I love MAU so much. I actually wake up looking forward to work. Every request from the radiologist or discussion with microbiology is a learning experience. It’s more like working in a family business where everyone helps each other. For example, I had a difficult patient to bleed which the SHO and Reg also struggled with before the Reg eventually got it. I asked for his advice. Simply by paying attention to gravity and going “fast” into the vein rather than slow (which would have forced vein aside by the incoming needle), I then bled a patient on the first attempt who admitted she was notoriously difficult. I even look forward to the commute to work as I work out the most fuel efficient cruising speed on my Golf. Something has to be right.

Today’s highlight was the most unusual ABG I have come across so far, but one that you can work through and work out so much from.

A man in his mid 60s with extreme COPD was referred by his GP for extreme shortness of breath. The referral note also mentioned a potassium of 2.9.

By extreme COPD, I mean on home oxygen for most of his waking hours and on regular salbutamol, ipratropium, fluticasone, salmeterol and carbocysteine.

By extreme shortness of breath, I mean bedbound for the last 3 days.

His early warning score was 9 (that’s bad – 15 is virtually a cardiac arrest and 5 needs senior input). His oxygen saturations were 69% on 3L of O2. His RR was 32. His pulse was around 80 and irregular, feeling more like frequent ectopics than AF (i.e. regular for a while, then a missed beat). His BP was around 140/90. His temperature was 37.5.

This called for an ABCDE approach.

A – patient talking.

B – We put the oxygen up to 6L, targeting 88-92%. A brief listen to the chest revealed widespread wheeze and crackles in the lung bases, more on the right than left. The right lower zone was dull to percussion. We gave salbutamol and ipratropium nebulisers. An ABG was needed.

Should we have gone straight to 15L O2? That would be in line with the latest BTS guidelines. However, this patient got to his target on 6L, and was a known retainer of CO2. Please comment if you have any views either way on this, would love to hear them.

C – His fluid status wasn’t too bad, although capillary refill was around 3 seconds. An ECG showed U waves and flattened T waves, with multiple wide complex ectopics. We took routine bloods (FBC, U&E, LFT, CRP, Clotting) and started IV fluids with KCL added.

D – Alert, just. Clearly pretty confused. BM = 8.

E – nothing of interest.

The outreach nurse recognised this patient met the SIRS criteria as well as having a site of infection, defining sepsis and so the sepsis six was started:

“Give 3, Take 3”

1. Give oxygen (done)

2. Give fluids (done, with potassium added based on ECG and GP referral with potassium of 2.9. Of note, the maximum concentration of K that should be given is 40mmol/L, and the maximum rate is 10mmol/hour.)

3. Give antibiotics (done immediately, each hour delay costs 7.6% mortality)

4. Take blood cultures (ideally before antibiotics, but not if this would delay the start of antibiotics by more than a few seconds)

5. Take Hb/lactate (basically an ABG)

6. Take a urine output (which usually means catheterise the patient)

He was too drowsy and confused to get much meaningful history. With the limited opportunities to get him talking, I tried to think about my differential and what would alter management. I realised that every question I asked that he replied to would be making him more uncomfortable. I asked 8 questions:

“Do you have any allergies?”
“Yes, penicillin”
“What happens when you take penicillin?”
“Rash”

“Is there any chest pain?”
“Yes”
“Where?”
*Points to right lower ribs*
“Is the pain affected by your breathing?”
“Yes”
“How long has it been there?”
“3 days”

“How has your health been recently?”
*No reply*
“Have you been bedbound recently?”
“Yes, 3 days”

That was all I could get at this stage.

When I ran this ABG at A&E, they were convinced it was venous. It actually was probably arterial, as the predicted saturation at a pO2 of 4.0kPa is 67%, and the patient has sats around 69% at the time the sample was taken.

The most unusual thing about this ABG for me was not the hypoxia or hypercapnia, which would be standard for many COPD exacerbations, but the degree of alkalosis. This may reflect the patient’s longstanding COPD. He was probably a long term CO2 retainer, for whom a PCO2 of 8kPa may not be that far from normal. He has metabolically compensated over the years, so that despite the pCO2 of 8.1kPa this patient is actually still alkalotic. The base excess is phenomenal.

This also meant that although acutely hypokalemia must be treated to avoid arrythmia, it is worth bearing in mind that the low plasma K may actually reflect K redistributed intracellularly (be it from alkalosis or salbutamol) and our treatment may be increasing total body potassium quite a bit. The patient had not been vomiting or had any diarrhoea, nor been on any diuretics, so it was unlikely that the K had left the body altogether. This meant that we should look out for rebound hyperkalemia later on as the underlying problem leading to the alkalosis/high salbutamol requirement resolves. It is almost like the reverse of DKA where you look out for hypokalemia as insulin drives potassium intracellularly.

Further treatment being discussed was BPAP. The ceiling of treatment had to be established before this was considered, as well as whether or not he would be suitable for intubation.

This case highlighted that even if you do not know the underlying diagnosis, you can still stabilise the patient.

This was an exacerbation of COPD, probably secondary to an infection. Other possibilities included a pneumothorax and PE.

A chest xray was the next most suitable investigation.