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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.