Clinical Case 27: Part B – what actually happened..
September 15, 2011
Thanks for all of your comments and plans. Lots of good ideas – wish I had thought of a few of them!
So here is how I managed the man with severe COPD, ?AF and severe AS:
- NIV – BiPaP, started ASAP with a lowish pressure settings and wound it up as long as the BP / conscious level allowed
- Phenylepherine infusion – a 200 mcg bolus, then infused and repeated the bolus. Try to keep the BP up and hopefully induce a reflex bradycardia?
- No DC cardioversion – the man was too awake to shock, and I was too scared to give him any sedation that might have knocked off his respiratory drive. In my head – there is no way I could do as good a job with ventilation as he was doing. Even a minute or two of sedation would have left us in dire straights with his resp. failure crashing quickly.
- IV bolus of Amiodarone 300 mg – aim to get back to SR or at least some B-blockade / slowing.
And almost like magic after about half the amiodarone was in and as the 2nd phenyl epherine bolus went in – he flipped into SR at ~110/min. He turned pink and felt a lot better – he was still puffing away, but happier! I am not sure which drug or God did the trick – but it worked – good enough for me!
After this we loaded with some broad lung ABs and steroids. we gave IV MgSO4 to ward off a return of whatever SV tachyarrthmia was there intitially.
In terms of palliation vs. intubation – we have the unique scenario of being a long way from and ICU – so you decision-making here is sharpened – you have to decide on this early. Personally, in this type of case I think a good trial of NIV with medical optimisation either works or it doesn’t – if the patient does not respond I think the prospect of intubation and the week – months of ventilator-dependency that follows is not a good way to die.
It can be tricky to have “the chat” in such extreme poor situations – and I am always disappointed that the doctors who care for these chronic problems do not discuss these very real and inevitable scenarios with the patients before – when they are ‘well’ and in a better place to decide how they feel about palliation as an option. Making a patient NFR in the middle of a crisis is not the way to go – good palliation should begin much earlier!
My 2 cents. Casey
Oh, I found this article from J Emerg Trauma Shock. 2010 on treating tachyarrythmias – has a flow diagram that seems to lead to DC cardioversion in all groups!
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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
11 Comments
Sounds about right…crank up the BiPAP with a sympathomimetic infusion running and trickle in vitamin A hoping to get rate control…
If he’d crashed, would you have intubated? Presume were set up ready-to-go in cae.
I share your frustration with the difficulty of discussing treament ceilings in the middle of a crisis…and evwn though I sit on both sides of the fence (local primary health care office doctor as well as oncall in ED), it can be difficult to communicate the ‘what ifs’ and encourage patients to consider treatment ceilings before they end up in the doo-doo.
Currently I am back in the hospital system doing some anaesthetic upskilling…it amazes me that not much seems to have changed over the past decade since I last was in the tertiary system…people with advanced dementia still sent in via ambulance form nursing home as no documented advance health plan and perception from nursing staff, family and sometimes locum GP cover that ‘something must be done’. People wit multiple major comorbidities who are shocked when I initiate discussion re: treatment options and limits prior to their major operation or when being considered for ICU admission.
I often point patients to a blog from a few years ago ‘a plan for the end’ which discusses some of these issues and helps patients consider their options – see http://www.ruraldoctoring.com/2008/09/case-a-plan-for-the-end.html
I guess what I am trying to say is that it is still relatively uncommon for these discussions to have taken olace befoer the shit hits the fan…even in small rural communities where the local doctors play both sides of the fence. Hence I am a huge advocate of having these discussions more frequently – on every hospital admission for a ‘flare’ of condition, prior to even elective anaesthesia/surgery ‘in case’ as part of my consent process/risk discussion…and particularly if I am drawing up one of those infernal ‘chronic disease care plans’ (item 721/723) where there is an excellent opportunity to discuss and document treatment ceilings for those with chronic disease.
Anyone got any thoughts on how better to iprove our discussion on treatment options prior to patients hitting resus?
Nice one guys
I will have to try the phenylephrine infusion trick one day..problem is we don’t carry it on the retrieval packs
Tim totally agree with you about the chronic disease care plans..I do heaps of them for Indigenous clients and not once have I entertAined the idea of discussing advanced care directives etc…what an excellent idea!
Casey,not sure about giving Magnesium after amiodarone..won’t hurt but not sure if it adds anything above the amiodarone?
I have always been nervous about the beta-blocking effects of amiodarone and it’s extremely long half life (and to a lesser extent it’s potential for pulmonary toxicity) when I think about using it in the COPD patient who seems to have a reactive airways component.
Perhaps it is just a theoretical problem, but I think about having a patient crash and then having to support them for months until even that single amiodarone dose is totally cleared….
Aaron
Good points-
I think the Mg was given for the bronchospasm and the level was lowish when we got bloods back. Also not much harm and might stabilise the myocardium a bit
Amiodarone appears to be one of those drugs that come in and out of favour – it is the mini-skirt of medicine. currently in favour here in Oz for AF. So it is used a lot in acute AF
I might need to look into the evidence abit
Tim – would I have intubated – well, probably not. Why? If I had spoken to an ICU early – they would have refused this patient point blank. I would if I were and ICU consultant. So intubating in Broome is a pointless task really if you have no longer term plan and I dout it would change the eventual outcome –
Any counterpoints? C
Just to reinforce the good decision not to cardiovert electrically as first option .Unless you are pretty sure the AF is less than48hrs old, there is risk of CVA due to clot formation and even more commonly the AF being refractory to cardioversion. Chronic AF is resistant to cardioversion in the main and a lot of times it’s hard to distinguish acute from chronic AF.
Casey, Don’t get me wrong amiodarone is by far the most commonly used anti-arrythmic drug in North America too. It is definitely at the top of the algorithm for atrial fib here as well. I am cautious it personally because it has multiple effects, in this case beta blocking effect in a potentially bronchospastic patient, and it has an extreme long half life (about 50 days). I personally prefer procainamide in general as an antiarrythmic, though it has downside in this case as well.
Minh, We will have to have a pleasant disagreement on this one! I think it is important to really get a good look at the ECG in this case. The rate well above 200 suggests it is probably not a-fib. It could be flutter, or SVT, but is probably multifocal atrial tachycardia (in this case it turned out to be a-fib but generally that rate suggests otherwise). If you can say with certainty that the ECG is MAT then I agree no cardioversion, but I think all three other rhythms must be shocked. There is certainly rick of CVA, but there is also risk of immediate cardiovascular collapse and death with the amiodarone bolus. There is a risk of death in this case no matter what we do, even if we stabilize this guy we have probably achieved nothing substantial, his 3 month mortality is probably >75%. There is simply no therapy in this gentleman that is not without substantial risk of catastrophe.
I am definetely not criticizing your or Minh’s suggestions in this case, rather pointing out that the case is such a nightmare that there are really no good options. I think 10 physicians could probably all do 10 different plans in a patient like this and still all fall under an umbrella of ‘reasonable decision making’.
Good call on making decision not to intubate early in the piece. Hacing said that, this guy did revert eventually and presumaby made it to discharge…if he’d becme obtunded and needed intubation for airway control, wold a brief period of ventilation have been appropriate?
Sadly I see many intubate early and fail to appreciate the downstream consequences (make it someone elses problem, usually ICU!)…
Bottomline, we should not be afraid to decide upon treatment ceilings early, and preferably agree these in consultation with patient and family
Of course, it gets trickier when patient/family expects full active measures yet treating doctor(s) feel inappropriate on grounds of futility. However we don’t always get what we want….I for one wold like a pony for Xmas….doesn’t mean I am going to get one!
Hi Tim. In response to your question – “can you use USS to differentiate pneumothorax from bullae?” Dr Goudie (see todays case) tells me that if you see good lung sliding on the USS then it is not likley a pneumothorax, however the absence of lung sliding is less specific – could be a pneumo or a bullae. So if you have an area of lung on the CXR which could be either – then do the USS and if it slides – it is probably a bleb / bulla, not apneumothorax – so don’t needle it!
Casey
I will email your query to the US gurus and see what they say.
Thanks Casey, that’s what I thought…so seems USS would be useful adjunct for that case (case 028)
Thanks for this great case! I recently had a case with some similarities, but much less hair raising/sphincter tightening. The patient came in with fever, severe tacky (~190) and hypotensive (SBP 60-80) with a history of sore throat and apparent trismus. I was obviously apprehensive about this patient crashing because of his difficulty opening his mouth, but in spite of his alarming vitals was incredibly well clinically, especially after I analgesed him with NSAIDS and some Decadron for what I feared might be a cellulitis or abscess (not seen on X-ray). His BP tempted me to electrocute him, but his clinical condition reassured me to stick to observation for a while. I rehydrated him with about 5 litres of IV NS, administered IV Abx and kept a super close eye on him. Like your patient, his tachycardia converted spontaneously after good rehydration/reperfussion (I like your phenylephrine solution – will consider in the future) He went to the ICU and was observed for a few days (during which he went into severe EtOH withdrawal, much to the annoyance of the nursing staff), but no dice on an infectious source (blood cultures were drawn pre Abx). Our internist posited a bizarre presentation of Coversyl allergy (which he had recently started).
Should also add that his bloodwork also belied sepsis, with normal WBC and differential and a reassuringly low, though abnormal, lactate.