some cardiology questions

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    The ER I am in right now uses a 3 electrode system. My patient had chest pain that correlated with st depression in v1-v2. After ntg, pain resolved, depression resolved. This process repeated a couple of times until the ntg started. The pain and depression consistently correlated.

    I was able to leave her hooked to the 12 lead ekg, but if I couldnít, I am pretty sure there is a way I could have monitored a v lead by moving electrodes. Anyone know the placements? Maybe shoulder leads in normal, red to v2? I suppose if I did this for one cycle of depression, it would confirm accuracy.

    Also- This lol was maintaining a sbp in the 140ís even with the ntg gtt. My thought was to titrate the gtt up to reduce afterload and decrease myocardial oxygen consumption. The receiving facility with the cath lab asked that the gtt be titrated down to pain free. I am not sure why. Any thoughts? No indication of right sided involvement.

    Also, an interesting wild card with this pt: she had herna pushing up on her diaphragm displacing her heart to the right. The apparent septal ischemia was more likely anteriolateral.
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  3. 7 Comments so far...

  4. 0
    Quote from hherrn
    The ER I am in right now uses a 3 electrode system. My patient had chest pain that correlated with st depression in v1-v2. After ntg, pain resolved, depression resolved. This process repeated a couple of times until the ntg started. The pain and depression consistently correlated.

    I was able to leave her hooked to the 12 lead ekg, but if I couldnít, I am pretty sure there is a way I could have monitored a v lead by moving electrodes. Anyone know the placements? Maybe shoulder leads in normal, red to v2? I suppose if I did this for one cycle of depression, it would confirm accuracy.

    Also- This lol was maintaining a sbp in the 140ís even with the ntg gtt. My thought was to titrate the gtt up to reduce afterload and decrease myocardial oxygen consumption. The receiving facility with the cath lab asked that the gtt be titrated down to pain free. I am not sure why. Any thoughts? No indication of right sided involvement.

    Also, an interesting wild card with this pt: she had herna pushing up on her diaphragm displacing her heart to the right. The apparent septal ischemia was more likely anteriolateral.

    There is really no way to monitor v leads with a 3 lead system. With the good old einthoven's triangle, the idea is that the three leads make a triangle which has a center point corresponding to the center of the chest. When looking at precordial leads, the V leads are one electrode and the "combination" of the standard leads are the other "electrode". Without all three leads that virtual electrode would not be in the center of the chest, so the precordial leads would not be looking "through" the heart.

    The reason to titrate the nitro to pain free is to resolve as much of the ongoing myocardial ischemia as possible. You kind of hit on it in your post when you said that the depression resolves when the pain resolves. They want the ischemia limited and also make the coronaries as dilated as possible.

    As a sidebar, with marked ST depression in V1 and V2 it might be more of either a right sided or even some posterior involvement. A septal infarct would more likely be seen in V3 or V4.
  5. 0
    Quote from hherrn
    i was able to leave her hooked to the 12 lead ekg, but if i couldn’t, i am pretty sure there is a way i could have monitored a v lead by moving electrodes. anyone know the placements? maybe shoulder leads in normal, red to v2? i suppose if i did this for one cycle of depression, it would confirm accuracy.
    what you are referring to is the “modified chest lead (mcl).” if you google modified chest lead there are several sites that discuss this. to monitor in a modified chest lead the right/left arm leads are placed in the normal position. the left leg lead is placed in the position of the precordial lead_ that you want to monitor, and you then monitor in lead iii. this is referred to as mcl_.

    while the qrs complex will not duplicate what you would get on a 12 lead ekg, the morphology is similar and might be useful for identifying changes, however you have to be able to place your monitor in diagnostic, rather than monitoring mode.

    personally, i think the best thing you could do is what you did: leave the 12 lead ekg attached an on. if you only have access to one machine, let someone take it if needed, and when they are done reattach to your patient.

    hope this information was helpful.
    Last edit by chare on Sep 11, '09
  6. 0
    Yes, you can perform modified chest lead monitoring with a three lead setup and even obtain a modified nine lead ECG; however, you need to look at your three lead monitor. You need to verify that the monitor can be placed into "diagnostic" mode. A XII lead machine does more than monitor XII leads, it also monitors these leads with diagnostic quality. If you cannot monitor your modified leads in diagnostic mode, you really cannot localize ischemic or necrotic changes. In essence, a non diagnostic strip is nothing more than a rhythm strip.

    Many people are not aware of the profound differences between a rhythm strip and a XII lead ECG.
  7. 0
    Quote from pianoman511
    There is really no way to monitor v leads with a 3 lead system. With the good old einthoven's triangle, the idea is that the three leads make a triangle which has a center point corresponding to the center of the chest. When looking at precordial leads, the V leads are one electrode and the "combination" of the standard leads are the other "electrode". Without all three leads that virtual electrode would not be in the center of the chest, so the precordial leads would not be looking "through" the heart.

    The reason to titrate the nitro to pain free is to resolve as much of the ongoing myocardial ischemia as possible. You kind of hit on it in your post when you said that the depression resolves when the pain resolves. They want the ischemia limited and also make the coronaries as dilated as possible.

    Just to clarify: She was pain free on a pretty low dose of ntg. My thought was to titrate up a bit to drop afterload reducing myocardial oxygen demand. (No signs of right sided involvment) The receiving facility wanted her on the minimal dose to control pain/ischemia. Her sbp of 140 wasn't adressed.

    As a sidebar, with marked ST depression in V1 and V2 it might be more of either a right sided or even some posterior involvement. A septal infarct would more likely be seen in V3 or V4.

    I'm thinking septal involvement shows in v1-v2, and v3-v4 are anterior.

    Here's another one for anyone who wants to field it: With depresion in only v1-v2, is a posterior (v6-9) indicated? In some ways I guess it is academic- If the depression was recipriocal, than any elvation went away when the depression went away. But, should I have done a posterior?

    I am in an ER now in which not all the providers are experienced in emergency medicine. Time to put my thinking cap on.
  8. 0
    You can never go wrong with obtaining posterior views. Posterior wall infarct is commonly associated with multiple areas of infarct. With right dominate circulation, inferior wall MI and posterior wall MI are associated. However, it can be associated with left sided infarcts as well. There can be significant cross over and sharing when it comes to the posterior wall.

    Regarding nitroglycerine, you really are not significantly dilating coronary arteries in many patients. NTG is not given to "open" occluded arteries as much as it is given to decrease preload and to some extent, after load.
  9. 0
    NTG's primary/intended effect is coronary vasodilation. It's unintended, possible side effect is peripheral vasodilation - look at the nitric oxide and where/how it works.

    Clinically I don't see where you'd want to decrease preload? It would merely compromise RA/RV function and the pulmonary consequences - a diurecitc would work better as far as I'm concerned. However, if I wanted BOTH preload and afterload reduced, I'd better off considerig a combined dilator like nitroprusside.
  10. 0
    Venous effects predominate with GTN. Yes, arterial dilation including coronary arterial involvement occurs; however, venous dilation is a major factor in the clinical pharmacology of GTN. Reducing preload offers potential benefits. Decreased preload leads to decreased left ventricular pressure, volume, & ultimately workload. Obviously, this decreases wall tension and may promote coronary perfusion.

    GTN is easier to titrate and potentially more predictable than diuretics. In addition, many diuretics can promote electrolyte imbalance, therefore GTN may be a better choice in some patients.


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