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Tom B.

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Posts posted by Tom B.

  1. What she said!

    Seriously, the most common mistakes I see are:

    1.) Placing leads V1 and V2 one intercostal space too high on the anterior chest (in some cases even higher)

    2.) Placing leads V1 and V2 too far apart (make a "peace sign" with your fingers and you should be able to touch both electrodes)

    3.) Placing lead V3 directly under lead V2

    4.) Placing lead V4 under the nipple instead of visualizing the midclavicular line

    Other common mistakes that aren't related to lead placement are failure to undress the patient from the waist up and leaving a female's bra on. Protect a female's dignity and get her covered up as soon as possible, but don't place leads down the front of a shirt or reach up under a bra. It's absurd. STEMI patients should be completely undressed (similar to trauma) anyway.

    Beyond that it's just taking pride in your workmanship. Shave the chest (hopefully for male patients) and use the benzoin tincture. It works! Also, if you're using rectangular electrodes, line up the edges and make it all symmetrical. It helps keep you organized. There's no value in putting some lengthwise, some width-wise, and some diagonal.

    Make sure the leads aren't all tangled up. Strand them out individually to minimize artifact. Don't wrap the O2 line, the IV line, the ECG line, and the BP line together. It's a mess, it looks unprofessional, and it's harder to troubleshoot problems.

    Be sure the patient isn't holding him/herself up with his/her arms. The muscle tremors will be noted as artifact. The patient should be in a relaxed semi-Fowlers position and breathing normally. You can lay a towel and/or blankets on top once the electrodes are placed to minimize shivering or Parkinsonian tremors.

    If you don't settle for imperfection you will almost never have problems with poor data quality (which confounds computerized measurements and interpretations, makes nuanced interpretations more difficult, and harms the credibility of prehospital 12-lead ECG programs).

    Good luck!

    Tom

    • Like 3
  2. How about transport for evaluation when CP is the initial complaint ?

    Great Post btw.

    ps Are your certain your a Fire Man too ? shiftyninja.gif

    By all means transport patients who complain of chest discomfort to the hospital! LOL! :)

    Yes, I'm a firefighter! (But I was a medic first).

    Tom

  3. Something to keep in mind about LBBB. The GUSTO investigators (and subsequent studies of Sgarbossa's criteria) used elevated cardiac biomarkers as evidence of AMI. In other words, they combined STEMI and NSTEMI. That's why I think it's a mistake to suggest that Sgarbossa's criteria is an insenstive marker of acute STEMI if we accept that the ECG finding we call STEMI is a surrogate for an acute occlusive thrombus in an epicardial coronary artery.

    The criterion that has caused the most controversy is discordant ST-elevation > 5 mm. Even according to the original algorithm, this is only a score of 2 (probability of AMI 50%). That's because with LBBB the ST-T wave abnormality is proportional to the depth of the S-wave. A QRS complex that is 50 mm deep in lead V2 can have 5 mm of ST-elevation and the ST-elevation is only 10% the depth of the QRS complex, which is fine. A better approach is to say ST-elevation > 0.25 the QRS complex indicates acute STEMI (which was proposed by Smith et al. from Hennepin County Medical Center).

    The ECG provided shows a perfectly "normal" looking LBBB that does not satisfy any of Sgarbossa's criteria for AMI in the presence of LBBB. I would obtain serial ECGs and look for ST-T changes that suggest dynamic supply vs. demand characteristics. Absent that, there is no reason to transport this patient for primary PCI or give thrombolytic therapy.

    Tom

    • Like 1
  4. We actually received a letter from him to the service following that article and the response he received from medics. It was a three page explanation, the full text of which I don't have available where I am at the moment. Essentially his quote was with regards to the thombolysis study when the reporter asked him why we were interpreting for STEMI bypass but not the STREAM study. His explanation centered on the medico-legal issues with it being an ongoing clinical trial. I will try to remember to copy the relevant sections when I get back to work on Tuesday. At this time I'm not cynical enough to discount everything else we've been receiving based on a TorStar article. We were all still taken aback when we read that article around here, especially when compared to the latest feedback we were getting from the CCU/cath lab on the program.

    Official average pt. contact to balloon time from anywhere in the region I work = 82 minutes.

    It's interesting there was a backlash from the paramedics about that quote. Even more interesting that he cared enough to provide a detailed explanation! That says something. Thanks for the insight.

    Tom

  5. Here we bypass the ED entirely and go to the cath lab directly. Our STEMI protocol is to ID the STEMI in the field (on Paramedic's interpretation NOT machine), verify they meet conditions for PCI and begin transport to cath lab, bypassing local hospitals. On route the crew calls the cath lab hotline and calls a "Code STEMI" which activates the cath lab team. We transmit the ECG so that it is waiting for the cardiologist when he or she arrives but the activation and bypass is on our field diagnosis. Apparently it's working quite well with our pt. contact to balloon time actually beating the times for the Emergency Department within the same hospital as the cath lab. (Not by much, but a nice feather in the cap)

    Dr. Warren Cantor the Chief Interventional Cadiologist has continued to push the importance of Paramedic interpretation over transmission or machine interpretation as the most reliable method. In the first 100 STEMI patients enrolled in the bypass program EMS had a 13% false activation rate (including false positive ECG and cases where criteria for PCI were not met), which is comparable to the rates found in ED Physician interpretation. (His words, not mine.)

    Currently ACP crews do need to transmit a 12 lead for MD interpretation when enrolling a patient in the STREAM prehospital fibrinolysis study, but as per Dr. Cantor this is an issue of medico-legal concerns and research ethics, not Paramedic competency and if the study shows fibrinolysis followed by later PCI to be a better route it is expected that wireless transmission will continue to augment Paramedic interpretation.

    I think Dr. Warren Cantor is talking out of both sides of his mouth.

    "So what we're looking at is whether patients may benefit by getting the clot-busting medication in the ambulance," explains Cantor. "And in order to do that, you can't rely on a paramedic interpreting the ECG. A physician really has to confirm the heart attack."

    The full story is HERE.

    I see no reason whatsoever for there to be a medico-legal or ethical concern if the paramedics are competent to interpret the ECG.

    Tom

  6. Ottawa is like the rest of Ontario doesn't have a small number of Paramedics, it is an ALL Paramedic service, with a moderate number of Advanced Care Paramedics. Not sure of the exact percentage for Ottawa, but currently 36% of my service is ACP and growing as more PCP's are selected for ACP. Not truly important, just wanted to clarify.

    I should also clarify, I realize that terminology is different in Canada, and that you are all "paramedics" whereas we in the U.S. draw distinctions between EMT-B, EMT-I, and EMT-P (or whatever we're calling them these days). When I said "small number of highly trained paramedics," I was referring to your ACPs.

    Tom

  7. I'm not disagreeing with you, per se, but where would you place that line such that research, success and failure can be transferred between services and learned from? We don't want EMS systems to reinvent the wheel, but I don't think "not invented here" is as likely to cause repeat research as it is to encourage an attitude of "Sure it works for them, but our system is different. That's why we'll keep doing what we're doing." That attitude is all too common an excuse and the last thing we need is to legitimize it.

    I think the point is that you have to actually read the study and determine whether or not it can be fairly applied to your EMS system. An even more worrisome attitude than "sure it works for them, but our system is different" is the attitude that "it works for them, therefore it works for us" when the truth is that your system is probably different, and not in a good way. Let's take King County Medic One, Boston EMS, Austin / Travis County EMS, Hennepin County EMS, Wake County EMS, etc. as examples. If they produce research that shows paramedics can safely (insert whatever you like here) can that be extrapolated to EMS at large? Absolutely not! Why? Because EMS organizations that report their data and engage in EMS research tend to be in the very top tier of EMS systems in the country. They're good because they measure and create robust quality improvement mechanisms.

    On the topic of 12-lead ECG interpretation, if you actually read many of the studies, the conclusion is often that "paramedics can identify ST-segment elevation on the 12-lead ECG". Well, whoop-dee-doo. A monkey could do that. The question is whether or not they can identify the ST-segment elevation of acute STEMI with a high sensitivity and specificity. Yes, you can find an occasional study that says this, but more often than not it is from a place like Boston or Ottawa (small number of highly trained paramedics). You have to invest in education and training as well as meaningful quality improvement techniques to replicate results like that. So it's really not a whole lot different from my comparison of the Navy SEALs or Delta to recruits from Ft. Jackson. It's often said that if you've seen one EMS system, you've seen one EMS system.

    That's not to say that EMS research is unimportant, because it shows what is possible. Having said that, we shouldn't depend on results from other EMS systems for any other reason that to come up with a hypothesis for our own EMS system. That hypothesis should include a shared reality of how an EMS system achieved whatever it is they achieved. The devil is in the details, and too often we skip straight to the conclusion.

    Tom

  8. The idea is not to increase thoracic pressure with aggressive ventilations. Increased thoracic pressure decreases preload to the heart, and in a sense can cause blood to be stagnant.

    I definitely agree that ventilations should be given sparingly (every 6-8 seconds which is a long time if you count it out). As for increased intrathoracic pressure, that's where the ResQPod comes in. At least, that's the Wake County EMS approach, and it seems to be working quite well!

    Tom

  9. Prolly the same way you can buy a 2010 car... in 2009.. A new, projected, model.

    Implement the training now, retrain everyone to the new protocol.. and Enact it in 2010. Sounds like a fairly normal approach.

    It might be, except that the ILCOR Conference doesn't meet until February 2010. If the AHA follows the pattern from 2005, the new guidelines will come out as a supplement to the November 2010 issue of the journal Circulation.

    Tom

  10. AHA Guidelines 2010 . . . coming to a training center near you (late '09)

    How can the 2010 guidelines come out in 2009?

    Tom

    We implemented CCR protocols about a year ago. The roll out was less than sterling - some people didn't understand it was for pulseless Vtach/Vfib only and nurses in the ER would lose it when we brought in the patients with an OPA and non-rebreather instead of an ET tube. They eventually got on the same page with us.

    Why not capture the airway with a non-visualized airway like the King LT-D and deliver asynchronous ventilations with continuous chest compressions?

    Tom

  11. Transcript from Amal Mattu M.D.'s December 2008 podcast at EMedHome.com:

    Another concern that you need to be aware of is, if you have a patient who has AF with WPW, stay away from amiodarone. Even now, AHA continues to list amiodarone as a viable option, but it's not a viable option. In fact, the only published reports on using amiodarone in rapid AF and WPW have indicated that amiodarone is associated with adverse outcomes. There's a handful of case reports of patients that had rapid AF and WPW. They got amiodarone and they decompensated. There are, to my knowledge – and I've looked through the literature in detail multiple times – and I have yet to find even a single case report or a single case series or a published study saying, "I had a patient with rapid AF and WPW, I gave him amiodarone, and they did well." Not a single publication that I can find. The only publications on that particular scenario that have ever been published in the literature are "patient did worse" so my recommendation and a handful of other peoples' recommendations also; "Stay away from amiodarone if you're taking care of a patient with rapid AF and WPW."

  12. Actually, you can make a fairly accurate determination of what's normal for bundle branch blocks and paced rhythms. It's not as difficult as you may think. The problem with just stopping the interpretation is that patients with BBB receive the most benefit from reperfusion therapy (FTT Collaborate Group). I'm sure you'll still treat the patient, but will you deliver the patient to the right hospital? Many prehospital 12 lead ECG programs/STEMI systems exclude patients with QRS duration > 120 ms. A huge flaw, in my opinion! Just out of curiosity, why should it matter whether you're inside the hospital or outside when it comes to learning advanced 12 lead ECG interpretation skills?

    Tom

  13. Did you not read the preceding posts before reviving this dead post? It is a paced rhythm and thus you can make NO conclusions about ST segment - abnormal depolarization means abnormal repolarization - Look at V4, V5 for the spikes.

    That's not entirely true. You just have to understand the expected appearance of the ST segments and T waves in the context of paced rhythm (which is similar to that of LBBB). In the presence of paced rhythm, the ST segment and T wave should be deflected opposite the main vector of the QRS complex (which is also the terminal deflection). The concept is "appropriate ST segment and T wave discordance". Any ST segment elevation in a lead with an upright QRS complex is abnormal. In a lead with a negative QRS complex, the deeper the S wave, the higher the ST segment elevation (normal finding with paced/LBBB). When the ST elevation is greater than 0.25 the QRS complex, it's abnormal and usually indicates AMI. ST depression is a lead that shows a negative QRS complex is also abnormal and often indicates AMI (inappropriately concordant ST segment depression).

    Tom

  14. chbare asked the right question. Is this paced? That's the first thing to rule out (and it's easy to look for a pacemaker pocket).

    Since it isn't paced, I'm going to fall back on one of the most basic and important rules of electrocardiography. Wide QRS complexes are ventricular until proven otherwise. Now throw in occasional fusion complexes and it's double-plus ventricular until proven otherwise (that was for all you George Orwell fans out there).

    The wide complexes show an important abnormality (this has to be taken with a grain of salt because we're in monitor mode but it's still concerning). They show inappropriately concordant ST segments and T-waves (i.e., acute injury pattern).

    If I may make a friendly suggestion, you might want to consider changing your default leads to include at least one reciprocal lead (my recommendation would be lead aVL because it's the most sensitive). Monitoring leads II, III, and aVF puts all of your eggs in the "inferior" basket and it's a little bit redundant.

    Assuming that lead I shows an upright QRS complex and lead V1 shows RBBB morphology (a guess based on what you said regarding the physician interpretation) then the wide QRS complexes probably show bifascicular RBBB/LAFB morphology, which means the escape rhythm probably originates near the left posterior fascicle of the left ventricle. That's just gee-whiz information, and irrelevant to the question of what the heart rhythm is (some type of supraventricular rhythm with accelerated idioventricular rhythm and then ventricular bigeminy).

    Interesting rhythm strip!

    Tom

  15. fiznat -

    Rules for RBBB:

    -Supraventricular rhythm

    -QRS duration = or > 120 ms (0.12 sec)

    -Terminal R wave in lead V1

    -Terminal S wave in lead I

    Note that with RBBB the conduction delay is in the second part of the QRS complex (which represents delayed right ventricular depolarization)

    To identify bifascicular block RBBB/LAFB

    -Supraventricular rhythm

    -QRS duration = or > 120 ms (0.12 s)

    -Terminal R wave in lead V1

    -Left axis deviation (upright QRS lead I, negative QRS leads II, III, aVF)

    Note that RBBB with Q waves from inferior MI can pull the axis left. How do you tell the difference between bifascicular block (RBBB/LAFB) and RBBB with Q waves from inferior MI? You don't. You just identify that it's a bifascicular morphology and move on.

    To identify bifasicular block RBBB/LPFB (less common)

    -Supraventricular rhythm

    -QRS duration = or > 120 ms (0.12 s)

    -Terminal R wave in lead V1

    -Right axis deviation (negative QRS lead I, upright QRS leads III, aVF)

    Rules for LBBB

    -Supraventricular rhythm

    -QRS duration = or > 120 ms (0.12 s)

    -rS or QS complex in lead V1

    -Monophasic R wave (usually notched) in lead I

    Note that I don't use lead V6 to confirm RBBB or LBBB. That's because lead placement is too variable, and also because LBBB can show an S wave in V6 with RVH (or can be a normal variant). However, LBBB should not have an S wave in lead I.

    Rules for nonspecific IVCD

    -Supraventricular rhythm

    -QRS duration = or > 120 ms (0.12 s)

    -LBBB in precordial leads and RBBB in limb leads (most common)

    -Any other morphology not explained by typical RBBB, LBBB, or bifascicular pattern

    -Suggests hyperkalemia or cardiomyopathy

    Note that wide complex rhythms not known with certainty to be supraventricular should not be called bundle branch blocks. It's better to say that it's a wide complex rhythm "with RBBB morphology" or "with LBBB morphology" or "with bifascicular morphology" to avoid confusion/mistakes.

    Tom

  16. As a general rule, I think we can agree that UNSTABLE > CARDIOVERT (provided it is not a compensatory tachycardia).

    I also agree there's a fine line between symptomatic and hemodynamically unstable and the terms should not be confused!

    Tom

    Thanks, I got some reading to do :P

    All these phrases get tangled, Stable, Symptomatic, etc, etc.

    Basically I am being taught this: If the patint is unstable (hemodynamically comprimised, constant chest pain, etc etc) cardiovert.

    If the patient is syptomatic yet stable (light headed, exertional fatigue, transient angina, etc) go for the drugs.

    If the patient is neither (palpitations, or unaware) leave them alone.

  17. Because with bifascicular block, A-V conduction is limited to a single fascicle (in this case the left posterior fascicle of the left ventricle). If the chief complaint is syncope, you have to consider that the patient is probably having transient episodes of 3AVB. If the chief complaint is chest pain you have to worry about ischemia of the last remaining fascicle. Either way, you don't want to make the situation worse with an antiarrhythmic which could trigger 3AVB (and wipe out any ventricular escape rhythms).

    If the patient is stable, that's good! Why mess with a good thing?

    Tom

  18. Another excellent case that illustrates the value of prehospital 12 lead ECGs for rhythm analysis.

    Wide complex tachycardia, rate of 150, with bifascicular morphology (RBBB/LAFB). Atrial complexes clearly visible in several leads (especially aVR, V1 and V2). The trained eye can identify 2:1 atrial flutter in lead III.

    Conclusion: 2:1 atrial flutter with bifascicular block (RBBB/LAFB).

    Treatment: Assuming the patient is hemodynamically stable, supportive care.

    Not to beat a dead horse, but this is another heart rhythm you wouldn't want to treat with antiarrhythmics, especially if the chief complaint was chest pain or syncope.

    Tom

  19. I wouldn't go that far, ERDoc! :)

    I work in a system that sometimes allows me to use EBM to treat patients.

    Tom

    I hope I didn't come off as saying that there shouldn't be prehospital protocols. I am in full support of prehospital providers being able to clear c-spines. I think it is great that you work in a system that allows you to use EBM to treat pts.
  20. Reasonable people can disagree as to what constitutes a painful distracting injury, but I don't see how this is different than any other skill in the paramedic scope of practice (advanced airway, 12 lead ECG interpretation, etc.) If a paramedic makes a bad decision, then where are the quality feedback mechanisms? Every EMS system has sentinel events, regardless of protocols, regardless of how "progressive". A good EMS system apprehends fallouts as learning opportunities.

    We had a paramedic who once failed to backboard a head-injured patient because the neuro exam was "baseline according to the nurse" (the patient suffered from dementia). The Medical Director explained to the paramedic that anything that compromised the physical exam meant that the spine could not be cleared. I assume the paramedic in question won't make the same mistake again.

    Isn't that the point? If your idea of risk management and quality patient care is "100% oxygen and a backboard for everyone because it's easier than educating the staff" then I'm not sure it's the best possible approach to ensuring that our citizens are well taken care of.

    Tom

    You are correct. It is not difficult to learn the criteria. It probably takes about 30 seconds to learn the 5 NEXUS criteria, maybe a little longer to learn the CCR. The difficulty comes in appreciating the limitations of the studies and the clinical decisions rules that were developed.
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