Clinical Case 020: the ABC of APO
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!
About The Author
Casey Parker
I am a GP working in Broome, NW of Western Australia. I work as a hospital DMO (District Med Officer) doing Emergency, Anaesthestics, some Obstetrics and a lot of miscellaneous primary care. Also on the web as @broomedocs | + Casey Parker | Contact
Courageous. I’m not sure what else to say with your GTN admin.
No, just kidding.
In the Emcrit linked trial, the most anyone (anyone being the 12 patients) got was at 24hours – 150 +/- 86 mcg/min (unless I’ve misread this small trial), at 15 minutes they were on 41+/- 20mcg/min. I’m not sure where the 400mcg/min came from.
The guideline for Broome starts them off at 50mcg/min so I don’t know that we are all that homeopathic! Maybe there’s just some reluctance to uptitrate as the rationale for uptitration is perhaps not as clear as it is for someone with chest pain?
How long do you keep them on the infusion? Do you think development of nitrate tolerance will be a problem?
Very interesting re the Lasix!
Hi Roy
Thanks for your critique. Yes, 400 mcg/min – see link below on bolus GTN
The evidence I am looking at was at the following link:
http://crashingpatient.com/medicine-surgery/076-heart.fx.htm
Weingart referecnes a number of papers using high initial doses of GTN.
At these doses, i run it fast for a few minutes, have an art line in and watch the BP closely, titrating down after the initial bolus has had an effect. Like any short acting drug – you need a bolus to get into the therapeutic range, and achieve a steady state – this is hard to do with low dose- up titrate strategy as is traditional.
Anyone wo uses Lasix religiously is basically “full of piss”! (HAHAHHA)
I can’t fault your logic from a pharmacodynamic persepective!
Hi, just wondering your thoughts on the use of GTN in the hypertensive APO patient who is also in rapid AF at a rate greater than 180bpm? I’ve heard the GTN can be harmful due to the patient’s tachycardia.
Look forward to your response, great site by the way!
Denis
Hi Denis – a good question. If the patient has AF@180 and has a high BP they likely have a “sympathetic” basis or the problem, they need sympatholysis.
Agents of choice here would be beta-blockers, fentanyl or GTN. If left alone they will probably go into APO or drop their BP eventually.
If they look unstable then giving a more gentle titration of GTN IV seems like a good idea, as you can turn it off quickly. Small aliquots of metoprolol would also be OK
I would do this in a room with a defib applied as DC cv might be required if it goes south and they crash their CO.
Slow the pump, relax the pipes – but be careful not to do either too aggressively.
My guess is your colleagues have experienced “harm” if by give a big SL dose of GTN in these pts who are on the shoulder of their Starling curve.
Also god to know if the pt has serious AS etc prior to giving nitro!
Casey
excellent APO summary Casey, cheers
I do wonder about Morphine though. The associations with bad outcome may just be that it is used on the most severe patients. In fact in my clinical experience that is the exact patient that is used on – the one where CPAP and GTN has failed and they are considering intubation. I think that is the patient where it’s use could be considered quite reasonably. Anecdotally I’ve seen a patient in that exact category who was saved by a small dose of morphine and avoided intubation because of it. I wonder whether fentanyl v morphine. I think the reduction in sympathetic drive is probably the main mechanism of action here but perhaps the ventilation that can supposedly occur with morphine reducing preload is perhaps beneficial in a subset of patients. I don’t think using fentanyl makes any more sense and certainly not because it simply hasn’t been studied like Morphine has in APO. However there’s probably no downside in using it as an alternative.
Without RCT’s to demonstrate true benefit/harm but with that negative association noted, I think the peri-intubation patient who has failed CPAP/GTN is probably the right patient to trial it – if it fails and/or they become to sedated, you were going to tube them anyway so you’ve lost nothing.
Your thoughts?
sorry “ventilation” in my above post should read “venodilation”