1. Interpretation of ABG
Vijaya Patil
Professor
Dept of Anaesthesia, Critical Care and Pain,
Tata Memorial Hospital, Mumbai
2. What does ABG tell us
Three physiologic processes
◦ Oxygenation
◦ Alveolar ventilation
◦ Acid-base Balance
Mainly 4 approaches
◦ Boston approach- Henderson-Hasselbalch
equation
◦ Copenhegan approach (Base excess)-
siggard Anderson formula
◦ Anion gap based approach- widely used at
bedside
◦ Stewart Fencl strong ion difference approach
3. Anion Gap based approach
26 year old man with pain, vomiting and distended
abdomen for last 4 days
Presented to casualty
Suspected intestinal obstruction
For emergency laparotomy
In ED- started on oxygen supplements 8lt/min by face
mask
HR- 124/min, BP- 120/98mm Hg, RR- 32/min
ABG- pH- 7.21, PaO2- 80 mm Hg, PaCO2- 17mm Hg,
HCO3- 7
4. What are measured and what
are calculated variables?
PO2, PCO2 and pH are actually measured
HCO3 is calculated using henderson hasselbalch
equation
◦ pH= 6.1+log10 HCO3/0.0307x PCO2
SpO2 is also calculated
HCO3 Measured in biochem lab using total CO2
content
Machines with co oximtere measure saturation and
also give carboxy-haemoglobin and
methhaemoglobin fraction
6. Step -1 pH- 7.21, PaO2- 80, PaCO2- 17 , HCO3- 7
Assess oxygenation
Is this patient hypoxemic
Normal PaO2 80-100 mm Hg
Is his oxygenation process normal ?
Must always be interpreted in relation to FiO2 and age
104 - 1/3rd of age (on room air at sea level)
Normal P/F ratio- >400
Our patient is receiving supplemental oxygen
Probably his FiO2 is around 40%
P/F ratio- 80/.4=200
Our patient has significant shunt
D/D- bibasal atelectasis due to distended abdomen,
pneumonia due to microaspiration
7. What is his A-a gradient
PAO2 = ( FiO2(760 - 47)) - (PaCO2 / 0.8)
285.2- 21.25= 263.95
A-a gradient= alveolar – arterial PO2
263.95 -80=184
A normal A-a gradient is <10 mmHg, but
can range from 5-20 mmHg.
◦ Normal A-a gradient = (Age / 4) +4
A-a increases 5 to 7 mmHg for every 10%
increase in FiO2
9. Step- 3 pH- 7.21, PaO2- 80, PaCO2- 17 , HCO3-
7
Is it respiratory or metabolic
HCO3 moves in same direction of pH and CO2 moves
in oppos direction of pH
To decide direction of pH take neutral pH as 7.4
PaCO2- 17mm Hg; HCO3- 7
Primary cause is metabolic
CO2 is low due to compensation- acidosis stimulates
respiratory center via chemoreceptors
10. Step-4 pH- 7.21, PaO2- 80, PaCO2- 17 , HCO3-
7
Is primary disturbance compensated and if yes is
compensation adequate?
11. Rules of compensation
The general rule for all acid-base disorders is that the body's
compensatory response is almost never sufficient to return the
plasma pH to normal (7.4)
If the pH is normal then it suggests that a second, acid-base
disorder is present
Beware of prior interventions like mechanical ventilation or
bicarb infusion
Respiratory acidosis: <24 hrs : Δ[HCO3] = 1-2/10x Δ
PCO2
>24 hrs: Δ [HCO3] = 5/10 x Δ
PCO2
Respiratory alkalosis: 1 - 2 hrs: Δ [HCO3] = 2/10 x Δ
PCO2
> 2 days: Δ [HCO3] = 5/10 x Δ
PCO2
For metabolic acidosis: Expect PCO2 = (1.5 x [HCO3]) + 8 ± 2
(also known as Winters formula)
12. In our patient.. pH- 7.21, PaO2- 80, PaCO2- 17 ,
HCO3- 7
In metabolic acidosis Expected PCO2 = (1.5
x [HCO3]) + 8 2
(1.5 x 7) + 8 2 =18.5 2
In our patient-17
Adequate compensation
13. Causes of inadequate
compensation
Respiratory limitations
◦ Mechanical ventilation
◦ Problems with respiratory centre
◦ Lung pathology (COPD)
◦ Neuromuscular problems
Metabolic limitations- renal dysfunction
14. Step-5
What is cause of metabolic acidosis
Calculate anion gap
◦ Difference in cations and anions
No actual gap but amount of unmeasured anions
(proteins, sulphates, lactates etc)
[Na+] + [K+] - [Cl-] - [HCO3-]
Normal 12-16 mmol/lt
Albumin is a major element of anion gap
◦ Hypoalbuminemia- alkalosis
Corrected anion gap- Observed Anion Gap + 2.5 x
(Normal albumin- observed albumin)
Low albumin can lead to falsely low anion gap
15. Rule no-1
Never interpret acid base disturbances without
electrolytes and albumin
In our patient- S.Na 130,S. K 2, chloride 84, bicarb 7
Anion gap- 36
Diagnosis- raised anion gap acidosis
16. Acidosis -causes
Raised anion gap Normal anion gap
Ketoacidosis
◦ Diabetic
◦ Starvation
◦ Alcoholic(ethanol)
Lactic acidosis
Uremia
Toxins
◦ Methanol
◦ Ethylene glycol
◦ Propylene glycol
◦ Salicylates
◦ Paraldehyde
GI losses of HCO3
Proximal RTA
ATN
Distal RTA
Hypoaldosteronism
Infusion of ammonium
chloride or hyperelimentation
17. Step- 6
Compare anion gap with bicarbonate gap
Delta ratio = (Increase in Anion Gap / Decrease in
bicarbonate)
18. How to use delta ratio
Delta ratio Diagnosis
<0.4 Hyperchloraemic normal anion gap acidosis
0.4-0.8 Consider combined high AG & normal AG acidosis BUT note that the
ratio is often <1 in acidosis associated with renal failure
1-2 Usual for uncomplicated high-AG acidosis
Lactic acidosis: average value 1.6
DKA more likely to have a ratio closer to 1 due to urine ketone loss
(esp if patient not dehydrated)
>2 Suggests a pre-existing elevated HCO3 level so consider:
a concurrent metabolic alkalosis, or
a pre-existing compensated respiratory acidosis
19. Our patient…
Increase in Anion gap 22 (36-14)
Decrease in Bicarb 24-7= 17
Delta gap= 22/17=1.2
Diagnosis??
Remember your patient has intestinal obstruction,
is vomitting, is tachycardic
His BP is 120/98
Narrow pulse pressure- Certainly he is
hypovolemic
Lactic acidosis due to hypoperfusion
20. Management
Would you take this patient to OT?
Certainly not- fluid resuscitate well
Would you give bicarb for acidosis?
21. Use of bicarb in metabolic
acidosis
undesirable effects
Hypernatraemia (893meq Na/Lt of NaHCO3)
Hyperosmolality
Volume overload
Rebound or ‘overshoot’ alkalosis
Hypokalaemia
Impaired oxygen unloading due to left shift of
the oxyhaemoglobin dissociation curve
Acceleration of lactate production by removal
of acidotic inhibition of glycolysis
CSF acidosis
Hypercapnia
22. Use of bicarb in metabolic
acidosis
Ventilation must be adequate to eliminate the CO2
produced from bicarbonate
Bicarbonate may cause clinical deterioration if
tissue hypoxia is present
Bicarbonate is probably not useful in most cases of
high anion gap acidosis
The preferred management of metabolic acidosis is
to correct the primary cause
Bicarbonate therapy may be useful for correction of
normal anion gap acidosis
23. Let us try to interprete this ABG?
pH 7.2, PCO2- 66, PO2- 75, HCO3- 26 on air
24. pH 7.2, PCO2- 66, PO2- 75, HCO3- 26 on air
Oxygenation- adequate
Acidemia
Respiratory
In acute resp acidosis HCO3 rise is 1-2 meq/10 CO2
Rise in CO2 -24, hence expected rise in bicarb
2.4meq
Adequate compensation
25. A healthy 45 yr old lady operated for open
cholecystectomy
At the end of surgery reversed and shifted to recovery
After 30 minutes nurse found her unresponsive
Diagnosis- acute respiratory acidosis probably due
to narcotic overdose/ residual recurarisation
26. 75 yr old man heavy smoker with bad COPD operated
for THR 4 days back under spinal epidural
Developed infection at surgical site and needs
debridement
Is febrile, tachypnoec with BP 90/70 mm Hg
27. pH 7.2, PCO2- 66, PO2- 75, HCO3- 26
Oxygenation- adequate
Acidemia
Respiratory
h/o COPD- expect chronic CO2 retainer
Previous ABG- PH 7.36, PCO2 56, HCO3- 30
Present bicarb is 26- 4 meq less than expected
suggesting probable metabolic component as well
This is a mixed disorder
Get electrolytes and calculate anion gap
Probably has lactic acidosis due to sepsis and
hypoperfusion and will need adequate rescuscitation
before proceeding for surg (source control)
28. Rule No -2
Never treat ABG isolated and always correlate
clinically
29. Patient in the recovery room has been
found to be Cyanosed with shallow
breathing .
SPO2 - 86 %
Following is his ABG on Room Air
ABG- PH 7.08, PCO2 79.5, PO2 36.5, HCO3
26
30. Is this sample arterial?
◦ For PO2 of 36.5 I expect saturation of 60-65%
◦ Saturation on pulse oximeter is 86
◦ Sample is venous
Oxygenation- 86% sats
◦ Expect PO2 around 50-55
◦ A-a gradient ( FiO2 (760 - 47)) - (PaCO2 / 0.8)-
PaO2
◦ (150- 100) – 50 =0
◦ There is no lung pathology
Acidosis- resp in origin
Compensation- acute postop problem
<24 hrs : Δ[HCO3] = 1/10x Δ PCO2
Bicarb should raise by 4
31. Few more examples….
52 yr old lady complained of head ache and seizures
CT brain- S/O SOL
Presented to TMH OPD
Referred to PAC for fitness for LN Bx
◦ In PAC –found to be extremely tachypnoec with altered mentation
Admitted to ICU
ABG –pH 7.5, pCO2 17, pO2 88 HCO3 13, Na 136, Cl
104, K 2.8
Alkalosis- respiratory in origin, AG- N
History of almost 8 days- suggestive of chronic alkalosis
Chronic respiratory alkalosis- drop in bicarb by 5 for
every 10 drop in CO2
Adequate compensation
32. Stewart approach
Also called as quantitative approach
Quantitative analysis of pH deviation
How much each element of acid base controller
substances will act pH deviation
Independent variables (PaCO2, SID, Atot )
Dependent variables (pH, H, HCO3,......)
33. Stewart approach
Acid-base abnormalities should be seen as resulting from
other biochemical changes in the extracellular
environment
◦ Strong ions (Na+,Cl-,K+,SO4 2-,Mg2+,Ca2+)
◦ Weak acids(albumin , phosphate )
◦ Carbon dioxide
To maintain electrical neutrality
[H+ ] is a function of SID, A TOT , PCO2 , and several
constants.
All other variables, most notably [H+], [OH-], and [HCO3 -
], are dependent and cannot independently influence the
acid-base balance
34. SID apparent = [Na+k+Ca+Mg] - [Cl+ lactate]
SID effective = [HCO3] + Atot
Strong ion gap (SIG)/NUI = SIDa- SIDe Normal Strong ion gap is
zero