Interpretation of ABG

Vijaya Patil
Professor
Dept of Anaesthesia, Critical Care and Pain,
Tata Memorial Hospital, Mumbai
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
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
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
Validation of report- a redundant step

H X HCO3/PaCO2 = 24 +/- 2 nmol/lt

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
What is his A-a gradient
PAO2 = ( FiO2(760 - 47)) - (PaCO2 / 0.8)
285.2- 21.25= 263.95
A-a gradient= alveolar – arterial PO 2
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
Step- 2- pH- 7.21, PaO2- 80, PaCO2- 17 , HCO3- 7

 Look at pH
 Acidemic (pH < 7.35) or alkalemic (pH > 7.45)
 Our patient pH 7.21- acedemic
 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
 Step-4 pH- 7.21, PaO2- 80, PaCO2- 17 , HCO3-
7
 Isprimary disturbance compensated and if yes is
compensation adequate?
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)
 For metabolic alkalosis: Expect PCO2 = (0.7 x [HCO3]) + 21 ± 1.5
In our patient.. pH- 7.21, PaO2- 80, PaCO2- 17 , HCO3- 7
In metabolic acidosis Expected PCO2 = (1.5 x
[HCO3]) + 8  2
(1.5x 7) + 8  2 =18.5  2
In our patient-17
Adequate compensation
 Causes of inadequate compensation
Respiratory limitations
◦ Mechanical ventilation
◦ Problems with respiratory centre
◦ Lung pathology (COPD)
◦ Neuromuscular problems
Metabolic limitations- renal dysfunction
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
 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
 Acidosis -causes
Raised anion gap Normal anion gap
 Ketoacidosis  GI losses of HCO3
◦ Diabetic  Proximal RTA
◦ Starvation  ATN
◦ Alcoholic(ethanol)
 Distal RTA
 Lactic acidosis
 Hypoaldosteronism
 Uremia
 Infusion of ammonium chloride
 Toxins
or hyperelimentation
◦ Methanol
◦ Ethylene glycol
◦ Propylene glycol
◦ Salicylates
◦ Paraldehyde
Step- 6
 Compare anion gap with bicarbonate gap
 Delta ratio = (Increase in Anion Gap / Decrease in
bicarbonate)
 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
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
 Management

Would you take this patient to OT?

Certainly not- fluid resuscitate well
Would you give bicarb for acidosis?
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
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
Let us try to interprete this ABG?

pH 7.2, PCO2- 66, PO2- 75, HCO3- 26 on air

 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
 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
 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
 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)
 Rule No -2

Never treat ABG isolated and always correlate clinically

Patientin 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
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
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
 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,......)
 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
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