Tom B.

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

If the patient has a normal level of alertness, a normal neuro exam, no signs of intoxication, no pain on palpation of the spine, no painful distracting injuries, and no pain with 45 degree lateral movement, flexion, or extension of the head, then no spinal injury exists. This is well supported in the evidence based literature. The spine is a bag of bones, and it hurts when it gets fractured. I don't put every patient with a MOI in bilateral traction splints, and I don't put every patient with a MOI on a LSB. Be a professional. Learn your job. Do it well. Or, find something else to do. Tom

As I explained in a recent interview with EP Lab Digest, the cardiologist who's "right" can generally provide an explanation of "why". Tomas Garcia MD used to remind us at the EKG Club that the most common reason cardiologists fail their 3-part board exam is ECG interpretation! Tom

Tom

Actually, the first box in the tachycardia algorithm says: Assess and support ABCs Give oxygen Monitor ECG (identify rhythm), blood pressure, oximetry Identify and reverse underlying causes In other words, the Hs and Ts are a higher priority than antiarrhythmics. Further down the algorithm, for stable wide complex tachycardia, the algorithm says: Consider expert consultation That's the first recommendation. It's worth noting that the ECC guidelines were written for physicians. In other words, it recommends that physicians consider an expert consultation (i.e., a cardiology consult) for stable patients. I don't believe that paramedics are expected to be automatons that blindly follow protocols. Algorithms, by their very nature, oversimplify complex problems. They are not a substitute for sound clinical judgment. My Medical Control Physician and Medical Director agree. Tom P.S. Congratulations on the save.

fiznat - Any ECG needs to be interpreted in light of the history and clinical presentation, but based on what I'm seeing with this ECG, I can tell you with 100% certainty that I would not give an antiarrhythmic to this patient. It's an irregular rhythm, with variations in QRS/T wave morphology. I don't know if the QRS is wide, or the complexes are a bizarre combination of QRS/T. Either way, this looks like a pre-morbid rhythm or a patient who has an underlying metabolic derangement. I wouldn't rule out acute STEMI or aortic dissection (elevated J points V2-V5) and I've seen acute STEMI create tombstones like we see in leads I, II, aVR, and III. Either way, and regardless of cause, if the patient is hemodynamically stable, then I'm falling back on the theory that "a perfusing rhythm is better than a non-perfusing rhythm or no rhythm at all". The patient should be worked up in the ED, and the Hs and Ts should be aggressively treated. Once hypoxia, acidosis, electrolyte derangements are treated, and serial ECGs or bedside echo are obtained, a treatment plan can be started that may include a trip to the cath lab. The last thing this patient needs is a drug like amiodarone, altering the shape of the cardiac action potential and prolonging the QT interval. Assuming this a polymorphic wide complex tachycardia (may or may not be true) I would get an expert consultation prior to treating with any antiarrhythmic (and I would hope the ED physician would do this same). You can't take it out once it's in. As a final thought, if the patient had an ICD, I would consider the application of a ring magnet to disable tachy functions. We had a similar case a few years ago and the ICD shocked the patient x2 into asystole and the patient was not successfully resuscitated. It turned out to be severe hyperkalemia. Tom

<s>It's the ghost rhythm. I've not seen it before</s>. I can see it now! Tom

Very cool! Excellent suggestion, fiznat. Tom Also, after you provide your interpretation I might ask for an explanation as to how you came up with your interpretation. This will help improve the educational quality of these posts. To view the strips larger you can usually click on them. If not, try holding the Ctrl key and scrolling your mouse wheel. Or hold Ctrl and tap + or - keys. Well enjoy, the next strip tease is coming really soon!

I've had good luck with Adenocard and Cardizem, too. If "good luck" is defined as terminating AVNRT or slowing the ventricular rate with AF. But what was the point? Looking back on my career (at a time when I had a much different outlook than I do today) I did these things because I could, and because it was fun, and because it meant that I was a "good" or "aggressive" paramedic. It wasn't about the patient. It was about me. In one of the few (if not the only) studies of prehospital Adenocard, it was given inappropriately 20% of the time, including regular wide complex tachycardia (5%) and irregular wide complex tachycardia (2%). I myself have seen Adenocard given for patients in acute pumonary edema with sinus tachycardia or AF with RVR. When asked why the paramedic gave Adenocard, they both said, "heart rates > 150 can't be sinus tachycardia". How many EMS systems educate and train their paramedics to the point where, 100% of the time, a 12 lead ECG is captured with excellent data quality documenting the arrhythmia, the print button is pressed prior to the administration of Adenocard to document the pause, and a 12 lead ECG is captured of the post-conversion rhythm? In my experience, not many. As for Cardizem, we recently pulled it off the truck. Why? Because how often do you have a patient with new onset AF with symptom onset < 48 hours who is stable? Not often. And how do you really know for sure that the symptom onset was < 48 hours? Usually when we see AF/RVR it's a heart failure patient with shortness of breath who needs oxygen, NTG, and CPAP. Not Cardizem. Why not allow the physicians at the hospital to risk stratify the patient, do a bedside echo to rule out a clot in the left atrial appendage, and heparinize the patient if necessary? I know some argue that Cardizem won't convert AF. Well, I've seen it many times as a cardiac monitoring tech on a stepdown unit. So no, I'm not a huge fan of prehospital antiarrhythmics. If the patient is unstable, then cardiovert. If the patient is stable, capture a 12 lead ECG with excellent data quality, start an IV, place the patient on oxygen, place the compo-pads as a precaution, and take the patient to the hospital. Documenting the arrhythmia in 12 leads is the most important thing you can do for the electrophysiologist who follows up on the case. If you must give an antiarrhythmic, you should do so cautiously, in accordance with your protocols, and with the understanding that any antiarrhythmic can be proarrhythmic, or even fatal if given in the wrong circumstances. That's why I wouldn't monkey around with AF/WPW in the field, except with electricity, and even then only if the patient was clearly unstable. Tom

The following is straight out of the Bob Page 12-lead book. Your primary survey of the WCT patient: 1. Measure the QRS width --- Good idea. If it's not "wide" it's not a WCT. 2. Determine the axis --- Should be a part of any 12 lead interpretation. Just be aware that axis cannot rule VT in or out. Does a right superior axis favor the dx of VT? Sure. But that should be your default dx anyway. 3. Look at morphology changes --- Here's where it starts getting dangerous. If you use morphology to "rule in" VT, then great! If you use it to "rule out" VT, then you're living dangerously. This goes for axis and morphology. 4. Look at concordance criteria --- Same feedback. 5. Look at signs of AV dissociation --- This is the best evidence that a rhythm is VT, but it's only present 50% of the time, and it's not easy to appreciate on most ECGs. 6. Get a good patient history --- A history of MI increases the probability that you're dealing with VT, but again, that should be your default diagnosis for a WCT. 7. Do a physical exam --- Goes without saying. Wide Complex Tachycardia > 150: Listed by ease of use, Often seen, & Specificity 1. Extreme right axis deviation (ERAD) & positve v1 2. QRS morphology in v1 3. QRS morphology in v6 4. ERAD & negative v1 5. Concordance in v1 through v6 6. RS interval > 100ms any V lead 7. QRS > 140ms if up & > 160ms if down in v1 --- Once again, ruling in VT is fine. Extreme right axis deviation: ERAD is also known as right-shoulder axis, northwest axis, intermediate axis or "no man's land". This is an axis > 180 degrees. --- I've seen it with nonspecific IVCD, RBBB/LPFB, and hyperkalemia. It's not always VT. But again, ruling in VT is fine. You can determine this simply by looking at leads 1, 2 ,& 3. If leads 1, 2, & 3 are all negative, the patient has ERAD. If v1 is positive with ERAD, the rhythm is ventricular in origin. It is still possible for a ventricular rhythm to present with ERAD and negative v1, this is just lest specific. QRS Morphology: 1. When you have the "bunny ear" shape in v1. Having the left ear bigger than the right ear indicates VT. This is also referred to as "big mountain/little mountain". --- Sort of like this case. Ruling in VT is fine. 2. A single peaked upright R wave in v1 is indicative of VT --- Negative. I've seen it many times with bifascicular block and even atypical RBBB. But ruling in VT is fine. 3. A single peaked upright R wave in v1 with slopped off end --- What does this mean? We've already listed a monophasic R wave as a rule-in VT criterion. 4. A fat (> 40 ms) R wave in negative QRS in v1 --- A slurred upstroke of the R wave does suggest VT. 5. A notched down stroke of negative QRS in v1 --- This is called "Jospehson's sign" and I've seen it in VT many times. 6. Any predominately negative complex in v6 suggests VT --- Or paced rhythm, or cardiomyopathy, or nonspecific IVCD. Concordance: 1. Negative concordance, meaning negative QRS complexes in v1 through v6, indicates VT or LBBB. --- That would actually be atypical for LBBB, although sometimes there is a persistent S wave in lead V6 with RVH. Regardless, if it indicates VT or LBBB then it's no help, right? It actually is more suggestive of VT, but that should be your default dx anyway. 2. Positive concordance indicates VT or WPW --- Or RBBB or nonspecific IVCD. Measurements: 1. Positive QRS in v1 > 140ms 2. Negative QRS in v1 > 160ms 3. RS Interval is highly reliable. From the start of the R wave to the nadir point of the S wave (the bottom point). > 100ms is VT --- Ruling in VT is fine. AV Dissociation: 1. Cannon A waves. These are waves of pressure seen shooting up the jugular veins. 2. P waves out of place and isolated 3. Different S1 (first hear sound). --- Ruling in VT is fine. Remember, we are trying to rule out VT. This means that if you have any of the criteria without strong conflicting criteria, call it VT. --- I missed it, Adam. Where are you ruling out VT? All toads are frogs, but not all frogs are toads! In other words, the inability to rule-in VT does not rule-out VT! That's why these criteria are dangerous. In the absence of compelling evidence to the contrary (e.g., obvious sinus P waves in a 1:1 relationship with the QRS complex and a normal PR interval, an "old" ECG for comparison that shows identical QRS morphology, occasional pauses that reveal flutter waves), regular wide complex tachycardias should be considered VT. There is no algorithm that can safely classify a wide complex tachycardia as SVT with aberrancy.

You could go even further and say that the impulse originates in the area of the left anterior fascicle of the left ventricle. Why? What type of bifascicular block presents with an upright QRS complex in lead V1 and a right axis deviation? RBBB and LPFB. With RBBB and LPFB, which fascicle depolarizes first? The left anterior fascicle.

For rhythm analysis, I like any lead that shows good P waves, QRS complex, and T waves. At least with a 12 lead, you've got your choice! Tom B.

My views on these types of topics are constantly changing. Five years ago, I wouldn't have had any idea what AF/WPW looked like, let alone how to treat it (or not treat it). I'm not a huge fan of prehospital antiarrhythmics in the first place. At least for regular wide complex tachycardia, you probably won't harm the patient by trying 150 mg of amio over 10 minutes. Of course, with AF/WPW you have the same concerns about symptom onset < 48 hours that you would have with any other AF. Like I said, I just don't care for prehospital antiarrhythmics, so I wouldn't feel comfortable monkeying around with AF/WPW. If it's unstable, I'll shock it. If it's stable, I'll let the ED physician (or a cardiology consult) figure it out. I wouldn't judge someone for giving amio since it's an option in the AHA ECC 2005 guidelines for irregular wide complex tach. I just wouldn't do it based on the possibility of causing harm with no clear evidence of benefit. Tom B.

Absolutely, and no hostile or pointless argument is desired. Thanks for the discussion! Tom B.

I'm not a guru, Adam. Just a guy with strong opinions. Some of them might even be right! Tom B.

In the absence of evidence that it helps, and with anecdotal reports of possible harm, why give it? Synchronized cardioversion is a perfectly viable option (and so is supportive care for hemodynamically stable patients). The first rule of medicine applies. Tom B.

I don't see how it provides evidence of anything. Most cases of VT present with other than right superior axis. Why should ventricular escape rhythms be any different? In my world, wide complex rhythms are ventricular until proven otherwise, and rate, axis, and QRS morphology are not sufficient evidence. Tom B.

I'm still curious to know how you differentiate between a junctional escape rhythm with LBBB and a ventricular escape rhythm. If wide complex rhythms are ventricular until proven otherwise, then you should consider this 3AVB with a ventricular escape rhythm. Or, 3AVB with a wide complex escape rhythm. There's no need to call it a BBB. Maybe it is, maybe it isn't. Tom B.

Adenosine might work for an antidromic AVRT, but it's a risky drug that can trigger VF, especiallly in the setting of AF/WPW. As for amiodarone, consider this 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."

This is a good example of why we need 12 lead ECGs. Can you imagine trying to diagnose this arrhythmia using lead II? Yikes! Tom B. With the exception of hyperkalemia, you're never wrong to presume that a broad complex rhythm is ventricular! The burden of proof is on the person who says it isn't. Tom B.

Just to play devil's advocate, how do you know the rhythm is supraventricular in origin? Tom B.

I'd like to make a minor correction. While a right shoulder (right superior) axis can be suggestive of VT, it's not true that rhythms with an other-than-extreme axis are unlikely to be VT. With VT, you can have a normal axis, left inferior axis, right inferior axis, or right superior axis. I apologize for nitpicking, but it's an important point. Tom B. Maybe I should have read through all the comments before I hit reply! Tom B. As a final thought, whenever the shortest R-R interval is 6 small blocks or less, there's an excellent chance you're dealing with an accessory pathway! My dept's protocols do not allow antiarrhythmics in the presence of delta waves, heart rates that = or > 250, or shortest R-R interval of 240 ms or less. Tom B.