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?)