2nd Example – ABG Report of the Patient

Example: (2)

A patient of constrictive pericarditis, who had breathlessness on slight movement from one month admitted in stuporosed condition in emergency department of DMCH on 15/01/15.

ABG Report of the patient

ABG was done on 15/01/15 at 9.39 PM.

ABG Analysis:

 (i) Gas Analysis

Step:1
PaO2 – 49.8 mm of Hg–Moderate hypoxemia
SPo2 – 70.5 % – Severe hypoxemia

There is slight  left shift of the oxygen dissociation curve, most probably due to decrease in temperature.

Step:2
PAO2 – 49.8 mm Hg – low
So, either Fio2 low or PaCo2 high.

Step:3
P(A-a)O2 = (49.8 – 49.8) mm Hg.
= 0 mm of Hg – normal

Step:4
PaCo2 – 122.5 – Hypercapnea – hypoventilation
So, the patient has hypoxemia with Hypercapnea
i.e. Type 2 Respiratory failure.

Due to advanced stage of LVF.

Step:5
Here PaCo2 is increased, and P(A-a)O2 is not increased , so the cause is hypoventilation alone  and since the patient had no neuromuscular disease , so it is due to decreased respiratory drive due to critical illness.

Step:6
P/F index or hypoxemia index = 237.3
x-ray finding does not suggest progressive diffuse pulmonary infiltration , feature of pneumonia . So it can be due to heart failure or arterial hypoxemia.

Step:7
There is slight mismatch in the relation between SPo2 and PaO2.
Cause of mismatch is left shift of the oxygen dissociation curve most probably due to low temperature.

Step:8
Hemoglobin and HCT value are high indicating polycythaemia mosr probably due to hypercapnea . we calculate arterial oxygen content
CaO2= 16.4X10(gm/L) X 1.34 X 70.5 / 100 + 0.003 X 49.8
= 154.93 + 0.149
= 155.08 ml/L
Expected CaO2 in a 70 Kg person is 194.44 ml/L.

*************************************************************************************************************************************

(ii) Electrolyte Analysis
S.Na+  – 130.7 mmol/L  – low
S.Cl   – 86.5      mmol/l  – low
S.iCa – 0.915 mmol/L  – normal
S.K+   – 5.31      mmol/L    – high
Decrease level of   s.Na+ and Cl-is due to fluid retention.high level of K+ matches with the change  in pH due to acidosis.

Anion Gap :-
AG = [130.7]-[86.5+43.4]
= 130.7-129.9
= 0.8 mmol/l
Derived AG is 6.1 mmol/L
This increased level of AG is due to increased in unmeasured anion.

Delta Gap :-
= 6.1-12
=  -5.9
Delta gap + HCo3 = -5.9+43.4
= 37.5 – metabolic alkalosis.

Gap-Gap Ratio :-
= -5.9 /(24-43.4)
= -5.9/-19.4
= 0.30 <1

BE :-
BE= 43.4 – 24=19.4
So,metabolic alkalosis.

*************************************************************************************************************************************

(iii) Acid Base Analysis

Step:1

 

 

Step:2
Hco3 – 43.4 mmol/L – Metabolic alkalosis

Step:3
PaCo2- 122.5 – Respiratory acidosis

Step:4

Step:5

Expected cause of Acid-Base change in simple.
So, respiratory acidosis with compensated metabolic alkalosis.
Compensation of Hco3 In chronic condition
= 2.62 X 122.5/7.50 kpa=42.79
So, expected value of Hco3  = 24+42.79=66.70
Compensation of Hco3 In acute condition
= 0.75X 122.5/7.5 = 12.25
So, expected value of Hco3 = 24+12.25=36.25

So,respiratory acidosis with chronic compensated metabolic alkalosis.

*************************************************************************************************************************************

Final diagnosis
Respiratory acidosis with chronic compensated metabolic alkalosis with hypoxemia and dilutional huponatremia

*************************************************************************************************************************************

Causes of Respiratory Acidosis
In this case it is ventilatory failure due to decreased respiratory drive or due to respiratory muscle weakness.

 

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2 thoughts on “2nd Example – ABG Report of the Patient

  1. Dr. Weerasinghe August 28, 2015 / 6:20 pm

    Dear Sir,
    In here expected HCO3 is higher than Actual HCO3. Therefore body failed to increase HCO3 upto expected level. So this is uncompensated Respiratory acidosis. As base excess is there there should be metabolic alkalosis. So I suggest this as ” chronic respiratory acidosis with uncompensated metabolic alkalosis due to type II respiratory failure probably due to reduced respiratory drive with Heart failure causes dilution hyponaetrimia. Please correct if I am wrong.
    Thank you,
    Dr. Weerasinghe

    Liked by 1 person

    • Dr. R. K. Das September 13, 2015 / 1:30 pm

      Thanks DR. WEERASINGHE for pointing out the things.

      I am sorry to inform that I was busy in my important work ,so a delayed reply to the query.

      In this particular patient
      Expected HCO3 for the fully compensated metabolic alkalosis is higher than the actual HCO3. So it seems that it is a case of uncompensated metabolic alkalosis.
      But in chronic respiratory acidosis (>24 hours),renal adaptation is achieved and the bicarbonate increases. The serum HCO3 concentration usually does not increase above 38mEq/L,however.
      ref The Kidney, 9 th edition by
      Brenner and Reeter

      So the case to be considered as compensated metabolic alkalosis.
      Thanks again.

      Like

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