• A substance is an acid if, when added to asolution, it brings about an increase in thehydrogen ion concentration of the ...
• Consequently, strong cations—Na+, K+, Ca2+,Mg2+—act as Arrhenius bases (because theydrive hydroxyl out of, and hydrogen ...
• Bicarbonate• Haemoglobin• Plasma proteins• PhosphateMinimise the change in pHBUFFER
• tools that have evolved over the past 50years• None are entirely accurate, and each has adedicated group of followers• T...
Carbon Dioxide–Bicarbonate(Boston) Approach
• Siggard Andersen developed the concept basedeficit/excess• Base deficit/excess : Defined as the amountof strong acid or ...
• proposed ―whole-blood buffer base‖• The sum of the bicarbonate and thenonvolatile buffer ions(serum albumin, phosphate, ...
Acid-base nomogram using the Copenhagenapproach (Crit Care Med26:1173-1179,1998)
• Developed by Emmett and Narins• Anion gap = [Na+ + K+ - (Cl- + HCO3-)]• Sum of the difference in charge of thecommon ext...
Concept of anion gap
• Most critically ill patients arehypoalbuminemic, and many are alsohypophosphatemic• Consequently, the gap may be normal ...
• Electric neutrality• Dissociation equilibriums• Mass conservationDetermined the hydrogen ion concentration ofECF , by ap...
• Small advance from the ―anion gap‖ approach• Proposed ―SIG‖• SIG = Apparent SID –Effective SID(UMA)• Normal ―SIG‖ is 8 ±...
―ANION GAP‖ Vs ―SIG‖
• The strong ion difference (SID)• The total concentration of weak acids (ATOT).• The PaCO2Only three factors independentl...
• ([Na+] – [Cl-]) + ([H+] – [OH-]) = 0• [H+] = √Kw‘ +([Na+] – [Cl-])2 /4-([Na+] –[Cl-]) /2• [OH-] = √Kw‘ +([Na+] – [Cl-])2...
• The sum total of the charges imparted by strongcations minus the charges from strong anions.• SID=([Na+]+[K+]+[Ca2+]+[Mg...
Effect of changes in SID on hydrogen and hydroxyl ionconcentration. ( Can J Physiol Pharmacol 61:1444-1461, 1983.)
• weak acids are partially dissociatedcompounds• Albumin and phosphate• Stewart used the term ―ATOT‖ to represent thetotal...
• Exists in four forms: CO2 [dissolved CO2(d)],carbonic acid (H2CO3), bicarbonate ions(HCO3-), and carbonate ions (CO32-)....
LAWS EQUATIONSWater dissociation equilibrium [H+] × [OH-] = Kw‘Weak acid dissociation equilibrium [H+] × [A-] = KA × [HA]C...
• [ SID ] + [ H+ ] – KC ×PC/[H+] – KA - [ATOT]/(KA +[H+]) –K × KCPC/[H+]2 – KW‘/[H+] =0• [ H+ ] is a function of SID, ATOT...
• Alterations in arterial carbon dioxide (PaCO2)tension—respiratory acidosis or alkalosis• Alterations in blood chemistry—...
Terminology of Acid-BaseDisordersThe definitions of the terms used to describe acid-base disorders are suggested by the Ad...
• neurologic injury (e.g., stroke, spinal cordinjury, botulism, tetanus)• toxic suppression of the respiratory center(e.g....
• anxiety, central respiratory stimulation (asoccurs early in salicylate poisoning)• excessive artificial ventilationAcute...
• Respiratory acidosis : narcosis, incompletereversal of neuromuscular blockade• Respiratory alkalosis : anxiety• Metaboli...
• hypoalbuminemia (imp)• metabolic alkalosis that can mask significant lacticacidemia• Mechanical ventilation increases th...
• Respiratory acidosis occurs when there is anacute increase in PaCO2 principally resultingfrom respiratory failure• Cyano...
• Associated with alterations in transcellularion pumps and increased ionized calcium• Vasodilation, diminished muscularpe...
• In dysoxia and states of severe stress, lactateis produced• In diabetic-ketoacidosis—β-hydroxybutyrateand acetoacetate—a...
• In dilutional & hyperchloremic acidosisrelative ratio of cations to anionsdecreases(relative increase of anions).• In co...
• Hypoalbuminemia decreases ATOT, increasesSID and is associated with metabolicalkalosis.• SID=([Na+]+[K+]+[Ca2+]+[Mg2+]) ...
Abnormalities Acidosis AlkalosisRespiratory Increased PCO2 Decreased PCO2MetabolicAbnormal SIDCaused by waterexcess or def...
• The major source of acid in the body is CO2• Excreted by the lungs• Only 20 to 70 mEq of hydrogen ions areexcreted throu...
• Once Hemoglobin, becomes overwhelmedKidney excretes an increased chloride loadusing NH4+, a weak cation, forelectrochemi...
• Metabolic acid is buffered principally byincreased alveolar ventilation ,bicarbonate(imp), plasma proteins &phosphate• c...
CompensationA patient can be uncompensated, partiallycompensated, or fully compensatedWhen an acid-base disorder is either...
Correct Terminology forCompensatory ResponsesAccording to the Ad-Hoc Committee , Secondaryor compensatory responses should...
• Lactic acidosis is treated with volumeresuscitation and source control.• Diabetic ketoacidosis is treated with volumeres...
• A severe deficit (HCO3- < 10-12 mEq/L and pH<7.2)should be corrected with sodium bicarbonate• Useful if the acidosis is ...
• Key to managing acid-base disturbances liesnot in altering acid-base balance, but ratherin correcting the underlying def...
• Treat the primary cause.• Potassium and magnesium should bereplaced.• Dilute hydrochloric acid can be given orallyor int...
• Increase alveolar ventilation.• Associated hypophosphatemia should bemonitored.RESPIRATORY ALKALOSIS• Decrease in alveol...
How to take an ABG Sample?1. Site of puncture2. Equipment required3. Expel air bubbles4. Keep sample in ice5. Patient‘s in...
• pH = 7.36 to 7.44• PCO2 = 36 to 44 mmHg• HCO3 = 22 to 26 mEq/L• PaO2 = 80 to 100 mmHg• SaO2 = 94 to 100 %• Base excess =...
• Stage I: Identify the Primary Acid-Base Disorder• Rule 1: An acid-base abnormality is present if eitherthe PaCO2 or the ...
• Rule 3: If either the pH or PaCO2 is normal, thereis a mixed metabolic and respiratory acid-basedisorder (one is an acid...
• Metabolic acidosisExpected PaCO2 = (1.5 × HCO3) + (8 ± 2)• Metabolic AlkalosisExpected PaCO2 = (0.7 × HCO3) + (21 ± 2)St...
Disorder Acute ChronicResp. Acidosis pH decreases by 0.08HCO3- increases by 1pH decreases by 0.03HCO3- increases by 4Resp....
• Rule 4: If there is a primary metabolic acidosis oralkalosis, use the measured serum bicarbonateconcentration to identif...
• Example: Consider a patient with a PaCO2 of 23mm Hg and a pH of 7.547.40 + [0.008 × (40 - 23)] =7.54acute respiratory al...
• The anion gap helps to classify met.acidosis• The normal value is 12 ± 4 mEq/L• High AG : lactic,ketoacidosis,ESRF,metha...
• High AG metabolic acidosis, the gap-gap (AGExcess/HCO3 deficit) ratio is unity (=1)• Hyperchloremic acidosis, the ratio ...
• CASE 1: A 20 year old man is brought to theemergency room with a history of consumption ofa bottle of pills.• pH = 7.35•...
• Step 2: Evaluate the PaCO2 and narrow down toone definitive processPaCO2 < 40 mmHg ( metabolicacidosis is present)• Step...
• Step 4: Determine if any other processes arepresentThe actual PaCO2 is less than the predicted Respiratory alkalosisDia...
• A 44 year old moderately dehydrated man wasadmitted with a two day history of acute severediarrhea. Electrolyte results:...
• Look at the pH.The pH is low, (less than 7.35) therefore bydefinition, patient is acidemic.• pH & pCO2 change in same di...
• Calculate the anion gapThe anion gap is Na - (Cl + HCO3-) = 134 -(108+ 16) = 10Since gap is less than 16, it is therefor...
• 1) Is the "pH― normal?• 2) Is the "CO2― normal?• 3) Is the "HCO3― normal?• 4) Apply ―ROME‖• 5) Look for compensation• 6)...
• pH normal, PCO2 increased• Mixed disorder.• Primary Respiratory acidosis• Compensatory response?• 7.4 – (0.003×20)• [HCO...
• Conclusion• The use of physical chemistry principles permits abetter explanation of acid-base balance andprovides tools ...
• Miller‘s anesthesia 7th edition• The ICU book 3rd edition Paul L Marino• A practice of Anesthesia 7th edition Wylie• Lee...
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Acid base balance & ABG interpretation,Dept of anesthesiology,JJMMC,Davangere

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Acid base balance and ABG interpretation presented by Dr.Gopan.G,Post-Graduate student. Chairperson : Dr.Ravi.R,Professor, Department of Anaesthesiology & Critical care,JJMMC,Davangere.

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Acid base balance & ABG interpretation,Dept of anesthesiology,JJMMC,Davangere

  1. 1. DEPARTMENT OFANESTHESIOLOGYJJMMC, DAVANGERE.SEMINAR ON ACID BASE BALANCE AND ABG ANALYSISCHAIR PERSON PRESENTED BYDr.RAVI.R Dr.GOPAN.GPROFESSORDATE:14-6-2013
  2. 2. Over view1. Basics concepts2. History ;approaches3. Acid base disorders &regulation4. Treatment5. interpretation
  3. 3. In pure water at 25°C, the [H+] and [OH-] are 1 × 10-7mmol/L.A solution is considered acidic if the concentration ofhydrogen ions exceeds that of hydroxyl ions.A solution is considered alkaline if the hydroxyl ionconcentration exceeds the hydrogen ion concentration.H2O ↔ H+ + OH-Basic conceptsPhysical Chemistry of Water
  4. 4. • pH -the negative logarithm of the hydrogenion concentration• pH for pure water is 7.0• Physiologic pH, for the ECF, is 7.4, which isalkaline.• Henderson Hasselbalch equation :pH = pK + log [HCO3-]/αPaCO2Cont‘dBASIC CONCEPTS
  5. 5. • A substance is an acid if, when added to asolution, it brings about an increase in thehydrogen ion concentration of the solution• A substance is a base if, when added to asolution, it brings about a decrease in thehydrogen ion concentration of the solutionDefinitions: Acid & Base
  6. 6. • Consequently, strong cations—Na+, K+, Ca2+,Mg2+—act as Arrhenius bases (because theydrive hydroxyl out of, and hydrogen into,solution, to maintain electric neutrality)• Strong anions—Cl-, LA-, ketones, sulfate andformate—act as Arrhenius acids
  7. 7. • Bicarbonate• Haemoglobin• Plasma proteins• PhosphateMinimise the change in pHBUFFER
  8. 8. • tools that have evolved over the past 50years• None are entirely accurate, and each has adedicated group of followers• Textbooks and clinical practice have tendedto overestimate the importance of isolatedchanges in hydrogen or bicarbonate ionconcentration• Clinical significance of acid-base balance isdetermined by the underlying cause, ratherthan the serum concentration of hydrogenand hydroxyl ionsAnalytic Tools Used in Acid-BaseChemistry
  9. 9. Carbon Dioxide–Bicarbonate(Boston) Approach
  10. 10. • Siggard Andersen developed the concept basedeficit/excess• Base deficit/excess : Defined as the amountof strong acid or base required to return pHto 7.4, assuming a PCO2 of 40 mm Hg andtemperature of 38°C• Current algorithms for computing thestandardized base excess (BE for ECF) arederived from the Van Slyke equation• SBE = 0.9287 [HCO3- - 24.4 + (PH – 7.4)]• Ref:Miller‘s anesthesia 7th edition Pg:1564Base Deficit/Excess (Copenhagen)Approach
  11. 11. • proposed ―whole-blood buffer base‖• The sum of the bicarbonate and thenonvolatile buffer ions(serum albumin, phosphate, and hemoglobin)• [Na+] + [K+] - [Cl-] = 48-49 mmol/L• Buffer base increases in metabolic alkalosisand decreases in metabolic acidosis.Cont‘d
  12. 12. Acid-base nomogram using the Copenhagenapproach (Crit Care Med26:1173-1179,1998)
  13. 13. • Developed by Emmett and Narins• Anion gap = [Na+ + K+ - (Cl- + HCO3-)]• Sum of the difference in charge of thecommon extracellular ions reveals anunaccounted for ―gap‖ of -10 to -12 mEq/L• Anion gap is based on the law of electricneutralityAnion Gap Approach
  14. 14. Concept of anion gap
  15. 15. • Most critically ill patients arehypoalbuminemic, and many are alsohypophosphatemic• Consequently, the gap may be normal in thepresence of unmeasured anions• Anion gap corrected for albumin = calculatedanion gap + 2.5 ( Normal albumin in gm/dL –observed albumin in gm/dL )• Second weakness with this approach is theuse of bicarbonate in the equationFailure of Anion-Gap approach
  16. 16. • Electric neutrality• Dissociation equilibriums• Mass conservationDetermined the hydrogen ion concentration ofECF , by applying laws of :Stewart Approach
  17. 17. • Small advance from the ―anion gap‖ approach• Proposed ―SIG‖• SIG = Apparent SID –Effective SID(UMA)• Normal ―SIG‖ is 8 ± 2 mEq/L• Apparent SID = ([Na+]+ [K+]+ [Mg2+]+[Ca2+]) - [Cl-])• Effective SID = [HCO3-] + [charge onalbumin] + [charge on Pi]Stewart-Fencl Approach
  18. 18. ―ANION GAP‖ Vs ―SIG‖
  19. 19. • The strong ion difference (SID)• The total concentration of weak acids (ATOT).• The PaCO2Only three factors independentlyaffect acid-base balance
  20. 20. • ([Na+] – [Cl-]) + ([H+] – [OH-]) = 0• [H+] = √Kw‘ +([Na+] – [Cl-])2 /4-([Na+] –[Cl-]) /2• [OH-] = √Kw‘ +([Na+] – [Cl-])2 /4-([Na+] –[Cl-]) /2• hydrogen and hydroxyl concentrations aredetermined by the KW′ and the difference incharge between sodium and chloride• Dissociate completely.• Strong ions in the ECF areNa+,K+,Mg2+,Ca2+,SO42- and Cl-STRONG ANIONS
  21. 21. • The sum total of the charges imparted by strongcations minus the charges from strong anions.• SID=([Na+]+[K+]+[Ca2+]+[Mg2+]) – ([Cl-]+[A-])=40-44 mEq(1)STRONG ION DIFFERENCE
  22. 22. Effect of changes in SID on hydrogen and hydroxyl ionconcentration. ( Can J Physiol Pharmacol 61:1444-1461, 1983.)
  23. 23. • weak acids are partially dissociatedcompounds• Albumin and phosphate• Stewart used the term ―ATOT‖ to represent thetotal concentration of weak anions(2)Weak Acid ―Buffer‖ Solutions
  24. 24. • Exists in four forms: CO2 [dissolved CO2(d)],carbonic acid (H2CO3), bicarbonate ions(HCO3-), and carbonate ions (CO32-).• The concentration of CO2 in ECF is determinedby tissue production and alveolar ventilation.• As CO2 increases HCO3- also increases.(3)Carbon Dioxide
  25. 25. LAWS EQUATIONSWater dissociation equilibrium [H+] × [OH-] = Kw‘Weak acid dissociation equilibrium [H+] × [A-] = KA × [HA]Conservation of mass for weakacids[HA] + [A-] = [ATOT]Bicarbonate ion formationequilibrium[H+] × [HCO3-] = KC × PCO2Carbonate ion formationequilibrium[H+] × [CO32-] = K × [HCO3-]Electric neutrality [SID] + [H+] - [HCO3-] - [A-] -[CO32-] - [OH-] = 0Stewart combined six derivedequations to solve for [H+]:
  26. 26. • [ SID ] + [ H+ ] – KC ×PC/[H+] – KA - [ATOT]/(KA +[H+]) –K × KCPC/[H+]2 – KW‘/[H+] =0• [ H+ ] is a function of SID, ATOT, PCO2• [H+] , [OH-] and [HCO3-] are dependent andcannot independently influence acid-base balanceAlthough the above-listed equations look simple, theyrequire fourth-order polynomials for solution. This isimpossible without computer technology
  27. 27. • Alterations in arterial carbon dioxide (PaCO2)tension—respiratory acidosis or alkalosis• Alterations in blood chemistry—metabolicacidosis or alkalosis.Acid-Base AbnormalitiesClassification
  28. 28. Terminology of Acid-BaseDisordersThe definitions of the terms used to describe acid-base disorders are suggested by the Ad-HocCommittee of the New York Academy of Sciences in1965Simple (Acid-Base) Disorders are those in whichthere is a single primary aetiological acid-basedisorderMixed (acid-Base) Disorders are those in which twoor more primary aetiological disorders are presentsimultaneously.
  29. 29. • neurologic injury (e.g., stroke, spinal cordinjury, botulism, tetanus)• toxic suppression of the respiratory center(e.g., opioids, barbiturates, benzodiazepines)• neuromuscular disorders (e.g., Guillain-Barrésyndrome, myasthenia gravis)• flail chest, hydro-hemo-pneumothorax,pulmonary edema, and pneumonia.Acute respiratory acidosis:Acid-Base Disturbances in theEmergency Setting
  30. 30. • anxiety, central respiratory stimulation (asoccurs early in salicylate poisoning)• excessive artificial ventilationAcute metabolic acidosis• severe diarrhea,renal tubular acidosis• Dilutional acidosis• lactic acidosis, renal acidosis, ketoacidosisAcute respiratory alkalosisCont‘d
  31. 31. • Respiratory acidosis : narcosis, incompletereversal of neuromuscular blockade• Respiratory alkalosis : anxiety• Metabolic acidosis : Hypoperfusion,Hypotonicfluid administration & Hyperchloremia• Metabolic alkalosis : Massive bloodtransfusion & nasogastric suctioningAcid-Base Disturbances CommonlySeen Perioperatively
  32. 32. • hypoalbuminemia (imp)• metabolic alkalosis that can mask significant lacticacidemia• Mechanical ventilation increases the circulating volumeof antidiuretic hormone-dilutional acidosis• Nasogastric suctioning causes chloride loss, diarrhealeads to sodium and potassium loss• Surgical drains placed in tissue beds will remove fluidswith varying electrolyte concentrationsAcid-Base Disturbances in Critical Illness
  33. 33. • Respiratory acidosis occurs when there is anacute increase in PaCO2 principally resultingfrom respiratory failure• Cyanosis, vasodilation, and narcosis• Respiratory alkalosis occurs when there is anacute decrease in PaCO2 as a result ofhyperventilation• Light headedness, visual disturbances,dizziness, and hypocalcemiaRespiratory Acid-BaseAbnormalities
  34. 34. • Associated with alterations in transcellularion pumps and increased ionized calcium• Vasodilation, diminished muscularperformance (particularly myocardial), andarrhythmias• Oxyhemoglobin dissociation curve shiftsrightward to increase oxygen offload into thetissuesMetabolic acidosis
  35. 35. • In dysoxia and states of severe stress, lactateis produced• In diabetic-ketoacidosis—β-hydroxybutyrateand acetoacetate—are produced• In severe renal failure, SO42- and PO43- (―fixedrenal acids‖) are not excreted, causingacidosis• Severe metabolic acidosis is associated withincreased SIG(UMA)METABOLIC ACIDOSIS
  36. 36. • In dilutional & hyperchloremic acidosisrelative ratio of cations to anionsdecreases(relative increase of anions).• In contraction alkalosis relative ratio ofcations to anions increases• Doberer etal : acidosis develops because ofdilution of HCO3- (HCO3- in the blood isa"closed system") without there being adilution of acid in the form of CO2 gas (whichdue to its ability to be exhaled can beconsidered an "open system").Dilutional acidosis , hyperchloremicacidosis and contraction alkalosis
  37. 37. • Hypoalbuminemia decreases ATOT, increasesSID and is associated with metabolicalkalosis.• SID=([Na+]+[K+]+[Ca2+]+[Mg2+]) – ([Cl-]+[A-])• The presence of hypoalbuminemia may maskthe detection of acidosis caused byunmeasured anionsHYPOALBUMINEMIA
  38. 38. Abnormalities Acidosis AlkalosisRespiratory Increased PCO2 Decreased PCO2MetabolicAbnormal SIDCaused by waterexcess or deficitWater excess = dilutional Water deficit = contraction↓ SID +↓[Na+] ↑ SID ↑[Na+]Caused byelectrolytesChloride excess Chloride deficitChloride(measured)↓ SID ↑[Cl-] ↑ SID +↓[Cl-]Other(unmeasured) anions,such as lactate andketo acids↓ SID ↑[UMA-] —Abnormal ATOTAlbumin [Alb] ↑[Alb] (rare) ↓[Alb]Phosphate [Pi] ↑[Pi]Stewart approach for Acid-Base Disturbances
  39. 39. • The major source of acid in the body is CO2• Excreted by the lungs• Only 20 to 70 mEq of hydrogen ions areexcreted through the kidney each day• CO2 is buffered directly by hemoglobin and byplasma proteinsRespiratory failureRegulation of Acid-Base Balance in
  40. 40. • Once Hemoglobin, becomes overwhelmedKidney excretes an increased chloride loadusing NH4+, a weak cation, forelectrochemical balance• ―Metabolic compensation‖Acid base regulation in respiratoryfailure contd
  41. 41. • Metabolic acid is buffered principally byincreased alveolar ventilation ,bicarbonate(imp), plasma proteins &phosphate• coupling of bicarbonate and H2O produces CO2that is excreted through the lungs via anincrease in alveolar ventilation• Chloride is preferentially excreted by thekidneyAcid base regulation in metabolicdisorder
  42. 42. CompensationA patient can be uncompensated, partiallycompensated, or fully compensatedWhen an acid-base disorder is eitheruncompensated or partially compensated, thepH remains outside the normal rangeIn fully compensated states, the pH hasreturned to near normal rangeBody never overcompensates
  43. 43. Correct Terminology forCompensatory ResponsesAccording to the Ad-Hoc Committee , Secondaryor compensatory responses should NOT bedesignated as acidosis or alkalosis.Eg: A patient with diabetic ketoacidosis andcompensatory Kussmaul respirations should bedescribed as having a metabolic acidosis withcompensatory hyperventilation‘The use of the term ‗secondary respiratoryalkalosis‘ in this case would be wrong
  44. 44. • Lactic acidosis is treated with volumeresuscitation and source control.• Diabetic ketoacidosis is treated with volumeresuscitation and insulin.• Renal acidosis is treated with dialysis• Occasionally,treatment with intravenoussodium bicarbonate is necessary• (base excess × weight in kg)÷3METABOLIC ACIDOSISTREATMENT AND CORRECTION
  45. 45. • A severe deficit (HCO3- < 10-12 mEq/L and pH<7.2)should be corrected with sodium bicarbonate• Useful if the acidosis is due to inorganic acids• It is recommended that 50% of total deficit be givenover 3 to 4 hours. 7.5% NaHCO3- contains 0.9 mEq/ml• The usual initial target((desired HCO3- concentration):10 - 12 mEq/L, which should bring the blood pH to~7.20• IV-push administration should be reserved for CPRRef:Koda-Kimble M, Young LY, et al. Handbook of Applied Therapeutics.Lippincott Williams & Wilkins, 2006. P10.3(1104).When and how to correct
  46. 46. • Key to managing acid-base disturbances liesnot in altering acid-base balance, but ratherin correcting the underlying defect• Sodium bicarbonate is administered as an7.5/8.4% hypertonic solution and has aplasma-expanding effect that can lead to adilutional acidosis and increases PaCO2 as well• Over-alkalinization causes decreased affinityof hemoglobin for oxygen leading to tissuehypoxia and lactic acid production ,Sodiumoverload and hypokalemia.Use of sodium bicarbonate bolusesor infusions is controversial
  47. 47. • Treat the primary cause.• Potassium and magnesium should bereplaced.• Dilute hydrochloric acid can be given orallyor intravenously.• Acetazolamide can be considered.METABOLIC ALKALOSISTREATMENT AND CORRECTION
  48. 48. • Increase alveolar ventilation.• Associated hypophosphatemia should bemonitored.RESPIRATORY ALKALOSIS• Decrease in alveolar ventilation• Hypoxaemia is an important cause ofrespiratory alkalosis.• Administration of oxygen in sufficientconcentrations and sufficient amount isessential.RESPIRATORY ACIDOSISTREATMENT AND CORRECTION
  49. 49. How to take an ABG Sample?1. Site of puncture2. Equipment required3. Expel air bubbles4. Keep sample in ice5. Patient‘s inspired oxygenconcentration
  50. 50. • pH = 7.36 to 7.44• PCO2 = 36 to 44 mmHg• HCO3 = 22 to 26 mEq/L• PaO2 = 80 to 100 mmHg• SaO2 = 94 to 100 %• Base excess = -2 to +2 mEq/LNORMAL VALUES
  51. 51. • Stage I: Identify the Primary Acid-Base Disorder• Rule 1: An acid-base abnormality is present if eitherthe PaCO2 or the pH is outside the normal range• Rule 2: If both change in the same direction, theprimary acid-base disorder is metabolic, and if bothchange in opposite directions, the primary acid-basedisorder is respiratory (ROME)• Example: Consider a patient with an arterial pH of 7.23and a PaCO2 of 23 mm Hg• primary metabolic acidosisA Stepwise Approach to Acid-BaseInterpretation
  52. 52. • Rule 3: If either the pH or PaCO2 is normal, thereis a mixed metabolic and respiratory acid-basedisorder (one is an acidosis and the other is analkalosis). If the pH is normal, the direction ofchange in PaCO2 identifies the respiratory disorder,and if the PaCO2 is normal, the direction of changein the pH identifies the metabolic disorder• Example: Consider a patient with an arterial pH of7.4 and a PaCO2 of 55 mm Hg• mixed respiratory acidosis and metabolic alkalosis
  53. 53. • Metabolic acidosisExpected PaCO2 = (1.5 × HCO3) + (8 ± 2)• Metabolic AlkalosisExpected PaCO2 = (0.7 × HCO3) + (21 ± 2)Stage II: Evaluate CompensatoryResponses (winter’s formula)
  54. 54. Disorder Acute ChronicResp. Acidosis pH decreases by 0.08HCO3- increases by 1pH decreases by 0.03HCO3- increases by 4Resp. Alkalosis pH increases by 0.08HCO3- decreases by 2pH increases by 0.03HCO3- decreases by 5Compensation for 10 mmHg change in PaCO2in respiratory disturbances
  55. 55. • Rule 4: If there is a primary metabolic acidosis oralkalosis, use the measured serum bicarbonateconcentration to identify the expected PaCO2• Example: Consider a patient with a PaCO2 of 23mm Hg, an arterial pH of 7.32, and serum HCO3 of15 mEq/L.• (1.5 × 15) + (8 ±2) = 30.5 ± 2 mm Hg.primary metabolic acidosis with a superimposedrespiratory alkalosis
  56. 56. • Example: Consider a patient with a PaCO2 of 23mm Hg and a pH of 7.547.40 + [0.008 × (40 - 23)] =7.54acute respiratory alkalosisIf the measured pH was higher than 7.55a superimposed metabolic alkalosisRule 5: If there is a respiratory acidosis oralkalosis, use the PaCO2 to calculate expected pH
  57. 57. • The anion gap helps to classify met.acidosis• The normal value is 12 ± 4 mEq/L• High AG : lactic,ketoacidosis,ESRF,methanol• Normal AG : diarrhea,saline infusion,RTA• In hypoalbuminemia AG should be correctedANION GAPStage III: Use The “Gaps” to Evaluate MetabolicAcidosis
  58. 58. • High AG metabolic acidosis, the gap-gap (AGExcess/HCO3 deficit) ratio is unity (=1)• Hyperchloremic acidosis, the ratio (AGexcess/∆HCO3 ) falls below unity (< 1)• Therefore, in the presence of a high AGmetabolic acidosis, a ―gap-gap‖ (AGexcess/∆HCO3)ratio of less than 1 indicatesthe co-existence of a normal AG metabolicacidosis• In the presence of a high AG metabolicacidosis, a gap-gap (AG excess/∆HCO3 ) ratioof greater than 1 indicates the co-existence ofa metabolic alkalosis.The “Gap-Gap” ratio
  59. 59. • CASE 1: A 20 year old man is brought to theemergency room with a history of consumption ofa bottle of pills.• pH = 7.35• PaCO2 = 15 mmHg• HCO3- = 8 mmolL-1• Na+ = 140 mmolL-1• K+ = 3.5 mmolL-1• Cl - = 104 mmolL-1• Step 1: Evaluate pH and narrow down to twopossible processes• pH < 7.36  Acidosis (metabolicor respiratory)
  60. 60. • Step 2: Evaluate the PaCO2 and narrow down toone definitive processPaCO2 < 40 mmHg ( metabolicacidosis is present)• Step 3: Apply the formula for metabolic acidosisPredicted PaCO2 = 1.5 (HCO3-) + 8= 20mmHgActual PaCO2 = 15 mmHg
  61. 61. • Step 4: Determine if any other processes arepresentThe actual PaCO2 is less than the predicted Respiratory alkalosisDiagnosis: Mixed metabolic acidosis +Respiratory alkalosis• Step 5: Evaluate anion gapAnion gap = 140 - (104 + 8) = 28 (↑)• Step 6: Evaluate gap-gap ratioDelta gap= (28 - 12) / (24 - 8)= 16/16= 1• Conclusion: Combined high anion gapmetabolic acidosis and Respiratory alkalosis
  62. 62. • A 44 year old moderately dehydrated man wasadmitted with a two day history of acute severediarrhea. Electrolyte results: Na+ 134, K+ 2.9, Cl-108, HCO3- 16, BUN 31, Cr 1.5.• ABG: pH 7.31 pCO2 33 mmHgHCO3 16 pO2 93 mmHg• Based on the clinical scenario, likely acid basedisorders in this patient are:• Normal anion gap acidosis from diarrhea or• Elevated anion gap acidosis secondary to lacticacidosis as a result of hypovolumia and poorperfusion.Case 2
  63. 63. • Look at the pH.The pH is low, (less than 7.35) therefore bydefinition, patient is acidemic.• pH & pCO2 change in same direction(decrease)-metabolic acidosis• Is compensation adequate?• Calculate the estimated PCO2.Using Winters formula; PCO2 = 1.5 × [HCO3-]+8 ± 2 = 1.5 ×16 + 8 ± 2 = 30-34.
  64. 64. • Calculate the anion gapThe anion gap is Na - (Cl + HCO3-) = 134 -(108+ 16) = 10Since gap is less than 16, it is therefore normal• Since the actual PCO2 falls within the estimatedrange, we can deduce that the compensation isadequate and there is no seperate respiratorydisorder present.• Assessment: Normal anion gap acidosis withadequate compensation most likely secondary tosevere diarrhea.
  65. 65. • 1) Is the "pH― normal?• 2) Is the "CO2― normal?• 3) Is the "HCO3― normal?• 4) Apply ―ROME‖• 5) Look for compensation• 6) Are the "pO2― and the "O2― saturation normal?The 6‗ Easy Steps toABGAnalysis
  66. 66. • pH normal, PCO2 increased• Mixed disorder.• Primary Respiratory acidosis• Compensatory response?• 7.4 – (0.003×20)• [HCO3-] to be increased by 4• Respiratory acidosis withmetabolic alkalosis
  67. 67. • Conclusion• The use of physical chemistry principles permits abetter explanation of acid-base balance andprovides tools to apply to a wide variety of clinicalsituations. This does not suggest that the―traditional‖ approach is incorrect. There iscurrently no clear strategy to determine which ofthe ‗modern‘ approaches, the Stewart approach orthe bicarbonate-centred approach , is the correctone.
  68. 68. • Miller‘s anesthesia 7th edition• The ICU book 3rd edition Paul L Marino• A practice of Anesthesia 7th edition Wylie• Lee‘s synopsis of Anaesthesia 13th edition• Anaesthesia CME programme 2011 Mysuru• A simple guide to blood gas analysis PeterDriscoll• www.acid-base.com• www.acidbasedissorders.comBibliography

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