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ABG.pptx
1. ARTERIAL BLOOD GAS ANALYSIS
{ABG}
DR JO MARTIN KUNCHERIA
JR1 , MD PAEDIATRICS
TDMC, ALAPPUZHA
2. TOPICS COVERED
1. ACID BASE BALANCE
2. ABG ANALYSIS
3. ACID BASE DISORDERS
4. CASE SCENARIO
3. ABG
To know the acid base status ,oxygenation &
ventilation (CO2 elimination)
Done in Critically ill children, respiratory diseases,
kidney diseases
•Serial values-
-progression of the disease/response to
treatment
4. ACID – BASE PHYSIOLOGY
• BODY PH: 7.35-7.45
7.35 ACIDOSIS
7.45 ALKALOSIS
CONTROL OF ACID BASE BALANCE
1.BUFFER :
2.KIDNEY:
3. LUNGS- Hyperventilation/ Hypoventilation
5. BUFFER:
Molecules maintaining normal body PH on adding acids/bases.
Extracellular- Bicarbonate
- routinely monitored clinically
- high concentration in body
- it is an open system
Intracellular- Phosphates
- bind upto 3 hydrogen ion
Intra & Extracellular- Proteins
- due to AA Histidine
- Extra cellular include Albumin
- Intracellular include Hb
Bone - Basic
- Sodium bicarbonate & Calcium carbonate
- Can buffer an Acid load
6. • KIDENY
- Renal tubules reabsorb bicarbonate filtered by Glomerulus
- 85% reabsorbed in PCT & 15% in ascending loop of Henle
- Tubular secretion of hydrogen ion and its urinary excretion with
generation of bicarbonate
- Acetazolamide can impair bicarbonate reabsorption in PCT
- Phosphate & Ammonia are the principal urinary buffers
- Hydrogen pump cannot lower PH of urine in CD below 4.5, here
ammonia acts as a buffer
- Aldosterone stimulates H+ excretion in CD causing an increased serum
bicarbonate concentration
7. OUTCOME OF ACID – BASE
DERANGEMENT
• Underlying etiology
• Functional status of lungs & Kidney
• Condition severity
• Duration of derangement
11. • Clean the site
• 22-25 G needle ,Prick at 30 to 40 degree over artery
• Apply gentle negative suction
• Collect 2 to 3 ml blood in a heparinized syringe , cap with a cork, roll
gently with hand, place on ice, reach lab within 15 minutes
• No air bubbles in the sample{ Po2 & Pco2 will change to room air
values}- Don’t shake/agitate the sample, just roll
• Apply firm & direct pressure to the sample site
• Analyze without delay(Every hr PH 0.05U)
18. STEP 3
• Identify compensation
Metabolic Acidosis(winters formula)
PCO2= 1.5 * (HCO3-) +8± 2
Metabolic Alkalosis
Pco2 by 7 for each 10 mEq /L (HCO3-)
19. • For every 10mm of Hg change in PCO2
Respiratory Acidosis(Acute)
{HCO3-} by 1
Respiratory Acidosis(Chronic)
{HCO3-} by 3.5
20. For every 10mm of Hg change in PCO2
Respiratory Alkalosis(Acute)
{HCO3-} by 2
Respiratory Alkalosis(Chronic)
{HCO3-} by 4
21. FORMULA FOR FINDING RESPIRATORY PROBLEM AS ACUTE
/CHRONIC
• pH=0.08 × pCo2/10
• Expected pH = 7.4 - pH
• pH in ABG = Expected pH ----- Acute
• pH in ABG > Expected pH ……. Chronic
22. STEP 4 - ANION GAP
• AG is measurement of the (unmeasured anions) –
(unmeasured cations)
= (phos +sulfate +albumin +organic acid) -(Ca +Mg +K)
• (Na +K +Ca +Mg )-
(HCo3+Cl+phos+sulphate+albumin+organic acid) = 0
• Na+-(Cl + HCO3) =
(phos+sulfate+albumin+organic acid) -(Ca+Mg+K)
Anion Gap : Na-(Cl + HCO3)
Normal AG= 4-11mEq/L
23. ANION GAP CORRECTION
• 1g/dl decrease in albumin decrease anion gap
by 2.5mEq/L
• If albumin is not close to 4g/dl the anion gap
should be corrected for albumin concentration
• AG(corrected for albumin)=
Na-{(Cl + HCO3) + 2.5(4-albumin)}
24. STEP 5 – SUSPECT ADDITIONAL DISORDERS
• Absence of Compensation
• Excessive Compensation
• Long standing pulm/renal ds
• Assisted ventillation
{ Can be found by calculating Delta Ratio}
25. • Delta Ratio: Anion Gap - 12
24 - (HCO3-)
DELTA RATIO INTERPRETATION
< 0.4 Normal AG Met. Acidosis
0.4- 0.8 Mixed normal & high AG Met. Acidosis
0.8- 2 High AG Met. Acidosis
> 2 Metabolic Acidosis with Metabolic Alkalosis
26. OSMOLAL GAP
•Calculated S osm= (2 x serum [Na, in mmol/L])+
[glucose, in mg/dL]/18+ [blood urea nitrogen,
in mg/dL]/2.8
•>20 indicates presence of osmotically active
particles (methanol, ethylene glycol)
34. NORMAL AG METABOLIC ACIDOSIS
Loss ofBicarbonate
• Diarrhoea
• GI fistula
• Exogenous chloride load (saline over use , TPN)
• Carbonic anhydrase inhibitor (Diamox)
• Renal tubular acidosis
• Compensation for Respiratory Alkalosis
35. CLINICAL MANIFESTATIONS OF METABOLIC ACIDOSIS
• Impaired cardiac contractility & increased risk
of arrhythmia
• Persistent pulmonary hypertension
• Hyperventilation
• Impairs brain metabolism , lethargy & coma
36. TREATMENT OF METABOLIC ACIDOSIS
• DKA- Insulin & IV fluid
• Lactic acidosis- IV fluid
• Chronic renal failure/RTA- long term base therapy
• Salicylate poisoning- alkali administration
• Oral base therapy: Citrate solution for younger children,
bicarbonate tab. for older children
• IV sodium bicarbonate 1mEq /kg for rapid
response
• Haemodialysis- Methanol / ethylene glycol intoxication
37. METABOLIC ALKALOSIS
A}CHLORIDE RESPONSIVE (Urinary Cl <15mEq/L)
• Gastric loss as emesis/Nasogastric suction
• Diuretics
• Cystic Fibrosis
B}CHLORIDE RESISTANT(Urinary Cl >20mEq/L),
High BP
• Adrenal adenoma/ hyperplasia
• Cushings syndrome
• 11 beta Hydroxylase deficiency
• 17 alpha Hydroxylase deficiency
Normal BP
Bartter syndrome, Gitelman syndrome, EAST syndrome
38. CLINICAL FEATURES OF METABOLIC ALKALOSIS
• Cl responsive have symptoms of volume
depletion
• Cl unresponsive have hypertension
• Ionized calcium decrease cause carpopedal
spasm
• Hypokalemia cause Arrhythmia
39. TREATMENT OF METABOLIC ALKALOSIS
• Some children nasogastric suction is decreased or
discontinued
• Addition of PPI reduce gastric secretion
• Diuretics dose can be decreased / eliminated
• Potassium sparing diuretics can block the action
of aldosterone , decrease H+ secretion
• Acetazolamide decrease bicarbonate
reabsorption in PCT
• Nacl, Kcl – volume and K deficit correction
• Adrenal adenoma resected.
• 17 alpha/11 beta OHlase def-- Glucocorticoides
40. TREATMENT OF METABOLIC ALKALOSIS
• Liddle syndrome- Triamterene , Amiloride to
block Na Channel
• Bartter/ Gitelman syndrome: Na & K
supplementation
• Gitelman syndrome requires Magnesium
• Severe Bartter syndrome benefit from
Indomethacin
41. Case scenario 1
PH 7.51 ALKALOSIS
Pco2 38 METABOLIC
HCo3 by 7
PCo2 unchanged
HCO3 31
Na 144
K 4
Cl 108
Metabolic Alkalosis which is uncompensated
42. Case scenario 2
PH 7.46 ALKALOSIS
Pco2 26.9 RESPIRATORY
PCo2 by 13
HCo3 by 3
HCO3 21.2
Na 144
K 4
Cl 108
Chronic Respiratory Alkalosis with Adequate
compensation
43. Case scenario 3
PH 7.29 ACIDOSIS
Pco2 33 METABOLIC
1.5(HCO3)+8±2= 29-33 ( adequate compensation)
AG: (140+4) –(108+15) = 18 ( High AG Acidosis)
Delta Ratio : Anion Gap - 12 = 6/9 = 0.6
24 - (HCO3-)
HCO3 15
Na 140
K 4
Cl 108
High AG with Normal AG Metabolic Acidosis
44. Case scenario 4
PH 7.34 ACIDOSIS
Pco2 55 RESPIRATORY
HCO3 by 3.5 for every 10 PCo2
PCo2 by 15
HCo3 by 4
HCO3 28
Na 154
K 4.8
Cl 116
Chronic Respiratory Acidosis of Adequate Compensation
45. Case scenario 5
PH 7.1 ACIDOSIS
Pco2 19 METABOLIC
1.5(HCO3)+8± 2= 15-19 ( adequate compensation)
AG: (148+3) –(110+6) = 35 ( High AG Acidosis)
Delta Ratio : Anion Gap - 12 = 23/18 = 1.3
24 - (HCO3-)
HCO3 6
Na 148
K 3
Cl 110
High AG Metabolic Acidosis
46. Case scenario 6
PH 7.21 ACIDOSIS
Pco2 45 METABOLIC/ RESPIRATORY
1.5(HCO3)+8±2= 33-37 ( NO compensation)
AG: (144+4) –(108+18) = 22 ( High AG Metabolic Acidosis)
Delta Ratio : Anion Gap - 12 = 10/9 = 1.1
24 - (HCO3-)
HCO3 18
Na 144
K 4
Cl 108
High AG Metabolic Acidosis with Respiratory Acidosis
47. Reference-
1. Nelson21 st edition
2. Paediatric emergencies 2nd edition
Dr Suchitra Ranjith
• Thank you
