Arterial Blood Gases

Interpretation of arterial blood gases

• Check Machine

• Clinical History

• Oxygenation

• Ventilation

• Acid base status

Is the Machine correct ?Is the Machine correct ?

H x HCO3H x HCO3 = 24 = 24

PCO2PCO2• pH 7.4 H+ = 80 – 40 = 40pH 7.4 H+ = 80 – 40 = 40• pH 7.3 H+ = 80 – 30 = 50pH 7.3 H+ = 80 – 30 = 50• pH 7.5 H+ = 80 – 50 = 30pH 7.5 H+ = 80 – 50 = 30

Clinical HistoryClinical HistoryMetabolic Acidosis – DM, Renal failure, Metabolic Acidosis – DM, Renal failure, muscle over activity, hypotension, diarrhea muscle over activity, hypotension, diarrhea Diamox, Metformin , AlcoholismDiamox, Metformin , Alcoholism

Metabolic Alkalosis – Vomiting, RT Metabolic Alkalosis – Vomiting, RT aspiration, hypovolemia, diuretics, aspiration, hypovolemia, diuretics, hypokalaemia, Bicarb administrationhypokalaemia, Bicarb administration

Respiratory Acidosis – COPD, muscular Respiratory Acidosis – COPD, muscular weakness, post-opweakness, post-op

Respiratory Alkalosis – Tachypnoea, Respiratory Alkalosis – Tachypnoea, Sepsis, hepatic coma,Sepsis, hepatic coma,

• Derived from PaO2 (partial pressure of oxygen in blood) and Saturation

• PaO2- measured directly by the blood gas machine

• Saturation- calculated value

• Some ABG machines- in-built oximeter can give a directly measured value for saturation.

Oxygenation

OxygenationOxygenation

A-a gradient – FiO2x(760-47)-PCO2x1.25 A-a gradient – FiO2x(760-47)-PCO2x1.25 (normal 20)(normal 20)

Oxygen cost of breathingOxygen cost of breathing

Expected oxygen (PO2) = 500 x FiO2Expected oxygen (PO2) = 500 x FiO2

P/F ratioP/F ratio

SaO2 functional saturation SaO2 functional saturation OHbOHb OHb+RHb OHb+RHb

• Assessment of ventilation and acid base status go hand in hand

• pH and PCO2- directly measured by the ABG machine

• Bicarbonate and base excess- calculated values.

Ventilation & Acid-base status

ABGABGnormal valuesnormal values

pHpH 7.4 (7.35-7.45)7.4 (7.35-7.45)

PaCOPaCO22 35-45 mm Hg35-45 mm Hg

HCOHCO33-- 22-26 mmol/l22-26 mmol/l

BEBE +/- 5+/- 5

PaOPaO22 >80(>60) mm Hg>80(>60) mm Hg

pH & PaCO2 move in opposite directionspH & PaCO2 move in opposite directions

HCO3 & PaCO2 move in same directionHCO3 & PaCO2 move in same direction

pH values and equivalent [H+] for waterpH values and equivalent [H+] for water

[H+] is the physical chemistry expression of molar [H+] is the physical chemistry expression of molar

concentration H+.concentration H+.

pH value pH value [H+]; nmol.l)1[H+]; nmol.l)1-1-1

7.6 7.6 2525

7.5 7.5 3232

7.4 7.4 4040

7.3 7.3 5050

7.2 7.2 6060

7.1 7.1 8080

7.0 7.0 100100

6.9 6.9 125125

6.8 6.8 160160

Base ExcessBase Excess

Actual Base Excess (ABE)– calculated by Actual Base Excess (ABE)– calculated by Van Slyke/Siggard Anderson equation Van Slyke/Siggard Anderson equation (1948-50)(1948-50)

Standard Base Excess (SBE)– some base Standard Base Excess (SBE)– some base diffuses out of blood in vivo – correction diffuses out of blood in vivo – correction does not take into account plasma protein does not take into account plasma protein & PCO2& PCO2

Base ExcessBase ExcessThe base excess is defined as the quantity of The base excess is defined as the quantity of strong acid required to titrate blood to pH 7.40 with strong acid required to titrate blood to pH 7.40 with a PaCO2 of 40 mmHg (5.33 kPa) at 37 Ca PaCO2 of 40 mmHg (5.33 kPa) at 37 CIn practice, acid is not titrated as suggested but In practice, acid is not titrated as suggested but calculated using a variety of established formulae calculated using a variety of established formulae or normograms. or normograms. The base excess thus ‘removes’ the respiratory The base excess thus ‘removes’ the respiratory element of acid-base disturbance and identifies element of acid-base disturbance and identifies the metabolic contribution to interpret with pH and the metabolic contribution to interpret with pH and [H+]. [H+]. The standard bicarbonate is broadly similar and is The standard bicarbonate is broadly similar and is the calculated [HCO3] at a PaCO2 of 40 mmHg the calculated [HCO3] at a PaCO2 of 40 mmHg [5.33 kPa]. [5.33 kPa]. Although the base excess allows a metabolic Although the base excess allows a metabolic acidosis to be diagnosed, it provides few clues as acidosis to be diagnosed, it provides few clues as to the pathophysiology or underlying diagnosis.to the pathophysiology or underlying diagnosis.

Steps for Acid Base StatusSteps for Acid Base Status

Calculated Actual Anion GapCalculated Actual Anion Gap

Acidosis or AlkalosisAcidosis or Alkalosis

Respiratory or MetabolicRespiratory or Metabolic

If Respiratory – Acute or ChronicIf Respiratory – Acute or Chronic

Metabolic Acidosis – Anion GapMetabolic Acidosis – Anion Gap

Other Metabolic DisordersOther Metabolic Disorders

Respiratory Compensation for metabolic Respiratory Compensation for metabolic DisordersDisorders

When pH & PaCO2 change in same When pH & PaCO2 change in same direction the primary problem is Metabolicdirection the primary problem is Metabolic

When pH & PaCO2 move in opposite When pH & PaCO2 move in opposite directions & PaCO2 is normal the primary directions & PaCO2 is normal the primary problem is Respiratoryproblem is Respiratory

If HCO3 & PaCO2 change in opposite If HCO3 & PaCO2 change in opposite direction then it is a mixed disorder (pH direction then it is a mixed disorder (pH may be normal with abnormal PaCO2 or may be normal with abnormal PaCO2 or abnormal pH & normal PaCO2abnormal pH & normal PaCO2

RespiratoryRespiratoryThe likely hood of complete compensation in The likely hood of complete compensation in chronic respiratory acidosis if PaCO2 > 60 is chronic respiratory acidosis if PaCO2 > 60 is <15%<15%

Acute compensation occurs within 6-24 hrAcute compensation occurs within 6-24 hr

Chronic compensation occurs within 1-4 dChronic compensation occurs within 1-4 d

In clinical practice it is rare to see complete In clinical practice it is rare to see complete compensation.compensation.

Maxm compensation of pH 50-75%Maxm compensation of pH 50-75%

In Ch respiratory alkalosis pH may be normal In Ch respiratory alkalosis pH may be normal

COMPENSATIONSCOMPENSATIONS

Compensation in same direction Compensation in same direction dec. in pCOdec. in pCO22 dec in HCO dec in HCO33

Acute ChronicAcute ChronicInc. PaCOInc. PaCO22 10 10 dec. pH dec. pH 0.08 0.03 0.08 0.03Inc. PaCOInc. PaCO22 10 10 inc HCO inc HCO33 1 3 1 3dec. PaCOdec. PaCO22 10 10 dec. HCO dec. HCO33 2 4 2 4

Inc. HCOInc. HCO33 1 1 inc. PaCO inc. PaCO22 0.5(0.5-1.0) 0.5(0.5-1.0) dec. HCOdec. HCO3 3 11 dec. PaCO dec. PaCO22 1 1

lowest 7 -8 lowest 7 -8

Bicarb CompensationBicarb Compensation

pCO2 change 10

Respiratory Acidosis

Respiratory Alkalosis

Acute 1 2

Chronic 3 4

Ionic components of plasma including Ionic components of plasma including electrochemical equivalentselectrochemical equivalents

Principal cations Principal cations (mEq.l)1(mEq.l)1-1-1))

Na (140)Na (140)

K (4)K (4)

Ca (2)Ca (2)

Mg (2)Mg (2)

Total 148 mEq.l)1Total 148 mEq.l)1-1-1

Principal anions Principal anions (mEq.l)1(mEq.l)1-1-1))

Cl (100)Cl (100)

HCO3 (25)HCO3 (25)

Protein (15)Protein (15)

Phosphate specie (2)Phosphate specie (2)

Sulphate (1)Sulphate (1)

Organic acids (5)Organic acids (5)

Total 148 mEq.l)1Total 148 mEq.l)1-1-1

Anion Gap (1975) Anion Gap (1975)

Proteins – Proteins – 1515 K+K+ 4.54.5

Org acids -Org acids - 5 5 Ca+Ca+ 5.05.0

Phosphates -Phosphates - 2 2 Mg+Mg+ 1.51.5

Sulphates - Sulphates - 1 1

TotalTotal 2323 1111

Anion Gap = 23-11=12Anion Gap = 23-11=12++44

Anion Gap = (Na+) - (HCO3 + Cl)Anion Gap = (Na+) - (HCO3 + Cl)

Anion Gap with K+=8Anion Gap with K+=8++44

Calculated Anion GapCalculated Anion Gap

AG influenced by Albumin & pHAG influenced by Albumin & pH

Change in Alb(4 gm) by 1 gm changes AG Change in Alb(4 gm) by 1 gm changes AG by 2by 2

Acidosis decreases AG by 2Acidosis decreases AG by 2

Alkalosis increases AG by 4Alkalosis increases AG by 4

Delta AG = AG – expected AGDelta AG = AG – expected AG

Metabolic AcidosisMetabolic Acidosis

Metabolic acidosis is a non-respiratory process Metabolic acidosis is a non-respiratory process which has a tendency to produce a metabolic which has a tendency to produce a metabolic acidaemia, acidaemia,

The correct term when plasma pH < 7.35 The correct term when plasma pH < 7.35 ([H+] =45 nmol.l)1([H+] =45 nmol.l)1-1-1). ).

Strictly, during acidosis the pH may be in the Strictly, during acidosis the pH may be in the normal range. normal range.

Clinically, a metabolic acidosis may be Clinically, a metabolic acidosis may be distinguished from a respiratory acidosis when distinguished from a respiratory acidosis when alveolar hypoventilation is not the primary cause.alveolar hypoventilation is not the primary cause.

Metabolic Acidosis - CausesMetabolic Acidosis - Causes

Normal Anion GapNormal Anion GapDiarrhoeaDiarrhoeaIntestinal/Pancreatic FistulaIntestinal/Pancreatic FistulaRenal Tubular AcidosisRenal Tubular AcidosisFluids with high Chloride(DKA+NS)Fluids with high Chloride(DKA+NS)

High Anion GapHigh Anion GapLactic AcidosisLactic AcidosisKetoacidosis (diabetic, starvation)Ketoacidosis (diabetic, starvation)Renal FailureRenal FailurePoisoning (salicylates, ethanol, ethylene glycol)Poisoning (salicylates, ethanol, ethylene glycol)

Disorders with low AGDisorders with low AGLab Error Most frequent

Hypoalbuminemia Second most common

Multiple Myeloma Corresponds with S paraprotein

Lithium, Bromide, Iodide Lithium 4

Hypercalcemia

Hypermagnesemia Theoretical

Polymyxin B

Underestimation of S Na Hypernatraemia, hypertriglyceredimia

Overestimation of S Cl Rare

Overestimation of S Bicarb

Organic acidsOrganic acidsPrincipally lactate and ketones. Principally lactate and ketones.

Several thousand millimoles of lactate and Several thousand millimoles of lactate and ketones are metabolised per day (e.g. lactate ketones are metabolised per day (e.g. lactate 1500 mmol.day)1) traditionally attributed to 1500 mmol.day)1) traditionally attributed to the liver. the liver.

Kidney contributes a large component of the Kidney contributes a large component of the body’s metabolic disposal of lactate, perhaps body’s metabolic disposal of lactate, perhaps up to 25–30%. up to 25–30%.

Hepatic urea production itself generates 2H+ Hepatic urea production itself generates 2H+ for every molecule of urea producedfor every molecule of urea produced

Inorganic acidsInorganic acids

Sulphate and phosphate are the two most Sulphate and phosphate are the two most important & generated in the range of 1.5 important & generated in the range of 1.5 mmol.kg)1.day)1mmol.kg)1.day)1-1-1. .

Bioproducts of dietary protein and amino acid Bioproducts of dietary protein and amino acid metabolism.metabolism.

Sulphur-containing amino acids methionine and Sulphur-containing amino acids methionine and cysteine produce around 70% of the body’s total cysteine produce around 70% of the body’s total fixed acid per day in the form of sulphuric acid. fixed acid per day in the form of sulphuric acid.

In chronic renal failure, sulphate may contribute In chronic renal failure, sulphate may contribute up to 5 mEq.l)1 to the anion gapup to 5 mEq.l)1 to the anion gap

High AGHigh AG

Renal Failure Ph, Sul Protein catabolism

BUN/Creat

Diabetic B hydroxybutarate Fatty acid met Urine ketones

Alcoholic Ketoacids

Starvation Acetoacetate

Lactic acidosis lactate Lactate

Exogenous Salicylate

Lactate Res & Met alkalosis

Gap Gap AcidosisGap Gap Acidosis

Delta AG/Delta HCO3Delta AG/Delta HCO3

1 = Met Acidosis with high AG1 = Met Acidosis with high AG

> 1.5 = Met Acidosis + Met Alkalosis> 1.5 = Met Acidosis + Met Alkalosis

< 1 or 0 = Met Acidosis with normal AG< 1 or 0 = Met Acidosis with normal AG

Metabolic Acidosis & AlkalosisMetabolic Acidosis & Alkalosis

Gap-gap ratio > 1(AG:BE) Gap-gap ratio > 1(AG:BE) (in presence of high AG acidosis (in presence of high AG acidosis when alkali is added the decrease in when alkali is added the decrease in HCO3 is less than the increase in AG. HCO3 is less than the increase in AG. In high AG Metabolic Acidosis gap- In high AG Metabolic Acidosis gap-gap ratio >1 indicates co-existence of a gap ratio >1 indicates co-existence of a Metabolic AlkalosisMetabolic Alkalosis

Stewarts Physico-Chemical Approach Stewarts Physico-Chemical Approach

Sum of all +ve ions = sum of –ve ionsSum of all +ve ions = sum of –ve ions

Aqueous solution is always neutralAqueous solution is always neutral

Dissociated H+ exerts chargeDissociated H+ exerts charge

Neutral pH – amount of dissociated H+ Neutral pH – amount of dissociated H+ &OH- is equal at 25oC & 1 Atm pressure&OH- is equal at 25oC & 1 Atm pressure

Strong Ion DifferenceStrong Ion DifferenceDisossiates more in solution than weak ionDisossiates more in solution than weak ion

Strong cations – Na+, K+, Ca+, Mg+Strong cations – Na+, K+, Ca+, Mg+

Weak cations – NH4, H+Weak cations – NH4, H+

Strong anions – Cl-, LactateStrong anions – Cl-, Lactate

Weak anions – HCO3-, PO4-, OH-Weak anions – HCO3-, PO4-, OH-

As strong cation increases in solution the As strong cation increases in solution the concentration of OH- increases more than the concentration of OH- increases more than the concentration of H+ ions – solution becomes more concentration of H+ ions – solution becomes more alkaline alkaline

Base Excess – change = metabolic Base Excess – change = metabolic

No change = respiratoryNo change = respiratory

Stewart approachStewart approachSID – Blood has more strong cations SID – Blood has more strong cations (Na 135) than strong anions (Cl 100) (Na 135) than strong anions (Cl 100) – pH is more alkaline than water– pH is more alkaline than water

Total Weak Acids –Albumin & PhosphatesTotal Weak Acids –Albumin & Phosphates

Solutions with greater SID generate more Solutions with greater SID generate more HCO3 & vice versaHCO3 & vice versa

More alkaline the blood, the more HCO3 More alkaline the blood, the more HCO3 generated & the more acidic the blood the generated & the more acidic the blood the less HCO3 generatedless HCO3 generated

Applications of Stewart’s Approach Applications of Stewart’s Approach

Sepsis & Septic Shock – metabolic Sepsis & Septic Shock – metabolic acidosis due to lactatemiaacidosis due to lactatemia

Hypoalbuminemia – metabolic alkalosis Hypoalbuminemia – metabolic alkalosis (can mask SID such as lactic acidemia)(can mask SID such as lactic acidemia)

Prolonged respiratory failure with Prolonged respiratory failure with associated hypercarbia leads to metabolic associated hypercarbia leads to metabolic alkalosis because of Cl loss in urinealkalosis because of Cl loss in urine

Applications of Stewart’s ApproachApplications of Stewart’s Approach

Mechanical ventilation increases the Mechanical ventilation increases the circulating volume of ANP & ADH resulting circulating volume of ANP & ADH resulting in increased total body water leading to in increased total body water leading to dilutional acidosisdilutional acidosis

Renal failure causes metabolic acidosis. Renal failure causes metabolic acidosis. Polyuric renal failure may be associated Polyuric renal failure may be associated with contraction alkolosis du to loss of Na, with contraction alkolosis du to loss of Na, K, & free water.K, & free water.

Applications of Stewart’s ApproachApplications of Stewart’s Approach

Nasogastric suctioning causes Nasogastric suctioning causes hypochloremic alkalosishypochloremic alkalosis

Diarrhoea causes acidosis by loss of Na & Diarrhoea causes acidosis by loss of Na & KK

Fever, sweating leads to insensible loss & Fever, sweating leads to insensible loss & contraction alkalosiscontraction alkalosis

Antibiotics diluted in Na rich solutions Antibiotics diluted in Na rich solutions increases SID & alkalosisincreases SID & alkalosis

Applications of Stewart’s ApproachApplications of Stewart’s Approach

Lorazepam large volumes of propylene Lorazepam large volumes of propylene glycol cause metabolic acidosisglycol cause metabolic acidosis

CRRT clears acidosis of renal failure by CRRT clears acidosis of renal failure by removing strong ions & phosphate removing strong ions & phosphate unmasks metabolic acidosis due to unmasks metabolic acidosis due to hypovolemiahypovolemia

Loop diuretics cause hypochloremia & Loop diuretics cause hypochloremia & contraction alkalosiscontraction alkalosis

Applications of Stewart’s ApproachApplications of Stewart’s Approach

Carbonic anhydrase inhibitors increase Carbonic anhydrase inhibitors increase CO2 levels causing respiratory acidosis & CO2 levels causing respiratory acidosis & cause diuresis leading to contraction cause diuresis leading to contraction alkalosisalkalosis

Contraction alkalosis should be treated Contraction alkalosis should be treated with free waterwith free water

Hypochloremic alkalosis should be treated Hypochloremic alkalosis should be treated by correcting Cl deficit using NSby correcting Cl deficit using NS

Applications of Stewart’s ApproachApplications of Stewart’s Approach

Mannitol causes dilutional acidosis. Mannitol causes dilutional acidosis. Contraction alkalosis follows due to Contraction alkalosis follows due to diuresisdiuresis

Normal & Hypertonic saline cause Normal & Hypertonic saline cause hyperchloremic acidosishyperchloremic acidosis

Diabetes insipidus can cause contraction Diabetes insipidus can cause contraction alkalosisalkalosis

Corrected HCO3Corrected HCO3

>24 Alkalosis>24 Alkalosis

<24 Acidosis<24 Acidosis

Actual HCO3 + delta AGActual HCO3 + delta AG

Urinary Anion GapUrinary Anion GapIn normal anion gap acidosisIn normal anion gap acidosis

(Na + K) – Cl (urinary pH < 6.5, no ketosis(Na + K) – Cl (urinary pH < 6.5, no ketosis

Neg UAG = GI, iatrogenicNeg UAG = GI, iatrogenic

Positive UAG (> 20-30) – RTA type I, II, IVPositive UAG (> 20-30) – RTA type I, II, IV

Urinary pH > 6.0 = distal type I RTAUrinary pH > 6.0 = distal type I RTA

Urinary pH < 5.5 = proximal type II/IV RTAUrinary pH < 5.5 = proximal type II/IV RTA

Hypokalaemia = proximal type II RTAHypokalaemia = proximal type II RTA

Hyperkalaemia = Aldosterone deficiency Hyperkalaemia = Aldosterone deficiency type IV RTAtype IV RTA

Metabolic Acidosis with Metabolic Acidosis with decreased AGdecreased AG

Multiple MyelomaMultiple Myeloma

HypoalbunemiaHypoalbunemia

HyperkalaemiaHyperkalaemia

HypermagnesemiaHypermagnesemia

HypertriglyceredemiaHypertriglyceredemia

Lithium ToxicityLithium Toxicity

Bromide Toxicity(pyridostigmine)Bromide Toxicity(pyridostigmine)

Metabolic AlkalosisMetabolic Alkalosis

Urine Cl < 10 mEq/l – saline responsiveUrine Cl < 10 mEq/l – saline responsive

Urine Cl > 20 mEq/l – saline unresponsiveUrine Cl > 20 mEq/l – saline unresponsive

Urinary Anion GapUrinary Anion Gap

Done in normal AG Metabolic AcidosisDone in normal AG Metabolic Acidosis

(Na + K) – Cl(Na + K) – Cl

Neg – GI lossNeg – GI loss

> 20-30 – RTA type I, II, IV> 20-30 – RTA type I, II, IV

Central Venous O2 Saturation Central Venous O2 Saturation (ScvO2)(ScvO2)

ScvO2 most valuable in identifying trends ScvO2 most valuable in identifying trends in the balance of DO2 & VO2in the balance of DO2 & VO2

ScvO2 <70% identifies a state of ScvO2 <70% identifies a state of inadequate O2 delivery relative to O2 inadequate O2 delivery relative to O2 consumption consumption decreased DO2–low CO, Anemia, Hypoxia decreased DO2–low CO, Anemia, Hypoxia increased VO2 - hypermetabolismincreased VO2 - hypermetabolism

Few ValuesFew Values

pHpH 7.30 7.30 PaCOPaCO22 60 60 PaO PaO22 101 101HCOHCO33 28 28

pHpH 7.228 7.228 PaCOPaCO22 45 45 PaO PaO22 100 100HCOHCO33 18 18

pHpH 7.55 7.55 PaCOPaCO22 26 26 PaO PaO228888 HCOHCO33 28 28

pHpH 7.50 7.50 PaCOPaCO22 40 40 PaO PaO22 98 98 HCOHCO33 36 36

A 60 year old male,known case of COPD was A 60 year old male,known case of COPD was admitted with history of acute exacerbation of admitted with history of acute exacerbation of breathlessness. The ABG:breathlessness. The ABG:pH- 7.204 PaCOpH- 7.204 PaCO22- 68 PaO- 68 PaO22- 65- 65 HCOHCO33 28 28

A 40 year old IDDM was admitted with breathless A 40 year old IDDM was admitted with breathless following Acute Gastritis.The ABG was :following Acute Gastritis.The ABG was :

pHpH 7.28 PaCO 7.28 PaCO22 18.4 PaO 18.4 PaO22 152 HCO 152 HCO33 8.5 8.5Na 127Na 127 K 3.3 Cl 101K 3.3 Cl 101 RBS 590mg% RBS 590mg% Urine Ketones -positiveUrine Ketones -positive

A 40 year old female presented with acute A 40 year old female presented with acute breathlessness .Chest was clinically clear. breathlessness .Chest was clinically clear. She had similar attacks in the past. The ABG was She had similar attacks in the past. The ABG was

pH 7.583 PaCOpH 7.583 PaCO22 15.9 PaO 15.9 PaO22 137.9 HCO3 14.5 137.9 HCO3 14.5

A 25 years old boy was admitted along with severe A 25 years old boy was admitted along with severe vomiting following food poisoning. The ABG was :vomiting following food poisoning. The ABG was :

pH 7.52pH 7.52 PaCO PaCO22 45 45 PaOPaO22 94 94 HCOHCO33 32 32

Na 130Na 130 K 3.1 K 3.1 Cl 86Cl 86

Expected changes in pH and HCOExpected changes in pH and HCO33-- for for a 10-mm Hg changea 10-mm Hg change in in

PaCOPaCO22 resulting from either primary hypoventilation (respiratory resulting from either primary hypoventilation (respiratory acidosis) or primary hyperventilation (respiratory alkalosis):acidosis) or primary hyperventilation (respiratory alkalosis):

ACUTEACUTE CHRONICCHRONIC

Resp AcidosisResp Acidosis

pH pH ↓↓by 0.07by 0.07 pH pH ↓ ↓ by 0.03by 0.03

HCOHCO33-- ↑ ↑ by 1*by 1* HCOHCO33

-- ↑ ↑ by 3 - 4by 3 - 4

Resp AlkalosisResp Alkalosis

pH pH ↑ ↑ by 0.08by 0.08 pH pH ↑ ↑ by 0.03by 0.03

HCOHCO33-- ↓ ↓ by 2by 2 HCOHCO33

-- ↓ ↓ by 5 by 5

* Units for HCO* Units for HCO33-- are mEq/L are mEq/L

SKM a case of complicated Falciparum Malaria was admitted with SKM a case of complicated Falciparum Malaria was admitted with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was pHpH 7.389 7.389 PaCO2 32.9PaCO2 32.9 PaO2 153PaO2 153 5l/m of O25l/m of O2 HCO3 19.2HCO3 19.2Urea 97.2Urea 97.2 Creatinine 2.8Creatinine 2.8He underwent HDHe underwent HDpHpH 7.407 7.407 PaCO2 38.4PaCO2 38.4 PaO2 52PaO2 52 5l/m of O25l/m of O2 HCO3 23.HCO3 23.CXR CXR ARDS . ARDS .He was on mech. VentilationHe was on mech. VentilationpHpH 7.406 7.406 PaCO2 34.7PaCO2 34.7 PaO2 101PaO2 101 FiO2 o.5FiO2 o.5 HCO3 21.1HCO3 21.19 days later after his 69 days later after his 6thth HD,he had a fainting attack,detected to have tachycardia HD,he had a fainting attack,detected to have tachycardia and hypotensionand hypotensionpHpH 6.962 6.962 PaCO2 39.8PaCO2 39.8 PaO2 271PaO2 271 FiO2 1.00FiO2 1.00 HCO3 8.8HCO3 8.8Immidiately ventilated and subsequently had malenaImmidiately ventilated and subsequently had malenaPost BicarbonatePost BicarbonatepHpH 7.136 7.136 PaCO2 42.1PaCO2 42.1 PaO2 273PaO2 273 FiO2 1.00 FiO2 1.00 HCO3 10.8HCO3 10.8Post HDPost HDpHpH 7.462 7.462 PaCO2 37.8PaCO2 37.8 PaO2 200PaO2 200 FiO2 1.00 FiO2 1.00 HCO3 26.1HCO3 26.1Post extubationPost extubationpHpH 7.442 7.442 PaCO2 52.9PaCO2 52.9 PaO2 225PaO2 225 FiO2 0.80 FiO2 0.80 HCO3 34.9HCO3 34.9pHpH 7.570 7.570 PaCO2 24PaCO2 24 PaO2 080PaO2 080 3l/m of 02 HCO3 21.3 3l/m of 02 HCO3 21.3

Case 1Case 1

A 28year female presented to the hospital with A 28year female presented to the hospital with fever for 2days & Status Epilepticus. She had an fever for 2days & Status Epilepticus. She had an cardiac arrest during a prolonged seizure & was cardiac arrest during a prolonged seizure & was immediately intubated, CPR was started, cardiac immediately intubated, CPR was started, cardiac rhythm was restored & she was connected to a rhythm was restored & she was connected to a ventilator. Her ABG done was :ventilator. Her ABG done was :

pH-6.788, pCOpH-6.788, pCO22-65,pO-65,pO22-392(FiO-392(FiO22-1)-1)

One hour later pH-7.175,pCOOne hour later pH-7.175,pCO22-23,pO-23,pO22-254(.8)-254(.8)

7hours later pH-7.456,pCO7hours later pH-7.456,pCO22-24, pO-24, pO22-300(.8)-300(.8)

Respiratory acidosisRespiratory acidosis

PCO2 65, expected pH-7.2PCO2 65, expected pH-7.2

Actual pH 6.788 – metabolic acidosisActual pH 6.788 – metabolic acidosis

Cause – post-tictal lactic acidosisCause – post-tictal lactic acidosis

Respiratory + Metabolic acidosisRespiratory + Metabolic acidosis

Case 2Case 2

A 48year male CRF patient presented with A 48year male CRF patient presented with bradycardia, hypotension & gasping bradycardia, hypotension & gasping respiration. ABG: pH-7.175, PCOrespiration. ABG: pH-7.175, PCO22-31,-31,

PaOPaO22-122(NC), HCO-122(NC), HCO33-11, Na-132,K-8.6-11, Na-132,K-8.6

Temporary cardiac pacing was done & Temporary cardiac pacing was done & patient sent for haemodialysis.patient sent for haemodialysis.

2hours later ABG: pH-7.262,pCO2hours later ABG: pH-7.262,pCO22-29.3, -29.3,

HCOHCO33-12.4,Na-139,K-6.2-12.4,Na-139,K-6.2

Case 3Case 3

A 82year male DM,HTN had 3 bouts of A 82year male DM,HTN had 3 bouts of vomiting, no urination for 12hours, gasping vomiting, no urination for 12hours, gasping respiration, bradycardia(CHB), respiration, bradycardia(CHB), hypotension(BP-80), & impending cardio-hypotension(BP-80), & impending cardio-respiratory arrest.respiratory arrest.

ABG:pH-6.9, pCOABG:pH-6.9, pCO22-19,pO-19,pO22-105(NC), -105(NC), HCOHCO33-3.7,Na-147, K-6.1-3.7,Na-147, K-6.1

9hours later ABG:pH-7.4,pCO9hours later ABG:pH-7.4,pCO22-14.5, -14.5, pOpO22-132(NC),HCO-132(NC),HCO33-17.2,-17.2,

Case 4Case 4

A 30year female with quadriparesis A 30year female with quadriparesis 15days developed respiratory distress.15days developed respiratory distress.

ABG:pH-7.275, PCOABG:pH-7.275, PCO22-116, PaO-116, PaO22-71, -71,

HCOHCO33-88.-88.

She was ventilatedShe was ventilated

ABG:pH-7.43,PCOABG:pH-7.43,PCO22-45,PaO-45,PaO22-80,HCO-80,HCO33-28-28

ABG samplingABG sampling

Transport of blood sampleTransport of blood sample

Heparin flushHeparin flush

Roll the syringeRoll the syringe

Transport in ice pack with ice all aroundTransport in ice pack with ice all around

Air free, Cork needle (do not bend or cap)Air free, Cork needle (do not bend or cap)

Excess heparin leads to metabolic Excess heparin leads to metabolic acidosis & increase in K+acidosis & increase in K+

Metabolic Acidosis with decreased Metabolic Acidosis with decreased ionized Caionized Ca

PancreatitisPancreatitis

RhabdomylosisRhabdomylosis

Tumour LysisTumour Lysis

Metabolic Acidosis with decreased Metabolic Acidosis with decreased GlucoseGlucose

Liver cell dysfunctionLiver cell dysfunction

ConvulsionConvulsion

MetforminMetformin

Adrenal insufficiencyAdrenal insufficiency

Starvation (protein calorie malnutrition)Starvation (protein calorie malnutrition)

Alcohol IntoxicationAlcohol Intoxication

ParacetamolParacetamol

MyxaedemaMyxaedema

Severe MalariaSevere Malaria

Metabolic AcidosisMetabolic Acidosis

Hypokalemia – RTA type 1Hypokalemia – RTA type 1

Metabolic AlkalosisMetabolic Alkalosis

Urinary Cl < 20meq/l – hypovolemiaUrinary Cl < 20meq/l – hypovolemia

Urinary Cl > 20meq/l – HypokalemiaUrinary Cl > 20meq/l – Hypokalemia

Hypokalemia – CushingsHypokalemia – Cushings

Salicylate poisoning Salicylate poisoning – + Metabolic acidosis + – + Metabolic acidosis + ↓↓Na + Na + ↑↑KK

Lactic Acidosis type-BLactic Acidosis type-B

MetforminMetformin

AlcoholAlcohol

SalbutamolSalbutamol

INHINH

MalignancyMalignancy

HypomagnesemiaHypomagnesemia

Reduced K+Reduced K+

Reduced Ca+Reduced Ca+

COMPENSATIONSCOMPENSATIONS

Compensation in same direction Compensation in same direction dec. in pCOdec. in pCO22 dec in HCO dec in HCO33

Acute ChronicAcute ChronicInc. PaCOInc. PaCO22 10 10 dec. pH dec. pH 0.08 0.03 0.08 0.03Inc. PaCOInc. PaCO22 10 10 inc. HCO inc. HCO33 1 3.5 1 3.5dec. PaCOdec. PaCO22 10 10 dec. HCO dec. HCO33 2 5 2 5

Inc. HCOInc. HCO33 inc. PaCO inc. PaCO22 0.7(0.5-1.0) 0.7(0.5-1.0) dec. HCOdec. HCO33 dec. PaCO dec. PaCO22 1- 1.5 1- 1.5

lowest 7 -8 lowest 7 -8

Case 1Case 1

Patient with H/O vomitingPatient with H/O vomiting

pH 7.52pH 7.52

PaCO2 41.25PaCO2 41.25

PaO2 92PaO2 92

Bicarb 36Bicarb 36

FiO2 0.21FiO2 0.21

Case 2 contd.Case 2 contd.

pH 7.52 - AlkalosispH 7.52 - Alkalosis

PaCO2 rises 1 for every 1 of Bicarb(36)PaCO2 rises 1 for every 1 of Bicarb(36)

Expected PaCO2 52(actual 41.25)Expected PaCO2 52(actual 41.25)

Metabolic Alkalosis + Respiratory Metabolic Alkalosis + Respiratory AlkalosisAlkalosis

Severe vomiting in pregnancy, Severe vomiting in pregnancy,

Diuretics/vomiting in cirrhosisDiuretics/vomiting in cirrhosis

Post cardiac arrest(hyperventilation, bicarbPost cardiac arrest(hyperventilation, bicarb

Case 2Case 2

74 yr COPD74 yr COPD

pH 7.55pH 7.55

PaCO2 56PaCO2 56

PaO2 63PaO2 63

Bicarb 48Bicarb 48

FiO2 0.21FiO2 0.21

Case 2 contd.Case 2 contd.

PAO2 = FiO2x(BP-47)-PCO2x1.25PAO2 = FiO2x(BP-47)-PCO2x1.25

PAO2 = 0.21x413 – 56x1.25 PAO2 = 0.21x413 – 56x1.25

A-a gradient 87.6-70=17.6 (normal)A-a gradient 87.6-70=17.6 (normal)

HCO3 48(48-24=24) HCO3 48(48-24=24)

Expected PaCO2 40+24= 64(56)Expected PaCO2 40+24= 64(56)

Metabolic AlkalosisMetabolic Alkalosis

Volume depletion, Hyperadrenalism, Volume depletion, Hyperadrenalism, Potassium depletion, Excessive alkali intakePotassium depletion, Excessive alkali intake

Case 3Case 3

pH 7.4pH 7.4

PaCO2 24.75PaCO2 24.75

PaO2 105PaO2 105

Bicarb 15.3Bicarb 15.3

FiO2 0.21FiO2 0.21

Case 3 contd.Case 3 contd.

HCO3 15.3(24-15.3=8.7)HCO3 15.3(24-15.3=8.7)

Expected PaCO2 (40–13( 8.7x1.5)=27 Expected PaCO2 (40–13( 8.7x1.5)=27 (actual 24)(actual 24)

Metabolic Acidosis with Respiratory Metabolic Acidosis with Respiratory AlkalosisAlkalosis

Sepsis, Combined Hepatic & Renal Sepsis, Combined Hepatic & Renal insufficiency, recent alcoholic binge insufficiency, recent alcoholic binge (alcoholic ketoacidosis with (alcoholic ketoacidosis with hyperventilation), Salicylate overdose hyperventilation), Salicylate overdose

Case 4Case 4

pH 7.15pH 7.15

PCO2 30PCO2 30

PaO2 105PaO2 105

HCO3 10.3HCO3 10.3

FiO2 0.5FiO2 0.5

Case 4 cont.Case 4 cont.

AcidosisAcidosis

HCO3 10.3, PCO2 30HCO3 10.3, PCO2 30

Expected PCO2(24-10.3=13.7) Expected PCO2(24-10.3=13.7) 40-13.7=19.45-26.340-13.7=19.45-26.3

Metabolic Acidosis & Respiratory AcidosisMetabolic Acidosis & Respiratory Acidosis

After Cardiac arrest or Severe Pulmonary After Cardiac arrest or Severe Pulmonary OedemaOedema

Case 5Case 5

pH 7.05pH 7.05

PCO2 15PCO2 15

PaO2 150PaO2 150

HCO3 4.1HCO3 4.1

Na+ 135Na+ 135

Cl 100Cl 100

FiO2 0.3FiO2 0.3

AcidosisAcidosis

HCO3 4.1, PCO2 15HCO3 4.1, PCO2 15

Expected PCO2 (24-4=20)20x1.25=25 Expected PCO2 (24-4=20)20x1.25=25 40-25=1540-25=15

AG=135-100-4=30.9AG=135-100-4=30.9

High Anion gap Metabolic AcidosisHigh Anion gap Metabolic Acidosis

Lactic Acidosis, Ketoacidosis, Renal Lactic Acidosis, Ketoacidosis, Renal failure, Poisoning(salicylates, methanol)failure, Poisoning(salicylates, methanol)

Anion GapAnion Gap

Proteins – Proteins – 1515 K+K+ 4.54.5

Org acids -Org acids - 5 5 Ca+Ca+ 5.05.0

Phosphates -Phosphates - 2 2 Mg+Mg+ 1.51.5

Sulphates - Sulphates - 1 1

TotalTotal 2323 1111

Anion Gap = 23-11=12Anion Gap = 23-11=12

Anion Gap = (Na+) - (HCO3 + Cl)Anion Gap = (Na+) - (HCO3 + Cl)

Case 6Case 6

pH 7.62pH 7.62

PaCO2 30PaCO2 30

PaO2 85PaO2 85

HCO3 30HCO3 30

K+ 2.5K+ 2.5

FiO2 .24FiO2 .24

Case 6 cont.Case 6 cont.

AlkalosisAlkalosis

HCO3 30(30-24=6), PCO2 30HCO3 30(30-24=6), PCO2 30

Expected PCO2(>40)Expected PCO2(>40)

Metabolic & Respiratory AlkalosisMetabolic & Respiratory Alkalosis

Severe vomiting in pregnancy, cirrhosis Severe vomiting in pregnancy, cirrhosis with diuretics or vomitingwith diuretics or vomiting

Case 7Case 7

pH 7.44pH 7.44

PCO2 63PCO2 63

PaO2 51.75PaO2 51.75

HCO3 42HCO3 42

FiO2 0.28FiO2 0.28

Case 7 cont.Case 7 cont.

HCO3 42(42-24=18), PCO2 63(63-40=23)HCO3 42(42-24=18), PCO2 63(63-40=23)

Expected HCO3(4x2.3=9.2)(24+9.2=33.2)Expected HCO3(4x2.3=9.2)(24+9.2=33.2)

Respiratory acidosis & Metabolic AlkalosisRespiratory acidosis & Metabolic Alkalosis

COPD plus diuretics or steroidsCOPD plus diuretics or steroids