PVC's, APC's No Treatment?

  1. We used to give Lidocaine for VPC's, especially if there was bigeminy, trigeminy, or even more frequent ectopy.
    I don't remember too much concern over APC's unless someone was in flutter and O2 was low. A fib got ablation or cardioversion. Now it seems very much nothing to treat. Same at your place?

    These days it seems that a good stress test and normal Holter, except for the above issues, means go home, good boy, good luck.

    Is it like that at your facility?
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  2. 6 Comments

  3. by   MunoRN
    Treatment generally isn't indicated for PVC's, this can be a fairly normal finding in the general population. Depending on the full clinical picture, ventricular ectopy generally indicates further assessment; electrolytes, cardiac function (echocardiogram), etc. Lidocaine is more of a last resort treatment, it's usually only used when ventricular ectopy is unstable/symptomatic and refractory to other treatments such as electrolyte optimization, cardioversion, and amiodarone. Individual paroxysmal PVCs, pairs, and often even bigeminy is not symptomatic, it's not unheard of for a patient to be in a persistent ventricular rhythm and tolerate it just fine, I've had patients in a persistent V-Tach that are just hanging out watching TV, this is often possible with a slow ventricular rhythm.
  4. by   CCU BSN RN
    With advances in medicine, heart failure patients are living longer. They have a lot of ectopy because their hearts suck.

    I'm not saying you shouldn't get lytes, and EKG, and keep your K>4 and Mg>2, and give your BB if it's indicated.

    Consider a few things about Lidocaine: can put your patient into VT and literally cause a code while you're pushing it. Also, lidocaine toxicity isn't too fun when they've been on a gtt for too long.

    Amio instead? Well, that's toxic to literally every organ, blows veins quicker than you can demand a central line, and has a half life of approximately 4 nuclear winters.

    A few ectopic beats (or even sustained bigeminy) in a mentating patient with otherwise stable vitals? Kind of seems like asking for trouble to aggressively treat that, don't you think?
  5. by   2210485
    Quote from CCU BSN RN
    With advances in medicine, heart failure patients are living longer. They have a lot of ectopy because their hearts suck.

    I'm not saying you shouldn't get lytes, and EKG, and keep your K>4 and Mg>2, and give your BB if it's indicated.

    Consider a few things about Lidocaine: can put your patient into VT and literally cause a code while you're pushing it. Also, lidocaine toxicity isn't too fun when they've been on a gtt for too long.

    Amio instead? Well, that's toxic to literally every organ, blows veins quicker than you can demand a central line, and has a half life of approximately 4 nuclear winters.

    A few ectopic beats (or even sustained bigeminy) in a mentating patient with otherwise stable vitals? Kind of seems like asking for trouble to aggressively treat that, don't you think?
    Respectfully disagree.. Aside from the elevated PVC burden that sustained Bigeminy can create, and subsequent risk for Electrically mediated cardiomyopathies down the line, Bigeminy alongside its cousins, couplets, triples, trigemini and quadrigeminy are all ominous signs for our patients.

    To better understand why it pays to ask, WHY are we in Bigeminy? PVC's like any other electrical phenomenon often have an underlying anatomic or structural point of origin. What sort of anatomy causes patterns of PVC's.

    The Answer: Re-Entry.. often in these sorts of situations anatomic sites of slow and fast conduction and native anatomy/ scar tissue are forming a circuit. The Bigeminal PVC can therefore be somewhat akin to an Echo Beat in AVNRT. The concern here of course being that these sorts of patterns could be the early indicators of re-entrant substrate formation that could support VT in the future. This is of exceptional concern in those patients that are at higher risk for VT in the first place (NYHA Class II+, HOCM, ARVD, MI, Surgical patients etc.)

    This hypothesis has been supported by studies that have suggested increased risk for VT development (Stable or unstable) in these patients.

    In my opinion the best management strategy for PVC's would be as follows:

    1. Patients with a documented burden over 15% (Symptomatic or not) receive aggressive medical management, with ablation to follow in the event of unsatisfactory control.

    2. Conservative medical management for symptomatic patients under 15%, with ablation to be considered only in extreme cases (prolonged impact on the patients mental health and ADL). To give a more specific example I've heard of patients coming in to appointments and break down into tears, saying they feel their life is unmanageable, they've been fired from their job and are contemplating suicide if they can't get their PVC symptoms under control.. I mean that's kind of hard to argue with. Just burn it.

    3. Aggressive management of all documented cases of patterns of PVC's as well as couplets or triplets, with the primary endpoint being the suppression of the possible Re-Entrant circuit as confirmed via 24 Hour Holter, Ablate if refractory. In my opinion regardless of patient symptoms here there is enough of a risk to justify this strategy.

    4. Prompt ablation in high risk patients with structural heart disease/ more advanced HF (NYHA III+ or EF <35%), where concern exists with regards to PVC burden contribution to hemodynamic status and disease progression.

    In terms of Medical Management, I think the progression here is pretty well established. Beta-Blockers are the first line. If unsuccessful there Flecainide has some good results, quite a few cardiologists here like going the Calcium Channel Route as well.

    Amio of course would be a bad plan in a lot of the higher risk patients, last thing you'd need is Pulmonary Toxicity in someone whos already fluid overloaded and in CHF. It can be a great option for the Bigeminy or Couplet type of patients who are perhaps a bit younger and absolutely refuse to pursue ablation. Preferably though if you get to the point where Amio is the drug of choice, you're probably already to the point where the Ablation will yield better results with comparable risk.

    In terms of acute management, not necessarily of pvc's per se but of arrhythmia in general, don't forget you always have ibutilide as an option to consider as well. Its a class III, without any of the nasty cosolvents, iodine concerns and toxicity risk of amio and studies have shown its actually more effective at terminating some of the same arrhythmias. What's more you dont have to worry about loading doses and infusion rates and pesky drug calcs, it's a straightforward iv push type of scenario.

    At my facility ibutilide has largely replaced amiodorone as the mainstay pharmacologic option in our EP lab. Of course the principle downside here being its low oral bioavailability. I can load a patient on amio and send them home with oral amio, no such option exists with ibutilide (house calls anyone?)
    Last edit by 2210485 on Nov 14
  6. by   Kooky Korky
    Wow, you guys really know your stuff! Thanks so much.
    The world has certainly taken a couple of spins since I worked Tele or ICU.

    Thanks for sharing your knowledge and experience. I will be looking up
    the meds and various abbreviations you all name.
  7. by   Susie2310
    Quote from 2210485
    Respectfully disagree.. Aside from the elevated PVC burden that sustained Bigeminy can create, and subsequent risk for Electrically mediated cardiomyopathies down the line, Bigeminy alongside its cousins, couplets, triples, trigemini and quadrigeminy are all ominous signs for our patients.

    To better understand why it pays to ask, WHY are we in Bigeminy? PVC's like any other electrical phenomenon often have an underlying anatomic or structural point of origin. What sort of anatomy causes patterns of PVC's.

    The Answer: Re-Entry.. often in these sorts of situations anatomic sites of slow and fast conduction and native anatomy/ scar tissue are forming a circuit. The Bigeminal PVC can therefore be somewhat akin to an Echo Beat in AVNRT. The concern here of course being that these sorts of patterns could be the early indicators of re-entrant substrate formation that could support VT in the future. This is of exceptional concern in those patients that are at higher risk for VT in the first place (NYHA Class II+, HOCM, ARVD, MI, Surgical patients etc.)

    This hypothesis has been supported by studies that have suggested increased risk for VT development (Stable or unstable) in these patients.

    In my opinion the best management strategy for PVC's would be as follows:

    1. Patients with a documented burden over 15% (Symptomatic or not) receive aggressive medical management, with ablation to follow in the event of unsatisfactory control.

    2. Conservative medical management for symptomatic patients under 15%, with ablation to be considered only in extreme cases (prolonged impact on the patients mental health and ADL). To give a more specific example I've heard of patients coming in to appointments and break down into tears, saying they feel their life is unmanageable, they've been fired from their job and are contemplating suicide if they can't get their PVC symptoms under control.. I mean that's kind of hard to argue with. Just burn it.

    3. Aggressive management of all documented cases of patterns of PVC's as well as couplets or triplets, with the primary endpoint being the suppression of the possible Re-Entrant circuit as confirmed via 24 Hour Holter, Ablate if refractory. In my opinion regardless of patient symptoms here there is enough of a risk to justify this strategy.

    4. Prompt ablation in high risk patients with structural heart disease/ more advanced HF (NYHA III+ or EF <35%), where concern exists with regards to PVC burden contribution to hemodynamic status and disease progression.

    In terms of Medical Management, I think the progression here is pretty well established. Beta-Blockers are the first line. If unsuccessful there Flecainide has some good results, quite a few cardiologists here like going the Calcium Channel Route as well.

    Amio of course would be a bad plan in a lot of the higher risk patients, last thing you'd need is Pulmonary Toxicity in someone whos already fluid overloaded and in CHF. It can be a great option for the Bigeminy or Couplet type of patients who are perhaps a bit younger and absolutely refuse to pursue ablation. Preferably though if you get to the point where Amio is the drug of choice, you're probably already to the point where the Ablation will yield better results with comparable risk.

    In terms of acute management, not necessarily of pvc's per se but of arrhythmia in general, don't forget you always have ibutilide as an option to consider as well. Its a class III, without any of the nasty cosolvents, iodine concerns and toxicity risk of amio and studies have shown its actually more effective at terminating some of the same arrhythmias. What's more you dont have to worry about loading doses and infusion rates and pesky drug calcs, it's a straightforward iv push type of scenario.

    At my facility ibutilide has largely replaced amiodorone as the mainstay pharmacologic option in our EP lab. Of course the principle downside here being its low oral bioavailability. I can load a patient on amio and send them home with oral amio, no such option exists with ibutilide (house calls anyone?)
    I'm guessing that the poster that you replied to may have been referring to patients who are elderly with significant heart disease and possibly multiple serious co-morbidities for whom medical management of PVC's could pose more problems; for instance patients for whom beta-blockers are contraindicated because their heart rate is too slow i.e. a resting heart rhythm of severe bradycardia with one or more bundle branch blocks who may need a pacemaker eventually, who also experiences runs of a wide complex tachycardia/other tachyarrhythmias. If this is the kind of situation the poster was referring to I can see their concerns. He/she also made the point, as I understood it, of a few PVC beats not warranting the risk of aggressive treatment when the patient is otherwise stable, which to my mind, as a nurse, makes sense especially if the above patient scenario applies.

    Would you be willing to tell us your clinical background, and could you provide a source on the internet so that I (and others who are interested) could learn more about the management strategy for PVC's that you mentioned?
    Last edit by Susie2310 on Nov 14
  8. by   2210485
    Quote from Susie2310
    I'm guessing that the poster that you replied to may have been referring to patients who are elderly with significant heart disease and possibly multiple serious co-morbidities for whom medical management of PVC's could pose more problems; for instance patients for whom beta-blockers are contraindicated because their heart rate is too slow i.e. a resting heart rhythm of severe bradycardia with one or more bundle branch blocks who may need a pacemaker eventually, who also experiences runs of a wide complex tachycardia/other tachyarrhythmias. If this is the kind of situation the poster was referring to I can see their concerns. He/she also made the point, as I understood it, of a few PVC beats not warranting the risk of aggressive treatment when the patient is otherwise stable, which to my mind, as a nurse, makes sense especially if the above patient scenario applies.

    Would you be willing to tell us your clinical background, and could you provide a source on the internet so that I (and others who are interested) could learn more about the management strategy for PVC's that you mentioned?
    Of course! My clinical background is that of a tech not a nurse, currently studying and working in the EP lab. Prior to this my background was in intensive care, where i took a liking to Cardiac Pacing and decided to go back to hitting the books.

    In terms of a source I would actually recommend a book if thats ok. "Clinical cardiac electrophysiology in clinical practice" by David T Huang ISBN-13: 978-1447154327. Its pretty short, 2 or 3 days to read, affordable and concise and would help gain a solid understanding of electrophysiology... Its certainly been a wonderful tool for figuring out whats going on in the ep lab.

    In terms of online resources theres not alot of 1 stop shops.. Scholarly articles are out there but theyre a bit tough to decipher, i could track some down later if you'd like though.
    Last edit by 2210485 on Nov 15

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