Acid Base Gas (ABG)

Dr Anju Gupta (Assistant Professor)

Anesthesiology, CNBC, Delhi
&
Dr Nishkarsh Gupta (Associate Professor)
Anesthesiology, DRBRAIRCH, AIIMS, New Delhi
 Outlines of talk
• What’s an ABG?
• Difference between ABG and VBG
• Blood gas sampling
• Acid/Base Physiology
• Compensation
• General approach to ABG
• Interpretation
• Case scenarios
• Take home message
 What is an ABG?
Blood Gas drawn from an artery to assess oxygen deficiencies
from primary ventilatory disturbances and/or metabolic acid-
base abnormalities

Oxygenation

Gas exchange

Acid-base
balance
 Why Order an ABG?
• Aids in diagnosis
• Provides clues about clinically unrecognized
disorders
• Helps guide treatment plan
• Aids in ventilator management
• Assess response to an intervention/ progress of
illness
• Acid/base status may alter electrolyte levels
critical to patient status
 Why an ABG instead of Pulse oximetry?
• Pulse oximetry does not assess ventilation (pCO2)
or acid base status.
• Pulse oximetry becomes unreliable when
saturations fall below 70-80%.
• Technical sources of error (ambient or fluorescent
light, hypoperfusion, nail polish, skin
pigmentation)
Radial artery- first choice
Which artery to choose?

Superficial

Collaterals

Compressible
Problems while
sampling for ABG
 Performing the Procedure:
Allen’s test vs modified Allen’s test
 Universal precautions
 Positioning (hyper-extending wrist)
 Palpate the arterial pulse & do ALLEN’s test
 Infiltrate 2% xylocaine
 Line the needle up with the artery, bevel side up
 Enter the artery & allow spontaneous fill of syringe
 Withdraw the needle & hold pressure on the site.
 Remove any air bubbles
 Gently mix the specimen by rolling it b/w palms
 Place the specimen on ice & transport immediately.
 Allen’s test
• The Allen's test assesses collateral circulation in the hand,
in 2 steps.
• First – suspected radial artery occluded at wrist for 3 min ,
hand colour compared with the other hand, if no change
means sufficient collaterals present through ulnar artery.
• Second – ulnar artery occluded for 3 min, change in colour
of hand is highly suspicious of radial artery occlusion.
• Positive test – presence of radial artery occlusion.
• Step 2 occludes the ulnar artery. A change in hand color
means the potential for radial artery occlusion is high.
• That is a positive Allen's test, which contraindicates radial-
artery puncture
 Modified allen’s test
• To assess ulnar artery collateral flow
• First – patient is asked to make tightly closed fist
• Second- pressure applied at wrist to compress both radial
& ulnar artery
• Remove obstructing pressure from ulnar artery while
keeping radial artery obstructed
• Flushing of palm within 5-15 sec- ulnar artery is capable of
supplying entire hand while radial artery is occluded.
• This normal flushing of the hand is considered to be a
positive modified Allen's test.
• A negative modified Allen's test is one in which the hand
does not flush within the specified time period. This
indicates that ulnar circulation is inadequate or
nonexistent
 Collection Problems
• Use of heparin
– Dilution effect -  HCO3- & PaCO2
• Air bubbles
• Specimen transport
– Sample to be analysed as soon as
possible
– Iced sample can be stored for 1 hr in
glass syringe and 15 min in plastic PO2 150 mmHg & PCO2 0 mm Hg in air
syringe bubble (room air)
– Blood is living tissue that continues to
consume O2 and produce CO2 Air
In vivo values
contamination

pH 7.40 7.45
pCO2 40 30
pO2 95 110
Plastic vs glass syringes
 Effect of Temperature
Increased Decreased
temperature temperature
pO2 Increase Decrease

pCO2 Increase Decrease

pH Decrease Increase

 Most clinicians do not remember the normal values of pH &

PCO2 at temp other than 37 C
 In pts with hypo/hyperthermia, body temp usually changes
with time (per se/effect of rewarming/cooling strategies) –
hence if all calculations done at 37 C easier to compare
 Values other than pH & PCO2 do not change much with temp
 WBC Larcency
• Rare phenomenon due to very high levels of
WBC(>50000)
• WBCs are metabolically active and consume the
oxygen leading to a fall in PaO2

• Solution: Get the ABG done within 5 min

• Others: Keep sample in ice / Add Potassium
cyanide
 Effect of Anticoagulation
 Amount of Heparin recommended Is 50U/ml of
blood drawn
 That is 0.05ml of heparin(1ml=1000U) for 1 ml
blood
 Dead space in a 5ml syringe = 0.2ml
 Thus you must take 4 ml of blood for correct
dilution
 Problems with over dilution: spurious fall in pCO2,
glucose, Hb and importantly electrolytes (esp
calcium)
 Best – Lyophilised Heparin coated syringes
Effect of anticoagulation
 ABG Vs. VBG
ABG VBG

pH 7.4 7.35

PCO2 40 46

HCO3 24 25

pO2 80-100 < 40

O2 saturation >95 60-85

Number of attempts Single Multiple

 Normal reference range

pH • 7.35-7.45
Acidosis Alkalosis
HCO3 • 22-26 mEq/L
PaCO2 • 35-45 mmHg
pH<7.35 pH>7.45
PaO2 • 80-100 mmHg
SaO2 • 96-100%
pCO2>45 pCO2<35
Base E/D • -2 to +2 mEq/L
Anion gap • 8-12 mEq/L HCO3<22 HCO3>22
A-a O2 • 5-25 mm Hg
 Principles of Acid-Base
• Acid base relationship is critical for homeostasis

• pH is maintained by 3 systems
– Physiologic buffers
– Lungs
– Kidneys

• Disorders in any of these systems leads to

alterations in blood pH
 Buffers:
Buffers in ICF Buffers in ECF
Intracellular Proteins Carbonate-Bicarbonate Buffer 53%

H2PO4-HPO4- system Plasma (35%)

Erythrocyte(18%)

Hemoglobin
Plasma Proteins
Organic & Inorganic Phosphates

Intracellular buffers are responsible for ~85% buffering in

Metabolic acidosis and ~35% in Metabolic alkalosis and almost
complete buffering in Respiratory acidosis and alkalosis.
 Lungs
• Changes in pH sensed by chemoreceptors
• Peripherally (carotid bodies)
• Centrally (medulla oblongata)

• Drop in pH-metabolic acidosis

• ↑ minute ventilation → ↓ PaCO2

• Increase in pH –metabolic alkalosis

• ↓ ventilatory effort → ↑ PaCO2
 Kidneys
• Play no role in acute compensation

• 6-12hrs respiratory acidosis

– Active excretion of H+
– Retention of HCO3-

• >6hrs of respiratory alkalosis

– Active excretion of HCO3-
– Retention of H+
 Arterial Blood Gas Machine

pH, PCO2, PO2

• The [HCO3-] and the base difference are calculated

values using Henderson-Hasselbach equation
 Blood Gas Report
• Acid-Base Information
– pH
– PCO2
– HCO3

• Oxygenation Information
– PO2 [oxygen tension]
– SO2 [oxygen saturation]
 Oxygenation Information
• PaO2 80 - 100 mm Hg
• SaO2 95 - 100 % is a normal saturation

pO2 (mm Hg) SpO2 (%)

Normal values on air >80 >95

Mild hypoxemia 60-79 90-94

Moderate hypoxemia 40-59 75-89

Severe hypoxemia <40 <75

 Inspired O2 – PaO2 Relationship

Predicted minimum PaO2

FiO2 (%)
(mmHg)
30 150

40 200

50 250

80 400

100 500

If PaO2 < FiO2 x 5, hypoxemic at room air

 pH
• Normal serum pH is maintained within a very
narrow range of 7.36-7.44
Acidosis (pH<7.35) Alkalosis
(pH>7.45)

Mild 7.3-7.34 7.46-7.5

Moderate 7.2-7.29 7.51-7.54

Severe <7.2 >7.55

Incompatible with <6.8 >7.8

life
 pCO2
• PaCO2: partial pressure of carbon dioxide
dissolved in the arterial plasma

– Normal: 35 - 45 mm Hg
– Is regulated in the lungs
– > 45 mm Hg = respiratory acidosis
– < 35 mm Hg = respiratory alkalosis
 Bicarbonate (HCO3-)
• Std HCO3-: HCO3- levels measured in lab after
standardizing at PCO2 of 40 mm Hg, temperature 37
degree C and SpO2 of 100%
• Actual HCO3-: HCO3- levels calculated from pH & PCO2
directly
• Reflection of non respiratory (metabolic) acid-base status
• Normal: 22 -26 mEq/L
• Is regulated by the kidneys
– < 22 = metabolic acidosis
– > 26 = metabolic alkalosis

Significance – in cases of respiratory acidosis,

actual bicarb > std bicarb
 Simple vs Mixed
• Simple/Primary acid–base disorders : when compensation
is appropriate
• A respiratory change is called “acute” or “chronic”
depending on whether a secondary change in the
bicarbonate concentration
• Mixed acid–base disorders
– When compensation is inappropriate i.e. the secondary response differs
from that which would be expected

Uncompensated Partially Fully compensated

compensated
Abnormal pH Abnormal pH Normal pH, other
values abnormal
  acid-base disorders
Disorder Primary Responses Compensation
Buffers
Metabolic  [H+]  PH  HCO3-  pCO2
acidosis (mins)

Metabolic  [H+]  PH  HCO3-  pCO2 Respiratory

alkalosis
(mins-24
Respiratory  [H+]  PH  pCO2  HCO3- hours)
acidosis
Renal
Respiratory  [H+]  PH  pCO2  HCO3- ( hrs-5days)
alkalosis

Respiratory acidosis  metabolic alkalosis

Respiratory alkalosis  metabolic acidosis
 For 10 mm Hg change in PCO2:
Change in HCO3
RESPIRATORY RESPIRATORY
ACIDOSIS ALKALOSIS

ACUTE 1 2

CHRONIC 4 4
 Metabolic Compensation
Compensation HCO3- : pCO2

• Metabolic Acidosis 1 : 1.25

• Metabolic Alkalosis 1 : 0.75

ABGs obtained
in the ICU

pH 7.18

PCO2 20
mmHg

HCO3 7
mEq/L
 Steps to
Solve
Acid-Base
Disorders
 Step-wise approach to ABG
1. Check ABG validity?
2. Assess oxygenation
3. Acidemic or Alkalemic?
4. Primary ds -- Metabolic or Respiratory?
5. For metab acidosis -- what is the Anion Gap?
6. If high-AG metab acidosis -- dHCO3?
7. Respiratory compensation for metab ds?
 ABG Validity
• Calculate [H+] : modified Henderson – Haselbach
equation
[H+] = 24 x [PaCO2] / [HCO3-]
• Normal [H+] = 40 nmol/L (pH=7.4)
• 1nmol/l change in [H+] changes pH by 0.01 in a
pH range of 7.1 – 7.5
OR
• Subtract the two digits after decimal point in pH
from 80
E.g. pH = 7.23 , [H+] = 80-23 = 57 nmol/L
• Calculated pH must be close to the measured pH
 Base Excess
• Normal value + 2 mEq/L
• HCO3 amount above or below normal content of
buffer base
• Depends upon entered Hb value and measured pH
and PCO2 values
• Negative BE also referred to as Base Deficit
• True reflection of non respiratory (metabolic) acid
base status
 ANION GAP
• AG = [Na+] - ([Cl-] + [HCO3-])
• Normal anion gap is 12 ± 4 meq/l
Anion Gap reflects the unmeasured anion and cations.

Unmeasured Anions Unmeasured Cations

Proteins (Alb) 15 mEq/L Calcium 5 mEq/L

Organic acids 5 mEq/L Potassium 4.5 mEq/L

Phosphates 2 mEq/L Magnesium 1.5 mEq/L

Sulfates 1 mEq/L

Totals: 23 mEq/L 11 mEq/L

 Unmeasured ions
Albumin, PO43-
Mg2+ Ca2+ K+ Acetate

Anion Gap

HCO3-

Na+
Cl-
 Bicarbonate gap (dHCO3)
• Only necessary if there is an AG metabolic acidosis.
• Does the increase in AG completely explain the ABG?
– Bicarbonate ↓→ presence of unmeasured anions
– For one molecule of anion, one molecule bicarbonate lost.
– Bicarbonate level can be therefore be calculated by formula=
(patient AG -12) – (24 – patient HCO3)
• +ve Bicarbonate gap:
– Met alkalosis
– Resp acidosis compensated by HCO3 retention
• -ve Bicarbonate gap:
– Non AG Met acidosis.
– HCO3 excretion to compensate for resp acidosis.
 Case 1
• A 66 year old man seen in emergency room. He has
had 8 days of severe diarrhea, abdominal pain, &
decreased intake, but adequate intake of liquids.
His medical history is significant for diabetes &
hypertension. Presently on enalapril, aspirin,
atenolol, metformin.Physical examination: B.P
105/70, Pulse 72/min, R.R 32.
• Lab report: Na 136, K 3.9, Cl 114, Creatinine 1.2,
Gluc:128
• ABG: pH 7.27 ; PO2 90; PCO2 27 and HCO3 13
• Which acid base disorder is present?
• pH low & ↓ HCO3 Metabolic acidosis.

Respiratory compensation :
• 1 mEq decrease in HCO3 compensated by 1.25 mmHg
decrease in pCO2
• Decrease in HCO3 = 24-13 =11
• Decrease in pCO2 = 1.25 x 11 =13.75
Expected PCO2 = 40-14 = 26 (Adequate)
• Anion Gap = 136– (114 + 13) =9

• Non-AG Metabolic Acidosis

 Metabolic acidosis
 Characterized by fall in plasma HCO3 & fall in pH and compensatory
decreased PaCO2

Normal Anion Gap Increased Anion Gap

1. Loss of HCO3 1. Metabolic disorders:

Diarrhoea, Lactic acidosis, DKA
Ureterosigmoidostomy,
Proximal RTA

2. Failure to excrete H+ 2. Addition of exogenous acids

Distal RTA Salicylate/ methanol poisoning

3. Addition H+ 3. Failure to excrete acid

NH4CL infusion Acute/chronic renal failure
• Clinical manifestations

Respiratory Kussmaul’s breathing

CVS Increased susceptibility to
arrythmia
Decreased response to
inotropes and secondary
hypotension
CNS Headache
Confusion
Coma
Kidney Renal failure
 Treatment of Metabolic Acidosis
1. Specific management of underlying disorder

2. Alkali therapy

Reserved only for selective patients with Severe Acidemia

Indications: pH< 7.15-7.2

HCO3 < 10meq/l

Amount of HCO3 required= (Desired HCO3 – Actual HCO3 ) X0.3 X Body

weight

Half of the correction is given followed by repeat ABG after 30 minutes

 Case 2
• ABG of a patient with CHF on furosemide
– pH 7.48
– HCO3 34 mEq/l
– PaCO2 48 mmHg

• Which acid-base disorder is present?

• pH  = alkalosis
• HCO3  = s/o metabolic alkalosis
• PaCO2  = s/o compensation
• Rise in PaCO2 = 0.75 x rise in HCO3 = 0.75 x (34-
24) = 7.5
• Expected compensation = 40+7.5= 47.5 mmHg ~
actual PaCO2 s/o simple acid base disorder
• So patient has primary metabolic alkalosis due
to diuretics
 Metabolic Alkalosis
• Characterized by ↑ HCO3 , ↑ pH,& compensatory ↑
in PaCO2
• Serum potassium & chloride low
• Urinary chloride estimation useful for diagnosis

• Clinical features:
• CNS- ↑ neuromuscular excitability leading to
paraesthesia, headache.
• CVS- hypotension & arrhythmias
• Others- weakness, muscle cramps
 Causes
• :
Chloride sensitive Chloride resistant
(urine CL- <20meq/l) (urine CL- > 40meq/L)

GI Losses Renovascular
Nasogastric suction hypertension
Vomiting Hyperaldosteronism

Renal acid losses

Penicillins Normotensive
Post-diuretic, Administration of alkali
Post-hypercapneic
 Treatment
• Chloride sensitive-
– IV normal saline volume expansion
– Discontinue diuretics

• Chloride resistant-
– Remove offending agent
– Replace potassium if deficit
– Extreme Alkalosis
– Hemodialysis
 Case 3
• Case scenario: Following sleeping pill ingestion,
patient presented in drowsy state with sluggish
respiration with rate of 4/min
– pH 7.1
– HCO3 28 mEq/l
– PaCO2 80 mmHg
– PaO2 42 mmHg

• Which acid-base disorder is present?

 Interpretation
• PaO2  = severe hypoxemia
• pH  = acidosis
• PaCO2  = s/o respiratory acidosis
• HCO3  = s/o compensation
• Rise in HCO3 = 0.1 x rise in PaCO2 = 0.1 x (80-40)
= 4 mEq/l
• Expected compensation = 28 mEq/l ~ actual
PaCO2 s/o simple acid base disorder

• So patient has primary respiratory acidosis

due to respiratory failure (sleeping pills)
 Respiratory Acidosis
Causes
CNS depression Sedatives, narcotics, CVA, brain trauma
Myasthenia gravis, tetanus, guillain barre
Neuromuscular disorders syndrome

Foreign body, tumor, reactive airway,

Acute airway obstruction obstructive sleep apnea, laryngospasm or
bronchospasm
Severe pneumonia, pulmonary edema,
Respiratory disorders pleural effusion, ARDS

Hemothorax, pneumothorax, flail chest

Chest cavity problems

Chronic lung disease

Obstructive or restrictive

Central hypoventilation OSA

• Clinical presentation:
– Headache, confusion, irritability, delirium

• Treatment:
– Treat underlying cause
– Establish patent airway & restore oxygenation.
– Treatment of pulmonary infection, brochodilator therapy, removal
of secretions.
– Oxygen therapy
– Mechanical ventilatory support
 Case 4
• A 15 year old boy brought from examination hall
in apprehensive state with complain of tightness
in chest.
– pH 7.54
– PCO 2 21
– HCO 3 21

• Which acid-base disorder is present?

 Interpretation
• pH ↑ = s/o alkalosis
• ↓ PCO 2 = s/o respiratory alkalosis
• ↓ HCO 3 = s/o compensation

• Expected compensation = 0.2 X (40- 21) = 4

• Expected HCO 3 = 24-4= 20 meq/l ~ actual HCO 3

• s/o simple acid-base disorder.

• so, the patient has primary respiratory
alkalosis due to anxiety.
 Respiratory Alkalosis
• Diagnosis:
– ↓ PaCO2 (<35mmHg)
– ↑ pH
– Compensatory ↓ HCO3

• Clinical features:
– Headache
– Arrhythmias
– Tetany
– Seizures
 Respiratory Alkalosis
Causes of Respiratory Alkalosis
Anxiety, pain, fever
Hypoxia, CHF
Lung disease with or without hypoxia – pulmonary embolus, reactive
airway, pneumonia
CNS diseases
Drug use – salicylates, catecholamines, progesterone
Pregnancy
Sepsis, hypotension
Hepatic encephalopathy, liver failure
Mechanical ventilation
Hypothyroidism
High altitude
 Treatment
• Reassurance
• Anxiolytic
• Sedation
• Pain control
• ↓ RR and TV when on mechanical ventilation
• Oxygen supplementation
 Case 5
• Known case of COPD develops severe vomiting
– pH 7.4
– HCO3 36meq/l
– PCO2 60mmHg

• Which acid-base disorder is present?

CAN A PATIENT WITH NORMAL pH
HAVE ACID BASE DISTURBANCES ?

YES

MIXED ACID BASE DISTURBANCES

 Interpretation
• pH normal = s/o either no acid –base disorder or
mixed
• ↑ PCO2 = s/o respiratory acidosis ( due to COPD)
• ↑ HCO3 = s/o metabolc alkalosis ( due to
vomiting)
• the patient has mixed disorder , respiratory
acidosis & metabolic alkalosis.
• Normal pH can be due to end result of opposite
changes caused by primary disorder.
 Case 6
• 35, woman, community 1. Assess oxygenation: Adequate
2. Acidemic or Alkalemic?:Acidaemia
acquired pneumonia, 3. Primary disoder?: Metabolic
brought with confusion. 4. AG 26
5. If high-AG -- dHCO3?
• TLC-24000  Excess anions= 26-12= 14
• Na-138, K-3.4, Cl-107  Hence, HCO3 should be 25-14 = 11
 But HCO3 6 less than predicted
• Urea-15mg/dl, Cr-0.8
Non AG Met acidosis.
mg/dl
• ABG 6. Respiratory compensation for metab ds?
Expected PaCO2 = 1.5 (HCO3-) + 8 + 2
– pH- 7.08 = 1.5 (5) + 8 + 2
– p CO2 -20mmHg = 15 + 2 = 13-17
Here PaCO2 is 20
– paO2 86
– HCO3- 5 mEq/l Additional respiratory acidosis
 Interpretation
• FINAL DIAGNOSIS
– Anion gap metabolic acidosis
– Non anion gap acidosis
– Respiratory acidosis
– Adequate oxygenation
 Key Takeaways
• Acid Base Homeostasis is all about maintenance of
normal H+ concentration.
• Valuable information can be gained from an ABG as to
the patient`s physiologic condition
• ABGs are frequently used to detect indices of
oxygenation, ventilation and acid base balance
• All intensivist, anaesthesiologist and physician must
know to analyze ABG report systematically
• ABG to be interpreted within 15 minutes of collection
to prevent false results
• Anion gap must always be calculated to decipher the
complex acid-base disorders in critically ill patients.
 THANK YOU

Any queries mail to:

drnishkarshgupta@gmail.com
 Base-deficit/excess {Copenhagen approach}

• Developed by Siggard- Anderson - 1948

• “The amount of strong acid or base required to
return pH to 7.4 assuming Pco2 of 40 mmHg &
temp of 38”.
• The initial use of whole-blood base excess was
criticized because of the dynamic activity of red
blood cells within the acid-base paradigm of gas
and electrolyte exchange.
• Was modified in the 1960s to use only serum
base excess, and the calculation became the
standardized base excess.