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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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slide2

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,
slide5

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
slide7

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
slide9
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
slide13

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
  • 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
  • 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

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)
  • 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
  • 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
  • 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

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
  • 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
  • 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
gap gap acidosis
Gap Gap 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
  • 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 Physico-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
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • 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
  • >24 Alkalosis
  • <24 Acidosis
  • Actual HCO3 + delta AG
urinary anion gap
Urinary Anion Gap
  • 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
  • Multiple Myeloma
  • Hypoalbunemia
  • Hyperkalaemia
  • Hypermagnesemia
  • Hypertriglyceredemia
  • Lithium Toxicity
  • Bromide Toxicity(pyridostigmine)
metabolic alkalosis
Metabolic Alkalosis
  • Urine Cl < 10 mEq/l – saline responsive
  • Urine Cl > 20 mEq/l – saline unresponsive
urinary anion gap1
Urinary Anion Gap
  • 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)
  • 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

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
slide45
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

slide46
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

slide47

Expected changes in pH and HCO3- 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

slide48
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
  • 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)
slide50

Respiratory acidosis

  • PCO2 65, expected pH-7.2
  • Actual pH 6.788 – metabolic acidosis
  • Cause – post-tictal lactic acidosis
  • Respiratory + Metabolic acidosis
case 2
Case 2
  • 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
  • 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
  • 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
  • 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
  • Pancreatitis
  • Rhabdomylosis
  • Tumour Lysis
metabolic acidosis with decreased glucose
Metabolic Acidosis with decreased Glucose
  • Liver cell dysfunction
  • Convulsion
  • Metformin
  • Adrenal insufficiency
  • Starvation (protein calorie malnutrition)
  • Alcohol Intoxication
  • Paracetamol
  • Myxaedema
  • Severe Malaria
metabolic acidosis1
Metabolic Acidosis
  • Hypokalemia – RTA type 1
metabolic alkalosis1
Metabolic Alkalosis
  • 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
  • Metformin
  • Alcohol
  • Salbutamol
  • INH
  • Malignancy
hypomagnesemia
Hypomagnesemia
  • Reduced K+
  • Reduced Ca+
compensations1
COMPENSATIONS
  • 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
  • Patient with H/O vomiting
  • pH 7.52
  • PaCO2 41.25
  • PaO2 92
  • Bicarb 36
  • FiO2 0.21
case 2 contd
Case 2 contd.
  • 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
  • 74 yr COPD
  • pH 7.55
  • PaCO2 56
  • PaO2 63
  • Bicarb 48
  • FiO2 0.21
case 2 contd1
Case 2 contd.
  • 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
  • pH 7.4
  • PaCO2 24.75
  • PaO2 105
  • Bicarb 15.3
  • FiO2 0.21
case 3 contd
Case 3 contd.
  • 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
  • pH 7.15
  • PCO2 30
  • PaO2 105
  • HCO3 10.3
  • FiO2 0.5
case 4 cont
Case 4 cont.
  • 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
  • pH 7.05
  • PCO2 15
  • PaO2 150
  • HCO3 4.1
  • Na+ 135
  • Cl 100
  • FiO2 0.3
slide72

Acidosis

  • 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
  • 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
  • pH 7.62
  • PaCO2 30
  • PaO2 85
  • HCO3 30
  • K+ 2.5
  • FiO2 .24
case 6 cont
Case 6 cont.
  • 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
  • pH 7.44
  • PCO2 63
  • PaO2 51.75
  • HCO3 42
  • FiO2 0.28
case 7 cont
Case 7 cont.
  • 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