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.
Probably not as good as we think. There are a lot of confounders – classically it can be tough to differentiaite APO from COPD clinically – large studies have shown this. So I just admit my shortfallings and get a CXR, it either looks like APO, or you find another cause for the SOB (pneumonia etc). Get a few ECGs, troponins and make sure you have thought about the other “reversible” causes. Oh and BNP – it is only helpful if negative – if the BNP is low – it is probably not APO!
The Oxford Handbook of Medicine lists the treatment of APO using the LMNOP mnemonic. So lets look at the evidence for these interventions.
No good evidence. Never been shown to improve short or longer term outcomes. Based on the flawed assumption that the patient is “fluid overloaded” which is usually not true – especially for the SCAPE patient. I almost never use Lasix in the acute setting, unless there is clear overload, and the patient is on it long term.
Morphine is bad! The ADHERE registry of APO patients showed that morphine was independently associated with increased mortality. Sure it might make the patient feel better – and that is fine if your goal is palliation, but not if you want to fix them! I don’t ever use morphine in APO. There are better options for sedation if you need that.
Nitrates are good. especially in the SCAPe with BP up high. The problem with GTN infusions is that we have all been trained to use homeopathic doses. If you really want to get the patient better quick, use GTN in a proper dose – 400mcg/min to start (see Emcrit for references
). I put 50 mg of GTN in 100 ml, and start it at 48 ml/hr for a few minutes and tirate back by 6 -12 ml/hr until I have a MAP around 80. If you do this well, the true SCAPE will be better in an hour. An art line is great – makes titration so much easier.
Oxygen is good – but we can do better. All the recent studies show that NIV is superior to oxygen. So if your patient can tolerate it – go with CPAP, if not, then O2 is good.
Along with GTN, CPAP is the thing that will get your patient better quickly and mean you don’t even have to consider an ETT. I start with 10 cm and titrate to RR and effort. Beware the low BP / floppy heart / super dry patient – they might crash with the combo of GTM and CPAP. If so – they are probably a type 2 patient – tough scenario. Oh, and the studies show no difference between CPAP and BiPAP – so I only use BiPAP if I think there is a ventilation / COPD component or hypercapnea.
Well ACE inhibitors are probably useful, they get at the neuro-hormonal axis that can be the cause of the SCAPE syndrome.
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!