STEMI on 3 lead
Can you?
Sometimes you can see ST elevation in 3 leads... sometimes you can't, right? Remember how Dubin characterizes a 3 lead vs. a 12 lead? Like looking at 3 sides of a car, rather than walking all around it? Can you perhaps not see small amounts of damage with just 3 views?
12 lead has really become the accepted standard. And the cardiology folks WANT STEMI door-to-balloon time to drop. There are many factors that make that happen... but diagnosis of STEMI prior to ED arrival is a HUGE factor to decrease the time.
The only factor, nationally, that decreases average times more is to have a cardiac surgeon onsite 24x7 - which doesn't happen at anything other than huge teaching hospitals.
Your'e right to a certain extent - 3lead gives us only partial view of the picture. Sometimes the changes are apparent straight up.
The most obvious example of suspected AMI on 3 lead analysis being ST elevation in leads two and three - the inferior. Most Paramedics would have come across this in at one time or another. Alternatively clinically significant ST depression (reciprocal ischaemia) in any of the limb leads should lead you to include an anterior infarct in your suspicions. Thus noting ST elevation is not the only way to to arrive at a differential diagnosis of infarct.
Lets not forget that "diagnosis" of infarct is made on the basis on three elements and requires at least two of those three to confirm diagnosis and invoke treatment protocols in the ED along those lines. (Though biomarkers now dominate diagnosis with Troponin rises being very sensitive and specific to demonstrating an acute event).
They are: 1. clinical history/presentation i.e. the pts story with S&S attached
2. 12 lead ECG changes. 3. abnormal Bio-chemical markers eg Troponin rises.
Now you could argue technically that with clinical history plus a twelve lead in the filed you can "diagnose" AMI. Having a 12lead in the field is definately a plus - provided the following don't mitigate its effectiveness in the process.
1. The operator is skilled at interpretation. Training, experience etc come in here. It's a pretty good idea to know, for example, the effect a LBBB or anterior hemi block will have your interpretation of AMI.
2. There is the time and practical circumstances to do a thorough analysis - try and do a good 12lead when the pt is throwing up big time as is common in the hypotensive inferior pt.
3. The patient isn't crashing in front of you necessitating a focus on treatment. Inferiors are classically unstable in the field with brady arrhythmia's, hypotension, severe pain etc. Anterior infarcts may cause PO as the LV fails requiring respiratory support.
Typically our most effective tool is clinically suggestive S&S. AMI is more often than not a catastrphic event with profound symptomology. We've all seen them - diaphoretic+++, acute pain++, rhythm disturbance, perfusion changes, anxiety++, SOB etc. (Of course they can also be subtle).
(And lets not forget about non STEMI's - 12lead useful in that?)
In the end the trick is to join up all the dots and recognise that even a singular piece of the pts story may alert you to AMI. For the ALS operator experience is definately a plus. As we all know S&S can be tricky, subtle or confusing.
For example, only recently I had an elderly man with no prior cardiac HX, who presented with severe, sudden onset central chest pain at rest whilst showering. He stated he felt particularly unwell, was frightened by the event and now felt nauseated. The pain apparently changed with deep inspiration.
His 3lead showed a mild sinus tachy. BP was normal. He was pale and "sweaty".
The BLS crew didn't join the dots. They were misdirected because his pain changed with breathing. 15% of AMI pts present to the ED with pain variability on inspiration. But the crew didn't know this, saw a normal ECG and differentiated the wrong way. They also assumed he was "sweaty" because he had just come out of the shower! Oops!!
For me the clue was the sudden onset at rest, the pts sense of impending doom and his description of the pain.
We did just 2 MCL's using our 3lead - 1 and 2 (V1&V2) - tombstones.
The point is I guess that the clinical assessment was useful in and of itself. The ECG tool was another dot joined (a very necessary one no doubt).
I'm not advocating that 12lead is superfluous -indeed it is not. But like so many things we do in the field components of any event create an index of suspicion that we must act upon. Spinal is another example - you know mechanism of the accident etc.
We don't have the time, the tools or the luxury of ED level analysis. !2 lead is an effective tool absolutely. But its also being adopted in the field for very specific reasons. Not just to diagnose AMI but to alert the cathlab/cardiologist to the type. This enables services to be used efficiently and maximally. Throbolysis or plasty. This is also why telemetry is also being added in the truck. With confirmation from both ends we can then introduce treatment even faster - say like throbolysing the pt in the ambulance.
Monitorisis is the way one of my old lecturers called it. Getting transfixed by the screen. I personally think we need to be very careful about getting preoccupied with electronic tools to the detriment of our skills as clinicians.
3lead - works for most pts - MCL's a nice little extra. 12 lead - even better but needs great care.
12lead will be the accepted standard I have no doubt -for equipment that is. But we operators need to be up to scratch to make it trully effective.
Incidentally MICA in Melbourne started out in 1973 as in field cardiac care. We are only just getting 12 leads. (hey - its aussie land - things go a bit slower here because of the gravity). Our time to balloon is worlds best practice.
(You have let us brag about something because we've only ever beaten you at the Americas cup and Michael Phelps didn't share very well with all those gold medals now did he?).
Cheers
MM
