The following arterial blood gas result was obtained from a 65-year-old lady with exacerbation of chronic obstructive pulmonary disease (COPD), day 7 in ICU following intubation and ventilation for respiratory failure.
Parameter |
Patient Value |
Normal Adult Range |
||
FiO2 |
0.3 |
|||
pH |
7.48* |
7.35 |
– 7.45 |
|
PCO2 |
42 mmHg (5.5 kPa) |
35 |
– |
45 (4.6 – 6.0) |
PO2 |
104 mmHg (13.7 kPa) |
|||
Total haemoglobin |
122 g/L |
115 – 165 |
||
SpO2 |
98% |
95 |
– |
100 |
Base Excess |
7.0 mmol/L* |
-3.0 – +3.0 |
||
Bicarbonate |
31 mmol/L |
22 |
– |
32 |
a) Interpret the arterial blood gas. (10% marks)
b) Give four possible reasons for the acid-base disturbance seen. (10% marks)
a)
Metabolic alkalosis
Raised A-a gradient
b)
Diuretics
Steroids
NG losses
Post hypercapnia
A systematic approach to this problem would resemble the following:
In summary:
Why would this be? One may refer to the list of causes for metabolic alkalosis. In a ventilated COPD patient with a normal-looking PaCO2 one could very easily point the blame at a posthypercapneic state.In fact, that is the only thing you can conclude from the bare minimum history the college has given. However, the question asks for four possible reasons. The college model answer offers diuretics, steroids and NG losses as potential contributors. Because of how little history is given, rhese differentials are at least as likely as the use of β-lactam antibiotics, Liddle's syndrome or clay ingestion.
Banga, Amit, and G. C. Khilnani. "Post-hypercapnic alkalosis is associated with ventilator dependence and increased ICU stay." COPD: Journal of Chronic Obstructive Pulmonary Disease 6.6 (2009): 437-440.