FL_Medic

Okay, this one isn't on my blog yet. Thought I'd get another one up quick because the last one was answered so quickly. Instructions for larger viewing from FireEMT: If you enlarge the image when you click on the part where it says to click to enlarge and it opens a new window click and hold the control key on your keyboard and then hit the + key. It will enlarge the image even larger as many times as your click it. If you do the same, but use the - key, it will make it smaller. This also works for normal web page viewing. It works in firefox, and internet explorer.

This is in fact A-fib with RVR and WPW. Didn't realize Fred got it about 5 minutes after I posted it. When you have a rhythm that is Fast Broad & Irregular consider this rhythm. Rule out torsades which is easy to do and then treat accordingly. Ventricular rhythms do not always present with extreme right axis deviation, be careful. STAY AWAY FROM AV SLOWING AGENTS. I wouldn't give any drugs to these patients. Shock them! Procainamide is the safest if you have to give drugs. Amiodarone is controversial, but second safest (if you are going to convert them you might as well zap them). C+ Channel blockers or Adenosine will effectively kill them. For more on WPW click here Sorry to those who read my blog first, I will try to post here first.

52 y/o male presents with chest palpitations.

On you getting a flash. When starting an IV you get a flash of blood when the open, beveled end, of the needle enters the vein. If you look at an IV catheter you will notice that the actual plastic catheter does not cover the entire needle. There is a very small measure between the end of the catheter and the needle. This requires that after you get a flash that you advance another "smidge". If not, your catheter may not advance and will probably kink up. The downside to this is possibly penetrating through the other side of the vein. This is the most common cause of a blown vein. You can still get a flash, and then blow it. An AC usually isn't as obvious when blown due to the amount of tissue in the area. Hands are very apparent and swell up nice and big for us before we get to the ER. The nurse in the room with you. A true cretin. The idea of fluids in but not out is only valid if you check it with a flush. The AC, as stated before, might require a larger flush. If you can't get blood out, you usually aren't in. What's the patients BP? If you have distal perfusion, you should have peripheral return right? On the nurse asking you if you started an IV. This doesn't matter at this point. We all miss IVs and I can't stand it when people try to point out others' misses. I don't know a single clinician that hasn't missed numerous IV starts. This nurse that asked you has no tact. You were doing a clinical, mistakes are expected! What do we do whenever we are administering anything into an IV line? Penetrate the medication access port, pinch the line, aspirate to check patentcy, and then push the med. Whoever administered the contrast was at fault and wanted to divert the blame. Don't worry about this. I know that feeling you have though.

ANSWER Bifocal Atrial Couplets & Left Anterior Fascicular Block ECG description: -Sinus rhythm with varied rate: 75-130 bpm -Premature Atrial Contractions (PAC) presenting in couplets -Left Axis Deviation (LAD). Cardiac Axis is deviated leftwards and superiorly at approx. 90° -Left Anterior Fascicular Block (LAFB) due to LAD, deep S in III, no sign of LVH or MI -Low Voltage in Limb Leads -Poor R Wave Progression (PRWP) Atrial Couplets, PACs and P waves After one sinus cycle, the rhythm is interrupted by a PAC (complex no. 3 from the left). The change in P wave axis and morhpology of this complex suggests ectopy. The P’ wave is inverted in leads II, III and aVF, suggesting that the ectopic impulse originates in the left atria, spreading in a retrograde fashion. Determining by the PR interval, which is 100 ms, the ectopic pacemaker is atrial and not junctional, and sits closer to the AV Node than the SA Node. The PAC is immediately followed by a new PAC, creating an atrial couplet. This second PAC seems to originate from another focus, as there is a change in P’ wave axis and configuration. The PR interval of this PAC is 110ms, and the P’ waves are upright in the inferior leads, suggesting that it spreads inferiorly and towards the left. The second PAC is followed by two sinus cycles, which is then followed by another PAC couplet. The PACs in this couplet seem to originate from the same ectopic foci as in the first couplet, although there is a variation in coupling interval length. Atrial couplets can be benign, but are less common in healthy hearts, and should increase suspicion towards onset of atrial fibrillation. Ultimately, one would prefer to print a longer rhythm strip at this point, to see the phenomenon over a longer time interval. Unfortunately this is not available for this particular case. The Postextrasystolic Pause With supraventricular premature impulses, the dominant automaticity focus (normally the SA Node, as in this case) is usually reset by the premature impulse. The supraventricular impulse usually activates the whole atria and thereby also the SA Node. The early activation of the SA Node interrupts the pacing function of the node, and causes a delay in impulse generation. The next impulse will then be slightly delayed, causing the following RR interval to be prolonged. This is called a noncompensatory pause. If the SA Node is not reset, then its pacing function will not be disturbed, and the following RR interval will be an exact multiple of the normal interval, resulting in a compensatory pause. PACs usually present with non-compensatory pauses, as ectopic atrial impulses will usually activate the whole atria, including the SA Node, and thereby interrupting the sinus pacing activity. In this EKG, the pause after the first PAC is interrupted early by another ectopic impulse, so this pause cannot be determined. The second PAC however (complex no. 4 from the left) is followed by a postextrasystolic pause that is prolonged, but still not an exact multiple of the normal sinus cycle length. This is a non-compensatory pause, which tells us that the SA Node has been reset. This helps to establish and diagnose an atrial origin for the ectopic beats. Courtesy of pqrst

I wouldn't say "a bunch", maybe more than one, but the QRS amplitude is otherwise pretty consistant.

Sorry I don't have any info on the patient. I stole this one from another site. I do have the answer however.

Stole these from a certain site. Thought they would be good for this. Answer will be revealed on 5/17/2009. Let me know what you think.

I have been working on a blog that will just be another source of EMS education. Go check it out, let me know what you think, and what I need. Paramedicine101.blogspot.com

CIPA is extremely deadly. I believe infection is the leading cause.

No problem. I don't mean to be critical, I just saw a moment to teach. Check out my blog sometime, and for some good EKG stuff.... ems12lead.blogspot.com.

That's actually not an incomplete LBBB. Note that the axis is around 60 degrees*. If you have a normal axis, you lack a hemifasicular block. Since LBBB is a block of both the left fasicles, you should be able to identify at least a single fasicular block to call it incomplete LBBB. Normal vectors, and R wave progression. That width you are seeing is probably due to early repol. Note notched J point most visible in V5(looks similar to osborn wave). *You can figure this out by considering aVL to be perpendicular to axis of depolarization because it is the most equiphasic lead(not predominately positive or negative. Since lead 2 is perpendicular to aVL than your axis is almost in line to lead 2. Since lead 2 is positive, and the positive electrode for lead 2 lies at about 60 degrees....abracadabra. If you already knew this, disregard.

Okay, more to come. Fiz, you're more than welcome to join in.

Ahh... increased digoxin levels. Very good!! The most common cause of atrial tachycardia with a 2:1 conduction like this one is increased digoxin levels. I am going to be posting more 12-leads on my blog, and I will be giving some great tutorials, if anyone is interested. I will try to keep the strip teases going, if there is a demand.

No gueses? What is a very common cause of atrial tachycardia with a 2:1 AVB?

You'll find it. I wouldn't worry about your first interpretation. I would bet money that the medic that left this strip in the ambulance didn't even see the extra p-waves. The fact that you are trying to learn more is what puts you in the top 15% in your field.

If by "march out", you mean stay consistent, you are absolutely correct.

Ahah... When you're thinking 3rd degree AVB, also known as complete heart block, there are some things to consider. First off, this rate would definitely make me question 3rd degree. You usually will have a pretty bardycardic patient with a complete HB. Next, the QRS. While these might just be > 120ms, you will usually have a more idioventricular looking complex(>150 ms). In complete HB the SA node has no say, meaning that your atria and ventricles are completely electrically unaffiliated. This means you will have p waves, and QRS complexes, but they will not be related. You can test this by checking your PR-interval. If you have a consistent PR-I, it aint 3rd degree. In 3rd degree your P-P interval will usually remain consistent, and your R-R interval will remain consistent. They will not be related though. So, since you have more P-waves than QRS complexes, and we have ruled out 3rd degree, it is a 2nd degree. 2nd AVB with 2:1 conduction ratio, as you stated, is correct. This is atrial tach with 2:1 conduction. Without knowing the PMHx, what do you think is the cause. There is a certain condition that is very common with this rhythm.

Well, that's a very common method. You have to be sure of the QRSd to use that method though, and this is borderline. Look at the late R-wave progression. R-wave progression is the transition in the chest leads. You usually start with an rS or QS wave in v1 & v2, and in v4 or v5 you will usually have an almost equiphasic QRS(negative and positive deflection almost even). That would be your transitional lead. The R wave becomes more prominant in v5 & v6 in a normal ECG. This 12-lead doesn't have transition until v5. Also, note the discordant T-waves. This is a normal finding in BBB, and is why LBBB are difficult to diagnose STEMI. Discordant means opposite(the t-waves are opposite the QRS) Also, pathological left-axis deviation was mentioned. This is indicative of a Anterior fasicular block. The left bundle branch has two fasicles anterior & posterior. A LBBB is a block of both these fasicles. So, knowing for sure that one is blocked, and having the left vectors we do, I'd say this is probably a LBBB. For more on axis deviation and hemiblocks check out EMS12lead.blogspot.com There is something else about this strip. It was almost caught, but diagnosed incorrectly.

I was just getting ready to tell you about -60. Remember your perpendicular leads. aVR is your equiphasic lead, and lead 3 has the biggest deflection(in limb leads). I bet you figured that out by now though. 3rd degree AVB has no AV association(regular PR interval). Ok, so those that are calling it LBBB, run me through your thought process. Let's say we are unsure if the QRS is 120ms.

Another strip for you to deduce. Unsure of PMHx, I found this laying in the ambulance.

My original angio is from a RAO angle, I looked at it again, and it was labeled RAO, duh... Fiznat, yours is pretty cool, you can actually make out the border of the epicardium.

No one has anything to add on this? Just wanted to raise this to the top one more time before it floats into the abyss.

Ok, but my statement was not based on opinion, feeling, attitude, or experience. It was based on research. It is my intent, throughout my career, to base my treatment decisions on evidence-based medicine. That was the point of my rebuttal.

Ok, I don't know where that came from. My age isn't in question here, I have the experience and knowledge. You're statement doesn't really dispute anything I said. I stand by not doing something just because you have seen a more experienced paramedic do it. That more experienced medic may not have read that shoving ammonia inhalants in someone's nares and putting your hand over their mouth, could kill them. Maybe that provider is burnt out, and really shouldn't be doing this job anyhow. Experience is never an excuse to stop educating yourself when it comes to this career. I do, however, attribute the medic I have become to all the medics I have worked with. Please don't lecture me based on my age, what statement have I made that has called my knowledge into question? As an instructor, I teach people much older than me all of the time, so the age argument is pretty pointless. I've been in the field since I was 18. May not be 20 years, but I have been doing this long enough to know a thing or two about a thing or two. It seems my age is in question a lot, even here on the job. All doubt goes out the window after they run the fist call with me, or ask me a question. That is why I get so defensive about this.