Clinical Case 098: the Falling Soldier
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
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
Tough situation … not your standard RAFF patient either … must be another pathology going on as the rate of 170 should not be enough to cause decompensation and LVF in a 26YO.
Considering intrinsic cardiac disease eg myocarditis; possibly AF with WPW (no 12-lead) as one R-R interval seems to give a ventricular rate of 300 which can only occur with an accessory pathway. Ischemia possible … would have to analyse the 12-lead. Other possibilities toxins.
Q1. He is in shock so does need emergent DCR. Given the hypotension I would go with ketamine 1.5mg/kg IV and 150J biphasic. Hypoxia needs addressing too … if he tolerates I would apply NIV: starting with 10cm H20 CPAP to treat presumed cardiogenic pulmonary edema. If he doesn’t tolerate wait until he dissociates.
Q2. To me the situation needs urgent action
Q3. Reasonable to perform rapid beside echo as described in the case. Don’t think any other bloods or imaging would be useful nor timely in this case.
Dramatically shocked I would proceed with electric cardioversion 120J than 200J biphasic for second attempt…In This case little sedation with Ketamine or If I haven’t it, just small propofol (see Emcrit on proced sedation) 0,25 mg/Kg.
This heart needs US, no doubt on that…
Jee!!!! certainly does not sound like a “small ED” from what I come across on your “case files”. What a wide variety of stuff you do 🙂
Its so great to interact with people with such wide practice scope.
Ok my two cents since I am just a GP in a remote rural town in Australia.
I will make only a quick comment,since there will be much smarter people talking in detail on this.
1) I would certainly sedate and do cardioversion. The guy is “unstable”.
2)I would want to look at the proper 12 lead ECG. My concern is that little slow slurring of the upstroke on QRS complex (“delta” wave) which, if its a real finding, would mean we are dealing with a WPW with AF -and the rythm is devolving into Vtach due to aberrant pathway and hence his repeated syncopes over years and years. Simple AF does not really explain it fully.Something else is going on here.
3) Regarding management:Any other med that slows conduction at AV node )Beta blcokers, calcium blockers, dig etc) could make him go into VF and cardiac arrest. The only “pharmaceutical” option in a stable patient would have been amiodarone and in an unstable patient (this one) – a DC shock .
I would use Fentanyl(relatively more cardiostable as compared to propofol) with some metaraminol to keep the BP up and perform Cardioversion.
Lets see what others have to say on this.
Thanks again for the case.
First apply trouser clips!
OK, I’d go for a DC cardioversion. Ideally I’d like more info but in reality he’s circling the drain fast. How to do it – 1-2mg midazolam and an apology. I suppose you could make an argument for ketamine given his BP but I’m not sure I want to add to his sympathetic surge any more…..
There are lots of signs that he has something very weird in the structure of his heart, so even if he was less sick the only drugs I would be comfortable about using would be Mg and amiodarone – and I don’t fancy amio with that BP.
I would want to know his electrolytes soon though (bedside VBGs?) and will be very interested in his echo when the probe comes back!
I totally agree. Some Midaz and a “this is going to sting a little”…. Speed of therapy shouldn’t be slowed by digging up bunches of sedatives…. Stinks for him but better than vfib.
Sedate with 5 mg Valium
Scratch your balls
cardiovert
after convert, omit 1 and 3
Aaahhhh!
Problem(s):
AF, LVF, shock, syncope, lack of information, in toilet…..
Action:
1. Internally berate myself for lack of anticipation and crap instructions to nursing team, whilst dragging large solider from loo.
2. Need 12 lead ideally…. rhythm strip: narrow QRS, irregular, rapid ventricular rate in places, ?slurred upstroke. What are we dealing with? WPW? Intermittent VT?
3. Assemble team, explain plan, assign roles, airway kit/drugs, metoraminol in pocket.
4. Pads on/paddles ready. Repeat numbers. Still hypotensive/hypoxic/dying…..
5. Try to fix hypoxia. NIV+ nasal cannulae for apnoeic oxygenation & CO2 monitoring
6. Ketamine 1mg/kg iv seems a good balance between sedation and CVS stimulation (vs sincere apology). Propofol a but wild for me with systlpolic 70.
7. DC cardiovert 150j synced biphasic. Amiodarone a bit bold with systolic 70 and shocked. Perhaps procainamide chaser if reverts…
8. Cross fingers……
– _SMALL_ dose of whatever the hell you like (ketamine, midazolam…) or homeopathic dose of propofol if you really must use the white stuff.
– DCCV 100-200 J biphasic & chuck it in SYNC mode if you’re feeling politically correct.
– Have some inotropes/pressors handy.
– Keep the pads on.
– Set up for the central line.
– Notify ICU.
– Do the echo or find someone who can.
Chris
Diagnostic clues might include the tan. He is a young fit guy in acute cardiac failure. Do we know K?
Awesome thought Lucy
Is he mid-Addisonian crisis with AF as a comorbidity – hence the profound hypotension / orthostatic syncope
I like it – thinking outside the box.
Would you throw a dose of hydrocortisone into the resus mix?
But….. no this was just the usual tourist tan… sorry
Casey – great case that always scares the crap out of us. Here’s my approach:
Circulation – ketamine and cardiovert at 200J. I like to start with maximal joules in sick patients so I don’t waste anytime with lower doses. If that doesn’t work, I’d try some push dose pressors with small doses of diltiazem for rate control hoping that rate control will improve forward flow. I would also consider dig loading (won’t work for a while but may help down the road). Magnesium is a consideration as well.
Airway/Breathing – start high-flow nasal canula and try NIPPV but I would have a low threshold to intubate since he’s looking a bit distressed.
This is one of the dangers with amiodarone that goes unrecognized. If the patient has underlying WPW, amiodarone may not be safe. There are no studies showing safety. Amiodarone has both beta blocking and calcium channel blocking properties. I would prefer using procainamide for rhythm control if using a drug. Have to say that the more I read about amiodarone, the less I think it has a role in the ED.
Hi Anand.
AV blockade?
Sure amiodarone Vaughan-Williams class II and class IV action so will cause AV node block.
Bad plan if WPW…. (Need 12 lead)
Digoxin and Diltiazem have similair AV blockade effect?
Class I Na channel blockade effect of amiodarone desirable, ? Better than isolated AV blockade
Still think procainamide best shot at influencing rate….
Why do you fancy Ca channel + dig?
Ben.
Not sure how many hospitals would have access to intravenous procainamide. Used to be one of those drugs which routinely got thrown away from resus kits rather than used because it went out of date. Do recall that the drug company (Bristol Myers) stopped importing it for a while ago. Seems it is now available under Special access scheme.
I was going to say the same thing – I think the nausea vomiting can be attributed to adrenal crisis. I would fluid load him, stat lytes and empiric IV steroids (hydrocortisone 100mg to start). The hypoxemia is probably because of low cardiac output, and might improve with fluids. Low threshold to DC cardiovert, but I don’t think he’ll stay in sinus. While waiting for lytes to come back, I’d start some peripheral K as well.
Sure, might be Addison’s. Might not. No Na/K info, no background history….
Aggressive fluid loading in context of arrhythmia and cardiac failure bit dicey….
Shock first….
USS would be helpful, determine fluid status, get echo (in my case, step 2: find better echo tech unless barn door obvious).
Probably cut to CVC unless really obvious echo…..
Have a chat with the ICU team (get argument about procainamide vs amiodarone vs any AV node blocker underway).
To paraphrase the best response so far…. Scratch, scratch…..
Is there anything in the ‘drinking beer all day’ – A US soldier on ops in Iraq could regularly be dehydrated and a young man back packing around Tropical Northern Aust drinking beer will be the same. Could explain AF ?
In England, they sometimes call AFib “Holiday Heart”, because frequently it presents after a weekend of binge drinking. Scratch, Scratch.
Yes, I’ve heard this term as well. That is the direction I was heading. I have had similar patients however they have remained in stable AF and have had improvements with oral fluids. U/A have shown some issues, some also have converted into A.Flutter. This case also does seem to show WPW in some complexes with delta waves… maybe more than one issue?
The holiday heart (often seen on Sunday morning shifts) patients I’ve seen have never been this unwell – usu present with unpleasant palpitations but nothing more. I also can’t explain the widespread murmurs with this, hence thoughts of something structural.
An arrhythmogenic cardiomyopathy? Any family history of collapse/sudden death?
1. Consider sedation with Ketamine or Fentanyl, I’d probably avoid Midaz due to hypotension.
Synchronized Cardiovertikn at 100, 200 then Max j
A 12 lead capture would be good prior to shock if it didn’t delay treatment. Fluid challenge and PEEP are additional considerations although not without their own fish hooks.
2. Her is unstable and needs some empirical treatment now. It would be good to get a 12 lead prior and after cardio version, or at least a couple of other leads.
3. Check electrolytes, temp, dipstux urine, check his bag for any meds presc/non presc, any history from his travel companions.
Very interesting case! For me the most interesting is that in an otherwise healthy, young man with a healthy heart atrial fibrillation alone (even with 170/min ventricular rate) should not lead to shock. The patient is definitely in shock now, probably cardiogenic. Maybe he has dilated cardiomiopathy, if in the past the army docs gave him “a bunch of pills” it could not be just for AF, also, the cause of the past syncopes would not be just the AF, so there is a probability of some undercurrent condition. Maybe there is some electrolite disturbance, or the shock has a septic component (though there was no fever).
So as a working diagnosis it is a young man with atrial fibrillation complicated by acute heart failure progressing to cardiogenic shock.
I would do sedation (etomidate+midazolam+morphine, if BP decreases, norepinephrine), then ETI, mechanical ventillation. After that the DC cardioversion, initally 200J, rising to 360J, if necessary, and amiodarone for rhythm control. Plus complete heart failure treatment, furosemid, morphine, inotropes.
Also, I think the echo will give us the answer, if not that, then the lab results. In the meantime blood gas if available, cultures. Did you do a 12 lead, or just the rhythm strip? I would definitely do a 12 lead before everything else.
Really curious about the end of the case! Also, I would hate if labour ward took the echo, too 🙂
Wow, nasty outcome! Do I get a point for cardiomyopathy though?
Was there any suggestion of what had made him decompensate acutely? The beers in Broome? Or did you come to the conclusion that he’d actually been getting bad for longer than he initially said?
Hi Kirsty
Yes, bonus points for your intuitive sleuthiness! Structural problem – either valve or muscle to explain the relatively poor physiological reserve in a young man.
I think this is a vicious spiral of chronic bad heart function, dilation with regurgitation of the LV valves. Add onto that acute / recurrent arrhythmia and a sympathetic surge all of which exacerbated the after load / demands on the failing LV.
I imagine that even small dose of sympatholytic agent (fentanyl + propofol) is enough to tip the balance and kill cardiac output quickly.
I think this is really a case of a terminal disease presenting in a young man – had he been 70 with chronic alcoholic cardiomyopathy – we all would have managed this in a more palliative manner.
Tough to do this in a young guy with little background data.
C
I agree that even microscopic doses of anything would probably have broken the camel’s back and I can’t see you had any other therapeutic options in the absence of ECMO/transplant.
I was wondering what decompensated him enough to trigger presentation – a final extra bit of MV dilation causing AF maybe?