High Blood Pressure: the basics

Hypertension, or high blood pressure, increases the amount of work the heart has to do. It’s like going to the gym and lifting heavier weights. Just like when you lift heavier weights at the gym to get bigger biceps, when your heart beats against a higher pressure it compensates by getting thicker. However, this compensatory mechanism can actually weaken the heart over time making it harder to perfuse the heart with blood and over time increases your risk of heart failure, heart attack, and stroke.

Some of my patients tell me, “but I feel fine”. And that’s the thing- high blood pressure is a silent killer. You can have elevated blood pressure for many years and not even ‘feel’ it. That doesn’t mean it can’t cause serious harm and increase your risk of future heart attack or stroke.


Defining Hypertension (high blood pressure)

A ‘normal’ blood pressure is <120/80. That means both the systolic (top number) and diastolic (bottom number) need to be below 120 and 80, respectively. Some people have lower blood pressures and that can be completely normal. The short and skinny of it is that you want your blood pressure less than 120/80.

Below are the different stages of hypertension. How we treat blood pressure depends on your individual circumstances and medical history. It is based on robust data summarized in a the 2017 ACC/AHA (American College of Cardiology/American Heart Association) guidelines.

If you have a normal blood pressure reading (<120/80) that doesn’t mean you’re off the hook. You should still get a yearly blood pressure reading. Sometimes you just hit a certain age where your blood pressure starts to creep up a little bit. This is a good reminder that having high blood pressure, like many things in medicine, is both genetic predisposition as well as some behavioral and lifestyle choices that can impact it. Having high blood pressure doesn’t mean you did anything wrong. Some of my patients are the healthiest individuals I’ve ever met. Except that hypertension runs in their family. We will get into some behavioral and nutritional choices you can make to help bring down your blood pressure in another post.

Elevated blood pressure is 120-129/<80. Notice the different goals for the systolic and diastolic (i.e. top and bottom numbers). Essentially, if your bottom number goes above 80 you are considered hypertensive. But if your diastolic remains <80 but your systolic is 120-129 we generally recommend rechecking your blood pressure in 3-6 months. This doesn’t mean you need medications but it does mean that we want to ensure you don’t develop high blood pressure. It’s also another chance to make some positive lifestyle habits and nutritional choices that can pay off over time. As many of my patients can attest, one of my favorite sayings is that many of the choices we make today can pay off over time. Like building a strong retirement fund with a good interest rate. In contrast, ignoring high blood pressure is like having bad debt. Either way- the interest is going to compound. So it’s always better to know if you have high blood pressure than to ignore it.

Stage 1 hypertension is either a systolic between 130-139 or a diastolic between 80-89. This is where working with your physician is important. In patients at higher risk of heart disease, like those who already have clinical evidence of atherosclerotic cardiovascular disease (i.e. prior stroke, heart attack) we often will initiate both lifestyle modifications and treatment with blood pressure medications. If you are a low risk patient we can consider lifestyle modifications alone and rechecking your blood pressure in a few months. If lifestyle modifications do the trick and bring down your blood pressure we can avoid using medications. But if you are doing all the right things and your blood pressure won’t budge then you likely will require medications to lower your blood pressure. Regardless, patients with stage 1 hypertension should be reassessed in 1 month.

Stage 2 hypertension is either a systolic >140 or a diastolic >90. In these patients we often jump to use medications while also initiating lifestyle modifications because the degree that lifestyle modifications will impact your blood pressure likely won’t be enough. Just like how you wouldn’t ignore a leak under your sink you should also not ignore high blood pressure-both will cause damage over time. This is where talking with your physician is important because not all patients are alike. If you want to avoid using medications I certainly don’t think it’s unreasonable to hold off if you are right on the borderline of stage 1 and stage 2 of hypertension as long as we have a plan in place and you continue to follow up. However, a blood pressure of 142/88 for instance is very different than a blood pressure of 180/100. For latter blood pressure (i.e. 180/100) would likely require initiation of medications right away. All patients with stage 2 hypertension should be also reassessed in 1 month (just like those with stage 1 hypertension).

The more uncontrolled your blood pressure is and the greater the period of time that it remains uncontrolled the greater your risk of heart disease (e.g. heart attack, stroke). Just because you have high blood pressure doesn’t mean you will have a heart attack and just because we treat your high blood pressure doesn’t mean you won’t. It’s all about decreasing that intrinsic risk.


Why you should check your blood pressure at home

In my clinical practice I like when my patients take their blood pressure at home for a few reasons. First, if you’ve ever been to a doctor’s office you know it can be a little anxiety inducing. That’s why I never make drastic changes based on a single blood pressure reading. Some patients can have white coat hypertension– when the blood pressure readings at your doctor’s office are always elevated but when you take them at home they are normal. These patients don’t need to be treated for high blood pressure!

Second, you can only go the doctor’s office so many times. Taking your blood pressure at home gives us additional data points to use to estimate your average blood pressure. Generally, I care the most about the your blood pressure trend. Let’s look at two patients as an example. ‘Patient 1’ consistently gets systolic blood pressure readings in the 140-150’s but occasionally gets a systolic blood pressure of 118. ‘Patient 2’ on the other hand gets consistent systolic blood pressure readings in the 120’s but occasionally gets a systolic blood pressure reading in the 140’s. In both patients I won’t ignore the occasionally high or low reading but I care more about where your blood pressure average tends to be.


How to take your blood pressure at home

Type of blood pressure cuff

Generally, arm cuffs are better than wrist cuffs. However the most important thing is that you use an appropriately sized cuff. Using the wrong size blood pressure cuff can give you falsely high or falsely low readings (shown below).

If you want to be accurate, the American Heart Association recommends a cuff bladder width 40% of the arm circumference and a bladder length 80% of the arm circumference. Use the middle part of your arm to check the circumference (shown below).

How to actually measure your blood pressure

If you don’t like reading I made a short TikTok video explaining how to actually check your blood pressure (shown below). The following tips aren’t to torture you- they are so we get accurate readings. The important things to remember are:

  • Blood pressure cuff should be bare to skin (not over clothing)
  • Keep your arm supported (don’t elevate it in the air)
  • Keep your feet flat on the ground
  • Don’t cross your legs
  • 30 minutes before taking your blood pressure do not smoke, drink caffeine, or exercise (life hack- take it first thing in the morning before your first cup of coffee or if you smoke before your first cigarette)
  • You can repeat the reading after waiting 5 minutes. I typically tell patients to take it once in the morning and once in the evening
  • WRITE DOWN YOUR READINGS IN YOUR PHONE OR NOTE PAD AND BRING THE READINGS TO YOUR NEXT DOCTOR’S VISIT

Don’t forget to bring your readings to your next doctor’s appointment

Every day after work when I leave the hospital I put my hospital identification card in my car. That way I don’t have to remember to take it with me to work the next day. Because believe me there’s nothing worse than getting to work and having to turn around and drive home to pick up your ID badge. Similarly, remove road blocks from bringing your blood pressure readings to your next doctor’s appointment by putting the information directly into your phone. This way you don’t have to remember to bring the notepad you’ve been writing your blood pressure readings in. If you choose to do it the old fashioned way with pen and paper that is perfectly fine. Just remember to bring it to your next visit. Remember to document both the top and bottom number in addition to your heart rate. Lastly, please do not rely on your memory to serve as a blood pressure log. I want to know what blood pressure readings you are getting at home and not just that it was ‘high’ or ‘normal’.


If you found this helpful then:

Most Commonly Used Tools Cardiologists Use For Palpitations

Palpitations are one of the most common reasons that I see patients in the inpatient and outpatient setting. Palpitations are abnormal the sensation of your heart beating. I explain them briefly in this TikTok video:

@marckatzmd

What are palpitations and other questions explained in greater detail on my 15min YouTube video #Cardiology #MedicalTikTok #Cardiologist #Palpitations

♬ original sound – Marc Katz, M.D.

Depending on the underlying diagnosis they can be completely benign or potentially life-threatening. I go into much greater detail in a much longer separate YouTube video here:


To understand the common tools we use to diagnose and treat palpitations you have to find out how frequently they occur. So let’s review the most common tools cardiologists use to evaluate palpitations.

If they’re happening right now- get an ECG! Sometimes an Apple Watch can even diagnose some abnormal heart rhythms like atrial fibrillation. But if palpitations are not happening when you get the ECG then you will not catch the rhythm. In the inpatient setting we often also use telemetry. This also underpins the importance of talking to patients to evaluate how frequent palpitations occur as different tools can be used for different durations of time. Sometimes even when we diagnose certain abnormal heart rhythms we use the next few tools to quantify the ectopic burden (how many extra beats are there) as this may influence treatment.

Holter Monitor: 24 – 48 hours

Holter Monitoring - SND Hospital Ropar

Holter monitors are 24-48 hour mini ECG’s, as depicted above. Patients wear them and document when they feel symptoms and we correlate the information we collect from the monitor. This can also help quantify how frequently someone is having a known abnormal heart rhythm to help guide other treatment choices.

ZioPatch Event monitor: 1 – 2 weeks

How Zio works | iRhythm

Event monitors are the next step up in duration. They can be worn for extended period of time, typically for 1-2 weeks. My favorite is the ZioPatch, shown above. It can be worn for weeks at a time (again, typically 1-2) and is small, goes on the chest, and records everything while being worn, and patients can even shower with this device. They click a button on the device to note when symptoms occur and then we go back to see what rhythm was happening at that time when we receive the report. It does not get transmitted in real time. Instead, as shown below, patients actually take it off at home and send it back to the company in the mail who then forward a report to the ordering physician.

The wireless future of medicine | zhiyaobme

Implantable Loop Recorder: up to 3 years

Implantable Loop Recorder

Lastly are implantable loop recorders (ILR). ILRs are less than 2 inches long and quite thin, as depicted below.ILRs are the only monitoring device that is actually implanted under the skin on the chest. They record everything and have up to a 3 year battery life! The ILR automatically records certain fast and slow rhythms but patients can also use an activator to save rhythms if they’re having symptoms. We often use these when the palpitations are infrequent or if we have a high suspicion of an underlying arrhythmia without a documented diagnosis that might change management. For example, I frequently use these in tandem with neurologists in stroke patients in whom we suspect but have not diagnosed atrial fibrillation (AF). If we see AF on an ILR then we would start a blood thinner but sometimes don’t want to treat empirically.  The location these are placed is shown below and often can be safely removed.

Just like any test these tools aren’t perfect. First, patients can have palpitations a few days a week but for whatever reason don’t have any symptoms when wearing the monitor. Depending on the clinical scenario sometimes we will redo the test. Second, these monitors should not be ordered unless clearly indicated. If you were to place Holter monitors on 100 random individuals you are certain to find some abnormal heart rhythms that are completely benign. Thus ordering unnecessary cardiac monitoring for patients can lead to unnecessary follow up procedures, testing, and possible harm.


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Medications After a Heart Attack| Why Dual Anti Platelet Therapy Is So Important

When you have a heart attack, or a myocardial infarction (MI), one of the most common outcomes is the placement of a stent inside your coronary arteries, or the arteries that supply the heart itself. The most common type of stent we use today are drug eluting stents (DES). Two medications cardiologists routinely prescribe together after DES placement are dual anti platelet therapy (DAPT).

DAPT is composed of two medications. The first is aspirin and the second is either Plavix (Clopidogrel), Brilinta (Ticagrelor), or Effient (Prasugrel). They are supremely important after a having a stent placed in the heart because they keep the stent open. DAPT keeps stents open by preventing clots from forming inside the stents.

The history behind coronary stents starts several decades ago when balloon angiography was the only direct mechanism we had to combat sudden heart attacks. We used to insert a balloon inside the clogged artery and open it up. However this only worked for a short period of time and at 6 months the artery was often narrowed again almost 50% of the time. Additionally when we deflated the balloon the natural physiology and physics of the balloon angiography would cause the artery to recoil and often would be even more narrow than before. This is visualized below on the left hand side

Elastic recoil and neointimal hyperplasia after stent placement

That’s why bare metal stents were created. The metal inside a stent kept the artery wall from recoiling. However these stents also closed up with time. The reason they closed or narrowed over time was due to neointimal hyperplasia. Neointimal hyperplasia is shown above on the right hand side. It is the process of normal smooth muscle cells inside of the coronary arteries abnormally being deposited inside the inner layer of the artery wall. That’s why drug eluting stents (DES) were created.

DES are the same metal stents but they are coated in a drug that slowly seeps into the artery wall and prevents neointimal hyperplasia and thus prevents the slow narrowing of the artery from happening. However this causes the metal struts of the stent itself to be exposed to the bloodstream for a longer period of time and results in an increased risk of in-stent thrombosis- or clots to form inside the stent. This is where dual anti platelet therapy (DAPT) comes in. DAPT keeps stents from having clots form inside the stent itself.

In the video below I go into greater detail about what happens during a heart attack inside the coronary arteries, a brief history on how heart attacks previously used to be treated, why we developed new types of coronary stents, and ultimately the importance of taking your dual anti platelet therapy after a heart attack and stent placement, and possible side effects of the medications to watch out for I also briefly explain the duration of DAPT therapy, side effects patients should look out for, other medications to avoid after a heart attack, and I stress the importance of never stopping your medications without first talking with your cardiologist.

Dual Anti Platelet Therapy After Myocardial Infarction and Coronary Stenting

***This video is intended for educational purposes only. This content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have heard or read online***

Should You Attend A Caribbean Medical School?

The most frequently asked question that I receive from students from around the world is ‘should I apply to a Caribbean medical school?’. There are plenty of blog posts on the internet that provide advise without objective evidence. So before I give you my unfiltered opinion I want to first present the cold hard facts surrounding the topic as well as some information that is not common knowledge to many pre-med students, most individuals outside of medicine, and future Caribbean graduates. My hope is to arm you with data so that you can make an informed decision about applying to Caribbean medical schools and how best to prepare yourself for success when attending a Caribbean medical school. Before jumping into the benefits and drawbacks of these programs let’s first take a step back and look at the journey of becoming a doctor in the United States.


Part I: Becoming a doctor in the United States

‘What do you call someone who graduates at the bottom of their class in medical school? Unemployed.

In order to apply to medical school in the United States you are required, at a minimum, to have completed your pre-med requisite courses which include one year of biology, one year of physics, one year of english, and two years of chemistry (usually general and organic chemistry). Many medical schools are also now requiring molecular genetics and biochemistry. For school specific requirements you can check out the Medical School Admission Requirement website. On top of your pre-med course requirements most American medical schools require a stellar MCAT score, extracurricular activities inside and outside of the medical field, and shadowing experiences of some sort. For the sake of brevity this blog post will not cover the lengthy topic of how to get into medical school.

There are two types of medical schools in the United States- allopathic and osteopathic. Students who graduate from allopathic medical schools earn an ‘M.D.’ which stands for ‘medical doctor‘ and students who graduate from osteopathic medical schools are a ‘D.O.‘ which stands for ‘doctor of osteopathic medicine’. There are differences between the two in certain aspects of their training and the standardized tests they have to take but in clinical practice they are quite synonymous and are otherwise both ‘doctors’ in every modern sense of the word.

In general, medical school in the United States is four years. This includes both MD and DO programs. However to make matters slightly more complicated there are also many medical schools that offer dual MD/PhD programs (generally speaking these are 7 year programs) as well some schools that offer or even require an additional year of research. Other medical schools also offer dual degrees. Some schools offer an MBA or MPH alongside their medical degree. So generally speaking medical school is a four year process but clearly there are exceptions to the rule if you choose to pursue a different path.

After graduating from medical school you are now a doctor, in name at least. In the United States you cannot practice medicine independently without completing residency training. This is worth repeating. In the United States you cannot practice medicine independently without completing residency training. This is the crux of issue regarding Caribbean medical schools. Acceptance into medical school ≠ a job. Acceptance into medical school guarantees you two fancy letters at the end of your name but without landing a residency position you will never practice medicine as a physician. In the remainder of this post I will explain that, based on prior residency match data and from personal experience, by attending a Caribbean medical school you put yourself at a distinct and intrinsic disadvantage in your ability to obtain a residency position in the United States compared with graduates from stateside MD and DO medical schools.


Part II: The Match

‘Like speed-dating but worse’

If we are going to understand why Caribbean medical graduates are at a disadvantage historically compared to American medical graduates we have to first understand the National Resident Matching Program (NRMP), or ‘the match’. 

Near the end of the third year of medical school students begin applying for residency. The program known as ERAS, or the electronic residency application system, is the online application students use to apply. It is a common application that almost every residency program uses and makes applying for residency simpler. After uploading your application and appropriate paperwork all you have to do, generally speaking, is click which school you want to apply to.

After the application deadline passes residency programs begin downloading applications. Many programs have hard cut offs. For instance, some programs require you to have a step score above a certain value and if your score is not up to par then your application simply won’t be looked at. Next the residency program picks who to send interview invitations to. Interview season generally lasts 3-4 months from October to January but varies from specialty to specialty. After interview season concludes both students and programs must submit ‘rank lists’. Rank lists are exactly what they sound like. Applicants rank which programs, from the ones they interviewed with, that they want to go to with their most highly sought after program at number 1 and then rank each subsequent program down the line. Programs do the same with applicants. Eventually a computer system attempts to ‘match’ students and programs together to make the best possible fit based on each respective applicant and programs choices. The following video is the best one that I could find that explains this quite complex process as succinctly as possible.

On the Monday of ‘match week’ applicants find out if they have matched or not. They find out where they matched on Friday. The reason for this is that if a student does not match they can participate in the SOAP, or supplemental offer and acceptance program. This is a second chance to try and match into a residency position that went unfilled. More information on the SOAP can be seen at The NRMP website.

This is why medical students ‘match’ into residency spots. It isn’t as simple as a job application. And Caribbean medical students match into residency at a far lower rate compared to their stateside colleagues.


Chapter 3: Raw Data

‘Without data you’re just another person with an opinion’

So now that we kind of understand what it means to ‘match’ into residency let’s finally take a look at the raw data from the 2018 main residency match. The NRMP data is widely available and I encourage you to take a look yourself here. The data describes Caribbean graduates with the term ‘international medical graduates’ or an ‘IMG’. These are further split into two categories: US citizen IMG and non-US citizen IMG. So if you are a US citizen and went to a Caribbean medical school then you are considered a US IMG.

In 2018 there were 37,103 active applicants and 30,232 first year and 2,935 second year residency positions. The following are the match rates for each type of applicant:

  • US allopathic graduates (MD’s): 94.3%
  • US osteopathic graduates (DO’s): 81.7%
  • US IMG: 57.1% 
  • Non-US IMG: 56.1%

If you only remember one thing from this post then this should be it. Only 57.1% of US IMG’s, or people like me who are US citizen Caribbean medical graduates, match into residency positions versus 94.3% of US allopathic grads and 81.7% of US osteopathic grads. This is terrifying! Imaging going through four years of medical school, accumulate a crushing amount of debt, only to end up without a job or the ability to practice as a physician (check out prior interview posts with individuals who went through that exact experience).

An interesting graph from the NRMP data shows that not every specialty ranks equally.

This graphic shows that the specialty in which the highest percentage of US IMG’s were able to match into was pediatrics at 69.8% of applicants matching while psychiatry on the other hand was the most difficult specialty for US IMG’s to match into at 30%.

So why do Caribbean graduates have a greater difficulty matching? Let’s take a look at NRMP data from a survey of program directors. This survey is also widely available and I encourage you to analyze it yourself here. The survey was sent to 209 program directors (PD’s) and 78 responded, or 37.3%.

The data shows each individual factor that program directors find important when they choose applicants to interview and rank for residency. As you can see below the USMLE step 1 score, based on this data, is by far the most important factor for choosing applicants to interview.

So a strong STEP 1 or COMLEX 1 score gets your foot in the door but it does not necessarily get you the job. Now let’s use the data from pediatric program directors (PD’s) for the next few graphs. This next graph shows the most important factors that pediatric PD’s felt were the most important factors when ranking applicants.

This graph clearly shows that the more important component of how medical students are ranked on a program’s rank order list is how an applicant interacts with residents and faculty on interview day. Again, a strong USMLE step 1 score seems to be of critical importance in helping get an applicant’s foot in the door but how they interacted on interview day earns medical students the opportunity to walk through it. Of note, each specialty seems to vary slightly in what they rank as most to least important but grossly these trends seem consistent across the board.

The issue however is that getting a stellar USMLE step 1 score isn’t the only obstacle when it comes to matching into residency for Caribbean medical students. At the end of the day all medical students learn the same science but not all medical students have access to the same residency programs.

The same survey of pediatric PD’s (and the same specialty that in 2018 had the highest successful match rate from US IMG’s) shows that some program’s won’t even consider an applicant if they graduated from a Caribbean medical school. The graph below shows that out of the PD’s who responded to the survey only 67% of them typically even interview US IMG’s.

Broken down even more we see that an even smaller percentage of programs will ‘often’ interview and rank candidates from Caribbean medical schools. This is another huge point that you should take away from this blog post.

Again, the match rate for US IMG’s in 2018 was 57.1% versus 94.3% and 81.7% match rate for allopathic and osteopathic grads respectively. I believe that part of that intrinsic disadvantage is that some residency programs simply won’t touch Caribbean medical school graduates. You simply can’t get a job if they won’t interview you for it.

Another unfortunate aspect of being a Caribbean graduate is that it seems to impact the fellowship match too, although to a lesser degree compared to the residency match. If we take a look at the results of the 2019 fellowship match data we can see a clear trend that does not favor Caribbean graduates. The following are the match rates for fellowships in 2019:

  • US allopathic graduates (MD’s): 89.4%
  • US osteopathic graduates (DO’s): 78.9%
  • US IMG: 68.5% 
  • Non-US IMG: 71.4%

For the sake of brevity I won’t delve too much into this data because the fellowship match is a little bit more complicated and not so clear cut. I’m not certain as to why Caribbean medical graduates have a tougher time matching into fellowships but I am certain that some fellowship programs won’t touch a Caribbean graduate just like how some residency programs don’t.


Chapter 4: Informed Consent

‘Without consent surgery would be considered assault’

In medicine before we perform any test or procedure we are required to get informed consent from our patient. Informed consent is the concept of understanding all of the possible consequences with full knowledge of the possible risks and benefits of said procedure. I think the same should be true about applying to Caribbean medical schools and after getting through all of that data I think we’re closer to fully understanding the implications of attending a Caribbean medical school.

Don’t get me wrong, I’m not trying to scare you away from applying. I graduated from a Caribbean medical school, matched into an internal medicine residency program, and successfully matched into a cardiovascular disease fellowship. There are plenty of success stories that originate in the Caribbean and I’ve interviewed nearly a dozen of my colleagues who matched into competitive specialties like emergency medicine and surgery. But Caribbean medical schools aren’t for everyone and you should understand that before you sign up or apply.


Chapter 5: The Caribbean Stigma

‘Some stereotypes originate in truth but are exaggerated by myth’

There is a common misconception in the pre-med community about the ‘Caribbean stigma’. This myth that there would be a doctor or nurse in the hospital you are rotating in that would choose not to work with you because of where you went to medical school. Or that Caribbean medical students are not as qualified as their stateside counterparts. Unfortunately the stigma is steeped in truth.

Caribbean medical students go to the Caribbean because they could not get into a US MD or DO program. That’s why I went to Ross University. I applied to 36 medical schools and Ross University was the only one that accepted me. Caribbean medical schools typically have lower standards and thus not every medical student makes it to graduation. I could not find the statistics on the attrition rate from stateside or Caribbean medical schools but I can speak from experience.

Out of the 440 students who started with me in my first semester of medical school only 76% advanced to their second semester. Although this is only one anecdotal piece of evidence and shouldn’t be used to grossly generalize against all Caribbean schools it does in fact happen. Furthermore, the fact that some Caribbean medical schools are for profit organizations is worrying to me and further underlines the fact that they accept too many students who otherwise wouldn’t be accepted into stateside medical schools. Not to mention that medical school in the Caribbean is just as expensive as medical school in the US. So if you are unable to secure a residency position you will be left with massive loans and a hard road ahead to paying them off.

So although the ‘Caribbean stigma’ exists when applying to and while attending medical school once you make to the hospital nobody cares where you went to med school. In the hospital I’ve met incredibly passionate, intelligent, and competent medical students, residents, fellows, and attending physicians from both Caribbean and allopathic and osteopathic medical schools. I’ve also met terribly incompetent individuals from Caribbean, allopathic, osteopathic medical schools too. Just because you attended a certain medical school doesn’t make you a better or worse doctor. Sure, it certainly impacts your ability to match into residency but there isn’t a single nurse, physician assistant, or doctor out there who will treat you any better or worse just because of what med school you went to.


Chapter 6: The Life of a Caribbean Medical Student

‘It doesn’t really matter where go to medical school because it’s always 72 and fluorescent in the library’

I won’t delve into the specifics of each individual Caribbean medical school and this list is not exhaustive but each of these schools share many similarities with the majority of Caribbean medical schools. In general when you go to a Caribbean med school only the first two years are spent ‘on the island’, or in the actual Caribbean. These first two years are spent in the traditional classroom where we are taught the same basic sciences that allopathic and osteopathic med students learn in preparation for USMLE step 1. It’s really not that bad. I enjoyed my time on the island. I remember being stressed out before my first major exam so I took a stroll on the beach to relax. After leaving the island most medical students rotate in hospitals across the US that each respective medical school has affiliations with. I rotated in hospitals in New York and Florida.


Chapter 7: The End Game

Measure twice, cut once

Your first choice should be to get into a US allopathic or osteopathic program. People who are not accepted at first often work on improving their weak spots in their resumé or work while they study to retake the MCAT. Often students will work a few years, do research,  get various master’s degrees, or do a post-baccalaureate degree. Others, like me, don’t want to wait and choose to attend a Caribbean medical school instead. 

This is a viable option for certain students but it might not be the right fit for everyone. Some residency specialties, like neurosurgery, orthopedic surgery, ophthalmology, otolaryngology, plastic surgery, urology, and dermatology, are some of the most competitive medical specialties that exist. Even US graduates often have difficultly earning these residency positions (my osteopathic colleague took three attempts to match into derm and he was a PhD too!). By attending a Caribbean medical school you are again giving yourself another uphill battle to fight. So if your heart is truly set on one of these specialties understand that although it is not impossible to match as a US IMG it will make it increasingly more difficult to do so. That being said, if you know you want to go into primary care fields like internal medicine, family medicine, or pediatrics then a Caribbean medical school might be the right fit for you. Again many residency, and fellowship, programs simply won’t look at you because you are a US IMG. So you might not be able to go to an ivy league internal medicine residency or fellowship program but you certainly can still become a doctor.

The ironic part of all of this is that in order to be a good doctor at the end of the day it really doesn’t matter where you went to medical school or what you got on your USMLE step 1 (as this blog post points out). In residency nobody care what your test scores were and when you are an attending your patients won’t care that you went to an ivy league school if you aren’t compassionate, kind, caring, or intelligent. And yet if you don’t do well on your exams, especially coming from the Caribbean, you hurt your chances of ever being able to treat future patients. Whether you like it or not this is the current status quo. So if you go to the Caribbean be ready to work hard, crush your step exams, and get great letters of recommendation.


I hope this post helped uncover some of the hidden curriculum of medical school and residency and didn’t scare you away from applying to Caribbean medical schools. Ross University was the only medical school I was accepted to and they gave me the opportunity to pursue my dream of becoming a physician. It’s up to you to make the best decision for your future career and then make the most of that opportunity. Hopefully now you can do so with confidence and informed consent.

You can also check out my YouTube video on the topic below:

Drop me any follow up questions that you may have below and be sure to subscribe so you don’t miss my next post!

What Happens When You Don’t Match Into Residency…Twice

Two years ago I interviewed a fellow Caribbean medical graduate. I interviewed him because of his failure. Specifically his failure to match into residency. I wanted to shed light on what the medical education community seems to shun and ignore- what happens after you fail to match into residency. Last year we were both hopeful that we would be able to share a comforting update on his path toward residency. His story was seemingly not yet ready to be told because for the second year in a row he heartbreakingly failed to match into a residency position. However, as the old adage goes, third times the charm.

 

 

It’s been two years since I interviewed you the first time. Back then you were recoiling from not matching into residency. Then you went through the match for a second time. What did you do during that first year after not matching your first time?

Hi Marc, it’s been quite some time and I’m happy to be back talking with you and answering your questions. After the first time of not matching, I began the process of getting my MBA in Health Services Management, studied for Step 3, and worked part-time for Ross University as a standardized patient. I also shadowed one of the pediatricians I worked with to keep my clinical skills fresh as she saw both adults and children.

 

 

How did you deal with the emotions of not matching for a second time?

To be quite honest, at first, I didn’t deal with the emotions. I was rather numb for a while and chose to ignore the feelings. But I started to really develop that anger more than I felt the depression stage of grief (Kubler-Ross knew what she was talking about). I had a hard time accepting the fact I did not match, considering what a program director told me, in which they implied that I was going to match at that program. I felt betrayed and became distrustful in the whole process.

 

 

What strategies did you change the second time around? Different specialties? How many interviews did you get the second time? Why don’t you think you matched the second time? 

I applied strictly to Family Medicine, which I definitely felt comfortable doing and I had wanted to really do it after attending the AAFP National Conference in July 2016. I met a lot of people and had some meaningful conversations with program directors. However, with all that said, I only had two interviews. It wasn’t that I was a repeat applicant that held me back, but it was the fact that I was never able to obtain a letter of recommendation from a board-certified Family Medicine physician. I do not believe that it was my interviews that did me in, but simply the numbers were against me.

 

 

So it’s your second match day and you find out you didn’t match, again. Take me through that week for you. 

It was a dark week. No…a dark couple of weeks. I was teaching our Ambulatory Care Competencies elective, which prepare MS-IV’s for Step 2 CS. We had finished around 10:45 AM and as I was walking to my car, I get the e-mail AGAIN that states “You did not match.” Again, there was no “oh hey girl” or “what’s going on” or anything like that. Just a simple “You did not match.” I immediately drove back to our school’s campus and got to work on SOAP. I actually had a phone interview at a university-based internal medicine program for a categorical position, which did not happen the year before. I spoke with three people and I naively felt very optimistic, thinking I was going to get the position. Well, the rounds of offers went by and there was nothing. It was very difficult to show up to work on Tuesday being surrounded by people who were celebrating having matched. In no way, shape, or form was I jealous or bitter. I knew that all of our journeys were our own and our applications were all different. However, it was just a little tough to be happy around them because I wanted to know what that feeling was like, so I took a break from social media. When I did that, the outpouring of support via text and email came from my former classmates and colleagues. So many people voluntarily reached out to me offering positive thoughts and were willing to put in good words for me for the next process. These people knew my work ethic and personality and were willing to put their reputation on the line by recommending me. That was a huge motivation for me to keep going and to get back on the horse again.

 

 

What did you do for the year after your second time not matching? Where did you work? 

I managed to get a full-time position with Ross University teaching for their Internal Medicine Foundations clerkship. However, I wasn’t even on their radar! According to the requirements, I was too far removed from graduation to be hired but they took me on the team on a per diem basis, if you will. I was working 40 hours a week, but just for the six-week clerkship. Unfortunately for one of the hires, he was unable to take the position and I had proven myself worthy of the position. They liked my teaching and mentoring style so much that they ended up offering me a full-time job and eventually, I became the Chief Clinical Teaching Fellow. I went from not even being considered for the team to becoming the team captain, which gave me the confidence going forward in the application process and it was something that I spoke about in my interviews.

 

 

Fast forward to your third time going through the match. You finally get a categorical position in internal medicine. What do you think was different this time around?

Well, my MBA was finished (and I graduated with highest honors) and my Step 3 score was in. I had taken Step 3 in January 2017, hoping to have it in time for the rank order list that was due in February 2017. Of course, I was part of the group of exams that wouldn’t get their score until May. May 2017 rolled around, and I passed so this showed that I am in good standing to eventually pass the boards, whether I ended up in Internal Medicine or Family Medicine. I also finally got that FM board-certified LOR for my application, which was a bonus since the writer is also a program director. Also, I was working on getting published in a medical textbook.

I knew that it was going to be very difficult to get residency interviews on my own, so I had to reach out to as many people as I could that were in residency programs. I asked people to talk about my character and work ethic. I looked at as many Family Medicine programs as I could and saw what scores they were looking for and narrowed Internal Medicine programs to the east coast and Chicago. Overall, I applied to 260+ programs. To my surprise, within the first week, I had my first interview offer and within four weeks of applying, I had four interviews lined up. I also constantly checked for new programs that were opening up and applied to those, which gave me some additional interviews. Overall, I had 3 IM interviews and 5 FM interviews (one of them was an interview I had last year, for which I was really grateful). Some of the interviews were from the help of people in the program, but that’s the main help I received. It helped me get my foot in the door, but I had to impress in the interviews. I did not take that help for granted and realized that I was not only representing me, but I was also representing them.

 

 

Do you know a lot of other students who didn’t match? What about people like you who didn’t match multiple times? What do people do who don’t match for a third time? What would you have done?

I have heard of a handful of students who matched after a third or fourth attempt. After I matched, I posted my story on Facebook and I got a huge number of messages with people asking for ideas on how to help them match and the best I could do was help brainstorm. Everyone’s application is different and since I don’t know what’s on their application or record, I could only speak on what I ended up doing.

To be quite honest, I don’t know what I would have done if I hadn’t matched a third time. I have been living in Florida already for my rotations and one thing that I was considering was applying for my ACN (Area of Critical Need) license. Since I had passed all the Step exams, I would’ve been able to practice medicine under the license of another primary care physician.

 

What general advise do you have for pre-med students researching Caribbean medical schools with regard to match rates? Did your medical school have resources available to you after you didn’t match?

Match rates are definitely useful, but you have to take them with a grain of salt, as you do with the match residency placements. Sure, Ross has matched at Yale and Duke, but you have to realize they are a rarity and have worked with the right people to earn that opportunity. However, use that as motivation to push yourself further to get that opportunity. Also, be aware of the school’s data. Take a look at what year the data came from because it may be slightly outdated. Take a look at where the graduates are able to practice. Even if you transfer into a “Big Four” (I guess Big Five school with AUA) medical school for your rotations, where you did your basic sciences will limit where you can obtain licensure so keep that in mind before you go to a cheaper Caribbean medical school. The extra cost is completely worth it.

 

 

What advise do you have for medical students who don’t match? What about if they don’t match twice?

Excellent question, Marc. Simply do not give up. It’s not a matter of if you will match, but rather WHEN you will match. Do not be afraid to reach out to colleagues who are in residency programs. I was hesitant at first because I wanted to earn it on my own merit, but if other industries interview people based on reference from those within the company, why can’t we do it in medicine? I know many people who got residencies because their parents knew people. My parents are not physicians. No one in my family is a physician. However, my friends from medical school could vouch for me, which in my opinion, carries more weight as there is no obligation to push for me.

Also, take Step 3!!!! You might as well get it out of the way, especially if you have lower scores like me, a failed attempt, or need a visa for residency. It can definitely open doors because every single interview mentioned that they were glad I had Step 3 done. One PD told me that it was a deciding factor in my application. In the words of Larry the Cable Guy, GIT ‘ER DONE.


To see our original interview after Steven’s first failed match check it out here- what happens when you don’t match.

Thank you again Steven for being so open and honest about your success and failures. I wish you only the best during residency and beyond.

 

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What happens when you don’t match

What happens to medical students who don’t match? Here’s what one unmatched psychiatry applicant had to say.

 

Thanks for letting me interview you Steven. You have a pretty unique story that my readers would love to hear about but before we delve in can you tell us a little bit about yourself? Who are you professionally? Did you go straight from undergrad to Ross? Who are you outside of the hospital?

My pleasure, Marc. I appreciate the opportunity to share my story as I feel people can learn from any experience in this process, both good and bad. I graduated from NYU in 2010 with a Bachelor of Arts in Mathematics. After graduation, I had about six months before starting with Ross University’s MERP (Medical Education Review Program) and I knew I needed to make money. So I took a job that any medical school bound person takes – working in the jewelry and diamond industry. I did mostly bookkeeping but I also prepared orders for a wholesale company that dealt with Macy’s, JcPenney, Sears, HSN, QVC, etc. It taught me a lot about dealing with large staffs and it was a nice break away from the science and math world I had spent so much time with in undergrad.

Professionally, I’m the one making jokes in the office but I focus on the patient when I’m in the room. I like to be a reason people enjoy coming to work, because they know it’ll be fun and productive. On the same token, I’m also someone who isn’t afraid to call someone out for their BS because I expect someone to do the same to me if I ever act out of line. I also am one of the first people to teach someone how things run in the office, how to order labs, do procedures, etc. Not only do people feel comfortable if it’s a peer teaching them but it helps me better my skills as well.

 

 

What specialties did you apply for? How many programs in each specialty? What was your reasoning for that number of programs?

I applied to psychiatry, internal medicine, and internal medicine-psychiatry combined. For psychiatry, I applied to 76 programs. For internal medicine, I applied to 10. And for IM-psych, I applied to all 9 programs in the country. My step scores weren’t that competitive and there are only 196 psychiatry programs in the country. I went through each program on FREIDA and checked to see if I matched their step requirements. If I did, I tried to see who the residents were. If there were zero or one Caribbean grad in all the PGY positions, then I didn’t apply as I felt that that one particular Caribbean grad may have had a connection there or had stellar scores. Plus, why would I spend money on programs that were going to outright reject me?

For IM, I applied to where I had rotated and since I could apply up to 10 for one fee, I applied to some hospitals in the NY/NJ area (which is where I’m from). And for IM-psych programs, there were only 9 so it made the most sense to apply to all of them.

 

 

How many interviews did you end up receiving? How did you feel your chances were at matching?

Formally, I received three interviews, but in total, I ranked four positions. I received 2 for psychiatry and I was taken off the waitlist for 1 IM-psych program. All of them were university-based programs. At the IM-psych program, I had mentioned that I had also applied for a psychiatry categorical position at the same place and I wanted to know if I had to come back for another interview, which I was totally willing to do. Ten minutes after that mini-interview, I had an impromptu meeting with the program director of psychiatry and she told me that she will see what the other four interviewers had to say about me from that day and she would let me know if I needed to come back or not. Two weeks later, I’m notified that she had enough to consider me for a position. Throughout the next two months prior to match day, I had received several emails about how the psychiatry program is expanding and there’s new facilities and all these wonderful things. I didn’t think I was a shoo-in but I felt that maybe I had a great shot.

 

 

So, it’s Monday, March 14th. The day applicants find out if they matched. You open the e-mail and find out that you did not obtain a residency. What’s going through your head?

Before that day, I told myself whatever happens, happens. I actually slept well the night before! I was driving in Fort Lauderdale and taking care of some errands and I happened to look at my phone. For five seconds, I was completely numb. And then it hit me. My biggest fear came true. All that work, all that money, all the stress, and for what? Nothing.

*cue Kim Kardashian ugly crying*

I can honestly say that it is one of the most devastating experiences and I would not even wish it upon an enemy. The e-mail just says “you did not match”. Not even a “good morning” or “hey girl!” Just one line that says you’re not good enough to continue in your career. After quickly doing my errands and a few snot-filled tissues later, I sped home passing several cops on the way and began on SOAP.

Most of us aren’t familiar with the SOAP, or the Supplemental Offer & Acceptance Program. Can you walk us through your experience with it? (Here’s a link to the SOAP schedule for my readers)

SOAP is a chance for unmatched applicants to apply to unfilled spots in all fields of medicine. However, this means that you will have to come up with new personal statements in the matter of hours, which is exactly what I had to do for family medicine. As Markus said in a previous posting, the website was down and no one could send in applications (because like LOL, heaven forbid the ERAS website works when it needs to).

I spoke with a friend who match into IM the year before through SOAP and she guided me through the process while she was at work. She told me to apply to the IM prelim, IM categorical, and family med programs that had the MOST open spots. I had only 45 spots to pick from and I used 5 of them on psychiatry programs that were unfilled. Then I went through family medicine and internal medicine. In retrospect, I could’ve used those 5 on family medicine or IM spots but what’s done is done.

 

 

So on Monday you found out that you didn’t match. Then during the week you went through the SOAP.  Friday comes along and you find out that you didn’t SOAP into a residency. How did that feel?

By that point, I had already gone through the five stages of grief. Denial set in when I was in the car. Then anger when I was cursing at anyone on the road that was slowing me down from getting home (which is what I do on a regular basis and I’ve been trying to work on but YOU try driving on I-95 in Fort Lauderdale and Miami and tell me you don’t have road rage, but I digress…). Bargaining was SOAP. Depression set in when the 5th round of SOAP happened and I hadn’t received any offers. It continued for a week when all I saw on Facebook were my friends posting that they matched at their number one or number two choices. It wasn’t that I wasn’t happy for them. Every single one of us had a unique journey and even the people I didn’t like, I respected them enough in a professional sense to be proud that they get to continue their journey. It was more about the fact that I didn’t get to continue my journey with them.

Several months had passed and I hadn’t reached the acceptance stage of grief. It wasn’t until I went to the AAFP National Conference in Kansas City at the end of July that I had realized that I had been in the wrong field all this time. I realized within the first hour of the conference that I had such a wrong idea as to what family medicine and primary care entailed. There are so many opportunities for me as a family medicine doctor, whether it be to provide medical care for a whole family, work as a hospitalist, deal with mental health issues, or even perform procedures. After I didn’t match, I had told myself that something big was in store for me, and I finally believed it. Networking at the expo hall with the residency programs made me realize that I was a perfect fit for family medicine and that there are programs out there that WANT me. As I’m writing this, I can definitely say that I wasn’t supposed to match into psychiatry because I realized that I was meant to match into family medicine (I’m hoping). It feels good to be in that acceptance part of grief!

 

 

Why do you think you didn’t match? What were your step scores? Was your application particularly weak in any one specific area?

I had thought about not giving exact numbers here, but in all honesty, who cares? Step 1 was a 208, and step 2 CK was a 209 (yes, the EXACT passing score). Step 2 CS was a pass and everything was on the first try. I expected my Step 1 score but my CK was an absolute miracle. I had worked harder for CK than I did for step 1 and yet, I was not getting anywhere with my studying. I took a UWorld assessment two days before just to get more questions in and I had about 179. So in two days, my score JUMPED 30 points. (This is NOT a plan I recommend to ANYONE, by the way.) I know I’m a terrible test taker and that in rotations, I shined and my letters of recommendation reflected that.

In addition, I had failed one course in basic sciences, and THAT was a reason why a program didn’t take me. They were too worried that I may not pass step 3 (which I’ll go into below) and therefore, not be able to be licensed. However, my scores were good enough to get some interviews at university programs so I must have done SOMETHING right.

 

 

Do you think the fact that you attended a Caribbean medical school played a factor?

Not at all. The places I had interviewed at were very IMG friendly, as were the residencies I spoke with at the AAFP National Conference.

 

 

What do you plan to do while you wait to apply for the 2017 match?

I am currently a Clinical Teaching Fellow for Ross University. Some of my colleagues know it as “junior faculty” but teaching fellow is the formal title and you better believe I am using that on my CV. For those who don’t know what that is, my role is to act as a standardized patient for the incoming 3rd year medical students and assist other junior faculty in teaching how to handle difficult patients and certain common primary care cases, as well as how to begin to formulate an efficient style of medical interviewing. I also assist in Ross’s Ambulatory Care Competencies elective, where we prep the 4th year students for Step 2 CS by presenting cases and critiquing their notes.

Outside of Ross University, I tutor for Huntington Learning Center (which I have been doing since 4th year of med school), where I mostly do SAT/ACT math and high school subject tutoring in math as well. In addition, I’m getting my MBA in Health Services Management through Keller Graduate School of Management, which is one of the sister schools of Ross University. What’s great about that is that they have an “MD to MBA” program where I was able to get credit for 5 out of the 16 courses, so now I only need to complete 11 of them. In addition to working, I plan on taking Step 3 by the end of October. Needless to say, I only know one speed and it is full speed ahead.

 

 

How are you handling your loan debt?

Some of my loan debt could not be deferred or put into forbearance, so I have been paying that off. However, since starting grad school, I’ve been able to defer most of my loans while taking out more. Thanks, Uncle Sam!

 

 

What words of wisdom would you give to someone knowing what you know now?

Have plans A through Z ready to go from the jump. You don’t want to rely on them, but you want them ready if you have to execute them.

Go to as many networking conferences as you can. I know those things can cost money, but at the very least, go to the big ones run by the specialties to which you are applying.

But most importantly, it’s not a matter of “if” you become a resident, but rather it’s a matter of WHEN. 2016 was not my time and I realize that now. However, come 2017, I will be a better applicant and in a better frame of mind to continue on in the next chapter.

 

 

Thank you Steven for an informative and entertaining interview. I look forward to finding out where you match in 2017.

 

Next week I interview a Ross University graduate who matched into a categorical general surgery position. Be sure to subscribe to my blog, like me on Facebook, and follow me on Twitter so you don’t miss it!

Best Resources to Destroy USMLE Step 2 CK

*Disclaimer: Below are my favorite resources with associated links. If you like my blog please use the links to buy any books on Amazon or services (Picmonic, OnlineMedEd) as I receive a small referral fee that helps me keep this blog up and running! I only listed products I trust or and/or used*


Question Banks

The purpose of doing practice questions is to find your weaknesses in order to guide your study process and  to get you inside the head of question writers. Hopefully you figured this out already since you most likely already took step 1. However, I found studying for step 2 CK to be more difficult than step 1 because of the other obligations that MS3 requires. Question banks are also great on the go. Long subway to your friend’s apartment on the upper east side? Do a question set on the train. Bored in between lectures? Practice questions. Lost your resident and don’t feel like going back to the floor? Practice questions. Practice questions? Practice questions! Here are the practice questions I used.

USMLE World

Still the gold standard when it comes to practice questions. There is no way around it. You can read the message boards on Student Doctor Network and they all reiterate what I find to be true. That UWorld is the end all and be all when it comes essential resources for Step 2 CK. Some students will argue that UWorld and a review book are the only resources you need for step 2 CK and for the most part that is true. I completed UWorld in its entirety once. Then I completed all of the questions I got wrong (which was nearly half of them). Then I continued to do full question sets until test day so I ended up doing UWorld two and a half times. I highly suggest it.

Kaplan

Kaplan is the other major question bank out there. I used to do Kaplan questions with my friend who preferred not to ‘waste’ UWorld when he studied for his clinical clerkship exams. Just like step 1, a major advantage of Kaplan to UWorld is that they tell you exactly where this topic or subject is located in the most popular review books. I enjoyed using Kaplan but chose not to invest more money in another review book when I could borrow my friends’ PreTest books instead. That being said, I haven’t heard terrible things about Kaplan.

PreTest

I took step 2 during the second week of my first elective rotation in cardiology. So the bulk of my serious step 2 studying was done during my 8 week surgery core and subsequent 4 week surgery elective. I took a practice test and I did terribly. Like embarrassingly bad. And my worst subject was surgery. I had completed all of the UWorld surgery questions and ran through them all a second time. I wasn’t being lazy either. I read through and studied the answers to each question but I just wasn’t making any progress. My friend suggested I try pre-test and I loved it. Pre-test gives you over a thousand questions for each clerkship exam. In some regards they go into far too much detail than you actually need for your step exam and cover a much wider scope of subjects than UWorld alone…but that’s exactly why I used it. You can finish all of the UWorld or Kaplan questions for the smaller subjects like psych and pediatrics quite quickly. These books expose you to a lot more pathology that other qbanks don’t cover. I highly suggest using this resource for in between lectures, after you finish a specific section of UWorld, or if you just want more high quality practice questions. Just beware that they are not NBME format. So I would shy away from them when it comes closer to test day

Practice Tests

The purpose of practice tests are to find your weaknesses and to exploit them in order to maximize your score. Basically, study what you suck at! That’s the point of doing practice questions and that’s the point of doing a practice exam. So you can tell if your study process is working or not. For instance, after I started dedicating more and more time to study my weakest subject, surgery, my score began to creep up. I found that the number of questions I got wrong in other subjects continued to stay relatively stable but I was able to decrease the number of surgery questions I got wrong from 20, then to 12, then to 8, and on my last practice test I literally got zero surgery questions wrong. My point is that you can’t just keep taking practice tests to see what score you would get on step 2. That’s great and you should do that but you have to remember that the purpose of taking a practice test is to evaluate your weaknesses and to strategically focus on them. Okay, now I can get off my soap box.

NBME

NBME is the gold standard because they are written just like the real test. You have to use these wisely because there are only a limited number of them. Additionally, I believe that it is worth the ten extra dollars to purchase the expanded feedback. This option grants you the ability to see which questions you got wrong. Annoyingly, they don’t tell Sure you can screen shot every single question if you really want to (unlike UWorld Self Assessment) but this is so much easier and also doesn’t mess with your ability to recreate test day.

USMLE World- Self Assessment

The only reason this resource isn’t above the NBME practice exams is because there is only one USMLE World Self Assessment (UWSA). Both the NBME’s and the UWSA are only half as long as the real thing but the advantage of the UWSA is that they are like UWorld question sets. You are given full UWorld style explanations of each question, both the questions you get correct and incorrect alike. I chose to make this my last practice test because I was able to utilize these four individual question sets like they were new questions that I was able to review afterwards.

Review Books

I encountered a few problems when I chose which review book to utilize. My ideal review book would have everything in it already. Explanations from UWorld, differential diagnosis categorized by both chief complaint as well as pathophysiology, best initial test, most accurate test, best initial therapy, maintenance therapies, and alternative therapies. I never found that type of book. So go to the book store and check them out for yourself before you buy them.

Master the Boards (MTB)

I liked MTB for the same reason why I disliked it. Its brevity is nice when you just want a quick and dirty answer but it leaves you hanging at times when you want more detailed UWorld style explanations (seriously, why can’t someone just put UWorld in a book format already?!). Between UWorld and MTB you are guaranteed to pass step 2 because they cover all of the high yield stuff but be prepared to annotate the shit out of it. Bonus tip: use MTB for step 3 instead of the step 2 CK version. It’s got a few extra gems in there and it’s really not all that different from it’s step 2 cousin. This way you won’t have to start all over again for your next step.

First Aid for the USMLE Step 2 CK

First Aid was my step 1 bible but I didn’t use it for step 2 CK and I regret that decision. I borrowed this book a few times from my friends and I liked it. It mimics the step 1 version quite well. Again, I did not use this as a primary resource but I would encourage you to check it out.

Step Up to USMLE Step 2 CK

I used Step Up to Medicine (SU2M) for internal medicine only and did not use Step Up To USMLE CK because I disliked SU2M so much. If MTB has too little information then this is the complete opposite side of the spectrum. It has long winded explanations of every subject in bullet format. Some people liked that but it wasn’t for me.

Lecture Material

Lectures were less valuable to me for step 2 than for step 1. I just didn’t have enough time to sit down and watch video lectures. My favorite way to study was to simply review whatever disease my patients had that day. Every once in a while however I just didn’t know something and needed someone to spell it out for me. These are the resources I used for those moments.

Online MedEd

This is by far my new favorite resource that I utilized for step 2. Online MedEd uses a reverse classroom style of teaching with whiteboard based lectures. Lecture videos range in length and subject matter but are amazing resources for both step 2 and for the wards. For instance, one day I was feeling a little lost about fluid management so I went to the library and threw on the fluid management videos. I went back to the floors with a better grasp of what I was doing and didn’t feel like such an idiot. I especially liked the algorithmic way of thinking they employ. I watched every video and would do it again in a heart beat.

Doctors in Training (DIT)

I loved DIT for step 1 but it just didn’t do it for me for step 2. I didn’t have hours and hours to watch videos everyday, nor did I have the energy for it (that’s why I liked OnlineMedEd a little bit more because their videos were short and to the point). What I still loved about DIT was that they remind you of what you may have forgotten. The pre-lecture and post-lecture quizzes are gold. It wasn’t for me but doesn’t mean you shouldn’t at least check them out. Not to mention they’re great guys to follow on Twitter.

Kaplan Lecture Videos

I got my hands on these videos and they were fantastic. Conrad Fischer at his best. If you liked Kaplan for step 1 then you will like them for step 2.

 

Miscellaneous

The other stuff that doesn’t fit into a pretty category like the stuff I already mentioned.

The Successful Match: 200 Rules to Succeed in the Residency Match

This book is pure gold and I highly recommend it to anyone and everyone going through the match process. It provides analytical data on the match. The author provides objective data on a subjective subject like what characteristic traits different program directors like to see in their candidates the most in each respective specialty. This book provides advice on everything from writing your personal statement, the most commonly asked interview questions and the best way to answer them, what type of programs you should be applying to, who you should be asking for letter of recommendations from, and so much more. It was my most valuable resource before and during interview season. You won’t regret this investment. In fact, your friends are going to want to borrow it. Mine did.

 

UpToDate

Most medical schools provide this for you and it was easily my most often used resource during my third and fourth year of medical school. It’s like Wikipedia for medicine when Wikipedia doesn’t do a good enough job at explaining something. Or when someone points out that Wikipedia isn’t ‘a reliable resource’. Anyway, it’s amazing and I love it. Bonus tip: click the ‘summary and recommendations’ tab to get a quick snapshot of the article you’re checking out.

Picmonic

If you used Picmonic for step 1 then you should keep using it for step 2. I talked about Picmonic before and it still rings true. Every time I thought about brain tumors, tumors of the bone, any vasculitis, developmental disorder, and everything from biochemistry my Picmonic note cards would pop into my head. I’ll probably be that one resident who puts a Picmonic mnemonic in the presentation slides for morning report. I don’t ‘like like’ Picmonic. I love them.

*Use my link to get 30% off your Picmonic subscription!

Blueprints

Blueprints is like PreTest because they are good for shelf exams but not so much for dedicated step 2 CK studying. I highly disliked Blueprints because it was so long but others liked it for that exact same reason. Each chapter gives you a few bolded key words, tables and figures and explains the topic in great detail (again, too much detail in my opinion). The book ends with 100 NBME style questions with long explanations. I liked PreTest more because of how succinct it was but I have friends who, again, had the complete opposite opinion. To each his or her own.

Tablet > smart phone

If you don’t have a tablet already I would highly recomend purchasing one. If you are short on cash you do not need to purchase an iPad. There are tablets out there for under $100. Sure they aren’t as pretty but all that you realy need them for is accessing UWorld. Yes, you can simply use your smartphone instead of buying another piece of technology but unfortunately every time you have your phone out people will think you are texting. I remember once when I was on my phone doing a UWorld question set while I waited for the operating room to be cleaned and a nurse called me out for ‘texting instead of taking care of my patient’. Said patient was actually sitting next to me in her bed on her phone playing ‘2048’. She was trying to beat my high score and was failing miserably. Anyway, my patient kindly told the nurse to ‘kindly fuck off’. She was one of my favorite patients ever. Moral of the story: if you are on your phone people will think that you are texting no matter if you are using it to cure cancer or are actually texting.

High Yield Board Review for Cardiology Fellows: Vascular Diseases

Below are some of my high yield notes for the general cardiology board examination focusing on vascular diseases with easily sharable supplemental articles and tables my reference.

Aortic Aneurysm

  • Bentall procedure for surgical aortic aneurysm repair
  • Elephant trunk for surgical aortic aneurysm repair
  • thoracic endovascular aortic aneurysm repair

Location:

  • Ascending aorta/root: 60%
  • Descending aorta: 40%
  • Both thoracic and abdominal aorta: 5-10%

Surgical Indications for Thoracic Aortic Aneurysm Repair

ConditionSize Threshold
Aneurysm≥5.5 cm
Bicuspid AV (BAV)≥5.5 cm
BAV with risk factors + low surgical risk≥5 cm
BAC with AVR>4.5 cm
Marfan syndrome≥5 cm
Marfan syndrome + risk factors>4.5 cm
Loeys-Dietz syndrome4 – 4.5 cm
Familial thoracic aortic aneurysm syndromes (TAAD)4.5 – 5 cm
*Abdominal aortic aneurysm≥5.5cm
*Abdominal aortic aneurysm>0.5 in 1 year
  1. Patients with infrarenal or juxtarenal AAAs measuring ≥5.5 cm should undergo repair to eliminate the risk of rupture. (Level of Evidence B)
  2. Infrarenal or juxtarenal AAAs measuring 4.0 to 5.4 cm in diameter should be monitored by ultrasound or computed tomographic scans every 6 to 12 months to detect expansion. (Level of Evidence A)

US Screening for Abdominal Aortic Aneurysm

Patient Level of Evidence
Men 65-75 who have ever smokedB
Men 65-75 who never smokedC
Women 65-75 who have ever smokedI
Women who never smokedD
*B: high certainty of moderate net benefit
*C: selectively offer given moderate certainty of small benefit
*D: no net benefit or possible harm
I: insufficient evidence

Surveillance Imaging in Known Aortic Aneurysm

Abdominal Aneurysm SizeFrequency
25-29 mm4 years
30-39 mm3 years
40-44mm2 years
*≥45 mmYearly
Class IIa, LOE B
*Yearly in both thoracic and abdominal aneurysms if ≥45mm. Otherwise repeat thoracic imaging q2-3 years


Peripheral Vascular Disease

  • Risk factors and odds ratio (95% CI): CAD/CVD 2.27, smoker 2, former smoker 1.87, DM1 1.68, HTN 1.47, age 1.39
  • Clinical Presentation of PAD (i.e. angina of the legs): 50% asymptomatic, 33% atypical limb symptoms, 15% typical intermittent claudication, 2-3% critical limb ischemia
  • Patients at risk of PAD who should be screened (IIa rec): (1) age ≥65yo, (2) Age 50-64 with risk factors (DM2, smoking history, HLD, HTN) or FH of PAD, and (3) age <50 with DM2 and 1 additional risk factor for atherosclerosis
Location of claudicationLocation of disease
CalfFemoral-popliteal ±aorto-iliac
Buttock & calfAorto-iliac
ButtockInternal iliac

Ankle Brachial Index (ABI)

ABIResult
>1.4Non-compressible
1-1.4Normal
0.91-0.99Borderline abnormal
≤0.9Abnormal
*If borderline and good story for claudication: can perform stress ABI (exercise or reactive hyperemia) to augment blood flow through stenosis
** If >1.4: perform toe-brachial index. 20-30% increase is normal. >20 mmHg drop is abnormal
How to perform: use HIGHEST value from DP or PT

Screening for PAD

Treatment of PAD

Acute Limb Ischemia (ALI)


Medium and Large Vessel Vasculitis

ClassificationDiagnosisEtiologyManifestationsTreatment
Large-vessel vasculitisTakatasu arteritis
Age <50, > women, Asain, B-sypmtoms, ±erythema nodosum)– 70% aortic lesions
– Vascular inflammation ➡️ stenosis (long and tapering i.e. rat-tailing) ±aneurysm
– Arm/leg claudication, mesenteric ischemia, stroke, renovascular HTN
– Diastolic murmur, bruit, absent pulses
Steroids, IL-6i, TNFai
Large-vessel vasculitisGiant cell arteritisAge >50, >women, caucasian– HA, jaw claudication, visual disturbances, stroke
– ±Polymyalgia rheumatica (40-60%): stiffness, proximal muscle pain (RF, anti-CCP antibodies)
– Subclavian, axillary stenosis/aneurysm, carotid/vertebral involvement
Steroids

Tocilizumab
Medium-vessel vasculitisPolyarteritis nodosa
Men, ~age 50, rare, associated with HBV infection

Diagnosed clinically
B-symptoms, neurologic complaints (peripheral neuropathy), renal involvement, GI involvement, orchitis, cardiomyopathy, pericarditis, coronary involvementSteroids

±Cyclophosphamide or azathioprine

Antivirals if associated with active HBV infection
Medium-vessel vasculitisKawasaki disease<5yo, Asain children (>Japanese),5 days fever, BL conjunctivitis, mucositis, rash, erythma, or desquamation of hands/feet, cervical lymphadenopathyUntreated: ~25% develop coronary aneurysms

Acute: IVIG ± aspirin. Sometimes steroids

±Anticoagulation if large aneurysms
Variable vessel vasculitisBehçet’s disease
Variable vessel vasculitisCogan syndrome
Single-organ vasculitisIsolated aortitis
Vasculitis associated with probable etiologyInfectious aortitis: syphillis, mycobaterial aortitis, suppurative/mycotic infectious aortitis

Rheumatologic disease: IgG4-related disease, antineutrophil cytoplasmic antibody-associated vasculitis (ANCA), spondyloarthritis, Erdeim-Chester disease, relapsing polychondritis, sarcoidosis

Coronary CT for Cardiology Fellows

The basics of cardiac CT imaging

My notes on coronary computerized tomography (CT).

Anatomy

  • Coronary artery segmentation
  • Normal coronary course
  • Normal anatomy on CT
  • Common anomalous coronary arteries
  • Common anomalous coronary arteries

Classification of anomalous coronary arteries

  1. Anomalies of:
    1. Origin (>LCX from right coronary sinus most common)
    2. Course
    3. Intrinsic anatomy
    4. Termination
  2. Hemodynamic consequence: non/significant
  3. Coronary fistula
  4. Complete myocardial bridging (>LAD most common)
  5. Association with higher risk of sudden cardiac death (SCD)

Normal Anatomy

  • A normal CTCA has a high negative predictive value (98– 100%) for excluding CAD
  • Indications for CTCA:
    • Low-to-intermediate risk patients with acute chest pain and non-diagnostic ECG and serum biomarkers
    • Low-to-intermediate probability of CAD and unable to exercise or with inconclusive functional test results

Malignant Anatomy: associated with chest pain, myocardial ischemia, or sudden cardiac death

  1. RCA arising from left sinus
  2. Left main coronary artery (LMCA) arising from right coronary sinus
  3. LMCA arising from the pulmonary artery

RCA arising from left side- generally better prognosis

  • Right coronary artery originating from the left coronary sinus. RCA in red, Left main coronary artery yellow. The proximal RCA's acute angle take off passes through the pulmonary trunk and aortic root causing moderate compression.
  • Myocardial bridging of the mid LAD
  • Pulmonary trunk level showing LMCA originating from pulmonary artery (red asterisk)
  • Aorta gives rise to RCA. Pulmonary artery gives rise to LMCA, now dilated
  • Again showing aorta gives rise to RCA. Pulmonary artery gives rise to LMCA, now dilated
  • Again showing aorta gives rise to RCA. Pulmonary artery gives rise to LMCA, now dilated
  • Anomalous left coronary from the pulmonary artery (ALPACA or Balnd-White-Garland syndrome)

Ischemic Cardiomyopathy (ICM)

High risk calcification features associated with higher event rates:

  • Low attenuation plaque: <30 Hounsfield units
  • Positive remodeling: lesion with vessel area >10% larger than a proximal normal reference site (remodeling index >1.1)
  • Napkin-ring sign: low-attenuation core surrounded by a rim-like area of higher attenuation (but less than 130 HU)
  • Spotty calcification: <3 mm length calcifications comprising <90°
  • CTA plaque phenotype features
  • CTA plaque phenotype features
  • CAD-RADS scoring and modifiers

Coronary artery calcium score (CACS) of 0

  • Asymptomatic, independent of Framingham risk score: very low risk of events (0.10% per year), safety window of at least 5 years
  • No benefit from aspirin for primary prevention
  • Patients with abnormal lipid profile but CACS 0 have little benefit from statin
  • Stable symptomatic patients with low-to-intermediate pretest likelihood of CAD, a CACS 0 can safely exclude flow-limiting coronary disease
  • CACS of 0
  • CACS of 0. Minimal calcium in the aortic root and aortic valve

Abnormal coronary artery calcium score (CACS)

  • Symptomatic patients with CACS> 400 are at high risk of events (>2% per year), independent of risk factors and functional tests.
  • CACS>1000, even if normal stress testing, have significantly higher risk of major adverse events
  • CACS 1832
  • Bicuspid AV with aortic dilation, and non-obstructive mixed plaque with evidence of positive remodeling`
  • pLAD, mLAD, dLAD in cross section
  • Obstructive CAD in LAD

Coronary Dissection

  • Linear low-density intraluminal image suggestive of focal dissection
  • Moderate ostial RCA stenosis. PRedominantly non-calcified eccentric lesion with low-attenuation core
  • Moderate ostial RCA stenosis. PRedominantly non-calcified eccentric lesion with low-attenuation core

LAD calcification

  • Calcified LAD with severe dLAD lesion
  • Severe focal, eccentric, predominantly non-calcified lesion in mid-to-distal LAD with low attenuation core, positive remodeling, and napkin ring sign

CTO of LCX with RCA collaterals in patient with discordant normal SPECT but abnormal ECG stress (2mm ST-depressions) sent for CTCA to evaluate coronary anatomy

  • Diffuse calcification of D1 and CTO of LCX

ECG Reference Guide For Medical Trainees

A quick reference guide for diagnostic ECG criteria with examples. Will continue to update regularly.


P-Wave Abnormalities

Right atrial enlargement (RAE)

  • 2 things help me remember RAE. First, the normal P-wave on an ECG typically represents the left atrium because the right atrium is typically smaller and it’s electrical current is typically hidden in the left atrium’s electrical signal. Second, the SA node sits in the right atrium. So when the right atrium gets enlarged we start to see it on the ECG. The P-wave gets BIGGER! I think of it similar to what we see in left ventricular hypertrophy. Typically, in a normal QRS complex we only see the left ventricle because it’s size and electrical signal is so much larger than the right atrium (similar to our atria). However, in LVH the left ventricle gets even larger. So the electrical signal it puts out is even bigger too. This is just like what happens in RAE. The right atrium is able to be seen in the P-wave which manifests with TALL P-waves. Thus, the diagnostic criterion are:
  • Inferior lead P-waves: >2.5 mm in height (tall positive P-wave because the SA node is superior in the heart so the electrical signal in the inferior leads, the direction the electrical impulse goes toward, will be larger in size)
  • >1.5mm in V1, V2
  • Clinically can be seen in RVH, COPD, pHTN > CHD >>tricuspid stenosis

Left atrial enlargement (LAE)

  • Back to our discussion about P-waves. In normal physiology the SA node in the right atrium fires and then the signal has to travel all the way over the left atrium. We already know that on normal ECG’s that the P-wave represents the left atrium. Thus, if the left atrium gets enlarged you will see LONGER P-waves because it will take more time for that signal to reach the entirety of the left atrium. Or at least that’s how I remember it in my head. Thus, for LAE think “1 box deep, 1 box wide”. If you can fit 1 small box inside the negatively deflected P-wave you should be thinking about LAE. The diagnostic criterion are:
  • Terminal portion V1 > 1mm deep, >40ms duration
  • Inferior leads: notched P-wave > 120ms

Biatrial enlargement (BAE)

You can also have both diagnostic criterion met for both left and right atrial enlargement. In these cases we simply call it biatrial enlargement. Here’s a quick and dirty reference for atrial enlargement:


Ventricular Hypertrophy

Left Ventricular Hypertrophy (LVH)

There are a LOT of criterion for LVH but the most frequent ones that I use in clinical practice are:

  • aVL >11 (Sokolow-Lyon ‘stand alone‘ criteria)
  • Cornell Criteria: R wave in avL + S wave in V3 > 28mm in men/> 20mm in women (Easy way to remember: CorneLL has 2 L’s, aVL has 1 L. Add them together to remember you use lead V3)
  • Sokolow-Lyon Criteria: S wave in V1 + R wave in V5 or V6 > 35mm
  • Delayed intrinsicoid deflection in V5, V6 >50ms (interestingly this is the only non-voltage criteria for LVH)

LVH can also have a ‘strain pattern’ with T-wave inversions (TWI) as seen in the ECG below.

LVH with strain pattern in I, II, V5, V6

Right Ventricular Hypertrophy (RVH)

  1. RAD: mean QRS axis ≥ 100 degrees
  2. Secondary ST-T segment changes (STD, TWI) in right precordial leads
  3. (R/S ratio in V1 > R/S ratio in V5, V6) or (R/S ration in V6 <1) or (R wave > 7mm in V1)

Clinically, Posterior MI can mimic RVH

  • Factors that favor RVH diagnosis: concomitant RAD, TWI in V1-V2
  • Factors that favor posterior MI: presence of inferior Q-waves

Combined Ventricular Hypertrophy

  • Exists when criteria for both isoloated LVH) and RVH are met
  • Should be suspected when criteria for LVH is present but QRS axis is > 90 degrees or criteria for right atrial enlargement exist
  • R/S ratio approximately equal to 1 in both V3 and V4 (Kutz-Wachtel phenomenon)
Diagnosis: Atrial flutter, LAD, LVH, RVH, iRBBB

Intraventricular Conduction

Left Bundle Branch Block (LBBB)

  1. QRS ≥120 ms
  2. Terminal S-wave in V1 (late forces of QRS should be negative)
  3. I, aVL, V5, V6: Broad notched or slurred R-wave. Occasional RS pattern in V5, V6 may be attributed to displaced transition of QRS complex)
  4. No Q-waves in I, V5, V6 but in aVL a narrow Q-wave may be present without myocardial pathology
  5. Delayed onset of intrinsicoid deflection >60 ms from beginning of QRS to peak of R-wave in V5, V6 but normal in V1-V3 when small initial R-wave can be discerned

Left Anterior Fascicular Block (LAFB)

  1. LAD (QRS axis between -45 to -90 degrees) and mean QRS duration < 120 ms
  2. qR complexes in I, aVL
  3. rS complexes in II, III, aVF
  4. Prolonged R wave peak time in aVL > 45ms (from beginning of QRS complex to peak of R wave)
  5. *Absence of other causes of marked LAD such as inferior MI or LVH

Note: The entire left bundle conduction system of the heart is made up of two fascicles, one anterior and one posterior. The left anterior fascicle supplies fibers to the anterior and lateral walls of the left ventricle. The above criteria of left anterior fascicular block do not apply to patients with congenital heart disease in whom left-axis deviation is present in infancy.

Left Anterior Fascicular Block (LAFB)

Left Posterior Fascicular Block (LPFB)

  1. RAD (QRS axis 90 to 180 degrees in adults) with mean QRS duration < 120 ms
  2. rS complexes in leads I and aVL
  3. qR complexes in leads II, III and aVF
  4. *Absence of other causes of right axis deviation including lateral MI, dextrocardia, or RVH

Note: The entire left bundle conduction system of the heart is made up of two fascicles, one anterior and one posterior. The left posterior fascicle is shorter and thicker than the left anterior, and receives dual blood supply from both the left and right coronary arteries. Multivessel coronary artery disease is the most common cause of left posterior fascicular block.

Right Bundle Branch Block (RBBB)

  1. QRS ≥ 120 ms
  2. V1, V2: RSR’ with secondary R-wave usually wider than initial R-wave
  3. Minority of patients may have a wide and often notched R wave pattern in lead V1 and/or V2
  4. S wave duration > than R wave or > 40 ms in leads I and V6
  5. Normal R peak time in leads V5 and V6 but > 50 ms in lead V1

Of the above criteria, the first 3 should be present to make the diagnosis. When a pure dominant R wave with or without a notch is present in V1, the 4th criteria should be satisfied

ECG Right Bundle Branch Block RBBB 5

Incomplete Right Bundle Branch Block (iRBBB)

  1. Same criteria for RBBB but QRS < 120ms but > 100ms

Non-specific inter-ventricular conduction delay

  1. QRS ≥ 110 ms
  2. Specific criteria for RBBB, LBBB not met

Quick and dirty reference to compare LBBB and RBBB:

Bundle Branch Block : Mnemonic | Epomedicine

Atrial Rhythms

Sinus Rhythm

In medical school we are taught this incorrectly. The correct way to tell that a P-wave is of sinus origin is that they are:

  1. Upright in the inferior leads (remember the sinus node is in the right atrium so the electrical wave will go from the top down and thus be positive inferiorly)
  2. Biphasic in V1
  3. Axis between 0 to 75 degrees (i.e. upright in the inferior leads)

The number of P-waves before every QRS complex is irrelevant. You can have sinus rhythm but be in complete heart block. Or have sinus rhythm but have second degree type I or type II heart block. Generally however they should have the same morphology. A single P-wave with a different morphology can indicate a premature atrial complex (PAC) but if you have multiple different P-wave morphologies then you might be dealing with wandering atrial pacemaker (WAP) or multifocal atrial tachycardia (MAT). I think of WAP and MAT as the same rhythm across a spectrum ranging from a normal heart rate (WAP) to a fast heart rate (MAT).

Sinus Arrhythmia

Diagnostic criteria:

  • Normal P wave axis (0 to 75 degrees; i.e. upright in leads I and II)
  • P-P interval varies by > 10% or 0.16 seconds

tl;dr normal sinus P-waves (as above) but P-P interval varies by >10% or 160ms (4 little boxes). ECG intervals can vary with respiration but they shouldn’t vary by more than 10%. Often incidental without major clinical significance

High Yield Board Review Notes for Cardiovascular Disease Fellowship

The following are iterative notes that I take while studying for my general cardiology, echocardiography, and nuclear cardiology board exams. Making them public so I can access them on the go and help out anyone else looking for similar information.


Valvular Heart Disease

Aortic Insufficiency/Regurgitation (AI/AR)

Severe AI, indications for surgery

  1. Asymptomatic: EF ≤55%
  2. Asymptomatic: EF >55% + LVESD >50mm or LVESDi >25mm/m2
  3. Asymptomatic: EF >55% with progressive decline in EF to low-normal (55-60%) with LVEDd >65mm
  4. Symptomatic
  5. Other concurrent cardiac/aortic surgery

  • Severe AI surgical indications
  • Accurate measurements
  • Severe AI via echo
  • Chronic sever eaortic regurgitation (AI/AR) symptom progression
  • Severe AI: survival and LV function
  • Severe AI: survival and NYHA class

Aortic Stenosis

  • Prostehtic AV algorithm

Low-Flow Low-Gradient AS (LF-LG AS)

  • LFLG algorithm 2

Bicuspid Aortic Valve

  • Bicuspid AV algorithm
  • Frequency of bicuspid anatomy
  • Screening guidelines
  • Bicuspid AV imaging surveillance guidelines
  • Bicuspid aortic valve surgical intervention guideline recomendations

Surgical indications for dilated aortic root/ascending aorta

Aorta sizeIndicationClass recomendation
≥ 5.5 cmRisk factors for dissection (FH, growth rate >0.5cm/year, bicuspid AV)I
> 5.0 cmRisk factors and low surgical risk <4% (FH of dissection, growth 3-5mm/year, aortic coarctation, small stature)IIa
> 5.0 cmLow risk, experienced surgeon, expert centerIIa
> 4.5 cmBicuspid AV planning for surgical AVR for AS/AIIIa

*Aortic root measured at sinus of Valsalva

ACC Guideline: Aortic Surgery for Bicuspid AV

Mitral Regurgitation

  • Simplified asymptomatic severe primary MR algorithm
  • Primary mitral regurgitation (MR) algorithm
  • Qualitative and quantitative MR by echocardiography (TTE)
  • Mitral valve anatomy
  • Etiologies of chronic mitral regurgitation (MR)- acute and chronic
  • Pathophysiology of acute and chronic MR
  • Qualitative assessment of MR
  • Clinical workflow for diagnosis and management of MR
  • MR algorithm
  • Qualitative and quantitative MR by echocardiography (TTE)
  • Medical therapy for chronic MR
  • Surgical interventions for asymptomatic chronic primary MR
  • Surgical interventions for asymptomatic chronic primary MR
  • Surgical interventions for asymptomatic chronic primary MR
  • Transcatheter edge-to-edge repair (TEER) for severe primary MR

Mitral valve prolapse and flail

Carpentier Classification of MR

  • Type 1: normal leaflet mobility (primary: endocarditis, perforation, clefts; secondary: dilated annulus)
  • Type 2: excessive leaflet mobility (prolapse, flail)
  • Type 3: restricted leaflet motion
    • 3a: in systole and diastole (Fibrosis of subvalvular apparatus: rheumatic, radiation, drug-induced injury, inflammatory conditions)
    • 3b: only in systole (Leaflet or chordal tethering: ICM, NICM causing LV dilation)

Mitral Valve Regurgitation Review Article

Chronic MR Algorithms

  • Qualitative and Quantitative Assessment of MR severity by echo
  • Recommended Treatment of severe secondary MR
  • Severe MR Algorithm
  • Recommended Treatment of severe secondary MR
  • Algorithm for Eligibility of Transcatheter Edge-to-Edge Repair (TTER) in severe MR
  • Semiquantitative parameters in MR
  • Quantitative measures for severe MR by PISA png
  • Pulsed Doppler Volumetric Quantification of severe MR
  • Indications for exercise stress testing in MR
  • Routine monitoring of MR via echo
  • MR treatment algorithm

Indications for TTE, TEE in MR

  1. Initial evaluation if suspicious for MV disease or MVP
  2. Initial evaluation of known ur suspected MR
  3. Annual evaluation in severe MR
  4. Reevaluation of MR with change in clinical status
  5. TEE to determine mechanism of MR and suitability of valve repair
  6. *Inappropriate: routine evaluation of MVP with (1) no or mild MR and (2) no change in clinical status

Mitral Valve Prolapse (MVP)

Arrhythmic MVP

  • Non-invasive markers associated with sudden cardiac death (SCD) despite not having severe MR
  • High density of PVCs, inferior TWI, spiked systolic high-velocity signal on echo (Pickelhaube sign), myocardial/papillary scar on MRI
  • Pickelhaube sign: peak systolic lateral mitral annular velocity ≥16 cm/s. More likely to have malignant arrythmia in those with myxomatous bileaflet MVP (‘B’ in image below)
Non-invasive markers associated with SCD in MVP

Acute Severe MR

  • Rapid equalization of pressure across LA/LV may only cause a short, unimpressive murmur (may only appear as mild MR)
  • *Suspect in acute heart failure with normal LV systolic function
  • *Suspect in decreased LVOT VTI despite hyperdynamic LV EF (suggestive of low forward flow- consistent with severe MR)

Mitral Stenosis

  • Stages of mitral stenosis (MS)
  • Stages of mitral stenosis (MS)
  • Wilkins Score for rheumatic mitral stenosis (MS)
  • Mitral stenosis (MS) pressure half-time
  • Mitral stenosis (MS) pressure half-time 2
  • Mitral stenosis (MS) mean gradient (MG)
  • Mitral stenosis (MS) PISA
  • Continuity equation for mitral stenosis (MS)
  • Mitral valve area via LHC
  • Gorlin formula: mitral valve area via LHC
Typical appearance of rheumatic mitral stenosis

2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease


Invasive Hemodynamics Review


Classic Valvular Murmurs

LesionTimingQualityRadiationSeverity
ASCrescendo-decrescendo

Gap between S1, murmur, and S2
Harsh, noisy
MRHolosystolic through S2

Starts with S1 through S2
Blowing, high pitchedAnterior prolapse/flail: axilla, left intrascapular area

Posterior: anteriorly along aortic outflow in left parasternal area (can be confused with SEM)
Weak correlation between intensity and severity

S3: increase in diastolic flow across MV orifice during rapid filling phase  

Increased P2 intensity: pHTN   Enlarged, displaced LV impulse: LV dilation
Post PVCMR changes little: high gradient between LA/LV in SR and post-PVC*AS murmur increases post-PVC as SV after PVC is greater (more flow)  
MVPEarly, mid-systolic click ➡️ systolic murmur±High pitched, ‘whoop’ sound Maneuvers on click and murmur:
– ⬇️ LV volume/preload (Valsalva, squat to stand): murmur/click occur earlier in systole
– ⬆️ LV afterload (squatting): murmur/click occur later in systole
Severe MVP: holosystolic murmur 
Differentiating AS from MR

Prosthetic Valves

Prosthetic Aortic Valves

Pressure recovery: due to small aorta causing falsely elevated mean gradient readings and thus low AVA

Prosthetic Valve Thrombosis

Prosthetic Valve Guidelines from JASE (Journal of American Society of Echocardiography)


Heart Failure

Non-Ischemic Cardiomyopathy (NICM)

2022 AHA/ACC/HFSA Guidelines

Abnormalities in Hepatic Vein Flow on Doppler

Amyloidosis

Diagnostic algorithm for diagnosis of amyloidosis

Figure 2.
99mTechnetium-pyrophosphate imaging for transthyretin cardiac amyloidosis

Treatment for ATTR amyloidosis

Medical therapies for amyloid

  • Tafamadis: amyloidosis but not NYHA IV
  • Patisiran: for ‘papa’- familial amyloid neuropathy

Pulmonary Hypertension (pHTN)

Peak TR jet velocity (m/s)Presence of other echo ‘PH Signs’TTE probability of pHTN
≤2.8 or not measurableNoLow
≤2.8 or not measurableYesIntermediate
2.9-3.4NoIntermediate
2.9-3.4YesHigh
>3.4Not requiredHigh

Echo Findings in Pulmonary Hypertension (pHTN)

VentriclesPulmonary ArteryIVC, RA
RV/LV basal diameter ratio >1RVOT acceleration time (AT) <105ms ±midsystolic notchingIVC >21mm, <50% inspiratory collapse with sniff (or <20% with quiet inspiration)
IVS flatteningEarly diastolic PI velocity >2.2m/sRA size >18cm2 at end-systole
PA diameter >25mm

Chagas Cardiomyopathy

Hypertrophic Cardiomyopathy (HCM)

Surgical options and complicationsSeptal myectomy –> LBBB
Alcohol septal ablation —> RBBB
DysopyramideQT-prolongation
Physical exam maneuversLouder murmur with Valsalva (decreased preload)Softer murmur with hand grip
High risk features for SCD1. First degree relative SCD
2. IVSd ≥30mm (IIa indication: ICD for primary prevention)
3. Unexplained syncope in past 6 months
4. LV apical aneurysm
5. EF <50%
6. NSVT: children (IIa), adults (IIb)
7. Extensive LGE on CMR (IIb)
8. Exercise induced NSVT or abnormal BP response to (drop ≥20mmHg) + high risk features (IIa- it is IIb if no high risk features)
HCM family screening in 1st degree relatives

Echo following septal myectomy for HCM with edge-to-edge (Alfieri) repair of the mitral valve

  • Anterior and posterior leaflets are sutured together in the mid portion giving the typical appearance of a double-orifice mitral valve
  • The color jet that can be seen on the septal wall represents flow from a coronary-LV fistula, a common benign finding after septal myectomy procedures
  • May lead to functional mitral stenosis (MS) requiring surgical interventions following edge-to-edge repair

Coronary Artery Disease

Guidelines/Review Articles

CABG (coronary artery bypass graft) Guidelines

UA/NSTEMI

  • TIMI risk score for UA/NSTEMI: predicts all-cause mortality, new/recurrent MI, severe recurrent ischemia requiring urgent revascularization through 14 days
  • GRACE score for UA/NSTEMI: predicts in-hospital mortality and death or MI
  • Risk stratification into ischemia guided, immediate invasive

NSTEMI: Early invasive strategy (within 24 hours) if:

  1. Elevated troponin
  2. Dynamic ST-changes
  3. Recurrent angina
  4. EF <40%
  5. Recent PCI
  6. Prior CABG
  7. DM
  8. Intermediate/high risk score (GRACE >140)

ACS Medications and Anti-Platelet Agents

NTg and PDE5i interaction

  • NTg contraindicated 24 hours of last use of sildenafil (Viagra, Revatio)
  • NTg cointraindicated 48 hours of last use of tadalafil (Cialis)

Coronary Microvascular Dysfunction

  • Coronary flow reserve (CFR) <2.5 indicative of microvascular disease in the absence of obstructive epicardial CAD
  • Treatment: ± beta blockers, CCB but not definitive guideline

Coronary Flow Reserve

  • iFR ≤0.89 or FFR <0.8

STEMI

  • RCA vs. LCX: STE III >II indicates RCA

Spontaneous Coronary Artery Dissection

  • Risk factors: fibromuscular dysplasia (FMD), postpartum status, multiparity, connective tissue disorders, systemic inflammatory conditions, and hormonal therapy
  • FMD screening: screen for extracoronary disease from brain to pelvis with CTA or contrast-enhanced MRA for aneurysms, dissections, and other areas of FMD
  • Renal aneurysms: treat when >2cm
  • Renal stenosis: balloon angioplasty > stenting. Stent reserved for procedural complications (i.e. dissection)


General Cardiology

Guideline Indications

TreatmentIndication
EntrestoHFrEF (≤40%) and NYHA II, III
IvabridineHFrEF (≤35%) at max tolerated dose of bb in SR with HR ≥70bpm
IV iron sucrose or ferric carboxymaltoseNYHA II, III and at least 1 of the following: 1. Ferritin <100 ng/mL2. Ferritin 100-299 ng/mL but iron sat <20%
PatisiranFamilial amyloid neuropathy
ICD, primary prevention1. EF ≤35%, NYHA II, III due to N/ICM
2. EF ≤30%, NYHA I, II, III
CRT indications1. LBBB with QRS ≥150 msec
2. EF ≤35%
3. NYHA II, III or ambulatory type IV
4. Already on GDMT
(LOE A for NYHA class III, IV and LOE B for NYHA class II)

ICD Indications

EFNYHAEtiologyClass Indication
≤35%II-IIIN/ICMI
≤35%INICMIIb
≤30%IICMI
≤40%Inducible VT/VF on EPSICMI
>55%Inducible VT/VF on EPS with extensive scarring on PET/MRIBrugadaIIb
>55%Inducible VT/VF on EPS with extensive scarring on PET/MRISarcoidIIa

Hypertension (HTN)

TypeDefinition
Resistent HTN≥130/80 on 3 meds for ≥ 1 month
Refractory HTNNot adequately controlled on 5 meds
PseudoresistentWhite coat HTN
MaskedNormal in office, high at home

Genetics

MutationAssociated Disease
Lamin A/CSkeletal muscle dystrophies
Notch 1Bicuspid AV, early AV calcification
T-box 5Holt-Oram syndrome (abnormal thumbs, ASD, VSD, HCM, conduction disease)
FBN1Fibrillin-1. 90% AD for Marfan syndrome
COL3A1Collagen- Ehlers-Danlos syndrome

Long QT-Syndromes

SyndromeGeneFunctional EffectAssociationInheritance
LQTS 1KCNQ1⬇️ IKSSwimmingAD; AR, ~30-35%
LQTS 2KCNH2⬇️ IKRStartleAD, ~25-30%
LQTS 3SCN5A⬆️ INASleepAD, ~5-10%
JLNS 1, 2KCNQ1, KCNE1⬇️ IKRDeafnessAR, very rare

Genetic Screening

  • Start with index family member with unknown or uncertain patterns (athletes with LVH or apical hypertrophy)
  • Idiopathic dilated cardiomyopathy without known mutation in family: first degree relatives TTE q3-5 years

Physical Exam

MurmurLesionLocation Best Heard
Fixed split S2ASD 
Single 2nd heart soundTOF 
Absent A2AS 
Absent P2Pulmonary stenosis 
Loud P2pHTN 
Worsens with ValsalvaHOCM (decreased preload) 
Diastolic murmur?Subaortic membrane 
Early systolic clickBicuspid AV (stiff but mobile)Left 2nd IC space, apex
Mid-systolic clickMVPLeft lower sternal border
Diastolic opening snapMS (and diastolic rumble)Left lower sternal border in LLD position

JVD Physical Exam Findings

DiagnosisJVD Finding
Constrictive pericarditisProminent Y descent, ±prominent X descent
TamponadeProminent X descent, absent Y descent
RV infarctionAbsent X and Y descent
VT, CHBVariable size A-waves (‘cannon A-wave’)

Vascular Diseases

Abdominal Aortic Aneurysm (AAA)

Society for Vascular Surgery recommendations, surveillance intervals for asymptomatic AAA:

  1. >2.5 cm but <3.0 cm, rescreen after 10 years
  2. 3.0-3.9, repeat imaging every 3 years
  3. 4.0-4.9, repeat imaging in 12 months
  4. 5.0-5.4, repeat imaging in 6 months

Indications for elective repair of an asymptomatic AAA include:

  1. >2.5 cm but ≤5.5 cm
  2. rapid expansion
  3. AAA associated with peripheral arterial aneurysms or peripheral artery disease.

May-Thurner Syndrome

PathophysiologyAnatomical variant: right common iliac artery overlies and compresses the left common iliac vein against lumbar spine
Risk factorsLeft lower DVT
Scoliosis
Female sex
OCP use or recent pregnancy
Left lower extremity swelling in absence of DVT
Clinical presentationYoung adult woman with left leg swelling and DVT
Diagnostic testMagnetic resonance venography of the pelvis
References
1. Peters M, Syed RK, Katz M, et al. May-Thurner syndrome: a not so uncommon cause of a common condition. Proc (Bayl Univ Med Cent) 2012;25:231-3.
2. Baglin T, Gray E, Greaves M, et al.; British Committee for Standards in Haematology. Clinical guidelines for testing for heritable thrombophilia. Br J Haematol 2010;149:209-20.
3. Society for Vascular Medicine. Five Things Physicians and Patients Should Question (Choosing Wisely website). 2015. Available at: http://www.choosingwisely.org/wp-content/uploads/2015/02/SVM-Choosing-Wisely-List.pdf. Accessed 03/22/2019.
May-Thurner Syndrome

Electrophysiology (EP)

CRT Indications

Antiarrhythmic Medications

*DFT: defibrillator threshold
SyndromeGeneMiscellaneous
ARVCPKP-2Plakophillin-2Intracellular calcium signaling abnormality
ARVCDSPDesmoglein-2Intracellular calcium signaling abnormality
ARVCDSC2Desmocollin-2Intracellular calcium signaling abnormality
ARVCJUPPlakoglobinIntracellular calcium signaling abnormality
MarfanFBN1Fibrillin-1Associated with aortic aneurysm, dissection
Ehlers-DanlosCOL3A1Collagen type 3, a1Associated with aortic aneurysm, dissection
Loeys-DietzTGFB1, 2Transforming growth factorAssociated with aortic aneurysm, dissection
CPVT1RYR-2Ryanodine receptorAD (>70% of cases, intracellular Ca-signaling)
CPVT2CASQ2CalsequestrinAR inheritence
LQTS1KCNQ1K current IKsbb (nadalol > propanalol)
***Associated with SCD while swimming
LQTS2KCNH2K current IKrK-supplementation (IIb rec)
LQTS3SCN5Aalpha-unit of INa±Mexilitine (IIb rec)
GAIN of function mutation
BrugadaSCN5ALOSS of function mutation
Hereditary PAHBMPR-2Bone morphogenic protein receptorAssociated with >70% of inherited pulmonary arterial HTN
DCMLamin A/C± skeletal muscle dystrophy
T-box5Holt-Oram (hand heart, ASD)
Notch 1Bicuspid AV, premature AV calcification
Genetic mutations associated cardiac conditions
Cardiac Genetics Chart

Supraventricular Tachycardia (SVT)

  • Focal AT- ongoing treatment options

Early Afterdepolarization (EAD) and Delayed Afterdepolarization (DAD)

Localizing VT Origin: LVOT vs. RVOT

  • Step 1: V1
    • LBBB: anterior to posterior- RVOT
    • RBBB: posterior to anterior- LVOT
  • Step 2: concordance
    • Positive: originates near base
    • Negative: originates near apex
  • LVOT VT
  • RVOT VT
  • RVOT: later R-wave transition (≥V3)
  • LVOT: earlier R-wave transition, LBBB, inferior axis

Bidirectional Ventricular Tachycardia (aka CPVT or catecholaminergic polymorphic VT)

  • Also known as Familial polymorphic VT
  • Inheritance: RyR2 gene mutation is AD, CASQ2 gene mutation is AR
  • Treatment: Nadolol (non-selective β1 and β2 agonist)
  • Dose: 0.8 mg/kg of nadolol ~ 1 mg/kg of metoprolol SR
  • Flecainide also used (ask EP)
Source: Leren, I., Saberniak, J., Majid, E., Haland, T., Edvardsen, T., & Haugaa, K. (2016). Nadolol decreases the incidence and severity of ventricular arrhythmias during exercise stress testing compared with β1-selective β-blockers in patients with catecholaminergic polymorphic ventricular tachycardia. Heart Rhythm13(2), 433-440. doi: 10.1016/j.hrthm.2015.09.029

2:1 AV Block

AV nodeHPS
Type of BlockMobitz I >> Mobitz IIMobitz II > Mobitz I
Conducted QRSNarrow (unless preexisting BBB)Wide (except intra-His block)
Escape rhythmReliable (narrow QRS)Unreliable (wide QRS)
PR on conducted beatsLongNormal
*Carotid sinus pressure Block worsensBlok improves
*Exercise/atropineImproves blockBlock worsens
Characteristics to identify site of block in 2:1 AVB

Stroke (CVA) Management

Blood Pressure

  1. If tPA used: BP should be lowered <180/110 prior to tPA administration
  2. After tPA: <180/105 for at least 24 hours post-tPA
  3. No tPA: only treat if >220/120
  4. Can treat if no tPA plus other reason to treat (Aortic dissection, pre/eclampsia, unstable CAD, acute HF)

CHA2DS2-VASc

  • 2 points: age ≥ 75 years and history of stroke/TIA/thromboembolism

Contraindications (CI) to tPA

AbsoluteRelative
History of hemorrhagic stroke or stroke unknown originTIA in prior 6 months
CVA within previous 6 monthsOral anticoagulation
CNS neoplasmPregnancy or first post-partum week
Major trauma, surgery, or head injury in past 3 weeksNon-compressible puncture site
Bleeding diathesisTraumatic resuscitation
Active bleedingRefractory HTN (sBP > 180)
Advanced liver disease
Infective endocarditis
Active peptic ulcer

Pulmonary Embolism


Cardiac Oncology

  • Dexrazoxane: prevent anthracycline-induced cardiotoxocity
  • Anthracycline cardiotoxicity: risk if >250mg/m2

Congenital Heart Disease (CHD)

D-Loop Transposition of the Great Arteries (D-TGA)

  • Atrio-ventricular concordance and ventricular arterial discordance
  • 2nd most common cyanotic congenital lesion (#1 is ToF)
  • Associated defects: VSD (~40%), pulmonic stenosis (PS), coronary artery anomalies
  • D-TGA anatomy
  • D-TGA Surgical Corrections
  • D-TGA surgical correction complications
  • Complications of arterial switch
  • Event free survival following atrial switch
  • Apical 4 chamber view showing anterior transposed aortic valve with posterior pulmonary valve behind it

Complications Following D-TGA Surgical Correction: Arterial Switch (Mustard/Senning Procedure)

  1. Arrhythmia: sinus node dysfunction, frequent SVT
  2. Systemic RV: 25% develop heart failure in their 30’s
  3. Tricuspid regurgitation (TR): functional due to annular dilation

Complications Following D-TGA Surgical Correction: Atrial Switch

  1. Supravalvular AS, pulmonic stenosis (AS), PPS (pulmonary artery stenosis)
  2. Coronary stenosis at re-implantation site
  3. Branch pulmonary artery stenosis
  4. Neo-aortic dilation and AI

L-TDA (or congenitally corrected-TGA)

  • Double-discordance (RA to LV to PA, LA to RV to aortia)
  • Non-cyanotic
  • Treat severe TR like severe MR in normal patients
  • Complications: TR, RV dysfunction, CHB (complete heart block)
  • L-TDA (ccTGA)
  • Complications of L-TGA


Biostats

TermDefinitionExample
Relative risk reduction (RRR)Rate in treatment/rate in placebo10%/20%=0.5
Absolute risk reduction (ARR)(Rate in placebo)-(rate in treatment)20%-10%=10% or 0.1
Number needed to treat (NNT)1/(ARR)1/(0.1)=10 so treat 10 patients over 2 years to prevent 1 event
Example: over a 2 year period therapy A has an event rate of 10% and placebo has an event rate of 20%

Echocardiography

Physics

Speed of sound propagation through tissue: 1540 m/s

Mitral Valve Leaflets on TEE

MV Leaflets on TEE

Stress Testing

Duke Treadmill Score= minutes of exercise – (5 x mm of ST-depression) – (4 x anginal index)

  • Anginal index: 0 for no angina, 1 for non-limiting angina, 2 for having to stop exercise due to angina
  • Positive score is good. Possible to get a negative score
  • Score ≤ -11 is high risk (79% survival at 5 years), -10 to +4 is medium risk (95% survival at 5 years) ≥5 is low risk (99% 5 year survival)
  • Consider LHC for high risk patients (≤ -11)

Nuclear Cardiology

Occupational Dose Limits

1 Rem = 0.01 Sv (international standard unit)

LocationRemSv
Whole body (organs)5 Rem0.05 Sv
Skin50 Rem0.5 Sv
Lens of eye15 Rem0.15 Sv
Pregnant workers
(Over gestation period)
500 mRem5 mSv
Fetus
(non-occupational worker)
500 mRem5 mSv
General public100 mRem1 mSv

Shielding

Alpha particles

Particle typeShield requirement
Alpha particlesSheet of paper
Beta particlesPlastic/clothing
Gamma raysInches/feet of concrete or lead

Common artifacts

  • LBBB: anterior septum (occurs least frequently with NM stress)

Abnormal TID (~1.36, exercise ≥1.29) with normal perfusion: special considerations

  1. HTN with LVH
  2. Difference in HR between rest and stress
  3. Technical difficulties in image acquisition

Lyme Carditis | How Lyme Disease Can Involve the Heart

I’m starting a new section on my blog and YouTube channel bringing you some cool cardiology related topics that you might not have heard about. To kick things off I wanted to talk about Lyme disease- and more specifically a possible complication of Lyme disease known as Lyme carditis. And if you prefer videos to reading check out my YouTube video on the topic and be sure to give it a like and subscribe!

Background: what is Lyme Disease?

Lyme disease is caused by the bacterium Borrelia burgdorferi (and rarely Borrelia mayonii). It is transmitted to humans through the bite of an infected tick, as depicted below.

Lyme Disease: Borrelia burgdorferi - YouTube

Why is it called Lyme Disease?

Lyme disease got it’s name from the small coastal town in Connecticut back in 1977 when Yale researchers identified clusters of what they initially called Lyme arthritis but then changed the name 2 years later to Lyme disease (1).

What are typical symptoms?

Classic Lyme disease typically causes a ‘bullseye-like rash’ on the skin on average 7 days after the initial tick bite but can happen anywhere between 3-30 days after the initial tick bite known. The medical term for this is erythema migrans. Erythema migrans can manifest differently, as below (2). It is rarely itchy or painful and can have a variable appearance. Additionally in dark skinned individuals it can be difficult to appreciate or visualize well.

Other symptoms that can happen anywhere from days to months after the initial tick bite include headache, neck stiffness, and severe joint pain and swelling that normally involve the knees and other large joints. So why is a cardiology fellow talkign about Lyme disease? Because a potentially serious and life threatening complication of Lyme disease is Lyme carditis.

What is Lyme carditis?

Lyme carditis occurs when the bacterium infects the heart tissue and disrupts the normal electrical conduction system of the heart. This can have a variable clinical expression. The most serious complication is complete heart block.

What is complete heart block?

To understand the complete heart block let’s look at what normal conduction of the heart looks like. To create a coordinated heart beat your heart conducts electrical impulses down a network of nerves. It goes from the SA (sino-atrial) node to the AV (atrio-ventricualar) node, then down to both ventricles, as below.

In complete heart block the top and bottom chambers of the heart are unable to communicate with one another and beat independently. This is also why complete heart block is also referred to as third degree AV block because the electrical impulses are unable to get through the AV node.

Why is complete heart block a big?

Normally the top chamber of the heart is in charge. It sends impulses down the electrical system of the heart and the ventricle does as its told. So what happens when the ventricle never receives any of those electrical signals? Your heart has a backup system for these very instances but it is far from perfect. This back-up system is normally inhibited by electrical impulses received from the SA or AV node but when it never receives those impulses it generates a ventricular rate of about 20-40 beats per minute. This means that you might only be able to sustain a heart rate of about 20-40 beats per minute! Additionally this back-up system isn’t always 100% and in Lyme carditis can lead to a fatal arrhythmia. It is serious and should be treated in the hospital.

What are the symptoms of complete heart block?

A slow heart rate also explains symptoms of complete heart block. Think about what happens everyday of your life when you stand up to walk around- your heart beats faster. If your heart can’t increase the rate that your ventricle beats then your brain is not going to get enough blood and you will feel faint, lightheaded, dizzy, and could even pass out. Passing out, or syncope, is your body’s way of making the heart not have to work against gravity but can also seriously hurt you or somebody else depending on how you fall. Other symptoms of complete heart block can include symptoms severe shortness of breath, palpitations, or chest pain.

How do we treat Lyme carditis?

The first thing we do is treat empirically for Lyme disease with antibiotics. The confirmatory lab tests can take a while to get back and some people don’t develop antibodies until a few weeks after infection. So we don’t waste any time and start treating as the benefit fo treatment often far outweigh the risk of the antibiotics. In the hospital we typically use Ceftriaxone and then switch to oral Doxycycline for a typical duration of about 21 days.

Not everyone who develops Lyme carditis develops complete heart block. There are varying degrees of heart block. About 4-10% of patients with Lyme disease develop some form of Lyme carditis (3). Out of the 4-10% of patients who develop Lyme carditis, about 90% of those only develop 1st degree atrioventricular block (AVB). 1st degree AVB is a benign form of AV block and can often be seen in normal otherwise healthy patients in the general population. However patients who develop new 1st degree AVB in the setting of Lyme disease infection should be watched in the hospital on continuous cardiac telemetry monitoring because it is a good predictor of those who might develop complete heart block.

If you develop hemodynamically significant heart block we often use a temporary pacemaker to ensure that your heart rate is adequate. We place place these through the jugular vein and depending on the type of temporary pacemaker that your receive are either floated to sit in the right ventricle or are screwed into the heart to ensure adequate electrical transmission. Depending on the type, temporary pacemakers are only able to stay in place between 2-7 days and are not a permanent solution.

The good news is that most people who develop complete heart block due to Lyme carditis fully recover with antibiotics and do not require a permanent pacemaker.

How do you prevent Lyme disease and where is it found?

The last teaching point I’ll make for is the importance of checking for ticks after you leave a heavily wooded area. Lyme disease is endemic to the northeast, north-central, and mid-Atlantic regions of the US but can be found elsewhere, as below.

U.S. map reported cases of Lyme Disease at a county-wide level

How do you remove a tick safely?

Now let’s say you notice a tick attached to you. What do you do? Try to get a small tweezers if you can and grasp it from as close to your skin surface as you can, as below.

Unfortunately if you just grab it from the body you can potentially rip off the body and leave its mouth stuck on you. The goal is to get the tick off you ASAP! So don’t use remedies like paints, nail polish, or petroleum jelly to wait for it to fall off. After you remove the tick you can flush it down the toilet, kill it in alcohol, or drop it in a sealed bag.

Then call your doctor

Questions we will ask will attempt to narrow the timeline of when the tick attached to you. Interestingly it takes about 36 hours being attached to you for the tick to transmit the bacterium to you. The reason for this is that the bacteria lives inside the tick gut and it takes about 36 hours for the tick to get so engorged on your blood that it actually vomits and in doing so transmits the bacteria before detaching and falling off.

So technically if you went hiking and noticed a tick one hour later then you might not need any treatment for Lyme disease. The reason why it’s important to call your doctor is that a prophylactic treatment for Lyme disease is a single dose of oral doxycycline which typically outweigh the risks of possible contracting and developing complications of Lyme disease.

Works Cited

  1. Delaware, T. (2020). Lyme Disease Information – Delaware Health and Social Services – State of Delaware. Retrieved 28 July 2020, from https://www.dhss.delaware.gov/dhss/dph/epi/lyme.html#:~:text=Lyme%20disease%20gets%20its%20name,the%20attention%20of%20Yale%20researchers
  2. Lyme disease rashes and look-alikes | CDC. (2020). Retrieved 28 July 2020, from https://www.cdc.gov/lyme/signs_symptoms/rashes.html
  3. Scheffold N, Herkommer B, Kandolf R, May AE. Lyme carditis–diagnosis, treatment and prognosis. Dtsch Arztebl Int. 2015;112(12):202-208. doi:10.3238/arztebl.2015.0202

I hope you guys enjoyed this post. If you liked this post drop a comment below and subscribe so you don’t miss my next post or drop a comment below if there’s something cardiology related that you think would make a cool post or YouTube video and I’ll see if I can make one for yah.

Echo Cheat Sheet For First Year Cardiology Fellows

When my co-fellow and started our cardiology fellowship we wish we had an echocardiography reference value cheat sheet. So we decide to make one for our new first year fellows! Our hope is that by having all of the reference values organized in one easily accessible place online that we can ease any new cardiology fellow into their new role. Instead of making it a Word document or PDF we wanted to share it with any other fellows who may find this useful. We will continue to update it with useful educational links, images, and videos over time. *Please only use this as a reference. The most reliable sources of information are ASE guideliens*

Echocardiography Reference Values

Normal Values for Aorta via 2D echo (Indexed to BSA)

Normal intervalIndexed interval
Aortic annulus20-31 mm12-14 mm/m2
Sinus of Valsalva29-45 mm15-20 mm/m2
Sinotubular junction22-36 mm13-17 mm/m2
Ascending aorta22-36 mm13-17 mm/m2
Aortic arch22-36 mm
Descending aorta20-30 mm

Aortic annulusSinus of ValsalvaSinotubular junctionAscending aortaAortic arch
AgeMenWomenMenWomenMenWomenMenWomenMenWomen
<3011.4 ± 1.211.4 ± 1.115.3 ± 1.815.5 ± 1.512.7 ± 2.313.5 ± 1.414.3 ± 1.615.1 ± 1.610.1 ± 1.310.7 ± 1.0
30-3911.4 ± 1.111.7 ± 1.015.7 ± 1.316.5 ± 1.613.3 ± 1.314.3 ± 1.514.5 ± 1.416.4 ± 1.810.8 ± 1.311.6 ± 1.6
40-4911.5 ± 0.911.7 ± 1.016.6 ± 1.516.8 ± 1.414.1 ± 1.514.6 ± 1.215.5 ± 1.516.4 ± 1.411.3 ± 1.311.5 ± 1.2
50-5911.5 ± 0.912.0 ± 0.916.8 ± 1.717.9 ± 1.614.1 ± 1.515.7 ± 1.316.2 ± 1.618.0 ± 1.411.3 ± 1.212.7 ± 1.1
60-6912.1 ± 1.011.7 ± 1.117.8 ± 1.617.5 ± 1.715.1 ± 1.614.7 ± 1.617.3 ± 1.717.6 ± 1.712.0 ± 1.112.5 ± 1.4
>7012.0 ± 1.011.6 ± 1.118.1 ± 1.718.2 ± 1.914.7 ± 1.615.5 ± 2.017.5 ± 1.418.2 ± 3.312.2 ± 1.312.7 ± 1.2
All11.6 ± 1.011.7 ± 1.016.6 ± 1.817.0 ± 1.913.9 ± 1.814.7 ± 1.715.7 ± 1.816.9 ± 2.311.2 ± 1.411.9 ± 1.5
Aortic Root Dimensions

Aortic Regurgitation

Primary Parameters
MildModerateSevere
Vena contracta (cm)< 0.30.3 – 0.6> 0.6
PHT (ms) – CW doppler> 500200-500< 200
Diast flow rev – PW desc AortaIf present, early diastolicEarly diastolicHolodiastolic
Primary Parameters

Quantification of Jet
MildModerateSevere
Jet-width / LVOT-width< 0.250.25 – 0.64> 0.64
Jet-area / LVOT-area< 0.050.05 – 0.59> 0.59

Qualitative Parameters
MildModerateSevere
Jet areaSmallVariableLarge if central, variable if eccentric
Coaptation defectMildModerateSevere
CW-profileWeakViableDense
LA sizeNormalNormal or enlargedEnlarged
LV sizeNormalNormal or enlargedEnlarged

PISA Parameters
MildModerateSevere
EROA (cm2)< 0.10.1 – 0.29≥ 0.30
Regurgitant volume (ml/beat)< 3030 – 59≥ 60
Regurgitant fraction (%)< 3030 – 49≥ 50

Aortic Stenosis

Disease Defining Parameters
MildModerateSevere
Valve area (cm2)> 1.51.0 – 1.5< 1.0
Indexed valve area (cm2/ m2)> 0.850.6 – 0.85< 0.6
Measured Parameters
MildModerateSevere
Mean gradient (mmHg)< 2020 – 40> 40
Peak gradient (mmHg)< 3535 – 65> 65
Peak velocity (m/s)2.6 – 2.93.0 – 4.0> 4.0
Dimensionless index (LVOT/AV)> 0.50.5 – 0.25< 0.25

Bioprosthetic Aortic Valve Stenosis

EOA (effective orifice area) index
  • Mild PPM: EOA ⩽ 0.85 cm2/m2
  • Moderate PPM: EOA 0.65–0.85 cm2/m2
  • Severe PPM: EOA < 0.65 cm2/m2
Practice Questions | Echocardiographic Evaluation of Aortic Valve Prosthesis
Prosthesis‐patient mismatch: definition, clinical impact, and prevention

Visual Assessment of LV RWMA 

Type of motionDefinitionWall Motion Score
Normal Normal thickening (>30% thickening end-systole to end-diastole)1
Hypokinesia Reduced thickening (10-30%)2
Akinesia Markedly reduced thickening (<10%)3
Dyskinesia Paradoxical thinning and/or outward motion during systole4
Aneurysmal Diastolic deformation5

LV Dimension and Volume

LV Dimension
 Women Men 
 Normal Mild Moderate Severe Normal Mild Moderate Severe 
Diastolic diameter 3.9-5.3 5.4-5.7 5.8-6.1 >6.2 4.2-5.9 6.0-6.3 6.4-6.8 >6.9 
Diastolic diameter/BSA cm/m22.4-3.2 3.3-3.4 3.5-3.7 >3.8 2.2-3.1 3.2-3.4 3.5-3.6 >3.7 

LV Volume
 Women Men 
 Normal Mild Moderate Severe Normal Mild Moderate Severe 
Diastolic volume, mL 56-104 105-117 118-130 >131 67-155 156-178 179-201 >201 
Diastolic volume/BSA mL/m235-75 78-86 87-96 >97 35-75 76-86 87-96 >97 
Systolic volume, mL 19-49 50-59 60-69 >70 22-58 59-70 72-83 >83 
Systolic volume/BSA 12-30 31-36 37-42 >43 12-30 31-36 37-42 >43 

LV Ejection Fraction (EF %)

Women Men 
Normal Mild Mod Severe Normal Mild Mod Severe 
54-74 41-53 30-40 <30 52-72 41-51 30-40 <30 

Right Ventricle Dilation

Base (RVD1)> 42mm
Mid (RVD2)> 35mm
Longitudinal dimension (RVD3)> 86mm
RV focused apical 4 chamber
PLAX Distal RVOT (left side)> 30 mm
PSAX Proximal RVOT (middle)> 35 mm
PSAX Proximal RVOT (right side)> 27 mm

RV dimensions
 Normal Dilated Moderate Severely 
RV diameter (RVD 1) 2.0-2.8 2.9-3.3 3.4-3.8 ≥3.9 
RV diameter (RVD 2) 2.7-3.3 3.4-3.7 3.8-4.1 ≥4.2 
Base-to-apex length 7.1-7.9 8.0-8.5 8.6-9.1 ≥9.2 

RV diameter
 Normal Mild Moderate Severely 
Above aortic valve 2.0-2.8 2.9-3.3 3.4-3.8 ≥3.9 
Above pulmonic valve 2.7-3.3 3.4-3.7 3.8-4.1 ≥4.2 

PA diameter
 Normal Mild Moderate Severe
Below pulmonic valve 1.5-2.1 2.2-2.5 2.6-2.9 ≥3.0 

RV size and function
 Normal Mild Moderate Severe
RV diastolic area, cm2 11-28 29-32 33-37 ≥38 
RV systolic area, cm2 7.5-16 17-19 20-22 ≥23 
RV fractional area change, % 32-60 25-31 18-24 ≤17 

Left Atrial Size and Volumes

Atrial dimensions
 Women Men 
 Normal Mild Mod Severe Normal Mild Mod Severe 
LA diameter 2.7-3.8 3.9-4.2 4.3-4.6 ≥47 3.0-4.0 4.1-4.6 4.7-5.2 ≥5.3 
LA diameter/BSA 1.5-2.3 2.4-2.6 2.7-2.9 ≥3.0 1.5-2.3 2.4-2.6 2.7-2.9 ≥3.0 
RA minor axis, cm 2.9-4.5 4.6-4.9 5.0-5.4 ≥5.5 2.9-4.5 4.6-4.9 5.0-5.4 ≥5.5 
RA minor-axis/BSA (cm/m21.7-2.5 2.6-2.8 2.9-3.1 ≥3.2 1.7-2.5 2.6-2.8 2.9-3.1 ≥3.2 

LA area (cm2)
Women Men 
Normal Mild ModSevere Normal Mild ModSevere 
<20 20-30 30-40 >40 <20 20-30 30-40 >40 

Atrial volumes
 Women Men 
 Normal Mild ModSevere Normal Mild ModSevere 
LA volume 22-52 53-62 63-72 ≥73 18-58 59-68 69-78 ≥79 
LA volume/BSA 22±6 29-33 34-39 ≥40 22±6 29-33 34-39 ≥40 

Mitral Regurgitation

Primary parameters
 Mild ModSevere 
Vena Contracta <0.3 0.3-0.69 ≥0.7 
EROA (cm2) <0.2 0.2-0.39 ≥0.4 
Jet size <4 cm2 or <20% of atrial size 4-10cm 2 or 20-40% of atrial size >10cm 2 or >40% of atrial size 
Jet orientation Central Variable Eccentric 
Pulmonary vein flow S-dominant Reduced S-wave Systolic flow reversal 

Qualitative parameters
 Mild Mod Severe 
Mitral valve apparatus Normal-mildly abnormal Often abnormal Abnormal, possibly flail 
CW-profile Weak Variable Dense 
Shape CW-profile Parabolic Variable Early peak, triantriangular 
LA sizeNormalNormal or dilatedDilated

Additional PISA-parameters
     Mild Mod Severe 
Regurgitation volume (mL/beat) <30 30-59 ≥60 
Regurgitation volume (EROA x TV)   
Regurgitation fraction (%) <30 30-49 ≥50 
PW-doppler A-dominant Variable High E values 

Miscellaneous parameters
    Mild Moderate Severe 
PW-doppler A-dominant Variable High E values 

Mitral Stenosis

Primary parameters
   Mild Mod Severe 
Valve area>1.5cm21.5-1.0m2<1.0cm2
Mean gradient<5mmHg5-10mmHg>10mmHg
PAP<30 mmHg30-50>50

Pulmonary Regurgitation

 MildModSevere
Pulmonary valve morphologyNormalNormal/abnormalAbnormal
Density CW-dopplerWeak, slow decalVariableDense, steep deceleration, early termination of diastolic flow
Jet width color DopplerSmall, <10 mm length, narrow originVariableLarge, wide origin
Ratio pulmonic to aortic flowNormalVariableSignificantly increased

Pulmonary Stenosis

 MildModSevere
Peak velocity (m/s)<33-4>4
Peak gradient (mmHg)<3636-64>64

Tricuspid Regurgitation

 MildModSevere
PISA radius<0.60.6-0.9>0.9
Vena contracta (cm_Not defined<0.7>0.7
Liver vein flowS-dominantReduced S-waveSystolic flow reversal, jet reaching liver vein

Additional Quantitative Parameters
 Mild Moderate Severe 
Jet size<5 cm25-10 cm2>10 cm2
IVC size<2.1cm, compressibleIn between>2.1cm, not compressible
 
Additional Qualitative Parameters 
 Mild Moderate Severe 
Coaptation defectMildModSevere
RV sizeNormalNorma/enlargedEnlarged
RA sizeNormalNormal/enlargedEnlarged
CW-profile tricuspid regurgitationWeak VariableDense
Shape CW-profile TRParabolicVariableEarly peak, triangular

Tricuspid Stenosis

Mean PG≥ 5 mmHg
Valve area ≤ 1cm2
VTI of TV inflow>60cm
Pressure half time≥190 ms
RASeverely enlarged
IVCElnarged

Pulmonary Artery Pressure

 RA pressure
IVC <2.1cm, >50% sniff3 mmHg
All others or if not visualized8 mmHg
>2.1cm, sniff <50%15 mmHg

Pulmonary HTN (pHTN)

Mild30-50 mmHg
Moderate51-65 mmHg
Severe> 65mmHg

LV Region Identification

Diastolic Function

Mitral Valve Leaflets on TEE

https://thoracickey.com/role-of-transesophageal-echocardiography-in-mitral-valve-repair/

Useful Websites

How To Interpret Inpatient Cardiac Telemetry

Continuous cardiac telemetry monitoring, or ‘tele’ colloquially, is how we remotely monitor patients’ heart rhythms while in the hospital. When it is used appropriately it is a valuable diagnostic tool that assists in diagnosing and managing specific abnormal heart rhythms. I use it everyday for post-myocardial infarction patients (those who just suffered a heart attack) to monitor for ventricular ectopic beats caused by ischemic myocardium (dead heart tissue). Unfortunately tele review is one of those lessons thrown into the hidden curriculum of medical training where people are often taught it on the fly without much guidance. Electrocardiogram, or ECG, interpretation is outside the scope of this post. Instead I will focus on a few helpful tips to help improve your ability to understand and utilize tele in a more meaningful and intentionally manner for any nurse, physician assistant, nurse practitioner, intern, resident, or incoming cardiology fellow. Lastly, don’t forget to subscribe so you don’t miss future posts!

1. Not everyone needs tele

Rule number one in medicine is ‘primum non nocere’ or ‘first do no harm’. Exposing patients to unnecessary monitoring can lead to further unnecessary testing and in turn possible harm. Not only is ordering unnecessary tele potentially harmful to patients but it is also costly. The average hospital bed is more expensive if telemetry is added on. It also can harm healthcare professionals through alarm fatigue. Think about how frequently those things beep along with every other alarm in the hospital. Not to mention how annoying actually wearing a tele monitor can be for patients (1). Inappropriate tele use is such a widespread issue in the United States that it is one of the cornerstones of the Choosing Wisely campaign from the Society of Hospital Medicine (2). Tele should be treated like any other imaging study and only be ordered for specific patients when indicated.

2. Evidence behind tele

No large randomized control trials have established standards of care for cardiac telemetry. However as the old adage goes you don’t need an RCT to prove that a parachute is useful when jumping out of an airplane. There are guidelines established by the AHA/ACC but they are just that- guidelines. In the end, you have to use your clinical judgement when ordering or discontinuing tele. Some of the obvious clinical scenarios when telemetry is useful include

  1. Syncope of unexplained origin (meaning if the patient has obvious vasovagal syncope then you don’t need tele!)
  2. Uncontrolled or unstable arrhythmias (AF RVR, VT)
  3. Following a STEMI
  4. ICU monitoring

3. Common reasons for inappropriate tele use

In residency I attempted to combat inappropriate tele use through a quality improvement project. While partially successful I found that there were a few common diagnoses that accounted for a majority of inappropriate tele use. In the New England Journal of Medicine (NEJM) Journal Watch, Dr. Winawer summarized my thoughts quite well in his post detailing top 10 reasons he has anecdotally seen over his career for inappropriate tele monitoring (5). Remember that these are anecdotes for tele use on the general medicine wards and exclude critical care units. Here are 5 of the most common reasons I see patients inappropriately placed on tele.

  • 1. Abnormal electrolyte derangements. You should not be using tele as a surrogate marker for electrolyte abnormalities. You should be managing the patient with frequent BMP’s. If they have ECG manifestations then they should not be on the general medicine floor and should be in a higher level of care. This include patients with End-Stage Renal Disease (ESRD) with chronically abnormal potassium levels without ECG changes.
  • 2. Low-risk chest pain. If you rule out ACS with negative serial troponin you can DC tele.
  • 3. Non-cardiac syncope. If a patient has a syncopal episode due to hypoglycemia or a seizure then tele has zero utility.
  • 4. Sinus tachycardia. Sometimes patients are admitted for non-cardiac issues and are found to have appropriate sinus tachycardia. This could be due to a fever, pain, anemia, or dehydration. Tele is sometimes used as a surrogate for ‘closer patient monitoring’. If a patient needs to be monitored more closely then they should be upgraded to a higher level of care. Tele is not an adequate replacement.
  • 5. History of atrial fibrillation. If a patient has a history of AF but is rate controlled they do not require tele monitoring. This often happens with patients admitted for something non-cardiac like cellulitis and placed on tele despite being hemodynamically stable.

4. Evaluate the need for tele daily

It is far harder to stop a medication than it is to start one. Same thing is true for tele. So each day that you check your patient’s tele remember to ask yourself if it is even necessary in the first place. This is a responsibility of everyone who interacts with the patient from bedside nurses to the advanced practitioner PA or NP, to both the primary physician and consulting physicians. Everyone has the ability to contribute to more meaningful tele use in the hospital- even our patients!

5. How to look at tele systematically

Okay, okay, okay. I get it. Only order tele when it’s indicated and discontinue it when appropriate to do so. So let’s say we have a patient on tele. Where do we start?

  1. Look at the live feed. See what rhythm your patient is in right now.
  2. Look at events. The computer typically will flag preset rhythms based on an algorithm. It has a high sensitivity so it often flags things that aren’t real arrhythmias. So you have to open each one to evaluate them. When in doubt print out the telemetry strip to have with you to review with your attending physician
  3. Look at the timing of the events. Did your patient have a run of atrial fibrillation last night? Look at the timing of the arrhythmia and ask your patient if they felt it. Similarly if your patient complains of chest pain or palpitations see if there are any events on tele that correlate with that timing.

6. Confirm with an ECG

Tele is great but sometimes it isn’t all that accurate. Always get a confirmatory ECG to compare the rhythm in question.

7. Print out the tele strip in question

I once had a patient who had an abnormal arrhythmia in the ICU. Unfortunately by the time we were able to see the patient they got transferred out of the unit to the floor. When this happened their telemetry data didn’t get transferred with them. So whenever you see something abnormal make sure you print it out and get it uploaded into the patient chart so we can see it in the future. This is also why I like to get an ECG to confirm abnormal rhythms so I make sure it gets uploaded to the EMR.

8. Call for help if you need it

This should go without saying but if you are concerned about a rhythm that doesn’t look right then call for help. If you are an intern and aren’t sure what to make of the tele strip then print them out, discuss with your senior, and on rounds. If you area a nurse then print out the strips and speak to the primary team.

9. But first evaluate the patient clinically

I understand that not everyone is a cardiologist but we are all medical professionals. It is not good enough to simply pass the buck and say ‘I called cardiology about it’. For instance, I’ve gotten calls to say “the patient’s heart rate is 40. What do you want to do?’. Well, it depends! Is the patient fast asleep, hemodynamically stable, and has had normal heart rate trends in sinus rhythm all day? Because a heart rate of 40 could simply be vagal tone brought on by sleep. Or is this a patient who just had a right coronary artery myocardial infarction and is now in complete heart block, feeling dizzy, and becoming hypotensive? My point is that one piece of isolated information is more valuable when put in the context of a clinical situation.


Now let’s go over some real life examples

This is the real meat and potatoes of this blog post. The following case presentations are not based on a single patient and are instead a culmination of many common threads I’ve experienced first hand. So let’s pretend you are a first year cardiology fellow and you are called to evaluate the following patients.

Case Number 1: it’s 3am and you are called because a patient is reported to be in ventricular tachycardia (VT) and the primary team wants to confirm if they should use 100J or 200J for the synchronized cardioversion. They send you a picture of the tele strip, below, while you’re walking to evaluate the patient. What do you tell them to do?

You can tell them to let you and the patient go back to sleep! Here’s why: on the telemetry strip you can see 3 rhythms strips. I labeled them 1, 2, and 3 in red, below. Strip number 1 on the top looks scary. It could be VT! But at first glance it doesn’t look quite right.

Now let’s just jump down to lead number 3 on the bottom. If you saw this lead all on it’s own you would never think “this is VT”. You can see clear cut narrow QRS-complexes. Now go back and look again at the blue circles.

Sinus rhythm with interference

Notice how the narrow QRS-complexes in the bottom lead are also present in the middle lead. Those are pretty easy to march out. The tough part is noticing that they are also present in the top lead. This brings us to our first major learning point. You cannot have an abnormal rhythm in one lead and a normal rhythm in another. If you have VT it should be present in every lead.

So what’s the above diagnosis? It’s tough to make out the underlying rhythm. It could be atrial flutter or just sinus rhythm with prominent T-waves. In the end however it is definitely not VT. The top lead is likely just interference!

Let’s drive this point home and look at another tele strip. Now that you are an expert at figuring out if it’s VT or just interference take a look at this one below.

This is another example where it can easily be mistaken for VT. But look smack dab in the middle at lead III. You can clearly see a regular rhythm with narrow QRS-complexes. You can also see narrow spikes in other leads that correlate with the timing of those sinus beats. The other leads simply have interference.

Now let’s take a look at another tele strip. What’s the rhythm?

In the above tele strip you can clearly see that there are 5 narrow QRS-complexes followed by 7 wide QRS-complexes. This is finally an example of non-sustained ventricular tachycardia (NSVT). In this tele strip the wide QRS-complexes are found in all 3 leads.

Ventricular tachycardia is a wide QRS-complex originating from the ventricle. It is considered non-sustained ventricular tachycardia (NSVT) when it lasts for ≥3 beats but for ≤30 seconds. The 30 second timing is kind of an arbitrary man made classification. But generally if the VT lasts longer than 30 seconds it is classified as sustained-VT. Sustained VT can be deadly because it can deteriorate into ventricular fibrillation (VF) which can be fatal.

To finish out this lesson lets take a look at a 12 lead ECG, below. This is an example of sustained VT.

Diagnosing and differentiating VT from atrial fibrillation with aberrancy is outside the scope of this post but I really like this Life In The Fast Lane blog post on this topic if you’re looking for more information.

Case number 2: you are consulted for ‘runs of sinus tachycardia’. What do you do?

Well first off (*using sassy cardiology fellow attitude*) tell them to try and figure out what the actual rhythm is first and then have them call you back . Okay okay, just kidding..kind of. Let’s dive into why you can’t have a ‘run of sinus tachycardia’.

First off, what should every primary team have done first before calling cardiology about actual sinus tach? The basic work up includes addressing underlying reasons for a patient to be tachycardic. This includes:

  1. Dehydration
  2. Acute anemia
  3. Pain
  4. Fever
  5. Hyper/hypothyroidism
  6. Holding a patient’s beta blocker

Fever tangent: What is Liebermeister’s rule?

Liebermeister’s rule is the appropriate increase in heart rate in response to a fever. In general for every degree abvoe 100F the heart rate should increase by about 10. So a fever of 101 can cause a heart rate of 110. A fever of 102 can cause a heart rate of 120, etc.

Conversely, what is the unusual diagnostic association of fever with bradycardia and what can it indicate? It is known as Faget sign. Faget sign can be seen with intracellular bacterial infections like legionella or mycoplasma pneumoniae as well as many other infections including yellow fever, typhoid fever, tularemia, brucellosis, and Colorado tick fever.

Now let’s say you did all of the above and still can’t figure out wyh on tele you are seeing runs of a fast heart rate. Sometimes looking at the graphic trend can help differentiate different rhythms.

First just think about what your normal heart rate does while in sinus rhythm. Throughout the day if you get up and move around your heart rate increases gradually to accommodate for increased cardiac output requirements. Think about when you walk up a flight of stairs or two. Your heart rate increases slowly. It doesn’t suddenly jump from 60 beats per minute to 150. It slowly climbs up to 65, then 70, then 75, then 80 and so on. Then in recovery after you finish climbing the stairs your heart rate similarly will slowly trend down and decrease slowly from 150 to 145 to 140 and so on. Below is an example of a patient who is in normal sinus rhythm without any arrhythmias.

The above graphic trend is for a 24-hour period. So the small spikes that you see are actually happening over a longer period of time. If we were to zoom in you would see a gradual upslope and then gradual down slope.

Now don’t get fooled. This can also happen in atrial fibrillation. Patient’s can be rate controlled pretty well and have gradual increases in their graphic trends. So just because the graphic trend is gradual it does not mean that it is sinus rhythm. Don’t forget the rules of telemetry. Get an ECG or check the rhythm yourself to figure out what you are dealing with.

Now our patient in question was having ‘runs’ of tachycardia, as seen below.

Above is the graphic trend over an 8 hour period. These bursts of fast heart rhythms are starting SUDDENLY and stopping SUDDENLY. This should not happen in sinus rhythm and indicates that you are likely dealing with some type of abnormal heart rhythm. Arrhythmias that can commonly do this include atrial flutter, atrial fibrillation, and atrial tachycardia.

The learning point here is that the graphic trend can be used to help guide your diagnosis. You cannot solely rely on the graphic trend to make a final diagnosis. You still have to go inside the event strip and FD, or full disclosure, strip in order to figure out what rhythm you are dealing with. When in doubt, print it out! And then call your friendly neighborhood cardiology fellow for some help to figure it out together.

Overnight I got called again abotu this patient’s heart rhythm. The primary team thought it was an SVT so they used adenosine to break the rhythm. Below is what they saw (sorry for blurry image).

In the above image the patient was going in a fast rhythm and adenosine was administered. Adenosine slows AV-nodal conduction. So all that it does it stops the atria from communicating with the ventricle. It does not necessarily stop whatever rhythm is happening inside the atria. In the above strip you can see that after the 5th narrow QRS-complex there is long pause until the next QRS-complex comes in. During that extended time period you can still see about 8 P-waves. This is highly suggestive of atrial tachycardia and is the first thing that comes to my mind when a patient is having ‘runs of sinus tachycardia’.

Atrial tachycardia can look like sinus rhythm, suddenly start, and suddenly stop. Again the full treatment of atrial tachycardia is outside the scope of this blog post but if you want to read more about it I like this LITFL blog post on atrial tachycardia.

Lastly, let’s take a look at another graphic trend, below.

Notice how this rhythm also suddenly goes fast and then suddenly goes slower. This is indicative of an underlying arrhythmia. I would be impressed if someone called me with a consult with this information at hand for assistance in rhythm identification. This is some ‘upper level senior resident who is interested in cardiology’ level of knowledge!

Again, graphic trends can be a valuable tool to help guide your ECG diagnosis but always get a 12 lead to confirm! And if rhythms and ECG’s are still tough for you then don’t worry because I still get them wrong at times. Medicine requires lifelong learning so use every one of your patient’s ECG’s as practice!

If you think this blog post helped then comment below and I hope be sure to subscribe so you don’t miss the next blog post!

Works Cited

  1. Henriques-Forsythe MN, Ivonye CC Jamched U, Kamuguisha LKK, Onwuanyi AE. Is telemetry overused? Is it as helpful as thought? Cleve Clin J Med [Internet]. 2009 Jun [cited 2012 Sep 4];368-372.
  2. SHM – Avoid continuous telemetry monitoring | Choosing Wisely. (2020). Choosingwisely.org. Retrieved 22 May 2020, from https://www.choosingwisely.org/clinician-lists/society-hospital-medicine-adult-continuous-telemetry-monitoring-outside-icu/
  3. When Should Hospitalists Order Continuous Cardiac Monitoring?. (2020). The-hospitalist.org. Retrieved 22 May 2020, from https://www.the-hospitalist.org/hospitalist/article/122074/when-should-hospitalists-order-continuous-cardiac-monitoring
  4. Drew BJ, Califf RM, Funk M, et al. Practice standards for electrocardiographic monitoring in hospital settings: an American Heart Association scientific statement from the Councils on Cardiovascular Nursing, Clinical Cardiology, and Cardiovascular Disease in the Young: endorsed by the International Society of Computerized Electrocardiology and the American Association of Critical-Care NursesCirculation. 2004;110(17):2721-2746.
  5. NEJM Journal Watch: Summaries of and commentary on original medical and scientific articles from key medical journals. (2020). Jwatch.org. Retrieved 23 May 2020, from https://www.jwatch.org/na44560/2017/07/06/dos-and-donts-telemetry-monitoring-telemetry-directors-top

Racial Disparities in Treatment of Heart Failure

Given existing disparities in access to health care the growing burden of heart failure in the US could disproportionately impact the African-American and minority community (1). 

Regardless of race or ethnicity, patients with heart failure (HF) have better outcomes when cared for by cardiology specialists than other specialties (e.g. internal medicine) (2,3).

However, prior studies on patients admitted for decompensated heart failure found those with lower incomes or patients who were AA were ‘significantly less likely to receive cardiology care when compared with younger, Caucasian, and more educated patients. Even after adjusting for severity of illness, social factors were strongly associated with receiving care from a cardiologist’ (4). 

In a larger database study published in 2018 of over 100k patients including over 20k AAs the authors found that Caucasians were 40% more likely to receive cardiology care than AAs(5).

As an editorial commented ‘can we continue to blame the disparity in care to lack of access or insurability? Is it not time to consider preconceived notions of access and inherent, although unrecognized, racial bias and stereotyping that lead to racial health disparities?’ (5).

I won’t pretend to be an expert in racial issues or healthcare policy but it is evident that generations of racial and socioeconomic disparities manifest in poor health and that we must recognize and challenge our own bias both personally and professionally.

For now, you can also head to https://justiceforgeorgefloyd.com/ or sign a petition to help get #JusticeForGeorgeFloyd.

Works Cited

  1. Piña, I. (2018). If It Is Not Health Care Access or Insurance Coverage, Then Why Do Racial Disparities Persist?. JACC: Heart Failure, 6(5), 421-423. doi: 10.1016/j.jchf.2018.03.013
  2. Uthamalingam S., Kandala J., Selvaraj V., et al. (2015) Outcomes of patients with acute decompensated heart failure managed by cardiologists versus noncardiologists. Am J Cardiol 115:466–471.Google Scholar
  3. Selim A.M., Mazurek J.A., Iqbal M., Wang D., Negassa A., Zolty R. (2015) Mortality and readmission rates in patients hospitalized for acute decompensated heart failure: a comparison between cardiology and general-medicine service outcomes in an underserved population. Clin Cardiol 38:131–138.Google Scholar
  4. Auerbach A.D., Hamel M.B., Califf R.M., et al. (2000) Patient characteristics associated with care by a cardiologist among adults hospitalized with severe congestive heart failure. SUPPORT Investigators. Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatments. J Am Coll Cardiol 36:2119–2125.FREE Full TextGoogle Scholar
  5. Breathett K., Liu W.G., Allen L.A., et al. (2018) African Americans are less likely to receive care by a cardiologist during an intensive care unit admission for heart failure. J Am Coll Cardiol HF 6:413–420.Google Scholar