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Yep acls manual, followed by critical csre nursing made incredibly easy and hemodynamic monitoring made incredibly easy. EKG skills need to be on point, get a good practice workbook and get started! Lastly consensus statements! 1 per day, everything relevant to your patient care starting on page 1, until repeat topics start showing up. They almost always include the latest and greatest advice on medical management. You need to know your drugs, know why they are given and what the best option is. JACC On that same note, download a pharmacology app on your phone. Research every new drug you come across, write them down, make flashcards etc. If you still have to check a reference to know if an infusion is incompatible, or if there are drug interractions you need to be making flashcards.

How in depth do you want to go? If you wanna get into the weeds and don't mind some intense reading, I found this book for only $18! I cant vouch for the distributer/source however, it just came up on my shopping results. I own a copy and it goes deep into the pathophysiology, helped alot! It does not go as deep into some of the practical elements however (pearls for a provider). Unfortunately this is a book that could take a long time to swallow: Cardiac Nursing Susan L Woods Isbn 97878179286 7817928 If you desire a book thats primarily focused on practice and interventions and not so much theory I have 4 recommendations: (Longer but easy to grasp conceptually, 1 - 2 weeks to read cover to cover) I am posting a link to the 7th edition, the most current is the 8th. I am doing this because honestly the changes are not significant enough to warrant spending the extra money on the book, used copies as cheap as $25. I have read all of the past 3 or 4 editions of this, I own this version. Some practices have changed a bit, but nothing that will necessarily bring harm to a patient by utilizing this edition.: Grossman's Cardiac Catheterization, Angiography, and Intervention: Donald S. Baim MD FACC: 78175567: Amazon.com: Books (Extremely short and easy, Was able to read cover to cover in 2 days) I own the newer edition, I have not seen the older one.. However, again, this will suffice I am sure. At the time of this post someone was selling one for $6: Textbook of Clinical Echocardiography 3rd edition: Catherine Otto: Amazon.com: Books (Easy and short, I read this in 1 day) Older edition selling for $5. Advanced EKG... Alot for extremely detailed information. Criteria and EKG findings you likely have never seen before. I know it's often easy to think "I've seen my share of EKGs", however I can not stress enough that this book is NOT your 'Dubins'. I'll even give an example of the type of differences here: Dubins wll teach you things like this: "A normal PR interval is .12- .20 seconds" This book will teach you things like: "V1 with RBBB pattern morphologic criteria presents as a rsr' in v1 withOUT the presence of a negative or 'true' S deflection." You won't be bored and you're almost certain to learn new things about EKG's. This book will absolutely help elevate your EKG skills, in fact a solid grasp on this book in addition to the next recommendation, honestly puts you at a level consistent with expectations of nurses in the EP Lab: Cardiac Arrhythmias: Practical Notes on Interpretation and Treatment: David Bennett: 9783487316: Amazon.com: Books (Extremely short and easy.. I read this in 1 day) at $46 this book is the most expensive I am listing! But its worth every penny! With a good rainy day worth of reading you will have a grasp on clinical electrophysiology to the extent where you can communicate with an Electrophysiologist without the burden of learning irrelevant details and procedure you will never see in your unit. A new publication designed to give non EP's a 'crash course' in the field; it is the most straightforward and streamlined outline I've read so far. It is a friggen AMAZING publication. 10/10 Clinical Cardiac Electrophysiology in Clinical Practice: David T. Huang MD, Travis Prinzi MD: 9781447154327: Amazon.com: Books (Long and difficult... "The Bible" of cardiology) older edition used running for $25. Its a textbook of cardiology... Goes without saying it will probably take a minute to read this thing fully. As a reference to fill in gaps left hy other suggestions though its great! Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, Single Volume, 8e (Heart Disease (Braunwald) (Single Vol)): Peter Libby MD PhD, Robert O. Bonow MD MS, Douglas L. Mann MD, Douglas P. Zipes MD: 97814164161: Amazon.com: Books Altogether these suggestions will run 115 + probably 35 S&H However for a $150 price tag (typically the price of a single book) you could leave with a wealth of cardiovascular knowledge. P..S All recommendations are considered to be 'Standard Curriculum' in training programs designed to train Cardiology Fellows, Cardiology Nurses and NP's and Cardiovascular Techs. They cover all of the topics mentioned by charge and the authors are considered the subject matter experts and are panelists that hold a good deal of weight at conference. You're in good hands with these.

If you're still looking for this stuff I would recommend 2 books for you, a workbook with practice strips and an instructional book: I found a copy of this first books last edition for only $6! Ill post a link, along with a link to the newer edition! For an instructional book on EKG interpretation, I have a great selection! This book is definately NOT your run of the mill 'Dubins'. It is designed for Cardiologists, Cardiac Nurses and Electrophysiology techs. It makes the assumption that you can already pick up a simple 12 lead EKG and interpret the Rhythm. It's this designed to introduce you to more advanced and intricate concepts that will aid in interpretation of real life EKG's at the level expected of a professional in the field of Cardiology. Sorry this is so long winded, I just wanted to stress the point a bit so it's not cast aside as "just another ECG guidebook". It can be found here: Cardiac Arrhythmias: Practical Notes on Interpretation and Treatment: David Bennett: 9783487316: Amazon.com: Books Or here: Bennett's Cardiac Arrhythmias: Practical Notes on Interpretation and Treatment: David H. Bennett: 97847674932: Amazon.com: Books For a workbook this is the best one! It has like.. 100 strips, each case being extremely complicated and reauiring as many as 15 answers.. Basicalky each EKG interpretation is a patient note. It comes with answers and explanations, usually 2 or 3 pages per ekg. It will keep you busy: The Complete Guide to ECGs: James H. O'Keefe Jr., Stephen C. Hammill, Mark S. Freed: 97812846634: Amazon.com: Books

I don't know the intricacies of Nursing, or how ya'll go about transfering. I do know what sort of expectations exist in the EP Lab however, and I don't see anything about that situation that would take away from your ability to perform in the EP lab. If you can work with Anesthesia patients, can manage conscious sedation and are willing to learn you'll get along just fine. In fact you could almost go so far as to say that a surgical or PACU/Recovery Unit nurse would actually be the best fit for the job, as opposed to ICU. Maybe some,experience with Ultrasound and Pacing would be a plus? Not mandatory though, No matter how you cut it... The EP lab is going to be an entirely different experience from just about everything else in the hospital. Theres noone who can walk into an EP lab and say "Oh yeah, I can figure out how to use this equipment! Its similar to my last ward!". Everyone entering EP should expect to be walking into an entirely different experience.. If you're excited about being involved in a new frontier of medicine. If the idea of working on largely theoretical rationale, going in to cases with literally no expectation as to what you're about to find, what tools you need or what needs to be done excites you, welcome. If you don't necesarily mind coming to work without knowing whether you'll go home at noon or midnight, or having to manage patients without any sort of clear algorithm to follow, if all this sounds good to you; you qualify.

Same here... I frankly don't care who comes after me or what they have to say about it. In an Emergency I'll do my best to render aid. I answer to a higher authority at the end of the day. As a more spiritual person I am amply convinced that if something needs to get done in the interests of preserving human life and I know how to do it; failure to do so would earb a conseauence far worse then whatever the legal system can dish out. I am committed to preserving life... Even if they imposed a life sentence for rendering such life saving care, I'd do it.

Dang.. Old school. I actually had to review the HRS consensus on this, another thing we don't do here. Do you ever actually see these? It would seem only the cox-maze 4 with accompanying ablation is the way to go. Big stigma with Maze in general due to its history/ high morbidity. There's just so many skeptics and so few new cases in this corner of the world that I kind if just assumed at some point they gave up on it. Behind the curve I spose.

Nope, sounds about right. If the docs familiar with the patient, confident in the anticoagulation strategy and familiar with the burden and onset of the afib they should know if TEE is necessary. Those at greatest risk for embolism are people who go into AFib at home, without any measure of their burden and don't have/are not compliant with an antithrombotic strategy. Once they've had a TEE however, if you can verify that they only just recently went into AFib (past hour or so) you know it is unlikely they've developed anything new. If you did everything right and anticoagulated after cardioverting you'll feel even better than that! If they have a pacemaker you can see precisely how often they go into the rhythm and be even more assured! The only thing I didn't necessarily like is the choice of Dig. Dig gets alot of shade thrown at it, lots of complications, drug interactions, mediocre performance etc. It has its place, unfortunately that place is more like a very fine niche. Noteworthy here is that the patient was already on amiodorone, which is highly effective at suppressing afib but comes with the drawback of limiting further treatment options and risking toxicity. As we all know theres also that half life consideration. Once you give Amio you're pretty much committed. Personally I am more fond of Ibutilide and Propafenone for Afib. Amiodorone would be the third pick. As an augment to electric cardioversion Ibutilide has been studied as had a conversion rate of 95%. It has a half life as low as 2 hours. Plus its a single dose vial delivered by IVP, so there's no messy dosage calculations and infusion rates/loading doses. You just take the drug out of the vial, put it into the body and you convert to sinus. Doesn't get much better. Oral Propafenone is not as effective as oral Amiodorone, but the advantage of Amiodorone sits at around 5% in most trials (regardless of the endpoint). Not really a significant margin.. Half life of around 10- 35 hours vs like.. Months. Now there is an exception to this: Emergency treatment, or cases where treatment might be delayed in favor of another drug. Amio is king here and I am a big advocate of just diving in head first on this one. It's common, relatively cheap, well known by all the staff, can go home with the patient and most importantly; it has the highest conversion rate. Ibutilide isn't a drug that you see being used on the floor too much... At my facility its' use is confined to the electrophysiology lab. But hey, you know what you won't find in the lab? Amiodorone.. Whatever's locked in the crash cart.. Probably approaching expiration and buried in sone drawer.. Only place we keep amio. That's saying something there. So in conclusion: Some choices were probably made with the drugs that could be different, but all in all looks fine.

Is it routine for you guys to use Bival at your labs? Going through school they hammered it into us.. Haven't seen it used since... What sort of protocol to you use to select appropriate patients for bival vs the run of the mill Heparin strategy? Or is it routine? Heparin Induced Thrombocytopoenia is an indication of course but the real prevelance of the disorder is .7% - .9% of patients who have recieved heparin in the last 48 hours. Essentially the most likely scenario would be a longer term inpatient or home care pt with HIT. These vulnerable populations constitute a fraction of cath cases and within that fraction less than 1% will present. So if HIT is the sole criteria I can't imagine you'd give it too often..

Yeah what?! Agreed with offlabel.. Theres numerous problems that could be going on. Paced patients are supoosed to have suppressed ventricles when they're being paced, not VT. Even if they have an ICD, burst pacing and shocks are ALERTS.. Events that need a doctors attention. Furthermore if the patient goes into a 'short run' of VT more than 4 times in 24 hours thats technically a VT Storm. Its very ominous and important. If a nurse called a doctor and said something like: "Your patient is in VT storm, but he's got a pacemaker so I didn't think it was too important to let you know..." Someone will go after that nurses license.. And rightly so. It would be no different then saying "The patients potassium was down to 2.1 but the doc already ordered a K+ infusion so I assumed he already knew what was going on.." These just aren't the assumptions anyone should be making. Next time that sort of thing happends if you feel. That, for whatever reason the patient isnt getting the attention they need you pick up,the ohone and call the physician and tell him. Especially if this is a cards patient.. Even if you're wrong and it's nothing, even if it hurts someones feelings or insults the charge nurse or whatever. The safety of the patient takes priority! If anyone really wants to give you grief about it they should take it up with the hospital administrators, Board of Nursing, JCO.. Im sure they'd love to hear about how they don't like nurses communicating safety concerns because it hurts their feelings. That discussion would end great for sure.

Well, of course 8- 10- 8ms would be virtually impossible to determine in a 12 lead or even an intracardiac electrogram. Even a diagnostic ep catheter has a margin of error and at least some degree of limitation. If however you see like.. 80ms, 100ms, 80 ms variations: It could be escape if the morphology (shape) of the wave is different. Possibly 2nd degree avb, sinus arrest with non conducting escape. That's a possibility. It could also be a disease superior to the AV Node and/or SSS. Conduction Disease can occur just about anywhere along the conduction pathway. Marching out the P waves as you did is a good plan. If you have a longer strip or a long term monitor watching for patterns in the P waves can help make sense of it sometimes. If you have a PAC or a pathway you can have concealed conduction creating the phenomenon as well. So gathering information about potential interactions between ectopics or abberency is always useful, as is a thorough understanding of patient history. Unfortunately with situations such as these theres just so many options that it's pretty difficult to develop a concise algorithm. Once you get the basics down and you've seen enough if these recordings to know what things look like: The only way to advanceg with this stuff, imo, is to stop thinking about EKG criteria, and a simple block of 3 components (pri, qrs, tu) and start thinking in terms of Anatomy and Physiology and electricity. Instead of seeing a P wave and associating it with 'atria' bear in mind that the atria can be futher subdivided into inconceivably small units and that each of those units plays a role in generating an ekg complex. Not sure if that helps or not, just my 2 cents on it.

Different strokes for different folks. Some,management strategies opt for rate control ithers are more heavy on rhythm control. For the rate control folks pacemakers are great for when you wanna ablate the AV Node (cause a 3rd degres Block) and just pace the ventricle. For Rhythm control Pacemakers are great at fighting Heart Failure and keeping AFIB from returning. Here are some things to remember about AFib (general info): 1. Most pacemakers have 'mode switching' features these days. That means when the afib starts only the ventricular component paces. 2. AFib as a disease is part of the same pathologic process that leads to AV blocks and Sick Sinus Syndrome. The majority of the AFib cases you see will likely have one of these other diagnosis. Thus many if these patients will already have pacemakers for some other indication when they start developing a noteworthy AFib burden. 3. Once a patient goes into AFib there pacemaker can't do anything about it. The only treatments from there are drugs, cardioversion or simply letting the patient break on their own. 4. AFib Ablation is the LAST line of defense. The procedure is transseptal and has a high rate of complication and failure. Afib ablation are also the most taxing procedures in terms of time and resources. They take anywhere from 4- 12 hours to complete and require almost twice the normal staff. 30% of procedures will have at least some form of complication. 30% of patients will ses the procedure fail and afib return in the next 10 years. 5. Once a patient is converted out of AFib an atrial pacemaker may assist in keeping the region responsible for the AFib suppressed for a longer period. 6. Frequent PAC's are associated with an impending episode of AFib and can give a rough estimate of how long a conversion will hold. 7. Best drugs to manage AFib are (in order of aggression, and often risk): -Class 3 Anti-Arrhythmics: Amiodorone (high success rate, but risk of toxicity) Ibutilide (IV preparation only, very expensive, short supply but the only drug that's been studied and proven to be more effective than Amio. This drug also carries a lower risk of complication. It is the drug of choice in the EP lab.), Sotalol (oral preparations available, common in most hospitals, less risky than Amio. Drug of choice to accompany a synchronized cardioversion) - Class 1c Antiarrhythmics Speaking from anecdotal experience class 1c seems to work better at controlling both AFib in addition to Ventricular ectopy. Propafenone seems to be a good selection for AFib, but Flecainide works as well. Flecainide would probably be best for PVC control of the two. -Calcium Channel Blockers Diltiazem and Verapamil.. Both very popular choices in Afib management. Diltiazem is the big winner here, common, affordable, patient can take it home. - BetaBlockers The tic tacs of antiarrhythmics. Appropriate for patients with low burdens or who need Beta Blockers to treat other issues such as hypertension anyways. 8. Thrombus and Stroke is a big risk for these patients. Most cardioversions, if not for immediately life threatening indications, will get a Trans-Esophageal echo prior to conversion. The TEE is vastly superior to the transthroacic ultrasound at visualizing the atrial appendages, which are the primary location where these thrombus like to hide. Exceptions to the TEE may exist in patients who only recently went into AFib on an inpatient unit, or those with aggressive anticoagulation stategies (e.g. INR over 1.8 for a long period). Local protocol will likely dictate the best course here. 9. Patients who do not wish to maintain their present anticoagulation strategy, have contraindications or in whom antithrombotic appraches fail may elect to have a 'Watchman' device implanted. Watchmans are basically just 'screens' or filters that sit in the appendage and prevent clots from embolising into circulation. 10. Afib and Aflutter are often confused. Having a regular rhythm doesnt really matter.. What if Aflutter has variable conduction? What if the variation is only 30 ms? The easiest way to identify the difference is to look at lead V1. Measure the wave you see there, is it LESS than 200ms or .20 (5 small/1 big box)? If so, your patient is in AFib. 11. Proper pad pacement for a cardioversion for all ages is anterior-posterior (pediatric placement standard). First, shave the areas I am about to describe. Clean the surface well with alchohol (not chlorohexidine or iodine) prior to pad application. Place 1 pad on the anterior surface of the chest, just barely to the right of the sternum (sternal border). Place the other pad on the back just to the LEFT of the spine. It should not be sitting over the shoulder blade.. Avoid contact with thick bones as much as you can. Look at your patient, do they look Small/Medium, Large or Huge? Set the defib to 100, 150 of 200 accordingly. Sync to the R Wave. Have someone place a pillow on top of the anterior pad and apply about 25 pounds of force (push hard). Shock. If unsuccessful, step up to 150 for small or medium folks, consider augmenting with Sotalol or Ibutilide for Large guys before stepping up to 200. Massive guys should get chemical augmentation jf they have not already. A second attempt at 200 can be tried. After that you will have to apply another set of pads and use a second monitor to deliver 2 shocks simultaneously. This all assumes biphasic shocks are the standard. 12. Scariest Afib ablation complication is pulmonary venous stenosis. Always watch your pt carefully when recovering a patient post Afib Ablation. 13. Afib is associated with CHF as well. Many Afib patients will need biventricular or 3 lead pacemakers to maintain ventricular synchrony. 14. Most Afib with RvR isn't an immediate life threat, however there is 1 exception: Afib in patients with WPW or accessory pathways is an inmediate, life threatening emergency. If your patient had delta waves, and they develop AFib don't hesitate to call a Code Blue, a Rapid Response or the doctors personal phone or duty phone as the situation allows. Without the AV Node to block excess impulses theres a chance that the afib will conduct directly to the ventricles. Afib conducting to ventricles without delay = Vfib =death. Its extremely serious and needs attention. In terms of pacing, I saw something mentioned in this thread that reminded me of some more pearls: If you suspect issues with pacing it's probably a good idea to just go ahead and draw up: 1. CMP 2. Blood Gas 3. Lactate Drugs that improve thresholds for both pacing and defib/cardioversion would include Catecholamines (Epi/Norepi) and Corticosteroids (Cortisol/Solu-medrol). Never hearts to recommend these things to the doc if you guys are at a loss.

I got 7 boxes on that qt personally, maybe 8. That's 280 ms, at a 240 ms coupling interval. I still land at 525 ms. Theres not even 10 boxes in that qt.. If the true uncorrected Qt was that long there would already be r on t occuring, assuming we're looking at the same set. You are correct though, its all irrelevant, rapid decisions for the patient are the most important. It does raise the question though.. What can we do for this patients qt interval? Id argue treating underlying cause, be it pericardiocentesis in the case of a confirmed tamponade, or via synchronized cardioversion for an afib scenario is the best course. As for showing off that's not the intention, rather these discussions are good practice. Folks post some good scenarios on these boards. The goal isn't to just bring up the points solely with the intention of proving someone wrong, rather engaging someone with your level of experience genuinely challenges ones critical thinking and offers some great reminders.. For example today I was reminded to be more careful in measuring the longest qt instead of just eyeballing them. The complex you measured wasn't the one I measured, and it occured to me that I didn't take the time to run over all of them. Technically I couldn't tell you which is the longest and that is an absolutely incorrect approach to ekg interpretation.

Madness lol.. It astounds me that such a program exists. Not that its bad, just sort of unfair.. Theres alot of folks in the medical community who are deprived of degree completion or bridge opportunities. I may be one of the few here thats not actually a nurse by trade... Ive been trying to find a reasonable program that will allow me to pursue mathematical biology and bioinformatics online or computational biology online.. Not only is it impossible to find, but its impossible to even start. It baffles me that schools can bridge lpn to bsn online, but i can't find online 3 or 4 level mathematics online. What could a professor possibly require of a student that absolutely requires face to face attendence in a course dealing with theoretical math? Alot of friends working in fields such as medical physics, are running into the same struggle to get to the next level. Within cardiology even, the techs physically don't have an established bachelors program in existance.. Online or in person. In short; Im glad they have these options available for you all.. But I'm also pretty jealous..

Second ekg is 100% afib though.. I opened it and said sss within like.. 2 seconds.. I'd be pretty stunned if proven otherwise.

So in terms of QTc his actual QTc based off the complexes i measured (the scary looking ones) is hanging out at roughly 520 ms. The key here is to actually determine the slope of the terminal t with a straight object, and meticulously identify the isoelectric line with the same. This ensures your measuring the true qt and not a q-p or q-u. Careful account has to be taken for heart rate as well, as in a tachycardia like this, a single box of error means a potentially large change in heart rate. Lastly try to measure qt on the same couple you're using for heart rate. This ensures in the case of a really irregular rhythm like afib, or an ectopic that youre correcting your qtc relative to the particular qt you measured. That said you are correct, 523ms is still an issue. When it comes to qt its best to just scrap whatever they teach in the textbooks and just go with the magic number, 500. Over 500 Qtc or any patient whos symptomatic with a qt approaching that limit needs some more attention. Likewise symptoms such as syncope with no other explanation should carry a high index of suspicion for lqt. Specifically for this patient a QTc of 520 effectively doubles their risk of a life threatening cardiac event (2.3x increase in risk to be precise). This is concerning, but compared to like... A run of VT.. It's not quite as worrisome. I do like that others pointed out meds might be a factor this is definately a possibility to consider, and it makes sense given the condition of the patient. Also a possibility is the fact that some patients with congenital lqts present with 'concealed' lqt. This lqt is typically unmasked during stress testing via treadmill or chenically through epinephrine; which is more effective than dobutamine stress for this purpose. With this in mind it stands to reason that a patient experiencing a tachycardia due to a pathology such as tamponade may find his lqts exposed. For this patient Id venture to say this morphology would fit best with lqt1 or lqt3. Lqt1 being more common overall, more likely to be concealed in the first place, and more easily unmasked with increased demand and sympathetic stimulii. However the shape of the t wave itsself could also point to lqt3, which is much less likely, but also arguably less dangerous in this circumstance. In any case I'm not entirely sold that correcting the qt should be the focus here. It is very likely that this patients qt will correct itsself if the heart rate goes down. Best way to do that of course would be to treat the underlying issue, if a restrictive tamponade or effusion type of situation is the primary suspect here, puncture.. If afib is suspected, cardiovert.. Hell do both if the situation really gives you the creeps. Which brings me to the most important question; the rhythm itsself. I know I'm sort of playing the devils advocate here, but theres not enough evidence to support this as afib based on the ekg provided.. In fact i would argue afib is inpossible throughout the entire period. There is at least 1 point in which the rhythm is absolutely reentrant, criteria for variability is not there during that run at the end of the reference strip. Further v1 typically will show some sort of flutter circus. Not having one doesn't necesarily mean its not afib, in fact it means that it would be afib in its purest form.. Complete chaos without flutter substrate. Not a rare finding but an uncommon one. Next id like to draw attention to the pattern here.. If you march out every larger/high voltage complex with the others its a pretty darn close match... Same can be said for the lower voltage complexes. Now granted afib variability is only 40 ms, and also granted that we have an absence of other criteria to truly base an afib diagnosis. Now one can say 'but theres no p waves!".. But the tricky thing is.. There are p waves! Or so it seems! If you look closely at morphologies youll spot a few inconsistencies.. Theres 1 that pops up just before a qrs complex. When you march them out you can see a few places where the morphology fits and a few where it does not.. It is however very easy to find yourself marching on t waves, a very prophetic sign toward svt.. The few inconsistencies however is compelling toward afib. Lets not also forget that in a coorifice afib type of situation yoh can have fib deflections that resemble p waves. Which is the basis of an argument against the marching p's that makes perfect sense as well. Im basing all of this on the assumption of course that the tamponade or effusion was confirmed by sonography.. If not theres the argument that this could be alternans or something else entirely. You gotta get that stat echo, or just get a fast exam for a parasternal long and see it to know.. Point being, i think theres evidence to point toward afib.. But its not slam dunk evidence.. Theres also not slam dunk evidence that any 1 particular etiology is implicated here.. This patient could have multiple things going on electrically speaking. With this in mind we have to take what we know: its fast.. Its not ventricular... We are unsure of the precise origin(s) therefore we apply an umbrella term of SVT.

Yeah lol, not gonna be pausing any lvads. At some point when i have more time ill probably wind up researching some more information from the manufacturers. Im sure they have a manual or a powerpoint or something to utilize. They probably have reps available to call to figure out the best resources to use I dont see an excessive quantity of lvad patients.. Maybe 3 per week? But it would probably be a good idea to learn more about how the device works so i know what im up against at least. Thankfully thus far i havent had one that was so difficult i had to call the electrophysiologist.. Just takes patience.

I can definately see icu as a great background in terms of how to handle a code, and for being able to rapidly mix and administer meds. You dont necessarily get the same kind of case load when it comes to cardiac arrest in the lab. At the lab where im at there wil maybe be a code every other month, whereas the icu and ed get them throughout the week. So yeah, in that regard absolutely agree icu is helpful. As for the other aspects: Anesthesia starts our art lines in the lab like 90% of the time, and the physicians jump in if they aren't available. I don't necessarily know what they do at other facilities, but at least where ive been ed and icu nurses dont set up fields or anything like that.. If a code requires operative intervention a team from the operating room comes down and handles all that. Edit: by this i mean like..full blown backfields, not like.. Drapes for central lines or foleys or something. They don't ever administer adenosine for ffr outside of the cath lab, and hemodynamic knowledge is limited to basic swan ganz monitoring (looking at pressures in 1 chamber) as opposed to the parameters involved in a full study/pullback. Point being; i feel like aside from the aforementioned code blue experience i feel like with a strong training/orientation program new nurses could be introduced to the required concepts in the lab straight out of school. As for ultrasound: We utilize sonosite, but the nurses can also be of value imo in adjusting settings such as gains and focus when using ice (the physician is sterile, and the techs are operating stimulators and 3d mapping, so the extra hand there can help). Also im not sure when the regulations are in terms of scope of practice in different areas, but nurses may be capable of doing tte or helping a physician with tee images in an emergency. This could potentially help in acquiring the required images early without having to wait for a tech to come in, or taking the attention of an extra physician. I know though it gets tricky in some countries, facilities or states. This board was actually the first time i had ever heard of a nurse being required to go through a formal training program just to use an ultrasound to get access.. I was literally dumbfounded by the bureaucracy and lack of logic involved.. How is allowing a nurse to stick blindly or off tactile input any safer then allowing a nurse to use an ultrasound with on the job instruction?

Cath lab if you can. I dont necessarily understand the benefit of working in icu first and i dont entirely understand why its a requirement. Aside from getting alot of code blue experience.. The skills learned in the icu hardly transfer... Care during the procedure and care after the procedure are 2 entirely different situations. If i had to pick a background that would be most beneficial in the lab it would be OR/ Anesthesia. The cath lab nurses primary job is going to be medication (specifically sedation) administration, patient monitoring and airway management and filling in as needed circulating. In a code yes, comfort with acls medications is a must but i feel like you can get that without necessarily needing experience in the icu. Working in an area where you get some ultrasound transducer time wouldn't hurt either. You can,never have too many people that know how to work an ultrasound machine in a cath lab.

Edit: ok so i downloaded it and was able to expand it a bit. 100% not flutter at any point. The cycle length is too short, basically it takes an electrical impulse a specific amount of time to travel from 1 area of the atria to another, if that time is not met the impulse is originating somewhere else. The majority of flutters follow the same track, so if we assume the case is typical we can predict whether the flutter is legit using this timing. Soo.. I stand corrected, its very likely afib. Change in qrs amplitute signals a rhythm change.. And the fact that it cleaned up with ectopy is suspicious. Afib can be identified by a-a (atrial to atrial) variability over 18 ms (we have that in those sawtoothed areas), r-r variability over 30ms not attributable to an absence of electrical activity (due to a pause, dropped beat or sinus arrhythmia variabilities.. Basically there should be an abundance of electrical activity and a definitely high atrial rate.. We have that.) and atrial waveforms less then 203ms (average flutter cycle length.. Were less than that). Whether or not you see a pwave or flutter wave or whatever isnt necessarily very important to identifying afib, as a fib can produce 'pseudo' pwaves or flutter waves in some circumstances, we can see this in the area in question, theres a convincing looking pri. Its still hard to see the strip on a phone, and without v1 to look at diagnosis is extremely difficult. V1 lies in close proximity to the right atria and generates an extremely useful map of the electrical vector there. So in an ideal situation 2 strips.. 1 of v1 and 1 from lead II taken during the same time period (as would be present in a 12 lead) is sufficient to distinguish a fib from flutter and to predict whether a circuit is typical or atypical clockwise or counterclockwise. Using 1 strip of unknown origin lowers my confidence by about half.

If you reguarly looked at and interpreted ecg's then yeah why not? If youre comfortable lookong at telemetry and the prior job gave you that comfort you're fine.

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.

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 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?)

Thanks for your reply dirpifan! As for mentioning pacers, i brought it up because one of our responsibilities here is pacemaker programming in the absence of the rep. We also handle outpatient programming for all the major brands. This is the setting where i seem to run in to lvads the most. They are noteworthy in this environment because the generate some sort of interference that impedes the ability of the programmer wand to obtain a connection with the device.. In other words, they are a pain to manage! You put the wand on and start trying to test or make adjustments but the wand loses its connection every few seconds and requires constant repositioning! Its kind of like trying to find that perfect spot in the room where you get a good cellphone connection... They are very rare to see in the lab itsself. All that said i am interested in the topic even if we dont work on the floor or in the operating room.. Simply because its kind of lame to have a gap in ones knowledge. With that in mind tamponade might not be something i would see, because the lvad patients i have are those who have already been sent home with the device.. However id imagine there are some complications that could still arise with these patients down the line that i could potentially run in to.. Such as a flow alarm, or perhaps even something as straightforward as an infection.

Hate to be 'that guy' but is it cool to backtrack to an even more basic level: From what I understand these devices are primarily bridges to transplant correct? I see these on extremely rare conditions... Mostly im only aware of them when they get in the way of pacemaker implantation. Dont even know who puts em in or what that process is like at all. On the invasive side i work cath, where patients are either gonna get an impella or if thats not the way we need to go then they just sort of.. Evaporate to some other part of the hospital and i never see them again. Anyone familiar with patient selection criteria for these? What sort of folks tend to wind up with these? How long do they typically plan for them to stay in? Are lvad implantations a significant operation? How does it vary in terms of the recovery process and demand on the nurses vs say.. Ecmo in the post op period. Anyone whos game to give the down and dirty id appreciate it. I realize i could just probably google these things, but id imagine some of,you folks can answer the question with ease and in a more concise manner.

Id recommend taking an anatomy and physiology class.. Whatever section of a&p you enjoy the most and get a really high score in is probably the field for you to be honest. Give everything a fair chance and you might find youre actually really well suited for another specialty.. Maybe you are crappy at reproductive and do better in genitourinary and renal.. Bam! A future in nephrology awaits.. Or maybe youll be really good at musculoskeletal.. Orthopaedic surgery might be your thing.. Or if you also love fitness it could move you in the physocal therapy/occupational therapy/rehab direction. Not a foolproof strategy but a good place to start.. If youre not interested in the science behind it and all you want is to "bring new life into the world" frankly you might struggle/ wind up very disappointed. Always remember you are a scientist first and foremost when you take on a career in patient care... Not just some extra pair of hands. Its like you're a singular neuron in the hivemind/collective brain we call a hospital. Personally i found my niche in cardiology.. granted i still have to have alot of knowledge about other systems to do my job mind you... But the bulk of the stuff i gotta know comes sort of naturally to me. It makes sense and just sort of allows everything else to fall into place. If youre in a field that fits you well, you'll find yourself understanding your patients conditions, the actions of your physicians, the protocols in place, and how to prioritize your tasks a bit better. Thankfully i was able to explore my options and find where i was comfortable, as opposed to some of my peers who maybe tried to jump into this field for the whole adrenaline filled, 'here to save lives' bs logic.