Basics of Arterial Blood Gas

Dr Arpit Gupta
Jr2 Medicine
 Components of the Arterial Blood
Gas
The arterial blood gas provides the following values:
pH: The normal range is 7.36 to 7.44
PaO2 The normal range is 80 to 100 mm Hg.
SaO2 :The normal range is 95% to 100%.
PaCO2 :The normal range is 35 to 45 mm Hg.
HCO3 : The normal range is 22 to 26 mEq/liter
B.E. The base excess indicates the amount of excess or insufficient
level of bicarbonate in the system. The normal range is – 2 to + 2
mEq/liter.
Anion gap : 12(+_) 4
 Acid-base Balance
Henderson-Hasselbalch Equation

[HCO3-]
pH = pK + log ----------------
.03 [PaCO2]

the H-H equation can be shortened to its basic relationships:

HCO3-
pH ~ ---------
PaCO2
METABOLIC ACID BASE
DISORDERS
Pathophysiology of metabolic acid
base disoders
• Dysfunction of the primary regulating organs
( kidney and gastrointestinal tract )
• Exogenous administration of drugs and fluids
that alter the body’s ability to maintain
normal acid base balance
• Abnormal metabolism that overwhelms the
normal defense mechanisms
METABOLIC ACIDOSIS
• Metabolic acidosis is a disorder characterized by a low
bicarbonate concentration and a low pH . The compensatory
reduction in PCO2 due to hyperventilation minimizes the fall in pH
• Compensation is calculated by
PaCO2=(1.5 HCO3)+8+-2
PaCO2=1.2 HCO3
PaCO2=HCO3+15

 If PaCO2(m)=PaCO2(e) –adequate compensation.

If PaCO2(m)>PaCO2(e) –concomittant respiratory acidosis
If PaCO2(m)<PaCO2(e) –concomittant respiratory alkalosis
 Metabolic acidosis can be produced by three
major mechanisms

Increased acid generation (ketoacidosis and

lactic acidosis)
Loss of bicarbonate via the bowel (diarrhoea,
small bowel fistulas) or via the kidneys
(carbonic anhydrase inhibitors, renal tubular
acidosis) and
Diminished renal acid excretion (renal failure
or type 1 distal renal tubular acidosis).
• Metabolic acidosis are categorized on the
basis of presence or absence of unmeasured
anions ( anion gap ) .
 Anion gap
• The anion gap represents the difference in charge between
measured cations and measured anions. The missing negative
charge is made up of weak acids (A − ), such as albumin and
phosphate, and strong unmeasured anions (UMAs), such as
lactate.

• Anion gap=([Na+]−([CL−]+[HCO3−])
 Factors which can affect the anion
gap
• Dehydration : AG will increase ( conc of ions will increase)
• Hypoalbuminemia : decreases AG ( for every 1g/dl
decrease AG will narrow by 2.5 to 3 meq/l)
AG=AG(CALCULATED ) + 2.5 ( Normal albumin – Observed albumin )
• Respiratory and metabolic alkalosis
• Others ( low Mg , low k , low ca , sodium citrate , sodium
acetate )
 Increased anion gap metabolic
acidosis
• Lactic acidosis
• Ketoacidosis
• Toxins ( ethylene glycol , methanol , toluene ,
salicylates , paraldehyde )
• Renal failure
 Example 1
• A patient with poorly controlled IDDM ,
missed his insulin for 3 days
• pH=7.1 , HCO3=8 meq/l , pCO2=20 mmHg
• Na = 140 meq/l , cl=106meq/l and urinary
ketones +++
• pH < 7.4 ( acidosis )
• HCO3 < 24 ( metabolic )
• pACO2 ( compensated ) = HCO3 x1.5+8(+_)2
= 8x1.5+8(+_)2
=12+8(+_)2
=18-22
• So compensation is adequate
Anion gap = 140 –(106+8)
=26
High anion gap metabolic acidosis ( compensated )
Example 2
A 30 year old female presented with chief
complaints of yellowish discoloration of eyes and
urine for last 20 days and A/S for last 2 days .
Her ABG is as follows

pH <7.4 ( acidosis )
HCO3 < 24 ( metabolic )
pCO2(compensation)= 4x1.5+8(+_)2
= 14(+_)2
=12-16

Anion gap = 25

High anion gap metabolic acidosis ( compensated )

Example 3
50 year old male presented with chief
complaints of breathlessness for last 2 days .
Pateint is known case of hypertension and on
irregular treatment .

pH<7.4 ( acidosis )

HCO3<24(metabolic)

PaCO2( compensation )=1.5x9+8+_2

= 16-20

Compensation is inadequate

So it is uncompensated metabolic acidosis

Delta gap
• This is used to compare the appropriateness of the change in
HCO3 compared to the change in anion gap
• Used to determine if another process is present in the high
anion gap metabolic acidosis

Delta ratio = change in AG change in HCO3

 Example 4
• A 21 year old man is brought in by his father with a one week history of
vomiting. He has been diagnosed with Hashimoto’s thyroiditis by his local
doctor 4 months previously. His blood pressure is 90/48 and pulse rate
104. These are his blood gas results:
pH 7.31
pCO2 39
pO2 72
HCO3- 19
BE -7
Na 108
K 6.2
Cl 72
Glc 3.3
• pH < 7.4 (ACIDOSIS)

• Given the low HCO3 and the normal pCO2 it is METABOLIC ACIDOSIS.

• Is there adequate compensation?

Expected pCO2 is [(1.5xHCO3) +8]+2 i.e.., [(~30) + 8]+2 = 38-39 so there is
adequate compensation

• What is the Anion Gap?

Na -(Cl + HCO3) = 108-(72 + 19) = 17 so raised anion gap metabolic
acidosis. (reference is 8-16)

• Is there any other process going on? Look at the delta gap.
change in AG/change in HCO3 = 17-12(use 12 as the expected AG)/24-
19(24 is the expected HCO3)
= 5/5 = 1 so this is a pure anion gap metabolic acidosis
 BDE
BDE ( base excess or deficit) is the amount of strong acid or base
required to return the pH to 7.4, assuming that P co 2 is constant
at 40 mm Hg and that the temperature is 37° C

In metabolic acidosis , the addition of UMA to ECF results in net

gain of H+ for each anion . This is buffered by HCO3 , for each
anion gained , cause decrease in HCO3

BDE=(HCO3−24.4+[2.3×Hb+7.7]×[pH−7.4])×(1−0.023×Hb)
• BDE(NaCl) = [ (Na+) – ( Cl-) ]
• BDE(alb) = 0.25 ( 4.2 – albumin )
• BDE(NaCl) – BDE(alb) = BDE ( calculated )

• BDE - BDE ( calculated ) = BDE ( gap )

Disturbance SBDE versus Pa co 2
Acute respiratory acidosis ΔBDE = 0

Acute respiratory alkalosis ΔBDE = 0

Chronic respiratory acidosis ΔBDE = 0.4 ΔPa co 2

Metabolic acidosis ΔPa co 2 = ΔBDE

Metabolic alkalosis ΔPa co 2 = 0.6 ΔBDE

 Normal anion gap metabolic
acidosis
• Gastrointestinal bicarbonate loss ( e.g. diarrhea , external
pancreatic drainage , drugs like calcium chloride , mgso4 )

• Renal acidosis
Hypokalemia ( e.g. proximal RTA , distal RTA )
Hyperkalemia ( e.g. type 4 RTA mineralocorticoid deficiency , mineralocorticoid
resistance , voltage defect
Normokalemia ( e.g. Chronic progressive kidney disease )

• Drug induced hyperkalemia (e.g. potassium sparing diuretics ,

pentamidine , ace and arbs , calcineurin inhibitors )
In normal anion gap metabolic Acidosis

LOOK FOR URINARY ANION GAP

To differentiate renal from extrarenal cause

 URINE ANION GAP (UAG)
(URINE Na+ + URINE K+ ) − URINE CL-

• POSITIVE GAP = Possibility of DISTAL RTA ( renal cause )

• NEGATIVE GAP = Met acidosis of extra renal
Cause eg. DIARRHOEA
 Example 5
40 year old female presented with pain
abdomen and bilateral lower limb weakness

ph = 7.1 , HCO3= 10 meq/l , pCO2=24 mmHg

Na=137 , Cl=118 ,
• pH<7.4 ( acidosis )
• HCO3 < 24 ( metabolic )
• pCO2 ( compensation ) = 1.5x10 +8+_2
• = 21 – 25
• Anion gap = Na –(Cl+hco3)
• =137-(118+10)
• =11

• Normal anion gap metabolic acidosis ( compensated )

 Example 6
A patient presented with multiple episodes of
loose stools for last 2 days . His ABG shows

pH=7.2 , HCO3=16 meq/l , pCO2= 32 mmHg

Na= 135 meq/l , Cl= 110 , HCO3 = 16
• pH < 7.4 ( acidosis )
• HCO3 < 24 ( metabolic )
• pCO2 ( compensation ) = 1.5x16+8+_2
• = 30-34
• Anion gap = Na –(Cl+ HCO3)
• = 135 – (110+16)
• = 11

• Normal anion gap metabolic acidosis ( compensated )

 NO Hyperchloremic RTA, Diarrhoea, Ileostomy,
Anion gap ( > 10 )
acidosis Diabetes, Excessive NACL

Type B1
Sepsis , malignancy, hepatic disease
, beri beri , phaeochromocytoma

Lactate > 2 mmol/l

Lactic Tissue TYPE B2
acidosis hypoxia Biguanides, streptozosin , fructose ,
sorbitol

Yes Diabetic
ketoacidosis Type A
cardiogenic shock , hypovolemic
No Starvation ketosis shock , hypoxemia , profound
Ketones Glucose high
anemia , seizures

No Alcoholic
ketoacidosis

Ehylene glycol , methanol ,

ethanol
Renal failure Osmolar gap >12
Aspirin , paraldehyde
METABOLIC ALKALOSIS
• Metabolic alkalosis is manifested by an elevated arterial pH,
an increase in the serum [HCO3-], and an increase in Paco2 as
a result of compensatory alveolar hypoventilation
PACO2=0.7 HCO3
PACO2=HCO3+15

• Metabolic alkalosis occurs as a result of net gain of [HCO3-] or

loss of nonvolatile acid (usually HCl by vomiting) from the
extracellular fluid
 Causes
• Effective ECFV contraction, normotension, K+ deficiency, and
secondary hyperreninemic hyperaldosteronism

 Gastrointestinal origin ( Vomiting ,Gastric aspiration ,Congenital

chloridorrhea ,Villous adenoma )

 Renal origin (Diuretics , Hypercalcemia/hypoparathyroidism , Mg2+

deficiency , K+ depletion ,Bartter’s syndrome (loss of function mutations
of transporters and ion channels in TALH) ,Gitelman’s syndrome (loss of
function mutation in Na+-Cl- cotransporter in DCT)
• ECFV expansion, hypertension, K+ deficiency, and
mineralocorticoid excess
• High renin: (Renal artery stenosis Accelerated hypertension ,Renin-
secreting tumor ,Estrogen therapy )
• Low renin : 1. Primary aldosteronism ( Adenoma ,Hyperplasia ,Carcinoma)
2. Adrenal enzyme defects (11β-Hydroxylase deficiency ,17α-Hydroxylase
deficiency)
3. Cushing’s syndrome or disease
4. Other Licorice ,Carbenoxolone ,Chewer’s tobacco

• Gain-of-function mutation of renal sodium channel with ECFV

expansion, hypertension, K+ deficiency, and hyporeninemic
hypoaldosteronism : LIDDLE SYNDROME
 Example 7
• Abg of patient with CHF on frusemide is as
follows
• pH=7.45 , HCO3=34 meq/l , PaCO2= 48
• pH > 7.4 ( alkalosis )
• HCO3 > 24 ( metabolic )
• PaCO2 (compensated) = 0.75 x rise in HCO3
= 0.75x10
= 7.5
expected pACO2 = 40+7.5
= 47.5

Metabolic alkalosis ( compensated )

 Example 8
A 1 year old male presented with multiple
episodes of vomiting and lump in the
epigastrium .
Abg pH= 7.50 , HCO3= 34 meq/l , pCO2= 42
mmHg , Cl=90 meq/l
• pH>7.4(alkalosis )
• HCO3>24 ( metabolic )
• pCO2( compensation ) = 0.7x( diff of HCO3)
• = 7 mmHg
• pCO2 ( compensated ) = 47 mmHg

• Metabolic alkalosis ( uncompensated )

RESPIRATORY ACID BASE DISORDERS
 Respiratory acidosis
• Due to inadequate CO2 elimination either due to mismatch between
alveolar ventilation and CO2 production or due to muscle weakness

• In acute condition , increase in PACO2 is mediated simply by dissociation

of H2CO3 into H+ and HCO3 and not by any active physiologic response .
There in no change in standard base excess

• In chronic condition , Cl- is removed from plasma space , primarily by

kidney , and SID increases to return blood pH to 7.35

• According to Henderson – Hasselbach equation , the increased pH will

result to an increase in HCO3 for a given PCO2
 Causes of respiratory acidosis
• Central {Drugs (anaesthetics, morphine, sedatives) ,Stroke
Infection}

• Airway (Obstruction ,Asthma )

• Parenchyma ( Emphysema, Pneumoconiosis, Bronchitis ,Adult

respiratory distress syndrome, Barotrauma)

• Neuromuscular (Poliomyelitis, Kyphoscoliosis, Myasthenia,

Muscular dystrophies)

• Miscellaneous (Obesity ,Hypoventilation ,Permissive

hypercapnia)
 Compensation

Acute
HCO3 will increase by 1mmol/l for every 10 mmHg rise in PACO2

Chronic
HCO3 will increase by 4mmol/l for every 10 mmHg rise in PACO2
 Example 9
Following sleeping pills ingestion , patient
presented in drowsy state with sluggish
respiration with RR=4/min

pH=7.1 , HCO3= 28 meq/l , PCO2= 80 mmHg ,

PO2 = 42 mmHg
• Ph < 7.4 ( acidosis )
• PCO2 > 40 ( respiratory )
• HCO3( compensation ) = 0.1x rise in PCO2
• = 0.1x40
• =4
• HCO3 compensated = 24+4
• = 28

• Acute respiratory acidosis ( compensated )

Example 10
65 year old male presented with chief
complaints of dyspnoea on exertion for last 3
years and cough for last 2 years . His ABG
is as follows

pH < 7.4 ( acidosis )

pCO2 > 40 ( respiratory )

HCO3 ( compensation ) = 0.4x rise in pCO2

= 0.4 x 44
= 17.6

HCO3 ( compensated)= 24 + 17.6

= 41.6

Chronic respiratory acidosis (compensated)

Example 11
A 50 year old male who is known case of COPD
presented to emergency with complaints of
cough with expectoration for last 10 days and
altered behaviour for last 2 days

pH< 7.4 ( acidosis )

pCO2 > 40 ( respiratory )

HCO3 ( compensation ) = 0.4x( rise in pCO2)

= 41.6

HCO3 (compensated ) = 24+41.6

= 65

Respiratory acidosis ( uncompensated )

 Respiratory alkalosis

Compensation
Acute
HCO3 will decrease by 2mmol/l for every 10 mmHg decrease in
PACO2

Chronic
HCO3 will decrease by 4mmol/l for every 10 mmHg decrease in
PACO2
 Causes of Respiratory alkalosis
Central nervous system stimulation (Pain, Anxiety, psychosis Fever,
Cerebrovascular accident, Meningitis, encephalitis ,Tumor ,Trauma)

Hypoxemia or tissue hypoxia (High altitude Pneumonia, pulmonary

edema, Aspiration Severe anemia)

Drugs or hormones (Pregnancy, progesterone Salicylates ,Cardiac failure)

Stimulation of chest receptors (Hemothorax, Flail chest, Cardiac failure,

Pulmonary embolism)

Miscellaneous (Septicemia, Hepatic failure, Mechanical hyperventilation,

Heat exposure, Recovery from metabolic acidosis)
 Example 12
• A 15 year old boy is brought from examination
room in apprehensive state with complaints of
tightness of chest
• pH= 7.54 , PCO2=21mmHg ,HCO3=20meq/l
• Ph > 7.45 ( alkalosis )
• PaCO2 <40 ( respiratory alkalosis )
• Fall in HCO3=0.2xfall in pCO2
• =0.2x(40-21)
• =3.8
• Compensated HCO3=20.2

• Respiratory alkalosis(compensated )
STEP WISE APPROACH
to
Interpretation Of
ABG reports
Six steps logical approach originally proposed by ATS
 STEP 0
Is this ABG Authentic?

STEP 1
ACIDEMIA or ALKALEMIA?

STEP 2
RESPIRATORY or METABOLIC?

STEP 3
If Respiratory – ACUTE or CHRONIC?

STEP 4
Is COMPENSATION adequate?

STEP 5
If METABOLIC – ANION GAP?

STEP 6
If High gap Metabolic Acidosis– GAP GAP?
 Is this ABG authentic ?
• pH = - log [H+]
• Henderson-Hasselbach equation

• pH = 6.1 + log HCO3-

• 0.03 x PCO2
The [HCO3-] mentioned on the ABG is actually calculated
using this equation from measured values of PCO2 and pH
• [H+] neq/l = 24 X (PCO2 / HCO3)
pH = -log [ H+]
pHexpected = pHmeasured = ABG is authentic
 STEP 1 ACIDEMIA OR ALKALEMIA?

 Look at pH
<7.36 - acidosis
>7.44 – alkalosis
 STEP 2 RESPIRATORY or METABOLIC?

Is primary disturbance respiratory or metabolic?

pH hco3 or pH hco3 METABOLIC

pH PCO2 or pH PCO2 RESPIRATORY

 RESPIRATORY-
STEP 3 ACUTE/CHRONIC?

If respiratory, is it acute or chronic?

Acute respiratory disorder ∆HCO3 = 0.1x ∆pCo2
(acidosis)

Acute respiratory disorder ∆HCO3 = 0.2x ∆pCo2

(alkalosis)

∆pH(e-acute) = 0.008x ∆pCo2

Chronic respiratory disorder ∆HCO3= 0.4x ∆pco2

∆ph(e-chronic)= 0.003x ∆pco2

Compare, Compare, pHactual (pHa) v/s pHexpected (phe)

 pH(a) =
pH(a) = pH(e- acute) between pH(e- acute) & pH(e- chronic) pH(a) = pH(e-chronic)

ACUTE RESPIRATORY PARTIALLY COMPENSATED CHRONIC RESPIRATORY

DISORDER DISORDER
 STEP 4 ADEQUATE COMPENSATION?

IS THE COMPENSATORY RESPONSE ADEQUATE OR NOT?

METABOLIC DISORDER PCO2expected

PCO2measured ≠ PCO2expected MIXED DISORDER

RESPIRATORY DISORDER pHexpected acute-chronic

pHa ≠ pHe range MIXED DISORDER

STEP 0 • Is this ABG Authentic?

STEP 1 • ACIDEMIA or ALKALEMIA?

• RESPIRATORY or METABOLIC?
STEP 2

STEP 3 • If Respiratory – ACUTE or CHRONIC?

STEP 4 • Is COMPENSATION adequate?

STEP 5 • If METABOLIC – ANION GAP?

• If High gap Metabolic Acidosis–

STEP 6 GAP GAP?
 METABOLIC ACIDOSIS-
STEP 5
ANION GAP?

• Normal Value = 12 + 4 ( 7- 16 Meq/l)

• Adjusted Anion Gap = Observed AG +2.5(4.5- S.Albumin)

 STEP 6 CO EXISTANT METABOLIC
DISORDER – “Gap Gap”?

C/O HAG METABOLIC ACIDOSIS,ANOTHER DISORDER?

 ∆ Anion Gap = Measured AG – Normal AG
Measured AG – 12

∆ HCO3 = Normal HCO3 – Measured HCO3

24 – Measured HCO3
Ideally, ∆Anion Gap = ∆HCO3
For each 1 meq/L increase in AG, HCO3 will fall by 1 meq/L

∆AG/ HCO3- = 1  Pure High AG Met Acidosis

 AG/ HCO3- > 1  Assoc Metabolic Alkalosis
 AG/ HCO3- < 1  Assoc N AG Met Acidosis
 Mixed Acid-base Disorders

In chronically ill respiratory patients, mixed disorders are probably

more common than single disorders, e.g., RAc + MAlk, RAc + Mac,
Ralk + MAlk.

In renal failure (and other conditions) combined MAlk + MAc is also

encountered.

Always be on the lookout for mixed acid-base disorders. They can

be missed.
 Diagnosing Mixed
Acid-base Disorders

1. Do not interpret any blood gas data for acid-base diagnosis without
closely examining the serum electrolytes: Na+, K+, Cl-, and CO2.
• A serum CO2 out of the normal range always represents some type of acid-base
disorder (barring lab or transcription error).
• High-serum CO2 indicates metabolic alkalosis &/or bicarbonate retention as
compensation for respiratory acidosis.
• Low-serum CO2 indicates metabolic acidosis &/or bicarbonate excretion as
compensation for respiratory alkalosis.
• Note that serum CO2 may be normal in the presence of two or more acid-base
disorders.
 In case of respiratory acidosis , look for metabolic compensation :

 If actual pH > expected pH  Respiratory acidosis + metabolic acidosis

 If actual pH < expected pH Respiratory acidosis + metabolic alkalosis

 In case of metabolic acidosis , look for respiratory compensation :

 If actual paCO2> expected paCO2 Metabolic acidosis + respiratory

acidosis

 If actual paCO2 <expected paCO2 Metabolic acidosis + respiratory

alkalosis
In case of metabolic alkalosis ,look for respiratory compensation :

• If Actual paCO2 > expected paCO2  Metabolic alkalosis + respiratory

acidosis

• If Actual paCO2 < expected paCO2 Metabolic + respiratory alkalosis

Example
25 year old male presented with chief complaints of
yellowish discolouration of eyes and urine for last 7
days and altered sensorium for last 2 days
ABG is as follows

pH < 7.4( acidosis)

HCO3 < 24 ( metabolic )
pCO2 ( compensated ) = 1.5xHCO3+8+_2
= 1.5x5.6+8+_2
= 14.4 – 16.4
So actual pCO2 is less than expected pCO2
concomitant respiratory alkalosis is also present
Anion Gap = Na –( Cl + HCO3)
= 35
High anion gap metabolic acidosis with metabolic
alkalosis
Delta ratio = anion gap HCO3
= 1.1
 Summary:
Clinical and Laboratory Approach to
Acid-base Diagnosis
Use a full clinical assessment (history, physical exam, other lab data
including previous arterial blood gases and serum electrolytes) to
explain each acid-base disorder. Remember that co-existing clinical
conditions may lead to opposing acid-base disorders, so that pH can
be high when there is an obvious acidosis or low when there is an
obvious alkalosis.
Treat the underlying clinical condition(s); this will usually suffice to
correct most acid-base disorders. If there is concern that acidemia
or alkalemia is life-threatening, aim toward correcting pH into the
range of 7.30 - 7.52

Clinical judgment should always apply

Thank you