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
- 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
PaO2
|
corresponding SpO2
|
> 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)
|
Step: 2
PAo2
(Alveolar oxygen content)
PAo2 is derived value and
is calculated as
PAo2=Fio2 (PB-PH2O)-PaCo2/R
Normal
value is 96-108mm/Hg.
Step: 3
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.
Step: 4
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.
Step: 5
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.
Step: 6
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 dystress syndrome (ARDS).
Step: 7
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.
Step: 8
Calculate
the arterial oxygen content(CaO2).
CaO2=Hb(gm/L)X1.34XSpO2/100+0.003XPaO2.
In a adult of 72 Kg the normal value of CaO2 is 200 ml O2/L
of blood.
O2 dissolved in plasma=3 ml/L. When the cardiac output is low,
we should calculate oxygen delivery=CoXCaO2 and then evaluate tissue
diffusion.
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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.
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.
AGc
=12+2.5(4.5-2)
=12+2.5X2.5=12+6.25=18.25
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-respiratory 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.
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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.
Step: 1
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.
Step: 2
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.
Step: 3
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
Step: 4
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.
Step: 5
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.
Step: 6
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 Hg
Chronic-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 Hg
Chronic-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.
Step: 7
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.
Step: 8
Final diagnosis.
Step: 9
Then we look for
the etiology of the A-B disturbances.
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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
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.
Response
to metabolic acid - base disorder
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 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
- 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(Normal AG
+ High Anion gap + low AG) + Alkalosis + Respiratory Acidosis/Alkalosis
Metabolic Acidosis +
Respiratory Acidosis - Leads to severe Acidaemia
- Poor outcome
Metabolic Acidosis +
Metabolic Alkalosis - Metaboli Acidosis
( patient may be normal or near normal pH,
AG increased )
Diabetic ketoacedosis + CRF - Metabolic Acidosis
Sedatives + salicylates - Mixed disorder
Triple
acid-base defect -> Alcoholic ketoacidosis may develop metabolic
alkalosis due to vomiting and superimpose of Respiratory Alkalosis.
