Storm delay

Thanks to the lovely slush-storm heading my way, school has been canceled for tomorrow and I get an even longer holiday weekend! I have a ton of things to write about from today, so rather than losing sleep tonight trying to get out a post, I'll take my time with it tomorrow. See you then!

To everyone traveling tomorrow: stay safe!

WILTIMS #219: All the fun facts!

It's funny and awkward being at this teenage stage of my medical education. An example is of how my vocabulary has changed in the last year and a half. Words that I once defined as part of my "TIL" facts last year are so familiar that I get in trouble forgetting to defining them to the uninitiated in current posts in this same blog. See below where, when trying to describe a pulmonary embolism, I used the word occlusion, which no one else in the room was able to use in a sentence. So, I've obviously learned a few things (and must make sure to check that I don't overuse jargon, both in this setting and during future patient care).

But at the same time, nearly every day a professor does the same thing to my entire class. She will use a very basic term from her discussed field, something that we simply have never had occasion to learn, and then have to stop and backtrack once she sees the confused looks and quiet whisperings between classmates. Today's word was claudication (just as angina means chest pain, claudication is leg pain).

TIL: There are two different nuclear dyes used in cardiac stress tests to image the heart. They each have their own pros and cons, but one was particularly entertaining. Depending on the location and travel plans of a patient, you may want to use technetium-99mTc instead of thallium-201 because, with the latter, the patient will be "nuclear" for a week. These two drugs have the same radioactive dose, similar cost, and the same effectiveness. But thallium has a longer half-life and will set off nuclear detectors (such as those in high profile airports or the Lincoln tunnel) for a week post-procedure.

Mitral valve prolapse (MVP) can cause premature ventricular contractions (PVCs). MVP is when the mitral valve, between the left atrium and ventricle, is pushed back into the atrium as the ventricle contracts, much like an umbrella inverting in a heavy wind. As it does this, it pulls on the cords and muscles that normally tether the valve in place. These papillary muscles stretch out and stress the wall of the ventricle, which can cause the heart muscle to send out an emergency wave of contraction (that's its somewhat knee-jerk response to pretty much any stress). This wave can result in a single weird beat of the heart, or more seriously trigger a dangerous arrhythmia.

The force parentheses were strong with this one, so lets take it without them first: More people die during or immediately following air travel due to pulmonary embolism as a result of a deep vein thrombosis than of airplane crashes. Ok, got the basic structure? One more time: More people die of pulmonary embolism (the occlusion (blocking off) of an artery in the lungs due to a piece of debris getting lodged in the progressively narrowing blood vessels) as a result of a deep vein thrombosis (a big blood clot forming in a large vein which often breaks off small emboli (chunks of stuff) when agitated (like during air travel)) than of crashes in commercial air travel.

Lastly, you can use right heart catheterization to measure left atrial pressure. This may not seem sensical at first, but hear me out. Think about where a balloon would travel if you let it into the right atrium. First, it would float through the tricuspid valve to the right ventricle. Then it would be pumped through the pulmonary valve to the pulmonary artery. Then it would wander into smaller and smaller arteries as it approaches the lungs before getting lodged (much like the pulmonary embolism we just discussed). Once it's stuck in the lung arteries, the downstream pressure will equalize all the way to the left atrium. This balloon has a sensor on it that measures this pressure and Voila! Left atrial pressure.

WILTYIMS #218: Listen up!

"Harvey": the cardiopulmonary patient simulator

The professor who taught us about cardiac murmurs today should take up beatboxing... wait... maybe he got his start as a beatboxer before becoming a doctor... so that he can use his powers of noise imitation to save lives through medical education! 

It's a little sad that the theme for the day was about how a super fancy mannequin can teach this material even better, but I honestly don't believe it. Over the next couple weeks we get to go in small groups to our school's new simulation center to practice doing a cardiovascular exam on "Harvey", a mannequin which can imitate heart and lung sounds, blood pressure and various pulses around the body. But I think Harvey has already been upstaged by our professor's uncanny ability to imitate any heart sound, at any speed, at a moment's notice.

In the words of one of the course directors, who was sitting behind me in lecture, I can't wait to see the transcription for this lecture:

Dr. M: And stenosis sounds more like [rhythmic noises] whereas regurgitation is more of a [other noises]. Now, if you have the patient make a fist, the sound will change from [quieter noises] to [louder noises]...

TIL: All about murmurs!

A murmur is essentially any unusual sound made by the heart and its surrounding vasculature. The most common murmurs are made from malfunctioning valves. For example, if the aortic valve gets all crusty and doesn't open all the way any more (aortic stenosis), then the blood will make a loud whoosh as it is squeezed through the smaller opening. Alternatively, if the mitral valve is leaky and lets blood flow backwards from the left ventricle to the left atrium (mitral insufficiency/regurgitation), you will hear a noise as the blood forces it's way back upstream.

Murmurs have a 6-level grading system for intensity:

1. barely audible - softer than the normal "lub-dub"
2. about the same intensity as the normal "lub-dub"
3. louder than "lub-dub"
4. you can feel the murmur with your hand
5. you can hear it distantly in the body via the skeleton (like putting your ear to the railroad track)
6. you can hear it without a stethoscope

That scale is crazy. If you can hear your own heartbeat through your chest (and not just through the arteries in your ears ('cause that's actually a-whole-nother problem)), you should probably go to the doctor.

WILTIMS #217: The EKGs Strike Back

Today we revisited a topic we covered back in physiology: EKGs. I definitely don't remember everything involved, but it's nice that at least the concepts are familiar this time. I'll need to really master interpreting those squiggly lines this time though, because now we are not just looking at what a healthy heart looks like, but how each of the innumerable heart dysfunctions look from an electrical perspective.

One totally useless slide from lecture today was particularly interesting to me: a ye olde EKG machine, circa 1895. The patient sat with three limbs in buckets of salt solution (these were the equivalent of the little sticky paper/metal leads of today) while the electrocardiographer looked through a viewer so as to draw by hand a vague approximation of what the electrical signal was showing.

TIL: A bunch of slight differences in terminology:

Sinus tachycardia vs supraventricular tachycardia: Tachycardia is an elevated heart rate. A sinus rhythm is simply any rhythm where all the peaks are in the right places. A problem comes, however, if an otherwise sinus rhythm is just too fast; the beats are so close together that they overlap and you can't see all the peaks distinctly. Since you can't at that point say whether it is or is not a sinus rhythm, you have to call it something else: the deceptively vague "supraventricular" tachycardia (because, just like in sinus rhythm, the rhythm generating pacemaker is in the atrium, hence supra- (above) the ventricle). 

Atrial flutter vs atrial fibrillation: A flutter occurs when the atrium is beating too fast and the ventricle can't keep up, so it only beats every 3 atrial beats (sometimes 2, sometimes 4, but always consistent). Afib occurs when the atrium is essentially beating non-stop so that there isn't even a signal that the ventricles can go off of. The ventricle then tries its best to keep a rhythm, but fails at it, resulting in an erratic heartbeat.

Atrial vs junctional vs ventricular escape: The heart has three normal pacemakers: the SA node, in the atrium; the AV node, between the atria and ventricles; and a baseline rhythm by the ventricles. The SA node overrides the AV node and either node overrides the ventricular rhythm, so that usually, the whole heart goes off the SA node. If for whatever reason, the SA node fails to fire, other nearby atrial cells can pick up the slack and make a new rhythm (atrial escape). If the whole atrium is slacking, then the AV node will lead the way (junctional escape). Lastly, if something is horribly wrong and nothing above is giving it a signal, the ventricles will beat on their own (ventricular escape).

WILTIMS #216: "P"s get MDs

Hopefully you correctly interpreted my week of silence as: EXAMS! This round of 7 hour testing was exclusively microbiology and antibiotic pharmacology. And assuming my math is right and I didn't catastrophically fail a miniboard exam, I think I'm finally done with micro!

Our micro professor after the final, celebrating with the home-brew we started during fungi

This marks a fun transition in our curriculum for pathology too. Up to this point we have mainly been studying "general principles" of medicine: inflammation, principles of cancer, anemias, etc. Now begins the organ systems: cardiovascular, renal, reproductive, etc. Today we started cardio and it was lovely. It felt like back in anatomy or physiology, when we were learning big, impactful medicine that was complex, but able to be reasoned-out. It is really hard to put this feeling into words...

It's not that the things we learn in biochem or the immunological parts of micro aren't important - in aggregate, all the tiny malfunctions of our biological underpinnings add up to untold suffering and death at the population level. But once you understand the cell biology involved, each of those conditions boils down to a very simple, typically unfixable problem - this enzyme doesn't work, that protein doesn't fold properly. Those tiny changes can have huge system-wide consequences, but because of how many of them we need to get through, we have to move on before discussing the complex treatment of and interplay between the larger effects.

When we deal with things on a organ system basis, we actually have time to riddle-out, not just that there are downstream effects, but how their nature changes given the disease process. It may just be the way I'm wired, but I love the diseases that result from entire organs failing. It reminds me that the entire body is actually connected; that it is a giant, moving, ever changing puzzle and we get to try to put the pieces back together.

TIL: Oxygen takes up 21% of the dissolved space in blood. That is exactly the same as the percent oxygen in the atmosphere. This makes some sort of very, very long term evolutionary sense.

Lovingly borrowed from WebMD

Bicuspid and unicuspid aortic valves can lead to aortic stenosis. The heart has four valves and they're all a little different. The aortic valve normally has three cusps (tricuspid) but there are rare birth defects that result in bicuspid or, far less commonly, unicuspid aortic valves. One of the main problems with this birth defect is that that the valve doesn't open as well which prevents blood from leaving the heart efficiently. This makes the heart work harder and can lead to several serious complications including left ventricular hypertrophy, where the left ventricle grows super big to compensate. But, this compensation usually does more harm than good in the longterm.

Mitral stenosis (hardening of the heart's mitral valve), has a "fish mouth" appearance upon gross examination.

WILTIMS #215: It's never lupus, but apparently always TB

Today was one of our last "lectures" in microbiology and instead of being talked at for another hour, we got to play to role of a (really bad) detective. The guest lecturer was a doctor who turned off the Powerpoint, and simply had us try to unravel a mystery. We were given an incredibly vague history of a fake patient and then were prompted to ask questions until we figured out what the patient had.

It was very slow going, but by using the facts we've learned this semester, we were able to come to a diagnosis of TB. Apparently TB has such varied and complex constellation of possible symptoms, that it should always be somewhere on one's differential diagnosis.

This was weird and awkward at first, but eventually very rewarding just to see how much we had grown this semester. We didn't immediately figure out the cause of the infection, but we knew how to rule-out some of the hundred of potential causes we had learned in the past few months. If someone asked, "Does the man have pets?" or "Are his lymph nodes swollen?" everyone knew the slew of diseases that the questioner was trying to rule in/out from that line of questioning. I'm calling that progress!

TIL: If a heroin user shows up at the ER with a fever and a chest x-ray showing a patchy infiltrate of the lungs, think staph aureus! This bug is found on the skin and enters the venous drainage via the heroin needle track marks. From there, it infects the heart, specifically the tricuspid heart valve, causing endocarditis. That infection of the valvar surfaces can cause chunks of virus-infected material to break off from the damaged valve and get caught in the lung, resulting in a patchy infection of the lung.

WILTIMS #214: Incoldenza

Thank you all for the kind response to yesterday's post. This probably isn't the best week to stay up writing, but I'm glad I did.

The highlight from today was a fantastic lecture on ebola from the director of our school's Center for Disaster Medicine. I won't bore you with the details, because this is already so saturated in the news right now. If you have any questions about anything ebola, write a comment or send me an email and I'd be happy to explain what I know, both about the disease and the response to it.

TIL: The cold is not the flu... unless it is. This is one of those big points that we try to ram home because it relates to low vaccination rates. People often confuse the cold and the flu, feeling that since a cold is no big deal, there's no need to get a flu shot. But the flu is WAY worse than a cold. The flu kills thousands to tens of thousands of people in the US every year. And these aren't just children, the elderly or people with weakened immune systems. The flu also kills perfectly healthy adults.

So all that being said, it's funny that one of the viruses that bears the influenza name, is actually better described as one of the (far less common) causes of the common cold. The influenza A and B viruses cause the full-blown, feel-like-you're-gonna-die flu. But the much rarer C-type of influenza virus causes symptoms so much weaker than its big, bad relatives, that it is considered one of the causes of the common cold. Most cases of the cold are caused by a rhinovirus or coronavirus, but several others can also cause those less-severe, non-specific symptoms, including RSV, adenovirus, coxsackievirus and others.