A 26 yo American backpacker presents to the triage of your small hospital ED complaining of palpitations.
He is traveling the globe after serving 2 tours of duty in Iraq and being discharged from the US Army. He is a bit reluctant to attend as he hasn’t much cash flow and is expecting he will be slugged for the visit. Fortunately this is not the USA [Ed: Ping Seth Trueger (@MDAware) here….]
Our former soldier is a tall, thin young man – well tanned from his travels in the north. HE states that the palpitations started this morning – maybe 4 hours ago. On questioning they may have been there intermittently over the past few days – though he didn’t want to interrupt his beachside relaxation to attend ED. HE denies any amphetamines etc, though has been drinking a lot of beer since hitting town.
On history – he says this has happened before and in fact he was “medically discharged” from the Army after experiencing a few episodes of syncope at the end of his last tour in Iraq. The Army doctors put him on “a bunch of pills” – which he stopped taking when he embarked on his round-the-world adventure with his buddies. When pushed he says he cannot recall exactly what the problem was…. When asked if he was diagnosed with any heart problems he says he thinks it was called “fibrillation, or something….”
So our young soldier is not really able or wiling to tell us too much.
He gets a bed in ED and attached to the monitors. Here is the rhythm strip…
Obs: Afebrile, BP is 100/50 laying, PR = 150, thready, hard to palpate at the wrist, SpO2 is 97% on air, RR is 18/min, BSL is 7.3mmol/l (131 if you are American). He does look a little pale, a few beads of sweat on his brow – though it is 100 F outside as always!
On further exam he has just a weird sounding heart – murmurs in all directions, going very fast – so tough to interpret – and lets face it, none of us are that smart. His chest is clear aside from bibasal creps…. odd for a young guy. No track marks or signs of endocarditis evident.
A quick bedside chest scan shows plenty ( > 6 ) B-lines per rib space in the lower chest zones – looks like lung oedema.
Normally I would do a quick look ECHO – just to see if there is anything grossly wrong – e.g.. big effusion, massive RV strain, flat LV or really obvious wall motion anomaly – but unfortuanltey the US machine with the ECHO probe has been taken down to the labour ward by mistake…. sorry , pet peeve – had to get that one off my chest ;-(
He gets a couple of lines and some blood taken for the usual… the spot troponin on the POC machine in the ED is negative. Being a small ED – it will be hours until the rest comes back.
There is no way to get any background data – he says he last saw a doctor in the base back in the USA a year ago. He never saw a civilian doctor and it is now 3 AM in the USA.
After collecting all that data – you decide to call your local friendly Cardiologist to get some advice – what now? As you call the secretary and wait on hold for your Cardiac colleague – you notice the nurse disconnecting him from the monitor for a toilet break… “Oh, goo looks like he is perfusing his kidneys, should make some aspects of therapy easier?” you think. Waiting, waiting, waiting….
After 5 minutes on hold and then 10 minutes chat – you reach the conclusion that this young guy is low risk from a CVA / CHADS-Vasc2 (MDCalc rocks!) perspective. The advice you receive is to try loading him with medical therapy – optimise his K+ and Mg++, then load with amiodarone 300 mg over an hour. This is pretty standard in many Australian EDs. You decide to ask the heart guru: “when would you consider using DC cardioversion in a young guy like this?”
The answer is – “I would only shock him if there was evidence of shock…” OK, so you hang up and write some drug orders, and decide to go and tell the patient what your Specialist advice recommended. But… he is not in the cubicle… Yep, it is one of those, “OH SHIT!” moments in ED!
You run to the toilet and can hear a groaning sound from within – it is impossible to open the door more than a crack as this 6 ft 4 guy has collapsed against the door and his legs are against the wall. He is moaning, and appears to be laying in a puddle of vomit with his pants around his knees.
Nothing a bit of brutacaine doesn’t fix. With the help of a burly orderly and a security guard you manage to haul him out of the john. Back up onto a bed. He is not looking good…
Obs: BP is now 70/40 – barely palpable at the wrist, the monitor still shows rapid AF – now 170/min. He looks really pale, a faint grey colour and has now developed marked work of breathing. SpO2 is 88% on 15l via non-RBM. He is waking up from his collapse and is now giving coherent but distressed answers, he looks scared.
This situation is spiralling… we need more info, why is this young guy decompensating so dramatically? You call the labour ward and request to swap machines – need to see that heart now!
OK, I am going to leave it there for now and ask these questions:
Q 1. Would you now crack on and go for a DC Cardioversion at this point?
1b. IF so, how would you proceed: sedation?, doses, DC joules?
Q2. Do we need to get any more information to make this decision, or is the situation enough to justify empirical treatment?
Q3. Any diagnostic ideas that might help?
THE CONCLUSION to this case…
Our patient was taken to Resus and pads applied. He was grey, sweaty – the pads were tough to stick due to the perspiration. This is fulminant sympathetic compensation for cardiac badness.
A decision to perform DC CV was taken. A homeopathic dose of fentanyl and propofol were injected… at which point he became unconscious – it took a moment to realise that the loss of consciousness was not due to the 10 mg of propofol – this was PEA arrest. CPR commenced – all hands on the chest.
Intubation and ventilation were quick and slick.
At this moment the orderly wandered in with the other US machine with ECHO probe
Thanks to Mike Stone / Sonocloud for the is FOAM clip Everything was massively dilated and the myocardium was moving, though clearly not pushing any blood out of the LVOT. Prolonged CPR eventually resulting in asystolic arrest.
This was severe, dilated cardiomyopathy. It was a long standing problem and the patient had decided to forgo any treatment. In the past he had been treated with various anti-arrythmics and warfarin – but had decided that that was not for him.
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