A 58 year old woman ventilated in intensive care for a week following a motor vehicle accident was noted to drop her oxygen saturation suddenly, requiring an increase in FiO2 from 0.4 to 0.6.
The nursing staff have performed an arterial blood gas.
|
Test |
Value |
Normal Range |
|
FiO2 |
0.6 |
|
|
pH* |
7.48 |
(7.36 – 7.44) |
|
PCO2 |
41 mm Hg |
(36 – 44) |
|
PO2 |
86 mm Hg |
Ventilator data
Tidal Volume 700 ml
Respiratory rate 14
Peak pressures 28 cm H2O
Plateau pressures 18 cm H2O
PEEP 7.5 cm H2O
SpO2 94%
EtCO2 28 mm Hg
a) What is the most likely diagnosis diagnosis? List your reasons for the diagnosis.
a) What is the most likely diagnosis diagnosis? List your reasons for the diagnosis.
The most likely diagnosis is a pulmonary embolus. The reasons are as follows:
Sudden onset of hypoxemia raises a number of possibilities – mucus plugging, pneumothorax, LVF, aspiration etc. However, the ventilation data indicate preserved compliance, normal peak pressures (argue against a pneumothorax or plugging or LVF) as well as there is increased dead space, (raised A-et CO2 gradient)
This question is identical to Question 13.4 from the first paper of 2014. It relies on the candidate to be able to quickly perform a calculation of the A-a gradient. However, even without maths, one can arrive at the conclusion that the PO2 is way too low for an inspired fraction of 60%.
One could rabbit on about the other causes, but the ventilator data is pristine. The patient has normal peak airway pressures, so nothing is blocked, and normal plateau pressures, demonstrating reasonably normal lung compliance. This is a defect of perfusion, not ventilation.
Lastly, the candidate is presented with an end-tidal CO2 measurement, which is substantially lower than the arterial CO2 measurement, suggesting that there is a large area of lung which is not participating in gas exchange, i.e. it is dead space.
Capnometry and the arterial-expired carbon dioxide gradient is discussed elsewhere.