"It cant be PEA if the rate is over 150" -- ??

[vs-eh?]

Perhaps your instructor was saying a narrow complex tachycardia without a palpable pulse but not actually in arrest? This comes into the whole stable/unstable tachycardia thing, which then leads to judgement calls on what is truly unstable (not just meeting the altered LOC/SOB/CHF/hypotension/CP thing) and what is stable. Whether you can rationalize giving drugs to first or electricity first.

The half life for certain drugs (specifically adenosine) for "treatable" pathological tachycardia's are very short (<10 secs) even with "optimal" cardiac output and peripheral circulation. The drug will simply not reach the heart fast enough to exert its desired effect with CPR perfusion.

As Rid said, they used to give Calcium gluconate for arrests before as first/second line drugs for PEA. It is still given (I have seen) for certain arrest types involving CCB's for obvious reasons. You would not want to potentially slow down the heart and diminish things like FOC in a post arrest situation (obviously a balance between maintaining CO and stability of the patient).

Look at hypovolemia as a prime example for a narrow complex tachy PEA. The rate is there with no volume to maintain adequate perfusion/oxygenation.

[AZCEP]

This rate and presentation should have pulses, you are right. Since the patient did not read the book on how to present, we need to evaluate the possibility of what is causing this problem.

Rate >175 and narrow QRS would lead me to believe hypovolemia, so a fluid bolus would be in order. Because the patient is pulseless, cardioversion would be indicated. Need to treat the rate first.

Adenocard is out, as has been shown, it won't be around long enough to work.

Back to causes. Hypoxia won't cause pulselessness at tachycardic rates. Acidosis is a possibility, but would be tied to electrolytes and ventilation. Hyperkalemia would cause a widening of the QRS so probably not. Hypocalcemia would tend to cause bradycardia. Hyponatremia would cause tachycardia, treating with hypertonic saline might be an option to consider. Has this patient experienced any trauma recently? Tension pneumo/Tamponade tend to show tachy-->brady progressions. Pulmonary embolus definte possibility related to history prior to arrest. Coronary thrombus could present this way, but we would see some ECG changes with it. For drug overdoses, any of the sympathomimetic drugs could cause this presentation as well.

So, we haven't really narrowed down the causes too much. Hypovolemia, PE, AMI if ECG changes are present, and Hx of sympathomimetic drug use would be at the top of my list.

Defib to stop the tachycardia, consider an antidysrhythmic to keep it slowed down, replace volume, look for ECG changes and drug use history.

[medic001918]

Now that I've read the post through some rested eyes and gotten some more information, it's a little easier to totally understand the scenario. I agree that at a rate of 175 BPM it will be hard to tell v-tach from SVT. The advice that has been given so far has been very good advice.

"Defib to stop the tachycardia, consider an antidysrhythmic to keep it slowed down, replace volume, look for ECG changes and drug use history." posted by AZCEP is excellent advice with great prioritization of interventions in this case.

I don't think the chances of finding a patient in a rythem as described is very likely at all. But we can all appreciate the thought process behind your question and wanting to know more. Good for you for wanting to expand your knowledge as much as possible. Keep up the good work.

Shane

NRMET-P

[vs-eh?]

Rate >175 and narrow QRS would lead me to believe hypovolemia, so a fluid bolus would be in order. Because the patient is pulseless, cardioversion would be indicated. Need to treat the rate first.

Defib to stop the tachycardia, consider an antidysrhythmic to keep it slowed down, replace volume, look for ECG changes and drug use history.

Sorry I may be reading this wrong again. Are you saying pulseless as in no palpable pulses, but not in arrest? Or are you saying pulseless and apneic (i.e. arrested)?

So if you come across a patient in a narrow complex tachycardia > X rate who has arrested you would do a synchronized cardioversion on them?

I agree that at a rate of 175 BPM it will be hard to tell v-tach from SVT.

This would go with the above. Fair enough that narrow complex tachycardia > X rate could be VT, you obviously don't do a 12 lead on an arrested or unstable patient. But in the case of an arrest, you treat as a VT arrest and defibrilate, not cardiovert...there is a difference.

And besides that argument could be used for any rhythm over X rate, though pathological re-entry rhythms in my experience are generally intrinsically faster than VT can be at times.

[AZCEP]

Sorry I may be reading this wrong again. Are you saying pulseless as in no palpable pulses, but not in arrest? Or are you saying pulseless and apneic (i.e. arrested)?

So if you come across a patient in a narrow complex tachycardia > X rate who has arrested you would do a synchronized cardioversion on them?

Whoops! Semantic error on my part.

Pulselessness associated with tachycardia needs treated with electricity, and quickly. The way it was explained to me by Dr. William McConnell was to treat the rate, then the rhythm, then the container/volume.

Local recommendations may vary.

[Punisher]

Because the patient is pulseless, cardioversion would be indicated. Need to treat the rate first.

No offense, but this doesn't seem to make a lot of sense.....at least in the case of overt hypovolemia. If they are in a physiologically appropriate rhythm (extreme sinus tach) as a compensatory mechanism, two things- one you are unlikely to "convert" them into a slower rhythm....except perhaps an IVR or asystole because of interrupting whatever low level of perfusion maybe occuring during the EMD. And yes, there is often some level of cardiac contraction involved with this- next time you are in the ED and they are coding someone in EMD, watch and you probably see them put up the ultrasound probe on the patient's chest to check for cardiac contractility.

Personally, this would be one of those cases where fluid boluses would seem indicated along with aggressive but appropriate vasopressor therapy, at least more so than electrical intervention. But as someone said, local interventions may vary. I'm going to post this to another forum I belong to and see what the EM docs suggest.

The other point I have is the suggestion of giving calcium channel blocking agents or beta blockers to arrest patients- are you three stops from West Ham? That might (MIGHT) slow the rate down, but once again- the underlying problem in many cases will still be present, and also is going to complicate maintaining cardiac output and tissue perfusion by reducing vascular resistance. IF the patient survives and obtains ROSC, it would be a further complication probably requiring higher doses of pressor agents to maintain a functional BP.

[vs-eh?]

I agree with what Punisher wrote.

I think we may be getting caught up somewhere in semantics, treatments for various tachydysrhymias, and what exactly "pulseless" means (i.e. dead or not dead just can't feel a pulse d/t hypotension)...

You obviously do not treat a extremely tachycardic patient with rate control drugs/cardioversion/defib if there is strong clinical evidence of hypovolemia/dehydration. That being said if I saw a dead patient with a narrow complex tachycardia at a high rate I would be looking at hypovolemia to be high on my list of differentials and would treat accordingly (with volume/epi/vasopressin and not electricity). If how ever the patient is not presenting clinically (as much as you can tell) with evidence of volume loss, etc...Then perhaps you could call it VT and treat it as such.

It becomes a fine line I guess at times and a chicken or egg thing...Tachy d/t hypovolemia or hypotensive d/t tachy...

Remember, it all comes down to how you can rationalize it to those men and women with the big M.D. after their name that allow you to practice.

[firefighter523]

So, anyway, I hope I didn't miss anything in this post. My two cents on this is, PEA is "ANY" rhythm without a pulse EXEPT V-fib and V-tach, and obviously asystole. PEA, regardless of rate, should be treated with fluids, fluids, fluids, along with Epi, and possibly Atropine. You can also think about 2 to 4 mg/kg of Calcium Chloride, also some Bicarb, along with a bilateral thoracostomys. Remember those H's and T's. You have nothing to lose if it is late in the code, try everything.

[TechMedic05]

No offense, but this doesn't seem to make a lot of sense.....at least in the case of overt hypovolemia. If they are in a physiologically appropriate rhythm (extreme sinus tach) as a compensatory mechanism, two things- one you are unlikely to "convert" them into a slower rhythm....except perhaps an IVR or asystole because of interrupting whatever low level of perfusion maybe occuring during the EMD. And yes, there is often some level of cardiac contraction involved with this- next time you are in the ED and they are coding someone in EMD, watch and you probably see them put up the ultrasound probe on the patient's chest to check for cardiac contractility.

Personally, this would be one of those cases where fluid boluses would seem indicated along with aggressive but appropriate vasopressor therapy, at least more so than electrical intervention. But as someone said, local interventions may vary. I'm going to post this to another forum I belong to and see what the EM docs suggest.

The other point I have is the suggestion of giving calcium channel blocking agents or beta blockers to arrest patients- are you three stops from West Ham? That might (MIGHT) slow the rate down, but once again- the underlying problem in many cases will still be present, and also is going to complicate maintaining cardiac output and tissue perfusion by reducing vascular resistance. IF the patient survives and obtains ROSC, it would be a further complication probably requiring higher doses of pressor agents to maintain a functional BP.

In an extremely hypovolemic patient, to treat the rate: Whouldn't we treat with fluid boluses? I don't know if I'm interchanging words, but treating a rhythym doesn't have to be with true 'medications' - And use things like oxygen and fluid.

Maybe I missed what you were trying to say, as well.

[fiznat]

Okay. i think you are having some confusion. Actually, most rates even of 175 (sure it is SVT NOT V-Tach ? Can you really see those P waves at 175 ? ) it may have a pulse.. just because the electrical rate is 175 there still maybe perfusion of .. 60.. 40.. etc.. That is why it is so important to take pulses, not just the reading the monitor.

Perhaps your instructor was saying a narrow complex tachycardia without a palpable pulse but not actually in arrest?

While I realize that the differentiation between a very tachy SVT and V-Tach in this patient would be difficult in the field, the question I'm asking is built around the assumption that the patient is indeed in a supraventricular tachy rhythm and has *no* pulse. I'm specifically asking about a PEA SVT, so yes I'm sure its not VT :wink:

Defib to stop the tachycardia, consider an antidysrhythmic to keep it slowed down, replace volume, look for ECG changes and drug use history.

This is mostly what I am thinking. Fix the rate, THEN go after causes (5 H's, 5 T's). ...Seems like we dont want to treat this like your regular old PEA, as going to epi right away is a bad idea- and jumping right to causes doesnt make sense cause the rate needs to be fixed beforehand. Perhaps this is why my instructor said that "it cant be PEA if the rate is over 150?" ...Because you cant begin following a PEA path of treatment until that rate comes down to something reasonable.

So if you come across a patient in a narrow complex tachycardia > X rate who has arrested you would do a synchronized cardioversion on them?

So the answer to this question is yes?

If they are in a physiologically appropriate rhythm (extreme sinus tach) as a compensatory mechanism, two things- one you are unlikely to "convert" them into a slower rhythm....

My understanding is that rates above 150 are NOT compensatory mechanisms. Sinus tach is one thing, a SVT at 170 or more is too quick to compensate for anything- it is it's own problem. Is this why everyone is leaning towards hypovolemia as a cause? Fluids I imagine are still probably a good idea, but why is hypovolemia such the popular choice?