Longer term goals.

[BushyFromOz]

Yeah i dont have any education in 12 leads, only what i have picked up myself. ST elevation in Ld II, III and aVF would tell me that there is an occlusion of a distal part of the left anterior descending arter. INferior AMI's have have a 45% to 55% (depending on what your reading) involvement of the righ ventricle. reducing preload any further and its reduction in ventricular stretch, reduction in left atrial and then left ventricular filling, you might not get enough left ventricular pressure on systole to open your aortic valve. ST depression in V3,4,5 and 6 would indicate some posterior involvement, diagnoal branchs of the left circumflex? You could move V1,2 and 3 and run a another 12 lead, re-labelling them for a 15 lead to get the posterior view.

Looked like a 1st degree block too.

Have o experience of fibrinolytic, but if the pt qualifies for it i'd give it, sounds like a hell of a long time to difinitve treatment for a STEMI.

As for the pain redcutionfrom increased B/P, i dont really know, im at the limit of my brains right now, had a terrible day at work :?

Feel free to correct me

[chbare]

Lets review the basics of coronary artery anatomy, assuming "normal" anatomy:

You essentially start with two arteries. The right coronary artery (RCA) and the left coronary artery (LCA). What area of the heart is typically supplied by the RCA? What about the LCA? Now, work your way down. What are the main branches off of the RCA? What structures are supplied by these branches? What are the main branches of the LCA? What structures are supplied by these branches?

Specifically, we have identified changes in II, III, & AVF. As stated, this signifies inferior wall involvement. With the knowledge gained by researching the questions above, what are we potentially dealing with? Does the patient's clinical picture fit with what we see on the XII lead?

Let us also talk about nitrates? We generally say these work by reducing preload. Is reducing preload a potential problem with the inferior wall MI patient. What did the fluid bolus do to our preload? However, are preload reducing agents absolutely contraindicated with every inferior wall MI?

Looking at the posterior wall is never a bad idea. What other areas not covered by a standard XII lead ECG would you want to look at, considering the location of this possible STEMI?

You are on the right track regarding the complaints of pain. What have we done by increasing blood pressure? It relates somewhat to the preload question above.

In addition, look closely at the XII lead. Look carefully at lead III. You do not have much to go on; however, focus on identifying P waves.

Take care,

chbare.

[Mateo_1387]

I may be a bit off, but this is what I am seeing with the 12 lead.

The heart rate is within normal limits, around 64 beats per minute.

There looks to be an almost R on T PVC, which is concerning.

There is ST segment elevation in the inferior leads, as well as some ST segment change in the anterior leads (V1-V3, as we cannot see V4-V6) This leads me to suspect a right ventricular infarction, involving the right coronary artery.

The patient also appears to have P wave and QRS disassociation, which is indicative of a 3rd degree heart block. What makes it interesting, is the QRS is narrow, which would mean the area of infarction would be affecting the AV node, and not the area below the AV node. Injury is below the AV node is usually seen with a wide QRS complex. If the patient develops bradycardia with hypotension, then we can use this information to know that Atropine may be used, instead of Transcutaneous Pacing.

Did you happen to do an 18 lead ecg? or a 15 lead?

[chbare]

Good call: The patient initially presented in a complete heart block. Subsequent XII leads and rhythm strips did a little better job of demonstrating this. The patient was initially anxious as you may remember from a prior post. The "PVC's" are in fact artifact from movement. V4R was positive. Posterior wall changes were identified as well. Does the patient's clinical condition and ECG changes support the diagnosis of inferior/posterior wall MI with RVI? Specifically, the AV block, low blood pressure, near syncope, and reported low heart rates. Is this all typical of this kind of MI. If so, why?

Would atropine be incredibly effective for a third degree heart block?

Would you go straight to pacing the patient in her current condition?

From what I gather, people would be comfortable with fibrinolytic therapy if available?

Take care,

chbare.

[aryan51]

Looks like I need to study my XII lead interpretation a little more. I totally missed that 3rd degree.

I'm thinking even though we still have borderline stable vitals I'd like to start pacing her due to the long transport time. She's going to need it soon enough anyway. Some new things to consider with this would be how our monitor is powered, and if it is by battery then we need to make sure we have enough for the entire trip. Also possibly thinking about some pain management for the TCP.

I have no knowledge on fibrinolytics beyond ACLS, and we don't carry them in EMS where I'm from, so I can't really say one way or the other with them.

[chbare]

I will tell you what happened: The patient was given fibrinolytic therapy in the form of TNKase as no specific contraindications were identified in the history. What things must we monitor following fibrinolytic therapy?

The patient was not paced; however, the patient developed an episode of bradycardia and near syncope. Atropine was given without any noticeable change in the heart rate. However, the bradycardia was transient and the patient developed the following shortly after fibrinolytics were given:

What do you think?

Take care,

chbare.

[CBEMT]

Looks like some ST-elevation? hard to tell from the small pic though so I can't count it out to see how elevated...

Click the pic- it gets bigger.

Try some dopamine too to help the pressure,

....According to the first set of vitals I saw, the pressure is over 90- why is dopamine even a consideration at this point?

I'm not trying to be an ass, but damn that's kind of heavy-handed don't you think?

[scubanurse]

ahhh... i couldn't figure out how y'all were reading it ... i feel blond ... and i must have had another blond moment reading the BP, but I think I was proposing the dopamine as an alternative to the fluid bolus to maintain pressure since it is a long flight and bladder control is an issue/i hadnt gotten a response on lung sounds. If they had been wet... could we use dopamine to keep pressure since a fluid bolus is contraindicated? j/w since i'm still learning.

[chbare]

Take a look at the prior posts, the patient's lungs are clear and remained clear following the initial bolus. Let us talk about dopamine? Are vasopressors a good think to automatically jump into when considering the MI patient? What will dopamine do to myocardial oxygen demand? In addition, consider the location of this MI. Are fluids in fact a better route given what we know about RVI and alteration in preload? No worries about bladder control. Always consider the risks and benefits of your treatments. We can always place a foley, use a bed pan, or improvise. With that, what about placing a foley in the patient? Would this be a wise choice considering the medications we have given?

What about "wet" sounds? Is this an absolute contraindication for a fluid challenge?

No problems with learning. This is the purpose of the scenario.

Take care,

chbare.

[aryan51]

Still on the topic of giving NTG to patients with XII leads indicating inferior MI's, would you withhold it deviating from most chest pain protocols? And what effects would moving on to morphine have? Would that also drop blood pressure as NTG would? Just trying to figure out what the alternate treatment would be, if any.