Arterial Blood Gas (ABG) is now widely done in hospitals. So direct measurement of pH, PaO2, PaCo2 are most precise in medicine .The value of such data depends upon the ability of the doctors to interpret the results properly and if the analysis is made systematically, it becomes interesting for the doctors and fruitful for the patient.
Analysed report of ABG helps the clinician in diagnosis, sometimes it has prognostic value and is important monitor in ventilated patients.
Before analysis patient’s history and clinical condition should be carefully reviewed.
ABG Analysis is done in three headings :-
- Gas Analysis
- Electrolyte Analysis
- Acid-Base Analysis
1. Gas Analysis:- Gas Analysis is done to decide the
- Type of respiratory failure
- Severity of hypoxemia
- Cause of hypoxemia i.e. FiO2, ventilatory defect, ventilation-perfusion mismatch, shunt, diffusion defect and finally decide arterial oxygen content.
For gas analysis we proceed in the following manner
Step: 1 We look for PaO2 (partial pressure of oxygen) and SpO2 (oxygen saturation) and compare
| > 80(80-100) mm of Hg
(60-80) mm of Hg
(40-60) mm of Hg
|97(95-100) % – Normal
(90-94) % – Mild Hypoxemia
(75-89) % – Moderate Hypoxemia (Clinical, symptom of tachypnea, hypotension, cold extremity)
|< 40 mm of Hg||
< 75% – severe hypoxemia (Clinical symptom of serious arrhythmia, brain damage and death may ensue in elderly)
PAo2 (Alveolar oxygen content)
PAo2 is derived value and is calculated as
Normal value is 96-108mm/Hg.
P (A-a)O2 (Alveolar-arterial oxygen difference)
Normally <15 mm of Hg, may be as high as 30mm of Hg in elderly. Other simple way to decide the normal value is Age/4+4, If this value is increased, Indicates parenchymal lung disease.
PaCo2 (Partial pressure of Co2)
Normal value is 36-45 mm of Hg and for the purpose of ABG analysis it is taken as 40 mm of Hg. More than 49 mm of Hg is considered as hypoventilation.
Now the type of respiratory failure is decided which is defined as type 1 when there is hypoxemia without carbon diaoxide retention and type 2 when there is hypercapnia. The calculation of the gradient between the alveolar and arterial oxygen tensions (A-a gradient) in type 2 respiratory failure will help to determine whether the patient has associated lung disease or just reduced respiratory effort. Examples of type 1 respiratory failure are consolidation, collapse, fibrosis, pulmonary oedema, pulmonary embolism, aspiration, atelectesis. Example of type 2 respiratory failure are COPD, Guillenbare syndrome, Myasthenia gravis, disease anywhere from brain to neuromuscular junction of respiratory muscle, drug toxicity, exhausted patient, critically ill patient may change from type 1 to type 2 respiratory failure.
Decision of the cause of hypoxemia from the value of PaCo2, P(A-a)O2 and the knowledge of response to O2 inhalation is done by the flow chart given below.
We calculate P/F i.e. PaO2/FiO2. It is known as hypoxemia index which is a measure of gas exchange. In the absence of pneumonia or heart failure, progressive diffuse pulmonary infiltration and arterial hypoxemia (P/F<300) indicates the development of Acute Lung Injury (ALI). More severe hypoxemia(P/F<200) denotes the acute respiratory distress syndrome (ARDS).
The relation between SpO2 and PaO2. It is decided by sigmoid saturation curve for haemoglobin which is also written in step1. If mismatch we search the cause of shift.
Calculate the arterial oxygen content(CaO2).
CaO2=Hb(gm/L)X1.34XSpO2/100+0.003XPaO2. In a adult of 72Kg the normal value of CaO2 is 200ml O2/L of blood.
O2 dissolved in plasma=3ml/L. When the cardiac output is low, we should calculate oxygen delivery=CoXCaO2 and then evaluate tissue diffusion. ************************************************************************************************************************************
2. Electrolyte Analysis: –
ABG gives us the status of Na+,K+,Ca++, and Cl–. The normal values of them are serum Na+ 136-145mmol/L,serum K+ 3.5-5.1 mmol/L,ionized (serum,plasma) Ca++ 1.15-1.33 mmol/L, Serum Cl– 98-107 mmol/L. Then we search the cause of hypo and hyper condition of different electrolytes.
In general sodium largely reflects reciprocal change in body water content. Chloride (Cl–) generally change in parallel with plasma Na+. It is low in metabolic alkalosis and high in metabolic acidosis. Potassium may reflect potassium shift in and out of cells-related to H+ ion. For each decrease in blood pH of 0.10, the plasma potassium should rise by 0.6 mmol/L. This relation is not invariable. Generally low level means excessive losses (gastrointestinal or renal). High level usually means renal dysfunction.
From the value of electrolytes and HCo3 we derive Anion gap, delta gap, gap-gap ratio and base excess/deficit.
Anion Gap (AG) :- Anion gap is calculated as AG=[Na+]-[(Cl–)+(HCo3–)] and is usually 12 mmol/L. AG increases most often due to increase of unmeasured anion and less commonly due to decrease in unmeasured cation (K+,Ca++,Mg++). Unmeasured anion are protein, phosphate, sulfate and organic anion. Albumin is the principal unmeasured anion and principal determinant of the anion gap. Since hypoalbuminaemia is present in as many as 90% of the ICU Patients. The following formula for the “Corrected AG” (AGc) has been proposed to include the contribution of albumin.
AGc=AG+2.5[4.5-(albumin in gm/dl)]
Example of a patient with a AG of 12 mmol/L and Plasma albumin 2gm/dl.
So, normal anion gap becomes high anion gap.
AG is useful to decide the cause of metabolic acidosis. AG should always be calculated for two reasons.
- Abnormal AG even if Na+,Cl–,HCo3– are normal.
- A large AG>20mmol/L supports a primary metabolic acid-base disturbance, regardless of the pH or Serum HCo3. A markedly rise of AG is never a compensatory response to a respiratory disorder.
So the cause of metabolic acidosis has been grouped as High, Normal and Low anion gap metabolic acidosis. In a patient all three can be present simultaneously and there can be simultaneous presence of metabolic alkalosis. To segregate these four, we take the help of delta gap, gap-gap ratio, BE and serum Albumin of the patient.
Delta Gap :-
Delta gap = pt’s AG-Normal value of AG.
= Pt’s AG-12.
When delta gap is added with measured HCo3, the sum value should satisfy the normal range of HCo3– i.e. 22-26 mmol/L. If this value is greater than 26mmol/L, indicates the additional presence of metabolic alkalosis and reduction less than 22 indicates non-anion gap metabolic acidosis.
Gap-Gap Ratio :-
Gap-gap ratio is calculated by comparing the anion gap excess(difference of measured and normal AG) to the HCo3 deficit(difference between the measured and normal HCo3 in plasma). Keeping in mind the normal
AG=12mmol/L & normal HCo3–=24 mmol/L.
AG excess/HCo3 deficit=(AG-12)/(24-HCo3).This ratio is sometimes called as gap-gap ratio because it involves two gaps (AG excess and HCo3 deficit).
Application of Gap-Gap Ratio :-
It gap-gap ratio is 1 – indicates high AG metabolic acidosis
It gap-gap ratio is <1 – indicates normal AG metabolic acidosis or treatment with N/S (hyperchloremic).
It gap-gap ratio is >1 – indicates associated metabolic alkalosis or when NHCo3 is added.
Base Excess(BE) :-
Base excess is defined as the fully ionised acid which could be required to return the patient blood pH 7.4 when Co2 has been adjusted to 40mm of Hg. It is calculated as
BE=HCO3(Measured)-24(Normal value of HCO3).
Positive value indicates metabolic alkalosis and negative value indicates metabolic acidosis. BE is true reflection of non-respriratory component of A-B balance. It is measure of metabolic acid level and normally is zero. A metabolic acidosis with base deficit>5 mmol/L requires explanation.
From the value of BE,NaHCo3 needed for neutralization can be calculated.
NaHCo3(mmol)=BE(mmol/L) X BW(Kg)/3
8.4% NaHCo3 solution contains 1 mmol NaHCo3 per ml.
Half of the amount is given and the ABG is done. Then calculate the amount required for final correction and administration.
In lactic acidosis,NaHCo3 decrease cardiac output and lowers blood pressure, so it should be used with caution.
3. Acid Base Analysis :-
The sole purpose of the A-B-analysis is to decide the primary disorder, compensatory effect (incomplete or complete in metabolic cause and acute or chronic in respiratory cause), disorder is simple or complex. If complex decide respiratory acidosis or alkalosis with metabolic alkalosis and/or metabolic acidosis. If metabolic acidosis decide high anion gap, normal anion gap, low anion gap. Lastly to conclude the aetiology of the defect. To conclude we proceed systematically in steps.
We look for pH and H+ simultaneously and decide acidemia/ alkalemia (net change present in blood). H+ is a derived value. It is calculated by simplified formula as H+ = 24XPaCo2/HCo3 .
- Normal value of pH 7.4 and H+ 40 nmol/L for all calculation of ABG.
- A normal pH can be normal, mixed defect or compensated defect.
- Severe acidemia (pH<7.25) reduce the efficacy of endogenous & exogenous administered catecholemine.
See for HCo3– . Its normal value for ABG analysis is 24mmol/L. It is increased >24 mmol/L in metabolic alkalosis. If it is decreased <24mmol/L in metabolic acidosis.
See for PaCo2. Its normal value for ABG analysis is 40 mm of Hg. If it is increased >40 mm of Hg – respiratory acidosis, if it is decreased <40 mm of Hg –respiratory alkalosis
We see the direction of movement of H+ and HCo3– . If H+ and HCo3– moves in opposite direction – metabolic cause, if H+ and HCo3 – moves in same direction – respiratory cause. If one is normal and another moves – moving factor decides the cause.
We see the direction of movement of PaCo2 and HCo3–. If the movement of PaCo2 and HCo3– is in the same direction – simple cause. If movement of PaCo2 and HCo3– is in opposite direction – mixed disorder. If one value is normal – simple cause. Other way to know about mixed disorder is to know the expected value of PaCo2 from last two digit of pH. If expected value and the actual value match – mixed disorder unlikely. If expected value and actual value differ – mixed disorder likely.
Compensatory change of Acid – Base disorder is decided by Rule of thumb for compensatory changes
Rule of Thumb
|Blood H+||Primary change||Compensatory response||Predicted compensation|
|Metabolic acidosis||>40||HCo3 <24||PaCo2 <40||PaCo2 falls = 1.2XHCo3– fall in mmol/L|
|Metabolic alkalosis||<40||HCo3 >24||PaCo2 >40||PaCo2 rise = 0.6XHCo3 rise is mmol/L|
|Respiratory Acidosis||>40||PaCo2 >40||HCo3 >24||Acute-HCo3 rise in mmol/L =0.75XPaCo2 rise in KPa.=0.1XPaCo2 in mm of HgChronic-HCo3 rise in mmol/L=2.62 X PaCo2 in KPa. =0.35 PaCo2 in mm of Hg.|
|Respiratory Alkalosis||<40||PaCo2 <40||HCo3 <24||Acute-HCo3 fall in mmol/L =1.50XPaCo2 fall in KPa=0.2 X PaCo2 in mm of HgChronic-HCo3 fall in mmol/L=3.75 XPaCo2 fall in KPa =0.5 X PaCo2 in mm of Hg|
Where 1 KPa=7.50 mm of Hg.
If Metabolic acidosis or mixed disorder, to conclude we take help of AG/Delta Gap / Gap-Gap ratio and BE. In mixed disorder respiratory acidosis and respiratory alkalosis do not Co-exist.
Then we look for the etiology of the A-B disturbances.
Causes of Metabolic Acidosis
There are two patterns of metabolic acidosis.
Pattern A – Normal anion gap i.e. hyperchloremic acidosis
Pattern B – Increased anion gap metabolic acidosis.
Pattern A i.e. normal anion gap metabolic acidosis may be due to (a) Inorganic acid (NH4Cl,HCl), (b) gastrointestinal base loss (loss of HCo3 in diarrhoea, small intestinal fistula) and (c) renal tubular acidosis (RTA) –urinary loss of HCo3 in proximal RTA and tubular acid secretion in distal RTA. So the diagnosis of RTA can be made if normal AG with no evidence of gastrointestinal disturbance and urinary pH is inappropriately high>5.5 in the presence of systemic acidosis.
Pattern B is high anion gap metabolic acidosis, causes of which are Methanol poisoning presented with blindness, Uraemia with obevious finding, diabetes mellitus as calculated by plasma glucose, Infection (CBC), Ischaemia(ECG), isoniazide toxicity(history), Lactic acidosis(s.lactate), ethanol toxicity, starvation and salicylate poisoning. Best pneumonic of it is (MUDPILES). Lactic acidosis is of two types. Type1 due to tissue hypoxia and the causes are peripheral generation of lactate as in patient with circulatory failure and shock. Type2 is due to impaired metabolism of Lactate as in liver disease, drugs (Metformin) and toxins.
Sometimes we get the low anion gap metabolic acidosis. The causes are hypoalbuminaemia and multiple myeloma. This condition is read by evaluating the corrected AG (AGc).
Cause of Metabolic Alkalosis
Abnormality that generate HCo3– are called “initiation factor” and abnormality that promote renal conservation of HCo3 are called “maintenance factor” . Metabolic alkalosis remain even after initiation factor have resolved.
Causes of metabolic alkalosis have been classified into two groups based on “saline responsiveness”. One group is saline responsive i.e. sign of extracellular volume contraction – most common pattern. They are vomiting , nasogastric suction , gastric fistula and diuretic therapy.
Another group is saline unresponsive metabolic alkalosis which implies excessive total body HCo3 i.e. HCo3 retention which can be associated with either euvolemia or hypervolemia and the causes are corticosteroid excess status eg . Primary hyperaldosteronism (conn’s syndrome), corticosteroid therapy, cushing’s syndrome and overuse of antacid salt for treatment of dyspepsia. Treat underlying cause. Response to metabolic alkalosis is decrease in minute volume by decreasing the respiratory rate. It starts 30-120 minute after and can take 12-24 hrs to complete.
It seems important to mention that in metabolic alkalosis compensatory increase in PaCo2 rarely exceeds 55 mm of Hg Higher PaCo2 values imply a superimposed primary respiratory acidosis. It is the most common abnormality found in critical care unit. Metabolically alkalotic patients may be sufficiently sick from their underlying disease, so the respiratory compensation is absent and hyperventilation may occur instead. Mortality with metabolic alkalosis in substantial. The mortality rate is 45% in patient with an arterial pH>7.55 and 80% when pH>7.66 . So, severe alkalosis should be viewed with concern.
Causes of Respiratory Acidosis
Common causes of respiratory acidosis are COPD (Type-II RF), ventilatory failure eg. Acute severe asthma, severe pneumonia, respiratory muscle weakness due to neuromuscular disorder, thoracic and skeletal deformaties , other causes are obesity which can make breathing difficult, sedative misuse including overuse of alcohol.
Causes of Respiratory Alkalosis
Common causes of respiratory alkalosis are L-Liver disease, E- embolism, D-drugs(eg. Salicylate, nicotine, xanthine derivatives and progesterone), A-Anxiety, V- patient on ventilator, P- pregnancy, H- heart failure other than this pleurisy, stroke, SAH, high fever, hyperventilation and those living at high altitude.
Response to metabolic acid – base disorder
The response to a metabolic acid-base disorder involves a change in minute ventilation that is mediated by peripheral chemoreceptor located in the carotid body at the carotid bifurcation in the neck.
Response starts within 30-120 m and take 12-24 hrs to complete.
Minute volume = Tidal volume X respiratory rate.
Response of Respiratory acid- base disorder
Secondary response to changes in PaCo2 occurs in the kidney. The renal response is relatively slow and can take 2 or 3 days to reach completion Because of the delay in the secondary response, respiratory acid-base disorder are separated into Acute and chronic disorder.
- Mixed disorder means complex disease.
- Independently co-existing disorders
- Not merely a compensatory response
- Dangerous extreme of pH
There can be combination of
Metabolic Acidosis + Alkalosis + Respiratory Acidosis/Alkalosis (Normal AG + High Anion gap + low AG)
Metabolic Acidosis + Respiratory Acidosis -> Leads to severe Acidamia – Poor outcome
Metabolic Acidosis + Metabolic Alkalosis (patient may be normal or near normal pH, AG increased) -> Metabolic Acidosis
Diabetic ketoacidosis + CRF -> Metabolic Acidosis
Sedation + salicylates -> Mixed disorder
Triple acid-base defect -> Alcoholic ketoacidosis may develop metabolic alkalosis due to vomiting and superimpose of Respiratory Alkalosis.