Myocardial infarction with acute pulmonary oedema

A 59 year old gentleman in the cardiology ward, enjoying a new LAD stent, suddenly complains of shortness of breath. On her arrival, the medical registrar finds him with a respiratory rate of 30 and coarse creps in both bases. A solid 80mg of IV frusemide is given; CPAP is commenced. Some hours (and litres of urine) pass before somebody compares the trend in ECGs and realises that the left bundle branch block is new.

This gas is aspirated from the femoral sheath once the patient is back to the cath lab:

Data to be interpreteted

Data to be interpreteted



Discussion and Interpretation

Assessment of tension-based and content-based oxygenation indices

Alveolar oxygen 171.275
A-a gradient 120.875
a/A ratio 0.29
PaO2/FiO2 ratio 168

There is significant hypoxia. Though the A-a gradient is raised, it does not offer a satisfactory impression of how profound this hypoxia actually is. The a/A ratio however demonstrates that only about 29% of the alveolar oxygen is ending up in the arterial blood.

The change in pH

There is a significant alkalaemia; the pH is 7.528.

The change in pCO2

The pCO2 is low, likely contributing to the alkalaemia.

However, if the pCO2 was the only acute contributor to the acid-base disturbance, the pH would be around 7.445 (as calculated by the Henderson-Hasselbalch equation, using a bicarbonate level estimated by the "2 for 10" bedside rule of acute respiratory alkalosis). There must also be a metabolic alkalosis lurking.

The change in Base Excess

The Actual Base Excess is positive, supporting the hypothesis that a metabolic alkalosis is also present.

Assessment of compensation

Copenhagen interpretation of acid-base compensation:

With this slightly alkalotic SBE, one predicts that the PaCO2 should be around 43.5mmHg. Since the measured PaCO2 is lower than this, there must also be a respiratory alkalosis.

Boston interpretation of acid-base compensation:

Note that this ABG machine reports the actual bicarbonate rather than the standard bicarbonate, which saves the Boston supporter from having to calculate the actual bicarbonate themselves. The actual bicarbonate for this scenario is 28.3mmol/L.

Using the "2 for 10" rule of acute respiratory alakosis, the expected bicarbonate for this scenario is 22.8 mmol/L; the actual bicarbonate is much higher (28.3), again supporting the idea that there is a metabolic alkalosis present. If we believed that the metabolic alkalosis is the primary disturbance, the expected PaCO2 would be 39.8mmHg - higher than the measured value. Thus, there is definitely both a metabolic and a respiratory alkalosis.

Assessment of oxygen-hemoglobin dissociation mechanics

The p50 is slightly left-shifted, which can be accounted for by the alkalosis, given that the dyshaemoglobin levels are within the expected range.

Additional remarks

This patient has a mixed alkalosis, with a minor respiratory and major metabolic components. The metabolic component can be explained by the vigorous diuretic therapy - that is probably also why the potassium is so low (2.9). The respiratory alkalosis seems counterintuitive (it's the opposite of what should be happening) until one recognises that the driving force behind the hyperventilation is hypoxia: this patient is drowning in pulmonary oedema fluid.