Current, including ischemic, is a Vector!

And it is exactly, keeping the following need, and the following kind of plaster wall in mind that we curated this article. After spending hours on highly detailed research and gathering of data, we made this article and a list of the best and top 6 tv wall mounts that are perfect for plaster walls. You can read our guides and information that will help you find the best kind, that suits your tv, at the bottom of the article. These guides are, what is the best tv wall mount? https://wallmountedhub.com/best-mount-for-plaster-walls/,

The clinical presentation and the abnormal ECG together with the patient’s background history suggest that we are confronting another acute coronary syndrome and YES! You are going to follow the algorithm suggested in the standard guidelines on managing ACS and consult cardiology, but the main questions here are:

1. Is this a patient that needs to go to the cardiac catheterization laboratory immediately?

2. If you are practicing at a non-PCI capable hospital and the nearest PCI capable hospital is hours away, potentially compromising your time to reperfusion targets, would you thrombolyze this patient?

Remember! Time is Muscle and every minute counts. Based on the standardized recommendations from the ESC and the ACC/AHA, the following time targets (max. time targets!) should be strictly followed:

But, why are we applying the STEMI time-to-treatment algorithms here! Let’s go back and look at the ECG a bit more carefully

The following is noted:

1. Prominent T waves in the inferior leads, suspicious for hyperacute T waves of acute ischemic injury. However, there isn’t enough STE (>1 mm in two contiguous leads) to pass this as an inferior STEMI + baseline wander doesn’t make this any easlier!! So perhaps will keep doing serial ECG(s) and see how these changes evolve.

2. Deep planar STD of 4-5 mm in the anterior leads. There are also pathological Q waves consistent with his previous TWO anterior wall MIs

ST-T wave changes in the lateral leads I, aVL, V5 and V6. Yes, they are abnormal! But I can’t pin-point any definite pattern to help me further and they don’t look like typical reciprocal changes either.

While your junior is hunting for the old ECG and doing serial ECG(s), I think all of us would be staring at those STD(s) and trying to see through them. Is this really anterior wall ischemia or something else?

Acute myocardial ischemia creates myocardial tissue with different depolarization and repolarization properties. As such, a CURRENT is generated. As the title suggests, CURRENT is a VECTOR and from basic physics you know that a VECTOR has a MAGNITUDE and DIRECTION, as shown in the diagram below

Seeing this diagram, one would wonder, if the STD(s) are actually a current of injury directed posteriorly toward the LV wall supplied by a dominant LCX (since the inferior lead changes are not that impressive!). To resolve this puzzle, the best next step would be to repeat the ECG with dedicated posterior leads

Note the following on this ECG done 5 minutes later:

1. There is no further evolution of the changes in the inferior leads

2. STD(s) previously described in the anterior leads persist

3. It is clear that the patient is suffering from an ISOLATED posterior LV wall STEMI. Those STD(s) seen in V1-V4 were actually reciprocal changes to the STE seen in V7-9!

4. Hang on! Shouldn’t you also be seeing tall R waves in the anterior leads to go with the posterior STEMI? That’s the classic teaching, but remember this patient had two prior anterior STEMI and has pathological Q waves in the anterior leads, which will likely cancel out the tall R waves you are used to seeing with run-of-the-mill posterior wall infarcts.

This is now a game changer! Yes you will be doing all the stuff you said you will be doing, but your priority here will be to get this patient to the cath lab for primary PCI or to administer thrombolytic therapy within the 10 minute time frame suggested above if you practice at a facility remote from PCI-capable hospitals.

Additional reading:

1. I highly suggest reading the following post by Dr. Stephen W. Smith http://hqmeded-ecg.blogspot.com/2012/02/five-primary-patterns-of-ischemic-st.html

2. A fun-to-read case-based discussion on causes of ST depression on the standard 12-lead ECG by Pollehn T, et al. The electrocardiographic differential diagnosis of ST depression. Emerg Med J 2002; 19: 129-135

3. There are a few other valuable ECG resources highlighted on Dr. Smith’s blog page that you can read to enrich your ECG knowledge further

sinus rythum

rate of 84

normal axis

incomblete LBBB

ST elevation inferior leads

hyperacute T wave in inferior leads

ST depression septal leads

reciprocal changes lateral leads.

next:

posterior ECG

Rt side ECG

CXR

ASA 300

Plavix 600

Fondaparinux: 2.5 mg

activate cathlap

Incomp lbbb

1 AV block

inferio STEMi

??? posterior stemi

need posterior ecg

stablization

cardiology consultantion

High risk background presented with severe typical chest pain.

ECG findings: Sinus rhythm  Hyperacute T waves at the inferior leads STD in anterolateral leads 1st degree AVB Impression:

Highly suspicious for inferior wall MI

Stabilize

Activate cath lab

Aspirin 300 PO

Heparin 5000 U IV

Do posterior ECG looking for Posterior extension 

Avoid nitrates

High risk pt + typical chest pain + ST changes , pt need to be stabilized, load with aspirin and plavix and emergent cardio consult for cath lab activation