INTERPRETATION OF  ARTERIAL BLOOD GAS  

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 INTRODUCTION

Arterial Blood Gas (ABG) analysis provides immediate and specific information regarding respiratory, circulatory and metabolic states of patient, which is useful in managing critically ill patients. Baseline ABG is also useful for patients who are at high risk for pulmonary complications.

Approach

The ABG report contains several pieces of information, most important of which are :-

ph

Arterial oxygen tension (Pa O2).

Arterial Carbon dioxide tension (Pa CO2).

Bicarbonate level (HCO3).

Base excess (B.E.).

In addition, serum electrolytes Na, K, Cl are also estimated.

pH

Þ    It refers to H+-ion concentration of blood.

Þ    pH 7.0 is neutral.

Þ    Normal pH of blood is between 7.35 and 7.45.

Þ    pH depends mainly on ratio of HCO3 (alkali or base) and carbonic acid (H2 CO3) which depends on Pa CO2 (acid). The normal bicarbonate (HCO3) level is around 25 mEq/litre. Normal PaCO2 is around 40 mmHg.

Þ    The bicarbonate level is chiefly dependent on kidney function, hence it is known as metabolic or non-respiratory component. PaCO2 chiefly depends upon lung function, hence it is known as respiratory component.

Þ    Any primary increase in HCO3 is alkalosis. Any primary decrease in HCO3 is acidosis.

Þ    A primary change is accompanied by secondary compensation.

Þ    Increased HCO3 will lead to an increase in PaCO2

Þ    Increase in PaCO2 in respiratory acidosis is accompanied by retention of HCO3 by the kidneys

Þ    Usually the respiratory compensation is seen immediately in few hours, whereas renal compensation takes few days.

Types of Acidosis and Alkalosis. They are :

·        Metabolic acidosis where in primary abnormality is reduction of bicarbonates (HCO3) due to loss of HCO3 or gain of H+.

• Metabolic alkalosis where in primary abnormality is increase of bicarbonate (gain of HCO3) or loss of H+. In both these abnormalities mentioned above, the compensation is respiratory.
• Respiratory Acidosis where in the primary abnormality is retention of carbon dioxide, CO2. Carbon dioxide is turned to carbonic acid, CO2 + H2O à H2 CO3.

·        Respiratory Alkalosis wherein the primary abnormality is wash-out of CO2 by   hyperventilation.

To Summarize

—Increased HCO3 is seen in metabolic alkalosis, which is compensated by respiratory increase in Pa CO2

—Decreased HCO3 is seen in metabolic acidosis, which is compensated by lungs with respiratory decrease in Pa CO2.

—Increased Pa CO2 is seen in respiratory acidosis, which is compensated by metabolic increase in HCO3.

—Decreased Pa CO2 is seen in respiratory alkalosis, which is compensated by metabolic decrease in HCO3.

Taking an example:

If HCO3 is decreased, the conditon is due to metabolic acidosis if pH is 7.2. If however pH is 7.5, the abnormality is compensated respiratory alkalosis. Again, if PaCO2 is 50 mmHg. (i.e. increased) and pH is 7.3 it is due to respiratory acidosis, whereas if pH is 7.5, the condition is compensated metabolic alkalosis.

Hence, on seeing the pH, HCO3 and PaCO2, we can recognize the simple acid-base disorder. Acid-base disorder can be "mixed", i.e., a combination of metabolic acidosis or alkalosis with respiratory acidosis or alkalosis. Occasionally, triple disorders are seen, i.e., respiratory acidosis with metabolic acidosis and metabolic alkalosis or respiratory alkalosis with metabolic acidosis and metabolic alkalosis.

Compensatory Mechanisms

There are mechanisms in the body to restore the pH back towards normal or near normal. These mechanisms are :

a) Cellular shifts of H+ and K+: e.g., in acidosis H+ shifts from vascular compartment to cellular compartment with K+ shifting in opposite direction. In alkalosis, H+ shifts from cellular compartment to vascular compartment.

b) Buffer pair compensation : The buffer most relevant in the clinical set up is bicarbonate (HCO3) and carbon dioxide (Pa CO2) pair. The other buffer pairs are phosphate and protein buffers.

c)       Respiratory compensation : Either retention or washout of carbon dioxide; this takes place in few minutes or few hours.

d) Renal compensation : Either retention of bicarbonate (HCO3) or its excretion takes few days; there are other renal compensatory mechanisms, like ammonia mechanism.

What Is Adequate Compensation?

In compensation, the body shifts pH towards normal. If the primary insult is metabolic, the compensation is respiratory and vice versa. To judge whether compensation is "adequate" or not, there are some formulas.

Metabolic Acidosis: In metabolic acidosis, the primary abnormality is reduction of bicarbonate (HCO3). The carbon dioxide (PaCO2) is lowered, i.e., in the same direction. In other words, carbon dioxide is washed out by hyperventilation (Kussmaul breathing). The degree of compensation is usually calculated as

Measured HCO3 + 15=-PaCO2

-Pa CO2-= -last two digits of pH

If in metabolic acidosis the HCO3 is 10 mEq/litre, then the expected PaCO2 should be 10 + 15 = 25 mmHg and the pH should be 7.25. The values are approximate. If however the PaCO2 is much higher than 25 (say, 35 mm Hg), additional component of respiratory acidosis is suspected. If PaCO2 is much lower than 25 mm Hg (say 15 mm Hg) then additional component of respiratory alkalosis is suspected.

Metabolic Alkalosis: In metabolic alkalosis, for each increase in HCO3 by 10 mEq/litre the Pa CO2 increases by 6 mm Hg — if the patient has prolonged vomiting due to pyloric stenosis/obstruction, and the HCO3 is 45 mEq/L (that is, 20 mEq/litre more than normal) then the Pa CO2 should increase by 12 mm Hg, for the compensation to be considered "adequate".

Respiratory Acidosis: In acute respiratory acidosis, increase in PaCO2 by 10 mm Hg is adequately compensated by retention of 1 mEq/litre of bicarbonate (HCO3). In chronic respiratory acidosis for each 10 mm Hg rise of Pa CO2, the compensatory rise of HCO3 is of the order of 3.5 mEq/litre.

Respiratory Alkalosis: In respiratory alkalosis, the primary abnormality is carbon dioxide washout. The compensation by kidney is by excretion of bicarbonate (HCO3). It differs in acute and chronic respiratory alkalosis.

The "adequate" compensation for acute respiratory alkalosis is as follows - for every fall of PaCO2 by 10 mm Hg, the HCO3 falls by 2 mEq/L;

For chronic respiratory alkalosis, it is as follows — for every fall of Pa CO2 by 10 mm Hg, the bicarbonate (HCO3) falls by 5 mEq/litre.

ANION GAP

It is the difference between serum Na+ on one side and sum of Cl- and HCO3- on the other. Usually it is 10 to 15 mEq/.

Anion Gap = Na+ - (Cl- + HCO3-)

Normal Na+ is 135-140 mEq/L

and Cl- is around 100 mEq/L,

HCO3 is around 25 mEq/L.

Hence anion gap is about 12 meq / L with a range of 8-16 meq / L

Anion gap is useful to classify the metabolic acidosis in two groups.

Usually due to gain of H+, it occurs in (high anion gap acidosis)

diabetic keoacidosis (DKA).

renal failure.

alcoholic acidosis.

lactic acidosis.

poisoning with salicylate, methyl alcohol etc.

Normal anion gap acidosis

It is usually due to loss of base in:-

renal tubular acidosis.

diarrhoea.

intestinal fistulae.

diamox therapy (Acetazolamide).

pancreatic fistulae

Usefulness of serum electrolytes in acid-base disorders

Þ    HCO3 increase means either metabolic alkalosis or compensatory respiratory acidosis; decrease of HCO3 means either metabolic acidosis or compensated respiratory alkalosis. The pH reading helps in differentiating between two.

Þ    K+ increase is usually seen in acidosis; K+ decrease is usually seen in alkalosis.

Þ    Chlorides are increased in hyperchloremic metabolic acidosis. Chlorides are decreased in metabolic alkalosis.

Usefulness of Venous Gases

Roughly in venous blood - Pa CO2 is about 6 mm Hg higher than in arterial blood. HCO3 is 2 mEq/L lower than in arterial blood. pH is 0.04 less than arterial blood

Buffer base

Buffer base includes - bicarbonates (HCO3) in plasma and red cells. phosphates (PO4) in plasma and red cells haemoglobin (Hb) and plasma proteins

Normal buffer base is 45 to 50 mEq/L; buffer base is mainly due to bicarbonates (HCO3) and Hb

·        increase in buffer base is due to metabolic alkalosis - Base Excess (BE)

·        decrease in buffer base is due to metabolic acidosis - Base Deficit (BD)

·        normally base excess is 0 to 2.5 mEq/L

·        Base excess is determined from the Siggard Anderson nomogram

(HCO3 above normal X 1.2 = Base Excess)

When acid H+ is added, the following events occur :-

1.     H+ + HCO3  -----------à H2O + CO2

2.     H+ + Protein -----------à H.Protein

Pa CO2

—hyperventilation can be inferred from the presence of hypocapnia

—main determinant is effective alveolar ventilation

—increase in ventilation decreases Pa CO2

—decrease in alveolar ventilation, increases Pa CO2

Pa CO2 — pH relationship

For every rise in Pa CO2 by 20 mm Hg, pH will decrease by 0.1 unit (i.e., becomes acidic) for every fall in Pa CO2 by 10 mm Hg, pH will increase by 0.1 unit (i.e., becomes alkalotic).

PaCO2 - HCO3 relationship

As mentioned earlier

(Acute increase in PaCO2 by 10 mmHg pH will increase the bicarbonates (HCO3) by 1 mEq/L

acute decrease in Pa CO2 by 10 mm Hg will cause decrease in bicarbonates (HCO3) by 2 mEq/L.

(Difference between calculated plasma bicarbonates (HCO3) value and actual bicarbonate value provides a rapid and easy assessment of metabolic component)

Oxygen

Oxygen is transported in two forms

(1)    oxygen dissolved in plasma - Pa O2

(2)     molecular oxygen bound to haemoglobin (Hb).

Oxygen content of the blood is the sum of above.

Oxygen content = (Pa O2 x 0.003) + (1.34 x 15)

Þ    (0.003 is a constant for oxygen dissolved in plasma)

Þ    (1.34 represents the amount of oxygen carrying capacity of one Gm. of Hb)

Þ    15 is 15 gm % the hemoglobin levels

Therefore Pa O2 100 mm Hg (i.e., oxygen dissolved in plasma) x 0.003 + 1.34 (oxygen carried in Hb) x 15 (saturation of Hb 100%) = 0.3 + 20.1 = 20.4 ml/ 100 ml (amount of oxygen carried in blood).

Decreased Pa O2 is hypoxia. Combination of decreased Pa O2 + decreased Hb results in decrease of oxygen content. Decrease in Pa O2 stimulates the respiratory centre through chemoreceptors in the carotid and aortic bodies.

Normal tissue oxygenation requires perfusion by blood adequate in oxygen content. Pa O2 provides a small contribution in plasma but more significantly exerts partial pressure (i.e., driving force) to saturate Hb molecules. This Hb fraction carries a far greater proportion of oxygen.

Pa O2 varies as much as by 10 mm Hg between supine and erect positions, it being higher in erect position, probably due to increased amplitude of respiratory excursions of diaphragm in erect position.

Pa O2 depends upon fraction of inspired O2 concentration (Fi O2).

Pa O2 = Fi O2 x 5,

 therefore Fi O2 21% should result in Pa O2 of 100 to 105 mm Hg (21 x 5).

Normal range of Pa O2 does not necessarily assure of adequate oxygen content of Hb, if Hb dysfunction exists. True oxygen saturation may be low inspite of normal Pa O2. Cyanosis can exist even with normal Pa O2 if more than 5 Gm of reduced Hb is present.

Hypoxaemia

The following are some important causes of hypoxaemia:

Þ    Decreased alveolar oxygen causing decrease of fraction of inspired oxygen (FiO2) concentration :

a)     in fire accident, where oxygen is used up so decreased alveolar oxygen results

b)    At higher altitudes, where air has lesser oxygen content.

Þ    Hypoventilation

Þ    Diffusion impairment.

Þ    V - Q (ventilation perfusion quantity) mismatch.

Þ    Increased pulmonary shunting.

Pa O2 more than normal (hyperoxia) occurs with

a)     supplemental oxygen administration;

b)    hyperventilation;

c)     increased barometric pressure

Concept of A —- a DO2

PAO2 - PaO2

PA O2 = Fi O2 (barometric pressure — water vapour pressure) - pressure due to CO2

Therefore, PA O2 = 0.21 (760 - 47) - (40/0.8) = 150 — 50 = 100.

Normal PA O2 —- Pa O2 = 5 to 15 mm Hg (on room air). A —- a DO2 varies with age, Fi O2, cardiovascular status;

Increase in A —- a DO2

It is seen in

1)     diffusion impairment;

2)     V - Q imbalance;

3)     increased shunt

Diffusion impairment is an infrequent cause of hypoxia at rest, which manifests as severe hypoxia during exercise.

Commonest cause of decreased Pa O2 is V - Q mismatch.

If Pa O2 remains low despite 100% oxygen administration, abnormal pulmonary shunt is suspected. Normally 2 to 2.5% of cardiac output bypasses the pulmonary bed via thebesius and bronchial veins.

Electrolyte and Acid-base Disturbances

Acidosis generally produces hyperkalaemia due to shift of K+ from intracellular compartment to plasma compartment, as H+ shifts from plasma compartment to intracellular compartment.

Occasionally one sees hypokalaemic acidosis, e.g., in diarrhoea where there is loss of bicarbonate (HCO3) alongwith loss of K+.

Alkalosis usually produces hypokalaemia due to shift of K+ from extracellular compartment to intracellular compartment; because of high bicarbonate (HCO3) levels, H+ shifts from cellular compartment to plasma compartment, as compensation.

A disproportionate rise or fall of chloride as compared to sodium levels may indicate metabolic acidosis or alkalosis respectively.

For example, normally sodium is around 140 mEq/L and chloride is around 100 mEq/L.

If sodium is 140 and chloride is, say, 85 mEq/L, this would indicate in all probability high HCO3 (Law of electroneutrality states that the sum of cations and anions has to be equal), which would suggest metabolic alkalosis.

If sodium is 140 mEq/L and chloride, say, 115 mEq/L, this would indicate, in all propability, a low HCO3, which would suggest metabolic acidosis.

Standard and Actual Bicarbonates

Standard bicarbonates represent the bicarbonate concentration in the plasma which has been equilibrated at Pa CO2 of 40 mm Hg and with oxygen in order to fully saturate the Hb. Since most of the buffering is done by Hb, unsaturated blood will show deficient buffering capacity. Normal bicarbonate is 24 mEq/L.

Actual bicarbonate and standard bicarbonate should be the same under ideal circumstances. Actual bicarbonate will be higher if Pa CO2 is more than 40 mm Hg (i.e., in respiratory acidosis). Actual bicarbonate will be lower if Pa CO2 is less than 40 mm Hg (i.e. in respiratory alkalosis). Normally the difference between standard and actual bicarbonates does not exceed 2 mEq/L.

SUMMARY

Formulae of adequate compensation

a.  Metabolic acidosis HCO3 + 15 = Pa CO2 (last two digits of Pa CO2 indicate last two digits of pH).

b.     Metabolic alkalosis For every 10 mEq/L above the normal value of 25 mEq/L of HCO3, compensatory rise of Pa CO2 is by 6 mm Hg.

c.      Acute respiratory acidosis for every 10 mm Hg rise above normal value of Pa CO2, compensatory rise of HCO3 is by 1 mEq/L.

d.    Chronic respiratory acidosis for every rise of 10 mm Hg of normal value of PaCO2, compensatory rise of HCO3 is by 3.5 mEq/L.

e.     Acute respiratory alkalosis for every fall of Pa CO2 by 10 mm Hg, compensatory fall of HCO3 is by 2 mEq/L.

f.       Chronic respiratory alkalosis for every fall of Pa CO2 by 10 mm Hg, compensatory fall of HCO3 is by 5 mEq/L.

Anion gap : normal anion gap is 10 to 15 mEq/L

Na+ is about 140 mEq/L

Cl is about 100 mEq/L

HCO3 is about 25 mEq/L

      Thus anion gap = Na+ - (Cl + HCO3) =

      140 minus (100+ 25) =  15 mEq/L

Buffer base — normally it is 40 to 45 mEq/L base excess - it is deviation of bicarbonates (HCO3) above normal x 1.2.

Thank You.

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