53 yo man with a history of hypertensive cardiomyopathy presents to ED at midnight with severe dyspnoea. No chest pain, no oedema, no fever, cough or signs of infection. On examination he has bilateral creps up to his scapulae, invisible JVP due to big neck / beard. ECG shows an old LBBB, same as previous. Obs – pulse 100 sinus tachy, BP 200/120, RR is 30, Spo2 = 90% RA – he looks sick, sweaty and scared. So what is the diagnosis? Well most of us would have no problem saying this chap has acute pulmonary oedema. But is it all that clear, and how should one treat APO? I have done a bit of research and come up with my own personal APO approach.
In my mind “APO” is usually one of 4 different clinical entities…
- SCAPE (Sympathetic Crashing Acute Pulmonary (O)Edema). Scott Weingart has a great podcast on this group at Emcrit. You diagnose this by looking at the BP – does this look like a patient who is running his own endogenous Adrenaline infusion? The case above fits into this group nicely. Often there is no history of CCF, no oedema, no clear ‘trigger’, normal LV function. This process is largely neuro-hormonal in aetiology and comes on pretty quickly – over hours.
- Acute-on-chronic (Acute decompensated HF). This group have a history of CCF, chronic poor LV function and likely are already on treatment (which hey have often missed!). They have low BP, poor urine output and borderline renal perfusion / function, they might have worsening peripheral oedema, and they tend to come on a bit slower – over days.
- The “Acute Cause” APO group. These are the folks who have a clear new cause for their APO – common causes: ACS / STEMI, rapid AF / arrhythmia, PE , acute valve rupture, high output state – sepsis, anaemia… These people might have a reversible cause or at least something you can try and fix / get to definitive care.
- Iatrogenic APO – uniquely occurs on surgical wards!! The old duck who has had a few too many litres of saline for her chronic low BP, This one is easier to pick, and might be a subset of group 2.
The Oxford Handbook of Medicine lists the treatment of APO using the LMNOP mnemonic. So lets look at the evidence for these interventions.
Magnesium – often low in CCF /AHF and can lead to arrythmia – so I like to load with Mag
Good Palliation: APO is sometimes the end of the line for a patient with severe heart disease. It is analogous to the COPD presenting in extremis in some cases. So before you embark on invasive manouvres you might want to have “the talk” with the patient and the family if it is clear that the underlying disease process is not remediable.
I aplogise for saying “studies show” but there is a lot of good data out there and a few great reviews – too many to go into in a quick blog. If you are keen to see them go to Crashing Patient and see the links.
The summary is: get them on the NIV ASAP, and hit em with a proper dose of GTN – they will get better quicker and you will intubate less people!