Tom B.

What is the process to change over to the hospital pacer following transport? Scenairo - in the field, find a patient in symptomatic brady, no response to medications, initiate pacing with good electrical and mechanical capture using the Lifepak 12. You arrive at hospital and the ER wants to continue to pace the patient. The ER also has the Lifepak 12, how do you switch Lifepaks and pads without losing capture?

Do you have the strips by any chance? It's so rare to see true electical capture achieved in the field I'm sure we'd all learn a lot from the case. In my experience the ED physician wants to see the underlying rhythm anyway. I remember on one occasion the pacer was turned off and there was (almost) nothing underneath. They turned it right back on and took the patient up to the cath lab with our LP12 attached. Not sure what happened when they got there but one of the nurses brought back our machine.

Lots of things "seem reasonable" but turn out to be harmful. Consider this video from the father of evidence based medicine.

Fast-forward to 5:00.

I fear there has been a bit of misinterpretation in what I posted.

Using lidocaine to reduce the development of ectopic beats, in the setting of a presumed AMI, is reasonable. It should not take precedence over managing the underlying problem, but reducing the occurrence of ectopic beats, and rhythm, should be a consideration. Limit the ischemia/injury, limit the development of dysrhythmias, and maximizing the cardiac output are still measures to shoot for with an active MI.

I was not talking about ACLS-EP. Also, it's about time (well past actually) that paramedic programmmes quit using ACLS as a standard educational tool. AHA develops guidelines based on a review of the science. The onus for good pre-hospital education sits squarely on our shoulders not AHA.

The AHA develops guidelines based on the evidence but it also produces educational materials. Many top performing EMS systems have eliminated the requirement of maintaining an ACLS certification because the video-driven ACLS course is so awful. We could talk all day about how the "onus is squarely on our shoulders" but the reality is that ACLS is a required certification for the vast majority of paramedics in the country but it no longer serves our needs. Perhaps you think that every EMS system should invent its own wheel but I'd rather see a thoughtful ACLS course be created by the AHA for EMS professionals. It's an opinion I've voiced to the Public Safety Team of the AHA and they seem interested in correcting this problem. I hope they do.

We look at other courses that focus on these situations. The FCCS course, for example, focuses on responding to these critically Ill and or injured patients. There exist many other courses as well. I'm not sure why people continue to think ACLS should be something it's not?

ACLS does encompass the critically ill periarrest patient. Why do you think it does not? The ACLS Reference Textbook and Experienced Providers Manual is a fantastic resource. The dumbed down video-driven basic ACLS course is an abortion and we should require more of our paramedics than to be resuscitation technicians who can follow a cookbook but are incapable of considering the Hs and Ts. The AHA has FAILED when it comes to prehospital emergency medicine. Period.

I could have sworn adenosine was contraindicated for WPW as well, but I can't recall exactly on that one.

Specifically AF/WPW where adenosine (along with CCBs) can induce VF. When you give adenosine it's a good idea to place the combo-pads first.

Rs complex in lead I with a tight R-wave so definitely not a LBBB.

I wrote a tutorial on axis determination here:

http://ems12lead.com/2008/10/04/axis-determination-part-i/

Good luck!

Tom

3rd degree AV block with junctional escape rhythm. Nonspecific ST-T abnormality. Notched J-point in several leads. Correlate with history and clinical presentation.

Tom

If the patient has no history of heart disease, and there are RS complexes in the precordial leads, and the start of the R-wave to the nadir of the S-wave is less than 100 ms, and AV dissociation is absent, and there are no fusion or capture complexes, and Wellens' criteria are not positive for VT in leads V1 and V6, then yes, VT is less likely, but cannot be safely excluded, especially when taking into account the problem of inter-observer agreement.

What about all of these together in one ECG? I understand that individually they can't be used to exclude VT, but if they are all present I would imagine VT is increasingly less likely....?

"I did not believe I was looking at VT as the axis is leftward (VT should be extreme rightward), there is no precordial concordance (as seen in VT), the morphology looks asymmetrical and abbarant (not VT), the rate is awful high for VT, and the patient was somewhat young."

This was a great case, but I'm going to clarify one point because it's very important. Ventricular tachycardia can have a frontal plane axis in any quadrant. A right superior axis helps support the diagnosis but absence of that finding does not exclude the diagnosis. Same thing with precordial concordance. There is no safe way to exclude VT based on QRS morphology. On rare occasions you might see ventricular flutter with a rate around 250 but you should suspect an accessory pathway whenever the rate approaches (or exceeds) 250. When it's a regular, monomorphic wide complex tachycardia, in theory it's okay to try adenosine, and in fact it may convert orthodromic or antidromic AVRT (or be diagnositc when the underlying rhythm is atrial flutter). Just remember to hit the PRINT button so you can see what happens during the asystolic pause. The drug of choice for this patient would be procainamide but in these types of situations "edison before medicine" is probably the wisest course of action for the hemodynamically unstable patient.

Thanks for sharing the case, fiznat!

It means that 1:1 atrial flutter is a strong possibility. It also means that the patient may have an accessory pathway.

Cool ECGs, fiznat!

Since the village elders are keeping their opinions to themselves I'll simply offer a couple of clues.

The 2010 AHA ECC Guidelines say "go right ahead" with adenosine for a patient like this but I wouldn't be comfortable doing it even though it could prove to be diagnostic in this case.

There's only one antiarrhythmic I'd consider and few EMS systems carry it because it's expensive and difficult to administer correctly (dosing and end points).

"Wide and fast" is VT until proven otherwise in my book right up until the rate pushes (or exceeds) 250. Then I'm forced to consider another possibility because that's a bit fast even for VT (although it could be so-called ventricular flutter).

Electrical cardioversion for unstable patients allows caregivers to avoid the potentially deleterious consequences of selecting the wrong antiarrhythmic which in some cases can be fatal.

For stable patients I'm a big fan of "supportive care and transport".

Tom

Now you guys have got me worried that I'm miss understanding the AVR criteria...I thought it was pretty straight forward (except for the last test, but even that one's pretty simple once you get it...unless I've missed something). Are there more intricacies than I know about? For instance, it was posted above that you have to pick the correct QRS when evaluating excursion. I hadn't heard that before.

In the first place I made a typo.

I wrote:

"44 had an initial voltage (in the first 40 ms of a bi- or multi-phasic QRS complex) greater than the terminal voltage (in the last 40 ms of the QRS complex)"

It should have read:

"44 had an initial voltage (in the first 40 ms of a bi- or multi-phasic QRS complex) less than the terminal voltage (in the last 40 ms of the QRS complex)"

Or as the paper itself describes it:

"[E]stimation of initial (v_i) and terminal (v_t) ventricular activation velocity ratio (v_i/v_t) by measuring the voltage change on the ECG tracing during the initial 40 ms (v_i) and the terminal 40 ms (v_t) of the same bi- or multiphasic QRS complex. A v_i/v_t >1 was suggestive of SVT and a v_i/v_t ≤1 of VT."

As for "selecting the correct QRS" call up the full text of the article. Here is one small excerpt:

"The v_i and v_t were measured in an individual QRS complex in any lead having a bi- or multiphasic QRS complex, in which the onset and end of the QRS were clearly visible and the initial ventricular activation was the most rapid (fastest). When either the initial or terminal 40 ms of the QRS complex displayed both positive and negative deflections, the sum of their absolute values (disregarding polarity) were used as the values of v_i and v_t. Because three channels were recorded simultaneously on the ECG tracings, the onset and end of the QRS were defined by the earliest and latest ventricular depolarization, respectively, among the three simultaneously recorded leads that included the lead with the fastest initial ventricular activation. Most frequently (in 87% of WCTs), the v_i was the fastest in the precordial leads and the leads most commonly used for analysis of v_i/v_t were v₃, v₅, and v₂ in decreasing order of frequency."

Also see the caption in Figure 1.

Does this really seem simple to you? I mean, I think I get it, but I'm a serious ECG dork.

Tom

Job13_5 -

Thanks for chiming in.

From an academic perspective there are things I like about this algorithm, but there are problems with it also. In the first place, can we honestly say it's simplified? Consider Fig. 7.

Out of 453 wide complex tachycardias:

35 showed AV dissociation > presumed to be VT

127 showed an initial R-wave in lead aVR > presumed to be VT

156 showed atypical BBB or bifascicular morphology > presumed to be VT (Note: Requires the clinician to understand typical vs. atypical patterns.)

Now we're down to 135 of the original 453.

44 have an initial voltage (in the first 40 ms of a bi- or multi-phasic QRS complex) greater than the terminal voltage (in the last 40 ms of the QRS complex) > presumed to be VT (Note: I am simplifying this criterion because the stipulations for selecting the right QRS complex are bewildering).

Do you think this criterion will be correctly applied by anyone other than EPs? I don't.

Even if by some miracle this final criterion is correctly applied in the field (and no other mistakes are made) 15 of the remaining 91 patients (16%) were misidentified as having SVT with aberrancy when in fact they were experiencing VT. Do you like those odds?

76 of the original 453 patients (17%) were correctly identified (by exclusion) as having SVT with aberrancy.

So again, the burden of proof is entirely on the person who says a wide complex tachycardia is something other than VT.

The most important criterion of all is "wide and fast" but sadly, that's the criterion more and more paramedics are willing to ignore.

The default diagnosis for a wide complex tachycardia should always be VT.

I have no quarrel with the idea that we should "treat the patient, not the monitor" but if that's your position then why do you feel the need to make the pronouncement that it isn't VT? Call it a wide complex tachycardia that is well tolerated by the patient and transport the patient to the nearest hospital.

That's a lot better than killing the patient with a calcium channel blocker.

Tom

Care to provide some more information on the highlighted parts? From what I read on the Brugada link by ER Doc, it is safe to rule SVT with aberrancy if the VTach criteria is not met. How do you know the criteria does more harm than good in the prehospital setting?

The problem is that mistakes are made (as high as 50% of the time) and there is poor inter-observer agreement (certainly the case every single time one of these threads hits the EMS bulletin boards). The most common error is misclassifying VT as SVT with aberrancy (as in this case) which has been proven to lead to clinical misadventure, including death. The algorithms have limited applicability for patients with preexisting intraventricular conduction defect (atypical right or left bundle branch block) and patients with an accessory pathway (antidromic AVRT). For a complete discussion about this see the ACLS Reference Textbook and Experienced Provider Manual (2003). Chapter 16: Stable Wide Complex Tachycardias. Some excerpts can be found here. I say the danger is greater in the prehospital setting because it's debatable as to whether or not antiarrhythmics are good or necessary in the prehospital setting in the first place. If the patient is hemodynamically unstable they should be cardioverted. If the patient is hemodynamically stable then there is time for expert consultation. Anitarrhythmic medications are dangerous and we should be handling them with the utmost respect.

Tom

Really? Because it looks to me that lead I is an up, not down. So, no it does not meet the requirements, as previously stated.

You cannot use the frontal plane axis to rule out VT. This kind of thinking is extremely dangerous. Wide and fast is VT until proven otherwise! This ECG shows RBBB morphology in lead V1 and left axis deviation. In other words, bifascicular morphology (RBBB/LAFB) which is the exact morphology we could expect if the VT originated in the left posterior fascicle of the left ventricle. In other words, one of the EXPECTED morphologies of VT. ERDoc used Brugada's critiera in the only responsible way, in my opinion, and that is to rule-in VT. Failure to rule-in VT does not rule-out VT and these criteria do more harm than good, especially in the prehospital setting.... by a large margin.

Tom

Thanks for answering, Tom.

What I meant is that VT by definition is ventricular, so I was confused when you suggested that 50% of VT might show AV association. I see now that you meant about half of them will demonstrate retrograde conduction, thereby associating P waves and QRS complexes even though the actual rhythm isn't originating supraventricularly.

Is that 50% stat a general illustration, by the way, or is that the actual percentage? Do about half of the AV nodes out there have some quality that allows retrograde conduction, and half do not?

Brandon -

The 50% statistic is cited frequently in medical textbooks and the peer reviewed literature. You can check out a Google search for examples.

I'm not sure why. Apparently some AV nodes allow antegrade AV conduction but not retrograde VA conduction. You'd think if it would allow one it would allow the other, but clearly that's not the case!

Tom

My apologies for the outrageous thread resuscitation, but these strip teases seem like they should be lasting resources. If Tom's still reading, I hope he'll be willing to add a little info.

Tom,

What do you mean by the above?

I agree that P-wave association is hard to note in most VT, but by saying it's only present 50% of the time, do you mean that some VT DOES have AV association? Surely that makes no sense unless you're thinking of retrograde conduction.

Brandon -

I'm not 100% sure I understand the question, but some VT does have AV dissociation. In other words, the ventricles are in a self-sustained ventricular tachycardia and the atria are in sinus rhythm (for example). So the ventricular rate might be 180 and the atrial rate might be 80. When that occurs, a trained eye might be able to march out the P-waves running through the VT. This is much easier sitting down inside the hospital with a rhythm strip laid out on the desk and a pair of calipers in your hand.

Other times, VA conduction is intact, so you will have retrograde activation of the atria. That's why a 1:1 relationship between atrial complexes and ventricular complexes is no help when differentiating between VT and SVT with aberrancy. If the episodes of a wide complex tachycardia are paroxysmal, you might say, "Then if the tachycardia ends with an atrial complex it must have been VT." Unfortunately, even that isn't true, since the tachycardia could end with a blocked atrial complex.

Does that answer your question?

Thanks,

Tom

To what extent do you feel that taking a little over a minute to intubate a cardiac arrest pt (refractory VF scenario), whilst compressions have been ceased, is acceptable/unacceptable.

It's not acceptable at all, and a major reason the survival rate for sudden cardiac arrest is so dismal in the United States and across the World. We know that continuous chest compressions are an important part of saving more people, so anything that interrupts chest compressions is bad, including tracheal intubation. Why not intubate without interrupting chest compressions or use a King LT-D to accomplish the same thing? It's working great in Wake County, NC where the survival rate for people observed to collapse from cardiac arrest with an initial rhythm of VF/VT approaches 50% in the City of Raleigh. They start compressions immediately, drop a King LT-D (with a ResQPOD and waveform capnography), defibrillate after 2 minutes, start a couple of IOs, and induce hypothermia for patients with ROSC and persistent unconsciousness. It's a simple and repeatable formula that is not so dependent on the experience level of the paramedics. But by God, we don't care how many people die in EMS! Just don't take away our authority to intubate!

Tom

I thought you guys might be interested in my interview with Keith Lurie, M.D. where we discuss the ResQPOD and the ROC PRIMED trial.

http://ems12lead.blo...h-lurie-md.html

Tom

Will try the scanning, but don't hold your breath. Further, since there was the LBBB, whether the QRS was slightly widened or not, and the faster heart rate, what would you do?

Option to look at the worst of the evils, the potential of significantly wide QRS and fast (VT) and the defibrillator going off. Would adenosine actually work in this case if there were reciprocal pathway causing the tachycardia? Could adenosine slow the rate down enough to realize the true underlying rhythm? Should antiarrythmic medications be given to stave of potential VT? Which med: Lido, Amio, or another???

How about doing the smart thing and running the EKG and 12 Lead at 50mm instead of 25mm standard?

Ah haaaaa..............

There's a world of difference between a confirmed LBBB and a wide complex tachycardia with LBBB morphology. In the absence of an old ECG for comparison, a wide complex tachycardia with LBBB morphology is VT until proven otherwise. Running an ECG at 50 mm/s may help pick up irregularity suggestive of AF or it may not. Either way you should leave your calcium channel blockers in the drug box. A slight widening of the QRS complex during faster rates is not unheard of, but it also poses the possibility of electrolyte derangement as someone else mentioned earlier in the thread. I'm afraid that doesn't help us pinpoint the exact diagnosis.

By all means let's look at the worst of the evils. Right now you have a conscious patient with a pulse. That's a good thing. Monkeying around with antiarrhythmics? Maybe a good thing. Maybe a bad thing! The first rule of medicine is "do no harm." If the patient had no ICD, would you be shocking? Would you be pushing antiarrhythmics? If not, then I see no reason to consider those options simply because an ICD is present.

I think this is a perfect example of a case where the paramedic should show restraint. Capture a 12-lead ECG. Monitor the rhythm. Consider deactivating the ICD. Start an IV. Draw labs. Supportive care. If you must give an antiarrhythmic, give amiodarone.

Tom

I'd like to clarify one extremely important point. A borderline wide complex tachycardia should be considered a wide complex tachycardia, particularly when the T-wave is deflected opposite the terminal deflection of the QRS complex. Wide complex rhythms are ventricular until proven otherwise.

Having said that, heart failure is a common indication for an ICD, and bundle branch blocks and atrial fibrillation are common manifestations of heart failure. Atrial fibrillation is the most common reason for an inappropriate ICD shock.

However, sometimes patients with an ICD are taking oral antiarrhythmics that slow down VT to below the lower rate limit for antitachydysrhythmia therapy. So correct rhythm interpretation is very important.

Regardless, if ICD shock number 5 doesn't convert the patient to sinus rhythm, it's doubtful that ICD shock number 6, 7, or 8 is going to convert the rhythm. So if you can document the pre-shock rhythm is essentially the same as the patient's baseline rhythm at the time of initial evaluation (with the exception of rate) then I wouldn't hesitate to deactivate the ICD with a ring magnet. You can always remove it.

I wrote a 3-part series on inappropriate or ineffective ICD shocks HERE.

It includes a case study similar to the one you mentioned as well as brand-specific instructions for applying the ring magnet.

Tom

P.S. Would you mind scanning the ECGs and posting them so we can take a look?

Let's also keep in mind that whether we like it or not, an abdominal exam is part of the EMT-B curriculum and, more importantly, the standard of care. I think it's a dangerous for a provider at any level to take the stances of some here regarding the limitations of EMT-Basics and put them into practice with patients in contravention of their regulatory oversight and medical direction.

A first-year law student could plant the idea in a jury's head that if Mr. or Miss EMT had only followed his training and performed an abdominal exam, Mr. Husband and Father of 3 would still be alive today.

Only if the EMT failed to transport the patient to the hospital, transported the patient to the wrong hospital, or neglected to notify the triage nurse at the hospital that the patient was complaining of abdominal pain.

You have to cause harm to be negligent.

Tom

Dust this is where I have to disagree with you. Again even if it changes no care in my ambulance it allows me to notify the hospital and perhaps even an uneducated description may trigger the doctor to be ready for more than the normal. Visualizing, palpating, and auscultating should be done even when it changes nothing in the ambulance. This is not tradition this is patient care.

If the patient is complaining of abdominal pain, the physician is going to do his own assessment whether you needlessly provoke additional pain in the prehospital setting or not.

I vote for leaving the patient's abdomen alone unless it's going to influence your transport decision or destination.

Tom

I was talking with a Paramedic who told me that he respond to a primary care clinic 30 minutes away from the hospital for a 50 year old white male patient who is 1 month S/P CABG. The patient went in for a routine appointment for palpitations. Upon arrival you find the patient on an exam table, on 2 liters of oxygen with saline lock in place & Dynamap in place. The patients vs were as follows HR 130, BP 110/50, RR 20, SPo2 95%, T 98.7. SAMPLE History was as follows: Hx of Palpitations. Allergies: NKA, Medications: Lopressor 100MG, Aspirin 325MG, Zocor 40MG, Lasix 40MG, Nitro SL, Plavix 75MG & Multi Vit. Past Hx.: CAD & HTN. Last intake breakfast. Events leading up to patient was resting at home. Enroute the patient was placed on 4 liters of oxygen, an IV of NS was started an additional 12 lead was obtained HR was 130 Atrial Flutter vs SVT, The Medical Command Physician ordered Adenosine 6MG IV x1 & the patients rate slowed to 113 with Atrial Flutter 3:1. If this was your patient what would you do?

In the first place, a heart rate of 130 with a BP of 110/50 should be left alone.

Secondly, I would question the diagnosis of atrial flutter. 2:1 flutter generally presents with a heart rate of about 150. While it's possible for 2:1 flutter to be 130, that would make the flutter rate 260 which would make 3:1 flutter about 86.

SVT is an umbrella term that includes all non-ventricular tachycardias, including sinus tachycardia, atrial fibrillation, and atrial flutter. Adenosine is specifically intended for reentrant tachycardias like AVNRT. If you give adenosine and it reveals flutter waves, you need to switch to another drug like diltiazem. That's if it's really necessary to treat the arrhythmia in the prehospital setting, which is debatable. After all, if it was hemodynamically unstable you'd be cardioverting.

One has to wonder sometimes whether we do things because it's good for our patients or because it's good for our egos!

Tom