ABG is the important diagnostic tools in Pulmonary & Critical Care setting. Here how to interpret its stepwise and significance each of the components of ABG in both Blood gas and acid base abnormality By Dr. Anirban Saha

1. ARTERIAL BLOOD GAS
INTERPRETATION
BY
DR. ANIRBAN SAHA
1ST YR PG RESIDENT
DEPT. OF PULMONARY MEDICINE
VIMSAR,BURLA

2. Introduction
 ABG is one of the most useful diagnostic test in both Respiratory & Critical care
settings to assess both the severity & causes of Pulmonary Gas exchange
impairment and acid-base disequilibrium & ABG is mandatory to establish the
diagnosis of Respiratory Failure
 Modern equipment to perform ABG assessment uses electrode to measure PaO2,
PaCO2 & pH. Other variables, such as bicarbonates, base excess, alveolo-arterial
gradient are computed using well-defined equations.
 ABG interpretation usually done using two step approach in clinical setting is
illustrated later

3. OBJECTIVES
 ABG Sampling technique
 Procedures & Precautions
 Interpretation of ABG
• Oxygenation status
• Ventilation status
• Acid Base status

4. INDICATIONS & CONTRAINDICATIONS
INDICATIONS
• Evaluation of the adequacy of a patient’s acid-
base(pH), ventilatory (PCO2), Oxygenation(PO2 &
oxyhaemoglobin saturation) status, the oxygen
carrying capacity (PO2, oxyhaemoglobin
saturation, total haemoglobin, and
dyshemoglobin saturation) and intrapulmonary
shunt
• Quantify the response to therapeutic intervention
or diagnostic evaluations.
• Assessment of inadequacy of circulatory
response- A high central venous- arterial PCO2
difference can indicate inadequate perfusion (as
observed in shock, & during cardiopulmonary
resuscitation)
CONTRAINDICATIONS
• Abnormal Allen Test
• Local infection or distorted anatomy
• Presence of arteriovenous fistulas or vascular
grafts( in which case arterial vascular puncture
should not be attempted).
• Known or suspected PVDs
• Relative Contraindications
• Severe Coagulopathy
• Anticoagulant Therapy
• Use of Thrombolytic Agents

5. ABG-Procedure
 Site-
• Radial Artery
• Brachial Artery
• Femoral Artery
 Procedure-
 Syringe should be pre-heparinized i.e, flushed with 0.5ml of (1:1000) heparin.Requires small amount of blood, So,
≤2ml syringe to be used.
 Position & Procedure-
 Wrist should be extended and locate the artery by palpating with index & middle finger, Under all aseptic condition
needle to be inserted at 30°-45° angle to the skin at the point of maximum pulsation of the artery, advance the
needle until arterial blood flushes into the syringe, arterial pressure will cause the blood to fill the syringe & after
removal of the syringe press the puncture site with gauge for 5 minutes. ABG analysis to be done immediately or
within 30 mins if cold chained maintained properly.

6. Modified ALLEN’S Test
 Instruct the patient to clench his or her fist; if the patient is unable to do this, close the person's hand tightly.
 Using your fingers, apply occlusive pressure to both the ulnar and radial arteries, to obstruct blood flow to the
hand.
 While applying occlusive pressure to both arteries, have the patient relax his or her hand, and check whether the
palm and fingers have blanched. If this is not the case, you have not completely occluded the arteries with your
fingers.
 Release the occlusive pressure on the ulnar artery only to determine whether the modified Allen test is positive
or negative.
 Positive modified Allen test – If the hand flushes within 5-15 seconds it indicates that the ulnar artery has good
blood flow; this normal flushing of the hand is considered to be a positive test.
 Negative modified Allen test – If the hand does not flush within 5-15 seconds, it indicates that ulnar circulation
is inadequate or nonexistent; in this situation, the radial artery supplying arterial blood to that hand should not
be punctured.

7. Modified ALLEN’S Test

8. Obtaining ABG sample

9. Complications & Precaution
 Arteriospasm or involuntary contraction of the artery: May be prevented simply by helping the patient
relax; this can be achieved, for example, by explaining the procedure and positioning the person
comfortably.
 Hematoma or excessive bleeding: Can be prevented by inserting the needle without puncturing the far
side of the vessel and by applying pressure immediately after blood is drawn. Due to the higher-pressure
present in arteries, pressure should be applied for a longer time than when sampling from a vein, and
should be supervised more closely, to check for cessation of bleeding.
 Nerve damage: Can be prevented by choosing an appropriate sampling site and avoiding redirection of
the needle.
 Fainting or a vasovagal response: Can be prevented by ensuring that the patient is supine (lying down on
their back) with feet elevated before beginning the blood draw.

10. Sampling errors
 Inappropriate collection and handling of arterial blood specimens can
produce incorrect results. Reasons for an inaccurate blood result
include:
1. Presence of air in the sample;
2. Collection of venous rather than arterial blood;
3. An improper quantity of heparin in the syringe, or improper mixing after
blood is drawn;
4. Delay in specimen transportation- Alteration of values PaCO2 & PaO2

11. ABG Electrodes
 pH (Sanz Electrode)
 Measures H+
ion concentration of sample against a known pH in reference electrode,
hence potential difference. Calibration with solutions of known pH (6.384 - 7.384).
 PCO2 (Severinghaus Electrode)
 CO2 reacts with solution to produce H+. Higher CO2  more H+  higher PCO2
measured.
 PCO2(Clark Electrode)
 O2 diffuses across membrane producing an electrical current measured as PO2.

12. ABG
ANALYSIS

13. BLOOD GAS COMPONENTS
 pH : It is a consistent with the concentration of hydrogen ions in arterial blood & inversely proportional to the
concentration of hydrogen ions.
 PaO2 : Measured the partial pressure of oxygen in arterial blood.
 PaCO2: Is the partial pressure of carbon dioxide in arterial blood
 HCO3: Calculated concentration of bicarbonate in arterial blood by Hasselbach equation.
 Base excess / Base deficit : calculated relative excess or deficit of base in arterial blood
 Sao2 : Calculated arterial oxygen saturation
 A-a gradient- Is a measure how efficiently mixed venous blood is equilibrated with alveolar gas, (i.e. diffusion across the
alveolar membrane, it is a measure of 𝑉
𝑄 mismatch., right to left shunts & very severe lung fibrosis.
 A-a Gradient =PiO2- (PaO2+
𝑃𝑎𝐶𝑂2
0.8
)
 All the Blood Gas component should be recorded along with FiO2

14. BLOOD GAS COMPONENTS
 pH
 pH is a logarithmic scale of the concentration of hydrogen ions in a solution. It is inversely
proportional to the concentration of hydrogen ions. Normally the body’s pH is closely
controlled at between 7.35 – 7.45. This is achieved through buffering and excretion of acids.
Buffers include plasma proteins and bicarbonate (extracellular) and proteins, phosphate and
haemoglobin (intracellularly).
 Hydrogen ions are excreted via the kidney and carbon dioxide is excreted via the lungs.
 Changes in ventilation are the primary way in which the concentration of H+ ions is
regulated. Ventilation is controlled of the concentration of CO2 in the blood.
 If the buffers and excretion mechanisms are overwhelmed and acid is continually produced,
then the pH falls. This creates a Metabolic acidosis.
 If the ability to excrete CO2 is compromised this creates a Respiratory acidosis.

15. BLOOD GAS COMPONENTS(contd.)
 Partial pressure (PP)
 Partial pressure is a way of assessing the number of molecules of a particular
gas in a mixture of gases.
 PaO2- Reflects the free oxygen molecule dissolved in plasma except those
bound to hemoglobin
 PaCO2 - Reflects ratio of metabolic production of CO2 to Alveolar
Ventilation
 PAO2- Partial pressure of oxygen in the alveoli, is calculated by
Alevolar Gas Equation: PAO2 = (Patm - PH2O) FiO2 - PaCO2 / RQ

16. Interpretation of oxygenation
 Oxygen Cascade & PAO2-
 Partial pressure is the pressure exerted by each gas in a mixture gas, the pressure exerted by the
mixture of gases is the sum of partial pressure of individual gases.
O2 Cascade

17. PaO2
 In the systemic arteries the partial pressure of O2 (PaO2) is about 95 mmHg,(This is due to a small amount of
deoxygenated blood is added to the systemic arteries (because of a small physiological shunt that normally exists in
the body).
 This ‘shunt fraction’ which represents about 2–5 % of the cardiac output, causes the systemic arterial oxygen to fall
fractionally−from 100 mmHg, to about 95 mmHg.
PaO2 Serves
as surrogate
measurement
of tissue
oxygenation
There is no
practical way
to measure
tissue
oxygenation
as such

18. Determinants of PaO2
 Age- Normal level of PaO2 declines with age
 PaO2= 109-0.43(age in years)
 FiO2- PaO2 will be increased with increased FiO2.
 PAO2-According to Henry’s law of diffusion increased PAO2 will increase PaO2 and
vice-versa
 Lung pathology
 Mixed venous O2 content
PAO2 is Determined by Alveolar Gas Equation

19. Alveolar Gas Equation & PAO2
 PAO2 = (Patm - PH2O) FiO2 - PaCO2 / RQ
PAO2: is the partial pressure of oxygen in the alveoli
Patm: is the atmospheric pressure at sea level equaling 760 mm Hg
PH2O: is the partial pressure of water equal to approximately 45 mm Hg.
FiO2: is the fraction of inspired oxygen.
PaCO2: is the carbon dioxide partial pressure in alveoli, which in normal physiological conditions is approximately 40 to 45 mm Hg,
RQ (respiratory quotient).
 PIO2 (Inspired PO2)= (Patm - PH2O) FiO2

20. Determinants of (PAO2)
 PAO2 (Partial pressure of alveolar oxygen) depends on Alveolar Gas Equation & it’s in turn depends
on the following,
 The fractional concentration of oxygen in the inhaled air (FIO2)
 The partial pressure of CO2 in the arterial blood (PaCO2)
 Barometric pressure(Patm), which is constant for a given altitude.
 The elevated PaCO2 will lower the PAO2 which will cause decreased PAO2 (Partial pressure of alveolar
oxygen) and it will lower the PaO2 that’s why hypercarbia is always associated with low PaO2 (Partial
Pressure of O2 in arterial blood)

21. Alveolo-Arterial Diffusion of Oxygen
 The A-aDO2 is the difference between the alveolar O2 tension (PAO2 ) and the arterial oxygen tension
(PaO2 ), it represents the ease with which the inspired oxygen diffuses into the blood, and therefore
reflects the efficiency of the lungs in oxygenating the blood.
• Normal
A-aDO2 on room air: 7–14 mmHg
• Normal
A-aDO2 on 100 % O2: Less than 70
mmHg
A-a difference reaches a maximum when PAO2
exceeds 350–450 mmHg, and then begins to fall
at higher PO2’s thus describing a Bell shaped
curve.
Therefore, between the two
extremes of inhaled FIO2 (0.21 and
1.0) the expected A-aDO2 level
(even in the normal subject!) is
difficult to predict.

22. Determinants of A-a Gradient
 In healthy person RBC takes time 0.25 sec, rapid heart beat reduces the contact
time, it is proved that over HR -240/min will reduce oxygenation.
 Disorders causing diffusion defects such as interstitial fibrosis retard the diffusion
of oxygen into the blood. RBC spends 0.75 sec in alveolar capillaries ,so more
diffusion time will cause in adequate oxygenation.
 Like the other causes of hypoxemia (other than shunt), a diffusion defect can be
easily corrected by administration of supplemental oxygen.
 Diffusion defect is the classical cause of hypoxemia in interstitial fibrosis but usual
mechanism is the V/Q mismatch.

23. Hypoxemia
 Four causes of Hypoxemia
 Hypoventilation
 Diffusion limitation
 Shunt
 V/Q mismatch

24. Hypoventilation
• Always increases alveolar & arterial
PCO2
• Decreases PO2 unless supplemental
O2 is inspired
• Easy to reverse hypoxemia by
supplemental O2
Respiratory
muscle
paralysis

25. Ventilation-Perfusion Mismatch
 Types of V/Q mismatch:
 Low V/Q mismatch: Ventilation low
relative to perfusion
 Right to left Shunt
 Obstructive airway disease
 High V/Q mismatch: Perfusion low
relative to ventilation
 Typically associated with Pulmonary
Embolism

26. SHUNT
 Shunt refers to blood that enters the arterial
system without going through ventilated
areas of the lung.
 Giving a patient with an intrapulmonary shunt
100% oxygen to breathe won’t increase the
PaO2 much
 If the shunt is caused by mixed venous blood,
its size can be calculated from the Shunt
equation.
Etiology of RIGHT –LEFT Shunt
• ARDS
• Cardiogenic pulmonary edema
• Lobar pneumonia
• Atelectasis
• Pulmonary thromboembolism (here, a shunt occurs by the reflex
closure of alveoli)
• Pulmonary arterio-venous malformations
• Intracardiac right-to-left shunts

27. Quantification of Hypoxemia
Expected PaO2 from given
FIO2
• Multiplying FIO2 into 5, gives the
approximate expected PaO2 for
the given FIO2
• If the FIO2 is 21 % (as in a person
breathing room air) the expected
PaO2 = 21 × 5 = 105
(approximately).
• If the measured PaO2 is
significantly below the expected
PaO2, there is a problem with the
gas exchange
The PaO2:FIO2 ratio
• It helps to comparison of
oxygenation status in different
FiO2 & correlation with disease
severity.
• The normal range for the
PaO2/FIO2 ratio is 300–500.
• In the appropriate setting a P:F
ratio of less than 300 indicates
acute lung injury (ALI)
• Less than 200 is diagnostic of
ARDS
The PaO2/PAO2 ratio
• PaO2/PAO2 ratio offers better
accuracy over a broader range of
FIO2 than the PF ratio.
• A better estimate of Oxygenation
than the P:F ratio.

28. PaCO2
Partial pressure of CO2 in arterial blood.
• PaCO2 is determined by respiratory equation
PaCO2 ∝
VCO2
VA
[VA= Minute Ventilation –VD(Dead space ventilation)]
PaCO2=
VCO2×0.863
VA
(0.863=converts VCO2 & VA in same unit)
According to the respiratory equation, CO2 will be expected to rise if:
 CO2 production (VCO2) is increased in the face of Unchanged Alveolar Ventilation (VA) –
1. Hyperthermia
2. Exercise
3. Rigor
 Alveolar ventilation (VA) decreases in the face of Unchanged VCO2-
1. Increased Physiological dead space, COPD
2. Decrease in Minute ventilation

29. Determinants of PaCO2
•,
•Compensatory to
met-Acidosis
•Tachypnea due to
hypoxic drive
•Hypothermia
•CNS Depression
•Neuro-Mascular
Disorder etc.
•Respiratory muscle
fatigue
•Fever
•Rigor
•Hypercatabolic state
Increased PaCO2=
Increased CO2
production
Increased
PaCO2=
Hypoventilation
Decreased
PaCo2=
Hyperventilation
Decreased
PaCO2=
Decreased CO2
Production

30. ACID-BASE ANALYSIS
 ABG analysis is to identify the acid base disorders based on the interrelationships between the
pH, pCO2, & Bi-Carbonate (HCO3-) concentration in plasma.
 Normal Blood Gas Parameters
• pH=(7.35 – 7.45)
• PaO2= 75-100
• PaCO2= (35-45)
• HCO3=(22-26)
• Base excess/deficit= (-4 to +2)
• (A-a) Alveolo-arterial gradient= (5-10 mmHg), (For every decade person was lived A-a gradient will increase by 1)
 Approaches
 Traditional approach
 Romanski Method of analysis ( most simplistic method of analysis)
 Stewart’s strong ion difference(Not done in clinical practice)

31. Clinical history
 While making an interpretation of an ABG clinical history is also have role like,
• A patient with a history of renal failure, uncontrolled diabetic status, of treatment with drugs
such as metformin is likely to have Metabolic acidosis
• A patient, with a history of diuretic use, bicarbonate administration, high-nasogastric
aspirate, and vomiting, is likely to have Metabolic alkalosis
• Respiratory acidosis would occur in COPD, muscular weakness, postoperative cases, and
opioid overdose, and respiratory alkalosis is likely to occur in sepsis, hepatic coma, and
pregnancy

32. ABG analysis by stepwise approach
 Step 1: Assessment of consistency of pH & [𝐻]+ by Henderson-Hasselbalch equation
determines validity of ABG.
 [H+] =
24(𝑃𝑎𝐶𝑂2)
[𝐻𝐶𝑂3−]
 Step 2: Is to look at the pH & assess for the presence of acidemia or alkalemia (using pH
cut off point 7.40)
 Step 3:The direction of change of P𝐶𝑂2 & pH if opposite direction ( P𝐶𝑂2 & pH ) it is
Primary Respiratory Disorder
 If P𝐶𝑂2 & pH changes in same direction ( P𝐶𝑂2 & pH ) it is due to Primary
Metabolic Disorder
 Step 5:Compensation for primary disorder

33. Acid-Base balance & abnormalities
 pH and H+
ion concentration are precisely regulated by following systems.
 At cellular level –by Buffer Systems
 By Organ Systems- Renal Regulation & Pulmonary Regulation

34. Acid-Base Regulation by Buffer System
 Bicarbonate buffer- CO2 is produced as a byproduct of the TCA cycle,combines with water to create
carbonic acid. Carbonic acid then dissociates into bicarbonate and a hydrogen ion:
 CO2 + H2O ↔ H2CO3 ↔ HCO3
−
+ H+
 This reaction resists dramatic changes in pH & to allow human body to remain within the narrow
physiological pH range (7.35-7.45).
 However, carbonic anhydrase is an enzyme that assists with this process. This reaction can and does occur
without an enzyme; It catalyzes the first reaction to form carbonic acid which can then freely dissociate into
bicarbonate and a hydrogen ion. Carbonic anhydrase is located in red blood cells, renal tubules, gastric
mucosa, and pancreatic cells.
 This buffer system is in equilibrium, that is, all components of the reaction exist throughout the body and are
shifted to the side of the equation appropriate for the environment.
 Other buffer systems in the human body include the
 Phosphate buffer system - is important for the regulation of urine pH
 Proteins buffer- Proteins assist with intracellular pH regulation
 Hemoglobin- Can bind both H+
& CO2 called Bohr effect & Haldane effect.

35. Acid-Base Regulation by Organ System
 Every organ system of the human body relies on pH balance; however, the renal
system and the pulmonary system are the two main modulators.
 Pulmonary system- It adjusts pH by exhaling CO2. As CO2 forming carbonic acid in the
body when combining with water, the amount of CO2 exhaled can cause pH to increase or
decrease. When the respiratory system is utilized to compensate for metabolic pH
disturbances, the effect occurs in minutes to hours.
 Renal system- It affects pH by reabsorbing bicarbonate and excreting H+ If bicarbonate is
reabsorbed and/or acid is secreted into the urine, the pH becomes more alkaline
(increases). When bicarbonate is not reabsorbed or acid is not excreted into the urine, pH
becomes more acidic (decreases). The metabolic compensation from the renal system takes
longer to occur: days rather than minutes or hours.

36. Acid-Base Abnormalities
 Acidosis- Is a process which tends to pH either by gain of H+
or by loss of HCO3
−
 Alkalosis- Is a process which tends to pH either by loss of H+ or by gain of HCO3
−
 If these changes will cause changes in pH then is called Acidemia or Alkalemia,
accordingly.

37. pH
Acidosis Alkalosis
P𝐶𝑂2 𝐻𝐶𝑂3− P𝐶𝑂2 𝐻𝐶𝑂3−
Respiratory
Acidosis
Metabolic
Acidosis
Metabolic
Alkalosis
Respiratory
Alkalosis

38. Determination of compensatory
Mechanism of Acid-Base Balance
 This is an adaptation to the primary acid-base balance intended to stabilize the
changing pH, A respiratory process that shifts the pH in one direction will be
compensated by a metabolic process or vice versa.
 Effect of compensation is to attenuate but not completely correction of the
primary change of pH
 Inappropriate compensation suggests presence of combined acid-base disorder

39. Compensation of Primary Acid-Base
Disorder (contd.)
Disorder Expected compensation
Metabolic acidosis PaCO2 = (1.5 x [HCO3-]) +8
Acute respiratory acidosis Increase in [HCO3-]= ∆ PaCO2/10
Chronic respiratory acidosis (3-5 days) Increase in [HCO3-]= 3.5(∆ PaCO2/10)
Metabolic alkalosis Increase in PaCO2 = 40 + 0.6(∆HCO3-)
Acute respiratory alkalosis Decrease in [HCO3-]= 2(∆ PaCO2/10)
Chronic respiratory alkalosis Decrease in [HCO3-] = 5(∆ PaCO2/10) to 7(∆ PaCO2/10)
 If the observed compensation is not the expected compensation, it is likely that more than one acid-
base disorder is present. Then Anion Gap to be determined.

40. Anion gap
 It estimates unmeasured plasma anions (fixed or organic acids such as, phosphate, ketones & lactate which are
hard to measure directly). It is calculated as the difference between plasma cations (𝑁𝑎+
& 𝐾+
) and anions
𝐶𝑙−
& 𝐻𝐶𝑂3−
.
 AG= [Na+]-( [Cl-] + [HCO3-] )
 A normal anion gap is approximately 10±2 meq/L.
 In patients with hypoalbuminemia, the normal anion gap is lower than 12 meq/L;
𝑨𝑮𝑪𝒐𝒓𝒓𝒆𝒄𝒕 = 𝑨𝑮 + 𝟐. 𝟓[𝑨𝒍𝒃𝒖𝒎𝒊𝒏𝑵𝒐𝒓𝒎𝒂𝒍 − 𝑨𝒍𝒃𝒖𝒎𝒊𝒏𝑶𝒃𝒔𝒆𝒓𝒗𝒆𝒅]
 Per each 1gm% deficit of albumin, a factor of 2.5 is to be added to AG to calculate corrected AG.
 If the anion gap is elevated, consider calculating the osmolal gap in compatible clinical situations.
If elevation in AG is not explained by an obvious case (DKA, lactic acidosis, renal failure),Toxic ingestion is
suspected

41. Anion Gap & [HCO3-]
 If increased anion gap is present, assess the relationship between change in anion
gap & change in [HCO3-]
 Ratio ∆AG
∆HCO3−
 This ratio should be between 1.0 and 2.0 if an uncomplicated anion gap metabolic acidosis
is present.
 If this ratio falls outside of this range, then another metabolic disorder is present:
• If ∆AG/∆[HCO3-] < 1.0, then a concurrent non-anion gap metabolic acidosis is likely to be
present.
• If ∆AG/∆[HCO3-] > 2.0, then a concurrent metabolic alkalosis is likely to be present.

42. Example 1. A patient with DKA has been vomiting prior to admission he has an AG = 20 &
[HCO3]=20
∆𝐴𝐺 = 10, ∆ 𝐻𝐶𝑂3 = 4
∆𝐴𝐺
∆[𝐻𝐶𝑂3]
= 2.5
Suggestive of an underlying metabolic alkalosis in presence of metabolic acidosis, explained by
vomiting.
Example 2. A patient admitted with fever & hypotension after a prolonged period of diarrhoea, she
has an AG=15, [HCO3]= 12 ∆𝐴𝐺 = 5, ∆ 𝐻𝐶𝑂3 = 12
∆𝐴𝐺
∆[𝐻𝐶𝑂3]
= 0.41
Suggestive of an underlying Non-Anion Gap Metabolic Acidosis, explained by diarrhoea.

43. Respiratory Acid-Base Abnormalities
 Acute respiratory disturbances will change pH 0.08 units for every 10 mmHg
deviation from normal
 Chronic respiratory disturbances will change pH 0.03 units for every 10 mmHg
deviation from normal
Therefore, in acute respiratory acidosis, the
pH will fall by 0.08 x [(PCO2 - 40)/10]
In acute respiratory alkalosis, the
pH will rise by 0.08 x [(40-PCO2)/10]
Therefore, in chronic respiratory acidosis,
pH will fall by 0.03 x [(PCO2 - 40)/10]
In chronic respiratory alkalosis, the
pH will rise by 0.03 x [(40-PCO2)/10]
Limits of compensation for respiratory acidosis
• The process of compensation is generally complete within 2 − 4 days.
• The bicarbonate is increased to a maximum of 45 mmol/L; a bicarbonate level in
excess of this may imply a coexistent primary metabolic alkalosis.

44. Chronic Respiratory Acidosis
A near normal pH
i.e, its compensatory Acidosis
Acidemic pH
Acute on Chronic Associated Metabolic
Respiratory Acidosis Acidosis

45. Respiratory Acidosis
Acute respiratory acidosis
(<24 h)
∆𝐻+
∆𝐶𝑂2
= >0.7
Acute on chronic respiratory
acidosis (<24 h)
∆𝐻+
∆𝐶𝑂2
=0.3-0.7
Chronic respiratory acidosis
∆𝐻+
∆𝐶𝑂2
=< 0.3
[H+] is measured by modified Henderson-Hasselbach’s equation, Normal [H+] =40 & normal PCO2 =40

46. Causes of
Respiratory Acidosis
or Hypercapnia
• In terms of CO 2 production and
excretion, alveolar hypoventilation is the
major mechanism for hypercarbia.
• Quite often however, increase in dead
space is an important mechanism

47. Respiratory Alkalosis
 Acute Respiratory Alkalosis (<12hr)
 Δ↑pH = 0.01 × Δ↓PaCO2
 HCO3– falls by up to 0.2 mEq/L for every
mmHg fall in CO2
 Chronic Respiratory Alkalosis (>12hr)
 Δ↑pH = 0.0003 × Δ↓PaCO2
 HCO3– falls by up to 0.5 mEq/L for every
mmHg fall in CO2
Limits of compensation for respiratory alkalosis
• The serum bicarbonate can fall to as low as 12 mmol/L; a lower bicarbonate level may imply a coexistent
primary metabolic acidosis.
• The process of compensation is generally complete within 7 to 10 days

48. Causes
of
Respiratory
Alkalosis
• Predominant
mechanism is
hyperventilation

49. Metabolic Acidosis
 Metabolic Acidosis is net gain of acid (hydrogen ions) or a net deficit of bicarbonate ions from the
extracellular fluid.
 In metabolic acidosis there is interrelationship between pCO2, pH & Base excess.
 PCO2 12 mmHg↔ pH 0.1 ↔Base excess 6 mEq/L

50. Base Excess
 It is an indicator of metabolic acid–base disorders.
 Positive” base excess:
 Metabolic alkalosis The amount of acid that needs to be addedto return the pH of 1 liter of an alkalemic blood sample to
7.40
 Negative base excess:
 The amount of alkali that needs to be added to return the pH of 1 liter of an acidic blood sample to 7.40.
 Base excess is expressed in mEq/L, and is normally zero (range: +2 to−2).Because of its lower SpO 2 , the BE of
venous blood (unless oxygenated) is higherthan that of arterial blood (2–2.5 mEq/L).
 following relationship holds between BE and changes in SBC (Standard Bicarbonate Concentration)
 𝐵𝐸 = 1.3 × ∆𝐻𝐶𝑂3

51. Total CO2 (TCO2)
 TCO 2 is the sum of all the species that can potentially generate CO2 .
 Like, Bicarbonate (HCO3-) (This is the only one of the CO2− producing species that is present in the body
in significant amounts), others are- H2CO3, CarbaminoCO2, Dissolved CO2
 It deferentiate Acute & Chronic respiratory Disturbance, With metabolic disturbances
Acute respiratory
disturbances
Chronic respiratory
disturbances
Metabolic
disturbances
In acute respiratory
disturbances, the
bicarbonate remains
relatively unchanged
result in a significant
alteration in bicarbonate levels
as a result of renal compensatory
processes.
It is the metabolic
disturbances that primarily
alter the bicarbonate.
Acute respiratory
disturbances produce
only minor changes in
TCO2 .
Chronic respiratory disturbances
produce appreciable changes in
TCO2 .
Metabolic disturbances
produce the greatest
changes in TCO2

52. Causes of
Metabolic
Acidosis
May present as
• High Anion Gap
Acidosis(HAGMA).
• Non Anion Gap
Metabolic Acidosis
(NAGMA)

53. Metabolic Alkalosis & Its interpretation
 A metabolic alkalosis is a primary acid-base disorder which causes the plasma bicarbonate to rise to a level
higher than expected.
 Predicted PCO2 & Metabolic Alkalosis
Predicted PCO2 = (0.7 × HCO3–) + 21
 Lower PCO2 values than predicted, indicate the presence of a coexisting respiratory alkalosis.
 Higher CO2 values than predicted, indicate a coexisting respiratory acidosis.
Limits of compensation for metabolic alkalosis
• The lungs are capable of hypoventilating such that the PCO2 rises to a maximum of about 60
mmHg.
• PCO2 levels in excess of this in primary respiratory acidosis may imply a coexistent primary
metabolic alkalosis.

54. Reference
Ashfaq Hasan
1. Handbook of Blood Gas/Acid-Base Interpretation Second Edition
2. West’s respiratory physiology : the essentials / John B. West, Andrew M. Luks. — Tenth edition.
3. Pramod Sood, Gunchan Paul, Sandeep PuriIndian J Crit Care Med. 2010 Apr-Jun; 14(2): 57–64.
doi:10.4103/0972-5229.68215PMCID: PMC2936733

55. THANK YOU