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Arterial Blood Gases. Interpretation of arterial blood gases. Check Machine Clinical History Oxygenation Ventilation Acid base status. Is the Machine correct ?. H x HCO3 = 24 PCO2 pH 7.4 H+ = 80 – 40 = 40 pH 7.3 H+ = 80 – 30 = 50 pH 7.5 H+ = 80 – 50 = 30. Clinical History.

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Presentation Transcript

Interpretation of arterial

blood gases

  • Check Machine

  • Clinical History

  • Oxygenation

  • Ventilation

  • Acid base status


Is the machine correct
Is the Machine correct ?

  • H x HCO3 = 24

    PCO2

  • pH 7.4 H+ = 80 – 40 = 40

  • pH 7.3 H+ = 80 – 30 = 50

  • pH 7.5 H+ = 80 – 50 = 30


Clinical history
Clinical History

  • Metabolic Acidosis – DM, Renal failure, muscle over activity, hypotension, diarrhea Diamox, Metformin , Alcoholism

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

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

  • Respiratory Alkalosis – Tachypnoea, Sepsis, hepatic coma,


Oxygenation

  • 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
Oxygenation

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

  • Oxygen cost of breathing

  • Expected oxygen (PO2) = 500 x FiO2

  • P/F ratio

  • SaO2 functional saturation OHbOHb+RHb


Ventilation & Acid-base status

  • 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.


Abg normal values
ABGnormal values

  • pH 7.4 (7.35-7.45)

  • PaCO2 35-45 mm Hg

  • HCO3- 22-26 mmol/l

  • BE +/- 5

  • PaO2 >80(>60) mm Hg

  • pH & PaCO2 move in opposite directions

  • HCO3 & PaCO2 move in same direction


pH values and equivalent [H+] for water[H+] is the physical chemistry expression of molar concentration H+.

  • pH value [H+]; nmol.l)1-1

    7.6 25

    7.5 32

    7.4 40

    7.3 50

    7.2 60

    7.1 80

    7.0 100

    6.9 125

    6.8 160


Base excess
Base Excess

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

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


Base excess1
Base Excess

  • The base excess is defined as the quantity of strong acid required to titrate blood to pH 7.40 with a PaCO2 of 40 mmHg (5.33 kPa) at 37 C

  • In practice, acid is not titrated as suggested but calculated using a variety of established formulae or normograms.

  • The base excess thus ‘removes’ the respiratory element of acid-base disturbance and identifies the metabolic contribution to interpret with pH and [H+].

  • The standard bicarbonate is broadly similar and is the calculated [HCO3] at a PaCO2 of 40 mmHg [5.33 kPa].

  • Although the base excess allows a metabolic acidosis to be diagnosed, it provides few clues as to the pathophysiology or underlying diagnosis.


Steps for acid base status
Steps for Acid Base Status

  • Calculated Actual Anion Gap

  • Acidosis or Alkalosis

  • Respiratory or Metabolic

  • If Respiratory – Acute or Chronic

  • Metabolic Acidosis – Anion Gap

  • Other Metabolic Disorders

  • Respiratory Compensation for metabolic Disorders


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

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

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


Respiratory
Respiratory is Metabolic

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

  • Acute compensation occurs within 6-24 hr

  • Chronic compensation occurs within 1-4 d

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

  • Maxm compensation of pH 50-75%

  • In Ch respiratory alkalosis pH may be normal


Compensations
COMPENSATIONS is Metabolic

  • Compensation in same direction

    dec. in pCO2 dec in HCO3

    Acute Chronic

  • Inc. PaCO2 10  dec. pH 0.08 0.03

  • Inc. PaCO2 10  inc HCO3 1 3

  • dec. PaCO2 10  dec. HCO3 2 4

  • Inc. HCO3 1 inc. PaCO2 0.5(0.5-1.0)

  • dec. HCO3 1 dec. PaCO2 1

    lowest 7 -8


Bicarb compensation
Bicarb is Metabolic Compensation


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

  • Principal cations (mEq.l)1-1)

  • Na (140)

  • K (4)

  • Ca (2)

  • Mg (2)

  • Total 148 mEq.l)1-1

  • Principal anions (mEq.l)1-1)

  • Cl (100)

  • HCO3 (25)

  • Protein (15)

  • Phosphate specie (2)

  • Sulphate (1)

  • Organic acids (5)

  • Total 148 mEq.l)1-1


Anion gap 1975
Anion Gap (1975) equivalents

  • Proteins – 15 K+ 4.5

  • Org acids - 5 Ca+ 5.0

  • Phosphates - 2 Mg+ 1.5

  • Sulphates - 1

    Total 23 11

    Anion Gap = 23-11=12+4

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

    Anion Gap with K+=8+4


Calculated anion gap
Calculated Anion Gap equivalents

  • AG influenced by Albumin & pH

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

  • Acidosis decreases AG by 2

  • Alkalosis increases AG by 4

  • Delta AG = AG – expected AG


Metabolic acidosis
Metabolic Acidosis equivalents

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

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

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

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


Metabolic acidosis causes
Metabolic Acidosis - Causes equivalents

Normal Anion Gap

  • Diarrhoea

  • Intestinal/Pancreatic Fistula

  • Renal Tubular Acidosis

  • Fluids with high Chloride(DKA+NS)

    High Anion Gap

  • Lactic Acidosis

  • Ketoacidosis (diabetic, starvation)

  • Renal Failure

  • Poisoning (salicylates, ethanol, ethylene glycol)



Organic acids
Organic acids equivalents

  • Principally lactate and ketones.

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

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

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


Inorganic acids
Inorganic acids equivalents

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

  • Bioproducts of dietary protein and amino acid metabolism.

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

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


High ag
High AG equivalents


Gap gap acidosis
Gap equivalentsGap Acidosis

  • Delta AG/Delta HCO3

  • 1 = Met Acidosis with high AG

  • > 1.5 = Met Acidosis + Met Alkalosis

  • < 1 or 0 = Met Acidosis with normal AG


Metabolic acidosis alkalosis
Metabolic Acidosis & Alkalosis equivalents

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


Stewarts physico chemical approach
Stewarts equivalentsPhysico-Chemical Approach

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

  • Aqueous solution is always neutral

  • Dissociated H+ exerts charge

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


Strong ion difference
Strong Ion Difference equivalents

  • Disossiates more in solution than weak ion

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

  • Weak cations – NH4, H+

  • Strong anions – Cl-, Lactate

  • Weak anions – HCO3-, PO4-, OH-

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

  • Base Excess – change = metabolic

  • No change = respiratory


Stewart approach
Stewart approach equivalents

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

  • Total Weak Acids –Albumin & Phosphates

  • Solutions with greater SID generate more HCO3 & vice versa

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


Applications of stewart s approach
Applications of Stewart’s Approach equivalents

  • Sepsis & Septic Shock – metabolic acidosis due to lactatemia

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

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


Applications of stewart s approach1
Applications of Stewart’s Approach equivalents

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

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


Applications of stewart s approach2
Applications of Stewart’s Approach equivalents

  • Nasogastric suctioning causes hypochloremic alkalosis

  • Diarrhoea causes acidosis by loss of Na & K

  • Fever, sweating leads to insensible loss & contraction alkalosis

  • Antibiotics diluted in Na rich solutions increases SID & alkalosis


Applications of stewart s approach3
Applications of Stewart’s Approach equivalents

  • Lorazepam large volumes of propylene glycol cause metabolic acidosis

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

  • Loop diuretics cause hypochloremia & contraction alkalosis


Applications of stewart s approach4
Applications of Stewart’s Approach equivalents

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

  • Contraction alkalosis should be treated with free water

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


Applications of stewart s approach5
Applications of Stewart’s Approach equivalents

  • Mannitol causes dilutional acidosis. Contraction alkalosis follows due to diuresis

  • Normal & Hypertonic saline cause hyperchloremic acidosis

  • Diabetes insipidus can cause contraction alkalosis


Corrected hco3
Corrected HCO3 equivalents

  • >24 Alkalosis

  • <24 Acidosis

  • Actual HCO3 + delta AG


Urinary anion gap
Urinary Anion Gap equivalents

  • In normal anion gap acidosis

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

  • Neg UAG = GI, iatrogenic

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

  • Urinary pH > 6.0 = distal type I RTA

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

  • Hypokalaemia = proximal type II RTA

  • Hyperkalaemia = Aldosterone deficiency type IV RTA


Metabolic acidosis with decreased ag
Metabolic Acidosis with decreased AG equivalents

  • Multiple Myeloma

  • Hypoalbunemia

  • Hyperkalaemia

  • Hypermagnesemia

  • Hypertriglyceredemia

  • Lithium Toxicity

  • Bromide Toxicity(pyridostigmine)


Metabolic alkalosis
Metabolic Alkalosis equivalents

  • Urine Cl < 10 mEq/l – saline responsive

  • Urine Cl > 20 mEq/l – saline unresponsive


Urinary anion gap1
Urinary Anion Gap equivalents

  • Done in normal AG Metabolic Acidosis

  • (Na + K) – Cl

  • Neg – GI loss

  • > 20-30 – RTA type I, II, IV


Central venous o2 saturation scvo2
Central Venous O2 Saturation (ScvO2) equivalents

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

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


Few values

2 equivalents

Few Values

  • pH 7.30 PaCO2 60 PaO2 101 HCO3 28

  • pH 7.228 PaCO2 45 PaO2 100 HCO3 18

  • pH 7.55 PaCO2 26 PaO288 HCO3 28

  • pH 7.50 PaCO2 40 PaO2 98 HCO3 36


  • A 60 year old male,known case of COPD was admitted with history of acute exacerbation of breathlessness. The ABG:

    pH- 7.204 PaCO2- 68 PaO2- 65 HCO3 28

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

    pH 7.28 PaCO2 18.4 PaO2 152 HCO3 8.5

    Na 127 K 3.3 Cl 101 RBS 590mg%

    Urine Ketones -positive


  • A 40 year old female presented with acute breathlessness .Chest was clinically clear.

    She had similar attacks in the past. The ABG was

    pH 7.583 PaCO2 15.9 PaO2 137.9 HCO3 14.5

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

    pH 7.52 PaCO2 45 PaO2 94 HCO3 32

    Na 130 K 3.1 Cl 86


Expected changes in pH and HCO .Chest was clinically clear. 3- for a 10-mm Hg change in PaCO2 resulting from either primary hypoventilation (respiratory acidosis) or primary hyperventilation (respiratory alkalosis):

ACUTE CHRONIC

  • Resp Acidosis

    pH ↓by 0.07 pH ↓ by 0.03

    HCO3-↑ by 1* HCO3-↑ by 3 - 4

  • Resp Alkalosis

    pH ↑ by 0.08 pH ↑ by 0.03

    HCO3-↓ by 2 HCO3-↓ by 5

    * Units for HCO3- are mEq/L


  • SKM a case of complicated Falciparum Malaria was admitted with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

    pH 7.389 PaCO2 32.9 PaO2 153 5l/m of O2 HCO3 19.2

    Urea 97.2 Creatinine 2.8

  • He underwent HD

    pH 7.407 PaCO2 38.4 PaO2 52 5l/m of O2 HCO3 23.

    CXR  ARDS .

  • He was on mech. Ventilation

    pH 7.406 PaCO2 34.7 PaO2 101 FiO2 o.5 HCO3 21.1

  • 9 days later after his 6th HD,he had a fainting attack,detected to have tachycardia and hypotension

    pH 6.962 PaCO2 39.8 PaO2 271 FiO2 1.00 HCO3 8.8

  • Immidiately ventilated and subsequently had malena

  • Post Bicarbonate

    pH 7.136 PaCO2 42.1 PaO2 273 FiO2 1.00 HCO3 10.8

  • Post HD

    pH 7.462 PaCO2 37.8 PaO2 200 FiO2 1.00 HCO3 26.1

  • Post extubation

    pH 7.442 PaCO2 52.9 PaO2 225 FiO2 0.80 HCO3 34.9

    pH 7.570 PaCO2 24 PaO2 080 3l/m of 02 HCO3 21.3


Case 1
Case 1 with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

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

  • pH-6.788, pCO2-65,pO2-392(FiO2-1)

  • One hour later pH-7.175,pCO2-23,pO2-254(.8)

  • 7hours later pH-7.456,pCO2-24, pO2-300(.8)


  • Respiratory acidosis with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • PCO2 65, expected pH-7.2

  • Actual pH 6.788 – metabolic acidosis

  • Cause – post-tictal lactic acidosis

  • Respiratory + Metabolic acidosis


Case 2
Case 2 with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • A 48year male CRF patient presented with bradycardia, hypotension & gasping respiration. ABG: pH-7.175, PCO2-31,

    PaO2-122(NC), HCO3-11, Na-132,K-8.6

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

  • 2hours later ABG: pH-7.262,pCO2-29.3, HCO3-12.4,Na-139,K-6.2


Case 3
Case 3 with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

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

  • ABG:pH-6.9, pCO2-19,pO2-105(NC), HCO3-3.7,Na-147, K-6.1

  • 9hours later ABG:pH-7.4,pCO2-14.5, pO2-132(NC),HCO3-17.2,


Case 4
Case 4 with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

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

  • ABG:pH-7.275, PCO2-116, PaO2-71, HCO3-88.

  • She was ventilated

  • ABG:pH-7.43,PCO2-45,PaO2-80,HCO3-28


Abg sampling
ABG sampling with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • Transport of blood sample

  • Heparin flush

  • Roll the syringe

  • Transport in ice pack with ice all around

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

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


Metabolic acidosis with decreased ionized ca
Metabolic Acidosis with decreased ionized Ca with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • Pancreatitis

  • Rhabdomylosis

  • Tumour Lysis


Metabolic acidosis with decreased glucose
Metabolic Acidosis with decreased Glucose with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • Liver cell dysfunction

  • Convulsion

  • Metformin

  • Adrenal insufficiency

  • Starvation (protein calorie malnutrition)

  • Alcohol Intoxication

  • Paracetamol

  • Myxaedema

  • Severe Malaria


Metabolic acidosis1
Metabolic Acidosis with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • Hypokalemia – RTA type 1


Metabolic alkalosis1
Metabolic Alkalosis with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • Urinary Cl < 20meq/l – hypovolemia

  • Urinary Cl > 20meq/l – Hypokalemia

  • Hypokalemia – Cushings

  • Salicylate poisoning – + Metabolic acidosis + ↓Na + ↑K


Lactic acidosis type b
Lactic Acidosis type-B with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • Metformin

  • Alcohol

  • Salbutamol

  • INH

  • Malignancy


Hypomagnesemia
Hypomagnesemia with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • Reduced K+

  • Reduced Ca+


Compensations1
COMPENSATIONS with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • Compensation in same direction

    dec. in pCO2 dec in HCO3

    Acute Chronic

  • Inc. PaCO2 10  dec. pH 0.08 0.03

  • Inc. PaCO2 10  inc. HCO3 1 3.5

  • dec. PaCO2 10  dec. HCO3 2 5

  • Inc. HCO3  inc. PaCO2 0.7(0.5-1.0)

  • dec. HCO3  dec. PaCO2 1- 1.5

    lowest 7 -8


Case 11
Case 1 with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • Patient with H/O vomiting

  • pH 7.52

  • PaCO2 41.25

  • PaO2 92

  • Bicarb 36

  • FiO2 0.21


Case 2 contd
Case 2 contd. with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • pH 7.52 - Alkalosis

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

  • Expected PaCO2 52(actual 41.25)

  • Metabolic Alkalosis + Respiratory Alkalosis

  • Severe vomiting in pregnancy,

  • Diuretics/vomiting in cirrhosis

  • Post cardiac arrest(hyperventilation, bicarb


Case 21
Case 2 with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • 74 yr COPD

  • pH 7.55

  • PaCO2 56

  • PaO2 63

  • Bicarb 48

  • FiO2 0.21


Case 2 contd1
Case 2 contd. with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • PAO2 = FiO2x(BP-47)-PCO2x1.25

  • PAO2 = 0.21x413 – 56x1.25

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

  • HCO3 48(48-24=24)

  • Expected PaCO2 40+24= 64(56)

  • Metabolic Alkalosis

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


Case 31
Case 3 with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • pH 7.4

  • PaCO2 24.75

  • PaO2 105

  • Bicarb 15.3

  • FiO2 0.21


Case 3 contd
Case 3 contd. with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • HCO3 15.3(24-15.3=8.7)

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

  • Metabolic Acidosis with Respiratory Alkalosis

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


Case 41
Case 4 with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • pH 7.15

  • PCO2 30

  • PaO2 105

  • HCO3 10.3

  • FiO2 0.5


Case 4 cont
Case 4 cont. with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • Acidosis

  • HCO3 10.3, PCO2 30

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

  • Metabolic Acidosis & Respiratory Acidosis

  • After Cardiac arrest or Severe Pulmonary Oedema


Case 5
Case 5 with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • pH 7.05

  • PCO2 15

  • PaO2 150

  • HCO3 4.1

  • Na+ 135

  • Cl 100

  • FiO2 0.3


  • Acidosis with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • HCO3 4.1, PCO2 15

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

  • AG=135-100-4=30.9

  • High Anion gap Metabolic Acidosis

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


Anion gap
Anion Gap with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • Proteins – 15 K+ 4.5

  • Org acids - 5 Ca+ 5.0

  • Phosphates - 2 Mg+ 1.5

  • Sulphates - 1

    Total 23 11

    Anion Gap = 23-11=12

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


Case 6
Case 6 with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • pH 7.62

  • PaCO2 30

  • PaO2 85

  • HCO3 30

  • K+ 2.5

  • FiO2 .24


Case 6 cont
Case 6 cont. with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • Alkalosis

  • HCO3 30(30-24=6), PCO2 30

  • Expected PCO2(>40)

  • Metabolic & Respiratory Alkalosis

  • Severe vomiting in pregnancy, cirrhosis with diuretics or vomiting


Case 7
Case 7 with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

  • pH 7.44

  • PCO2 63

  • PaO2 51.75

  • HCO3 42

  • FiO2 0.28


Case 7 cont
Case 7 cont. with SOB,decreased urination ,upper GI bleed & 2 episodes of sizzure.His ABG was

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

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

  • Respiratory acidosis & Metabolic Alkalosis

  • COPD plus diuretics or steroids


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