Treating PVC's

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Permalink Reply by blair4630 on November 1, 2009 at 2:01am

If the PVC's are not perfusing, then even if they were not replaced by sinus beats, the total cardiac output would be unchanged (remember CO=HRxSV).

That being said, look at what the ventricular beats are. If they are true PVC's, then yes, a antidysrhythmic may be appropriate, as knocking it out may allow the sinus node to continue on a normal rhythm, which is continual interrupted and reset by PVC's.

However, make sure they are premature...if there is a pause which is longer than the R-R interval, then these are not premature, and may actually be ventricular escape beats, due to sinus pause, block, or arrest. In this instance, it may not be the best thing to knock out lower level pacemakers (ie AV node, ventricular foci), as the SA node may be in trouble and not working properly.

Hope this helps, I'm sure I'm not thinking of everything there is to say on this matter. There are some great posters on this site for cardiac questions, I'm sure they will chime in over the next day or two.

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Permalink Reply by Jonathan Gilliam on November 1, 2009 at 5:49am

First I want to ask, what was your rate on the monitor? My comments are based on the rhythm being 40.

Ditto on the ventricular escape beats. Remember the intrinsic rates for your different pacemaker sites. SA node is 100-60, AV Junctional is 60-40, Ventricular rhythm 40-20. Another aspect to look at is what exactly the underlying rhythm is. Is it a sinus brady, or is it something else? With a rate down to 40, I doubt it's a sinus rhythm, so we're either looking at a low junctional rhythm or a ventricular rhythm, or maybe even an AV block. Look at the relation of P waves to QRS complexes. What is the ratio, and are they associated? What does the P wave and the QRS complex look like? So, since the patient is symptomatic, and is bradycardic, I'm assuming that what you see as PVC's are really ventricular escape beats. This patient would need TCP. As blair4630 mentioned, Lidocane given with these beats will knock out what bit of cardiac excitability is left and lead to cardiac arrest. With Atropine, it only works if the cause of the bradycardia is increased vagal tone. So, if you suspect a bradycardia is being caused by increased vagal tone, go ahead and try it, but don't delay on the TCP.

Now, let me run on with assumption number two. You have an underlying NSR with either multiple premature, ectopic QRS's or runs of V-Tach. If this is the case then yes, Lidocane is appropriate. Just remember to be ready to defibrillate if necessary. I'd place the combo pads on the patient just in case electrical therapy is necessary. Follow your V-Tach with a pulse protocol (either Lidocane or Amiodarone is appropriate in this case, depending on your service). Push a loading dose, hang a drip and rock on, just remaining vigilant that the patient doesn't deteriorate in to an arrest.

Hope this helps some. Just remember, when in doubt, consult the textbook. If that doesn't work, consult your instructor. Don't trust Google for medical searches, use something like MedScape. It's free to register, and has a wealth of information. This stuff will come to you, just keep at it.

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Permalink Reply by dr-exmedic on November 1, 2009 at 2:50pm

The other consideration is that it isn't healthy hearts that have PVCs. Treating with lido without searching diligently for the underlying cause is a little like giving Tylenol to someone with bacterial pneumonia--only in this case, actually worse, because the Tylenol won't affect your immune cells, while lidocaine will have its effect on healthy cells as well as the ectopic focus. In this case, you might be better off getting the underlying rhythm to go faster (i.e. atropine or pacing), as already noted--knocking out the PVCs will not automatically get the heart to fill the space with regular beats.

Also, it's hard to say what a "non-perfusing" PVC is without having an art line in. Sure, you may not be getting a pulse, but that doesn't mean you're not getting any forward flow--just not enough to feel.

As for searching, Google is OK (I use it all the time) but you have to be very, very careful about what links you end up following. You'll probably get a higher proportion of useful links from Google Scholar.

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Permalink Reply by Rob Theriault on November 1, 2009 at 3:01pm

Without a more complete picture it's difficult to judge but I am inclined to say no, don't treat the PVCs. Here's why:
1. PVC are generally a symptom of some underlying cause such as cardiac ischemia (variety of causes).
2. I would ask why is the patient bradycardic (if indeed he is) and condider treatment of the bradycardia
3. The heart rate is based on the pulse and not the cardiogram
4. I'd like to see the rhythm you're describing but I suspect the PVCs are in fact perfusing. Look at the distance between the R wave preceeding the PVC and the PVC. If the difference is equal to a heart rate < 150 then the ventricles likely have adequate filling time to produce output.
5. Lidocaine works best on ventriculr ectopy due to myocardial ischmia - amiodarone would be a better choice provided the patient is hemodynamically stable....but again I would not likely treat the PVCs at all in the case you described.
6. antiarrhthmics are only used to treat ventricular ectopy of they are occuring with such frequencey that they are are the root cause of hemodynamic compromise.

Hope that helps.

cheers
Rob (my blog)

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Permalink Reply by Jonathan Gilliam on November 1, 2009 at 3:13pm

Never even looked at Google Scholar, I'll have to check that out some time.

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Permalink Reply by Rob Theriault on November 1, 2009 at 4:25pm

...just to add to my previous comments....If you remove the PVCs from what might appear to be an underlying bradycardia, you can replace the PVC with a normal QRS that would fall exactly between the QRS wave before the PVC and the QRS after the PVC. This is assuming that the PVC is followed by a compensatory pause which is the case in most PVCs. In this case the heart rate without the PVCs would be normal.

I describe a dysrhythmia that is virtually identical to your case in my workbook and on my blog under "PVCs in various patterns". Just bear in mind that at one point in the narration I suggest that if you remove the PVC from the what appears to be a "tachycardic" rhythm...what I meant to say was "bardycardic".

cheers
Rob (Paramedic Tutor)

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Permalink Reply by Ben Waller on November 1, 2009 at 5:07pm

Rob, It's possible that may occur, but it's equally possible that you can just suppress the PVCs without a corresponding increase in heart rate. How is that helpful? It makes more sense to treat the underlying rhythm, which often resolves the PVCs without pharmacological intervention.


Without both seeing the patient and a look at the rhythm, it's going to be difficult to tell the difference between a simple PVC and ventricular escape beats. In the absence of more information, I believe it's more helpful to treat the bradycardia and to avoid treating PVCs that may spontaneously resolve if we can get the rate to a normal range.

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Permalink Reply by Rob Theriault on November 1, 2009 at 10:43pm

Hi Ben,
If these are in fact PVCs you can rest assured that intrisic beats will surface once the PVCs dissapear. We know that when there's a compensatory pause that this occurs because the ectopic depolarizes the SA node and resets the timing of the SA node. If these were inerpolated ectopics of escape beats that would be a different story. I assume, without the luxury of seeing the rhythm Derek describes, that he's referring to PVCs and and not escape beats. But in either case, and given the limited info we have to go on, I wouldn't treat the ectopics.....especially of course if they were escape beats....I think we're more or less on the same page.
cheers
Rob

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Permalink Reply by Ben Waller on November 1, 2009 at 11:43pm

Rob, thanks for clarification, and we are indeed on the same page. The norm is still "increase the rate" and see what happens with the PVCs prior to administering anti-arrythmics.

The emergency physicians and cardiologists here are increasingly reluctant to treat PVCs with antiarrythmics, too.

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Permalink Reply by Wes Seale on November 1, 2009 at 11:43pm

As others have said, be very cautious of treating a PVC at face value without thought to what is causing it. In this case lets look at the rate first. Is the rate drug induced (digoxin, beta blocker)? Increased parasympathic tone from a neurological insult or vagal stimulation? Are they infarcting the SA node? What is the underlying rhythm and is a block present (AVB, BBB, fasicular blocks)? A PVC is caused by myocardial irritability, typically some sort of ischemia, but can also be related to electrolyte imbalances and foreign bodies in the right ventricle such as a fractured or dislodged pacer wire or a PA cath that has floated back into the right ventricle. If someone has significant coronary artery disease (enough to cause a block with an associated rate in the 40s) it is likely that they are hypoperfusing the myocardium, causing the ischemia and irritability. Often simply increasing FIO2 will decrease or eliminate ectopic beats.

Lets look at this another way. What is going to kill the patient first- symptomatic bradycardia or the PVCs? More than likely the hypoperfusion and poor cardiac output of the bradycardia. Fortunately ACLS has a great algorythm for that. After oxygen, 12 lead, pacer pads and IV access I would consider 0.5mg of atropine if suspecting increased parasympathic tone. I would try dopamine for its chronotropic effect in someone with a functional pacing node or go straight to TCP in a high level block.

As the good doctor said, not all ectopic beats are non-perfusing. A premature ventricular contraction (PVC) may still eject blood and cause forward motion if the ventricles have had adequate filling time. Of course this will not be as efficient as a normally time contraction. Next time you do a clinical in ICU or ER watch a arterial or pulse ox waveform on a patient with PVCs. You will often see an associated waveform and even a compensatory pause. If the ectopy is so severe that it is the root of the problem then absolutely treat with an anti-arrythmic. Remember that the three most commonly used in EMS (amiodarone, lidocaine and mag sulfate) will often cause some drop in blood pressure. Keep that in mind and have your flexible treatment plan worked out.

Good question and keep up the critical thinking. It will serve you well.

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Permalink Reply by Wes Seale on November 2, 2009 at 12:33am

Just re-read what I wrote. Looks like I invented a new word. Meant to say parasympathetic not parasympathic.

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Permalink Reply by Chance Gearheart on November 2, 2009 at 7:47pm

What blair said, However: The PDR and every drug guide I have consulted has listed Lidocaine as a no-no when it comes to bradycardia. The reason being is those PVCs may actually be part of an underlying escape rhythm that may be attempting to compensate for AV/SA node failure, or blockage at the fiber junctions. Without invasive monitoring, (i.e. art line/swanz-ganz)it's nearly impossible in the field to differentiate non-perfusing with compensatory PVCs in bradycardia by just checking a peripheral pulse with reliablity, atleast in my meaningless opinion. Administering lidocaine to block the electrolyte channels can lead to a lethal, irreversable arrest when you take away that, that would require pacing to even have a chance at patient survival. It's better to worry about what's causing the problem first: Low HR and Hypoxia/ischemia/irritation of the heart. Remember your Hs and Ts. Bring the heart rate up, and treat the ischemia, and then see where you are at. Once you get the heart rate up, and the PVCs are still ongoing, then consider treating with lidocaine/amidoerone drip. You'll kill them faster with lidocaine over treating the bradycardia first - There is no field antidote other than pacing and diesel in liberal amounts, and if you block those sodium channels, pacing may not even work. By bringing up the heart rate, you might even increase cardiac output, and with high flow oxygen therapy to increase oxygen loading, you might even push enough oxygenated blood through the coronary arteries to eliminate your PVCs or decrease their frequency enough that lidocaine can be defferred until expert consultation.

Also, in cases like this, seek expert consultation early. This may not even be purely cardiac- PVCs can also be caused by traumatic injury to the myocardium or endocardium, endocarditis/pericarditis, drug overdoses, or electrolyte problems. If you have PVCs warrenting antidysrhythmic therapies, you need to be transporting rapidly to an intervention-capable facility and activating a cardiac team.

You always have your indications for Lidocaine/Amioderone Drip for PVCs- R-On-T Phenomenon, Frequent (>6 min) or multifocal PVCs, bigeminy or trigeminy, or couplet/triplet/etc; or symptomatic chest pain with PVCs (as evidenced by poor perfusion, severe ischemic chest pain, pulmonary edema etc) but always remember - Low heart rate is ALWAYS an absolute eliminator until you take care of that first.

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