TILIR #24 & 25: Hearts and poisons

Wednesday morning marked a milestone for our program. It was the first multidisciplinary conference to feature a cardiac patient since we started taking care of some of the cardiac service at the beginning of the academic year.  I had actually presented a cardiac patient for one of my multi-disc conferences last year and it was noticeably difficult for our residents and even attendings to work through what was going on with that patient because we simply never saw that pathology on the services we managed. Now we are actually starting to interact with this important subset of pathology regularly and our program can only be better for it.

WednesdayIL: DiGeorge (or 22q11.2 deletion) syndrome is a genetic condition associated with numerous cardiac problems, but a particularly pathognomonic one (a symptom that is very characteristic of a certain condition) is an interrupted aortic arch. This is like an extreme form of a coarctation where the aorta not only narrows but pinches entirely off. This is obviously bad, but not immediately incompatible with life as the body will force blood through collateral smaller arteries which widen in caliber as much as they can to accommodate the extra blood flow.

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Thursday we finally got to do a well known pediatrics mainstay: baby formula taste test! A couple of the hospital's registered dieticians gave a brief lecture on the numerous different types of formulas and dietary supplements for babies and toddlers. They then lead us in groups to the adjacent room to try small samples of most kinds of formula. We of course had to run upstairs afterwards for an ice cream chaser.

ThursdayIL: Alimentum tastes like poison. This is one of the least natural formulas in that it is basically pre-digested and thus marketed as hypoallergenic (along with the other big brand version, called Nutramigen). Nearly any baby is able to tolerate this formula so it's kind of our last line of defense before things get much more difficult (IV nutrition, etc). However, these formulas are crazy expensive, very physiologically dissimilar from regular breast milk, and they tastes awful, even to babies. Seriously, though, tastes horrendous. Stay away.

WILTIMS #428: Needing Beers to get through geriatrics

Last Tuesday I had a really good day. Today was less so. As much of the miserableness involved people who control my grade and my little blog is technically a public forum, I will just leave it at that.

This week I started my two week stay in the hospital's geriatric clinic. Not my particular cup of tea, but it should be survivable for the short duration. I had an interesting experience today looking back through the chart of a very elderly patient. Currently about 85 years old with several serious health conditions, she needed of a good deal of assistance with her daily activities. As with any patient, I read-up on her recent admissions and notes from the doctors who had taken care of her.  I learned a good deal about her medical history, but very little about her personal life - her story.

So then I dug into the social workers' notes. These provide great details about a person's living situation. I was surprised to find electronic records going back over ten years to when the patient was about 70 years old. And suddenly I realized that I had the documented history of one woman's journey into old age and frailty. each successive note showed how a heart condition or fall changed what she was able to do and how she was able to live.

I realize that the sorts of records have always existed in some form, but with the adoption of electronic medical records, it will become so much easier to essentially read the (very dryly written) story of someone's life through their interactions with the medical field.

TIL: AICD stands for artificial internal cardioverter/defibrillator.

The Beers Criteria is a list of drugs that should be used cautiously in the geriatric population. When it was first created in 1991 by Dr. Beers, it was a very simple, one-page tool to help prevent needlessly dangerous prescriptions. The most recent version is a dozen pages of very specific guidelines. Not sure if that's really serving the same purpose anymore...

While researching the Beers criteria, I learned what a non-anti-infective medication is. I'll let you read that one more time: non-anti-infective medication. What? Despite how it might seem, the negatives do not cancel out, which would make these simply infective medications. Actually these are medications other than those used to kill or weaken infectious pathogens such a bacteria, viruses, fungi, and parasites.

Endoscopic ultrasound is a nice alternative to MRCP for imaging choledocolithiasis.

Whereas gallbladder pain radiates to the chest and shoulder, the common bile duct radiates to the flank and back.

WILTIMS #413-14: A systemic problem

One of the more nebulous concepts I've learned this year is the interplay between correctional facilities, law enforcement, psychiatry, and medicine. The patients that have experience with the first two likely have a prickly relationship with the latter. The rule with the last three is that they will give you the benefit of the doubt if you're nice and don't heavily abuse any one part of the system. Of course biases exist, as studies (and experience) have shown over and over again. If your community's criminal or indigent population are socioeconomically distinct from the people taking care if them, they fare worse in the system.

Yesterday my medical team got a patient that had been spurned by the other three parts of the network. He was put in jail for drug charges, treated for opioid dependency with methadone while in jail and then released without any attempt to taper the medication or set him up with a rehab facility. In an attempt to get a fix, he immediately did IV heroin for several days while living on the street. Realizing he needed help, he came to our psychiatric ER looking for help detoxing. He was released a few hours later because there weren't enough beds to admit him for detox. He was given a MetroCard and directions to rehab shelters with instructions to go to an ER if he started showing any of the dangerous symptoms of detox.

Six minutes later he checked into our medical ER. At this point he complains of some vague detox symptoms and, oddly enough, pain in his finger. Over a month ago in prison, he had cut his hand. The wound had never healed and now was deep into the joint. Sadly, he probably should have been just bandaged up and sent on his way if one ER doctor hadn't heard a heart murmur when listening to the guy's chest. We never heard the murmur again, but it was enough to get him a bed for the night as we worked-up an unlikely, but potentially serious diagnosis of ok infective endocarditis.

I find it interesting and terrifying that these entities that are meant to help people can be so temperamental. One moment, a patient is our charge to be defended by the system when the next they are a burden to be pushed to the next sap that has to take them. People who need psychiatric treatment are arrested, in jail they are kept from the psychiatric and medical treatment they need, then they are released without any hope of recovering or surviving on their own and end up either in an ER or on the way back to jail. Don't get me wrong; sometimes the system does work. But in my very short experience in medicine, I've already seen it fail more times than should be allowed.

The benevolent connection between all four of the previously mentioned groups (corrections, police, psych and med) is social work. These are the only people that seem to bridge the gaps in this societal support system. They are also frequently the only people who help the patients navigate the time between the four services.

YesterdayIL: The frog-leg test is a way to test for asterixis (flapping movements indicative of a brain infection) when the patient is unconscious. 

TIL: For a P wave to be a P wave it must come from the SA node.

Cardiac pain is midline and lasts 2-20 minutes NOT seconds or hours.

Heart pain can cause a patient to tense their chest muscles to the point where they are sore. This is good to remember because a reproducible pain usually rules out heart problems, but the muscle sprain can be reproducible even after the heart pain has subsided.

WILTIMS #380-4: Family Med catch-up Part 1

I'm ok! Apologies for the unplanned hiatus; I apparently needed a break. Family medicine has been a lot of fun and the hours are superficially better, so one would reasonably assume that blogging through this clerkship would be no sweat after Peds or OBGYN. But though it's true that I'm no longer working 10-11 hour days and getting up at 4am, every minute of my 8 hour shift I am either in a patient room or running to the next one. 15-30 minute appointments are exhausting when you have 27 of them a day!

The clinic I'm working at for this rotation is frequented by the uninsured and underinsured. Most of the patients are immigrants, very few speak English, and almost all have chronic health problems exacerbated by their socioeconomic status and their previously sparse access to health care. I have already learned and revisited an amazingly diverse amount of medicine, and learned even more about the community I'm helping serve.

I will try to catch-up over the coming days and we'll see if I can stay up to date from here on out!

TuesdayIL: Chondromalacia patella is the erosion of the cartilage behind the kneecap. The only treatment is to limit activity (by cutting down on knee-strenuous activities, or losing excess weight).

WednesdayIL: When a patient is having an acute gout attack and reporting that indomethacin (an NSAID) and colchicine aren't helping, make sure to check the dose of the colchicine before adding a corticosteroid like prednisone. Many gout patients are on a maintenance dose of 0.6 mg colchicine daily, but an acute attack can be treated with up to 1.8 mg. So, make sure that they have tried that full dose before risking the complications of a whole new medication.

ThursdayIL: There are several ways of calculating whether a patient has left ventricular hypertrophy (LVH) based on a 12-lead EKG. Anyone who has studies EKGs knows a massively hypertrophied heart when they see one, but when it's a borderline case, how do you decide if it breaks the threshold? Here are some of the competing criteria:

• If the sum of the amplitude of the S wave in lead V1 and the amplitude of the R wave in V5 or V6 is ≥35 mm
• If the sum of the amplitude of the S wave in lead V3 and the amplitude of the R wave in aVL is >28 mm for men or >20 mm for women
• Other criteria break it down lead by lead (but you have to account for axis deviation).

FridayIL: Many people think that there exists some combination of vitamins that will give them strength and health at any age. Over the past week, we had several people - young, old, fit, obese, healthy, disabled - come in for a physical or because of some fairly benign health maintenance follow-up and ask for a "super-vitamin." Many of these same patients are against vaccines and traditional medications, and are very bad at watching their diet and exercising like we recommend. I'm sorry, but we have yet to discover a magic pill to make the 75 year old landscaper feel as strong as he did in his twenties, or allow the morbidly obese 40 year old to more easily walk down the street, or help the 92 year old not feel like an otherwise healthy 92 year old.

WILTIMS #332-3: My first goodbyes

Today was my last day at my first hospital. Tomorrow is a didactic day at our main hospital where all the psych clerkship students come back from their sites to review for our "shelf" exam on Friday. I get the feeling that this year is just going to fly by.

I've said goodbye to hospital staff before, when I worked and volunteered in various capacities at hospitals prior to med school. It's always a little bittersweet, but no different from other jobs. One of the things I'll miss about this bunch is their (dark) humor. The unit was getting pretty busy with more admissions today and few discharges. Someone joked that we should look into discharging patients to nursing homes around the South Bronx because the Legionnaires disease outbreak there is probably opening up beds...

But today I said goodbye to my first patients. When patients leave the hospital, it's great! They're usually doing better and often grateful for the work that we (read: almost entirely other people) have done. Today was different because I was leaving and the patient's were staying. There was no closure. I was sad to say goodbye, but more so, I was sad that I had to leave before my patients had gotten better. In a way, I almost felt like I was abandoning them to their fate; apparently it doesn't matter to my brain that I'm abandoning them to being cared for nearly exactly as they were when I was working, by wonderfully talented professionals. Still, it felt weird.

MondayIL: A diagnosis of rapid-cycling bipolar disorder is made if a patient experiences four or more mood symptoms (major depression, mania, hypomania, or a mixed state) in one year.

TIL: Brugada syndrome is a rare genetic heart anomaly caused by altered sodium channels that, among other things, may kill you at any time and makes you a pain to take care of for inpatient psychiatric care.

WILTIMS #230: ♫♪ And now, the end is near... ♪♫

Last WILTIMS post before winter break! Woohoo!
-or-
Last post before first semester finals of dooooooom!!! Woohoo?

Thank you for my first complete calendar year of getting to share the highs, lows, and science of med school with you. I know I've said that I write this partly for myself, but if I never got any views, I'm sure I would have ended this crazy run by now. So, unless I get ambitious and write over break, see you in 2015!

TIL: Kids with congenital heart malformations more often die from a fatal arrhythmia due to the scar from a life saving surgery than from the malformation itself. To be clear, very few of them die from this at all now and most would have died in infancy without surgery. But because we now do such a good job identifying and correcting the surgery, all of these kids outlive their malformation and a few eventually die from a rare long-term  complication from surgery.

Every heart attack patient is greeted in the ER by "MONA":

Morphine - for pain
Oxygen - to combat ischemia
Nitroglycerin - for vasodilation both of peripheral veins and coronary arteries
Aspirin - to prevent clotting and limit inflammation

The reason that heart valves specifically get endocarditis compared to other tissues of the heart is that they are nearly acellular. The white blood cells of the immune system can't get to this tissue to clear the infection. You might reasonably ask how blood cells have a problem getting to valves that are literally bathed in blood. This is where some immunology comes in handy. The way immune cells target and invade infected tissues involves a complex dance along the endothelial cells that line blood vessels. The fibrous tissue of the valves just doesn't have the external markers to slow down and hold on to white cells long enough for them to invade the tissue and do their thing.

WILTIMS #229: TIMI!

TIL: If you do a pericardiocentesis (use a big needle to drain the area around the heart of blood or other fluid) and are concerned you accidently pierced a chamber of the heart, there is quick way to tell. Splash the draining blood on the table and see if it clots. Blood in the pericardial space won't have any circulating clotting factors and won't clot.

A lot of people come into the ER with complaints that sound vaguely like a heart attack, but it would be ridiculous (and prohibitively expensive) to do a full diagnostic work-up on all of these patients. Extensive research has been done to show which risk factors are most predictive of an actual ischemic attack. The TIMI risk score correlates 7 groups of risk factors with the likelihood of death within two weeks.

The risk factors are:

1. Age >65
2. ≥3 coronary artery disease risk factors
3. Prior coronary stenosis of ≥50%
4. ST-segment deviation on EKG
5. 2 instances of chest pain within 24hrs
6. Use of aspirin within the last 7 days
7. Elevated cardiac blood test markers

Most of these probably make sense (or sound really jargon-y, if you're not medically inclined), but take a look at #6. Why would using aspirin, a very good drug for treating a heart attack, be a risk factor? Well, the patient is definitely complaining of something; that's why they're in the ER. And if they are in distress or have any of the other risk factors while already being on aspirin, then their underlying level of disease is probably worse than it appears.

If you have none of the TIMI risk factors after presenting with heart attack-like symptoms, then your chance of death in the next two weeks is 4.7% whereas if you have all seven, it's 40.9%.

WILTIMS #228: I'm not an ambi-dilator

TIL: "Coronary steal" is not the new look of Derek Zoolander, but a physiologic phenomenon caused by vasodilation medications (drugs that make your blood vessels expand). These drugs have a variety of effects on the cardiovascular system  but the one you might reasonably think would be useful is opening up the coronary arteries supplying the heart in a patient with athlerosclerotic plaques causing angina (chest pain) which could lead to a myocardial infarction (heart attack). But if you give these drugs to such a person, it will likely make the condition worse.

This counterintuitive result is due to the body being one step ahead of you. When the heart is ischemic (not getting enough nutrients via blood), the body automatically fully dilates the coronary arteries to maximize their blood flow. So, when you prescribe the vasodilator, it has no effect on the coronaries that you were targeting, but still works beautifully on all the other healthier blood vessels in the body. The other vessels widen and divert even more blood away from the coronaries, quite the opposite of the desired effect.

This seemingly nasty side effect (more like downright failure of the drug) actually has a silver lining; by administering this drug class in a controlled setting, you can test the heart's response to ischemic stress. This is one type of cardiac stress test.

WILTIMS #227: JVD or is your neck just happy to see me?

Today was one of our monthly-ish preceptor sessions, where we don our mini white coats and disperse among the real doctor folk of the area. It's really gotten fun at these sessions now that we somewhat know things. My preceptor is an adult general practitioner and most of his patients have either some infectious or cardiovascular problem and, luck would have it, those two topics are precisely what our big first semester final is on next week.

TIL: "Splinting" is a term for when a patient guards one side of their chest from expanding when taking a breath.

Jugular-venous distention (JVD) is a great external indicator of right-sided heart failure (as well as tricuspid valve stenosis and constrictive pericarditis). This is when blood backs-up in the large veins as it tries to come back to the heart. This pressure travels back up the jugular veins (among others) and causes them to visible bulge in the neck.

But the jugular can be visible normally, so how do you officially classify JVD? First, you must have the patient sitting back at 45° and at rest. If the jugular is visible 4.5cm above the sternal angle, then the patient is positive for JVD.

WILTIMS #225: Think before you think

I've noticed a change in the way that I think, and I'm not sure if I like it. I've started wanting an H&P (history and physical) on my friends and relatives. Now, I don't mean that I literally want to peek into their medical records; it's more that I have come to expect a certain amount of background information before addressing a problem. When I'm asked for advice by people I know, I go into "doctor mode" and immediately want more information than it's socially acceptable to ask for.

One of the most important things you learn early in medical school is that your ability to diagnose and treat is most directly affected by the quality of your history and physical. You can't rule out or rule in anything if you don't have all the appropriate information. Doctor-patient privilege is a powerful thing, allowing you to ask anything - with the understanding that the conversation is confidential, useful, and may help to solve the problem at hand.

I want that same ability for certain situations. I want to be able to call timeout on our normal relationship and deploy this higher standard of listening, but that's just not socially feasible most of the time. Now, I think this is usually fine when the problem is medical; people naturally expect to have to share details if they bring up a medical problem on their own. But with interpersonal problems, issues at work, or in academics, there is a level of discretion employed that you simply get to bypass in medicine.

If a friend is asking for serious non-medical advice, I go into "problem solving mode" (a close relative to "doctor mode"). It's fun. It turns even terrible situations into puzzles. If I can just see all the pieces, eventually I will solve it. But this is a false analogy. There are times when the broken pieces will never add up to a full picture. When problem solving doesn't help. When all a person needs is comfort and understanding. This is a scary route to desensitization and it is plotted out by the most benign and even well-meant reasoning.

For years we are trained to elicit a problem, break it down into useful pieces of information, elicit more info if needed, and then start offering solutions. That's great, usually. But in real life, we aren't hearing the problem from an exam prompt or even a patient in a clinical setting. These everyday questions come from friends, from family. They probably aren't telling you their troubles because you're a doctor or medical student, but because you are a person close to them who they can trust to listen and reassure them. Sometimes they already know the answer to their problem. Sometimes they aren't sharing everything because the problem is too personal and you figuring out the solution (using your mighty problem solving skills) will only bring more pain, not less.

To any med students reading this, try to keep in check the wonderful, powerful ability you are honing to someday save untold lives. Your ability to problem solve is part of what makes you special and able to apply the vast knowledge you are accumulating, but it also can isolate you from your fellow humans if you let it dominate your thought process.

TIL*: Uremic pericarditis kills dialysis patients in blizzards. This is part of why only certain vehicles are supposed to be on the road in snowstorms. The average healthy peron can go a couple days bundled up and playing board games. But if a person in renal failure can't get to a dialysis clinic (thanks to roads blocked by accidents or stranded cars) they die - often from this form of pericarditis (inflammation in the tissue and space surrounding the heart). Stay off the roads in an emergency!

*It's a new record! I'm three days late on posting this one, but I'll be damned if I don't maintain my post-per-day-of-class run. Apologies for the delay!

WILTIMS #226: Eye eye, captain.

Why do doctors always look in your eyes? It seems like whatever you go in for - a fever, a headache, high blood pressure - they need to peek in the peepers. Well, just as the eyes are your window to the world, they're our window to blood vessels. The blood vessels in the retina are the only ones in the body that can be viewed directly. It's like we can look straight through the skin and watch disease processes do their damage.

With hypertension, a fundoscopic exam (eye exam) is especially useful thanks to a whole spectrum of symptoms that can tell us about the progression of this widespread medical condition. AV nicking shows venous damage around intersections with hypertensive arteries. Cotton wool spots are tiny infarcts of retinal tissue due to blood vessels pinching off parts of nerve cells. Finally, the retina can hemorrhage causing tiny blobs of blood to escape the vasculature. These can be tiny and unnoticed (until a doctor sees them during an eye exam) or so large that they severely reduce the persons vision.

TIL: Stages of heart failure were recently renamed so that stage A heart failure is really just a warning of predisposing risk factors. Stage A means you don't actually have any symptoms or structural damage, but have one or more of the high risk warning signs that, if left untreated, are likely to cause the other, more legitimate stages of heart failure.

Pulsus alternans is an interesting, if ominous, effect of left systolic heart failure whereby the heart alternates strong and weak beats thanks to a poorly executed compensatory response. When the heart fails to pump out enough blood, some blood is left in the ventricular chamber. When the heart tries to refill that chamber, it now overfills it because of the leftovers from the previous beat. This stretches the muscle out (using the Frank-Starling mechanism) causing the heart to beat harder. This tuckers out the already failing heart and it pumps rather feebly the next time, starting the cycle over again.

WILTIMS #224: De-defects

As a nice little follow-up to yesterday's heart congenital defects post, today I learned about some of the repair procedures for these defects. Most of these conditions require multiple procedures because a baby born with one of these deformities is typically premature and would not survive the main surgical correction. So, frequently, a less invasive procedure is done as a stopgap measure to keep the baby alive long enough to develop and grow a bit more.

TIL: The stopgap procedure used for transposition of the great arteries is to purposefully punch a hole in the atrial septum. This is the malformation from yesterday where you need a shunt of some kind between the parallel circuits of blood flow in order to survive. To better the outcome and stall until bigger procedures can be attempted.

Seemingly paradoxically, the first procedure developed for the permanent fix of this condition involves the rerouting of the left and right atria to the opposite ventricles. I have yet to hear a good expansion for why they didn't start with what is now the more common procedure: simply switching the great arteries back to where they normally are.

I say simply, but this surgery is very complicated (I still don't think it's more complicated than construction two crisscrossing atrial chambers while maintaining proper pacemaker production through the heart, but hey what do I know?). The incision must be made above the great arteries valves which presents us with a problem; the coronary arteries, which supply the heart with nutrients, come off the aortic valve. That valve is being left behind and converted into a new pulmonic valve, which won't be able to oxygenate the heart tissue. So in addition to the switching off the aorta and pulmonary arteries, the coronary arteries must also be moved over to the old pulmonic valve.

WILTYIMS #223: Defects

We had a lecture today yesterday was on congenital heart defects. Here are some of the facts I found particularly interesting:

TIL: A person can be born with a double aortic arch. You might rightly think this shouldn't be a major problem because it's simply a redundant (if super large) blood vessel. Problems arise not because of blood flow, but because the second arch completes a circle around the the esophagus and trachea/bronchi. This leads to problems swallowing and breathing.

Coarctation of the aorta is a narrowing of the superior descending aorta and is one of the only things that will make you listen for the heart sounds through the patient's back. The aorta naturally arcs backwards and the stenosis occurs just on the downturn so that the noise of the blood whooshing through is best heard on the back, between the scapulas.

Ventricular septal defect (VSD) causes left sided volume loading because the volume ejected during systole never returns to the RV. Blood squeezed through the defect from left to right will go straight into the pulmonic valve and back to the left side.

A "tet spell" is a temporary event that occurs in children with the condition called tetralogy of Fallot, a fairly common constellation of heart malformations. Tet spells are caused by increased resistance through the pulmonary artery (it's not known why this happens) which causes all the deoxygenated blood longing for the lungs to go through a hole in the septum. The deoxygenated blood just cycles back to the body, causing the child to turn blue and faint.

And finally, when is the one time you want a septal defect? If you are born with a transposition of the great arteries (the aorta and pulmonary artery) you need a septal defect to survive long enough for surgery.Transposition of great arteries sucks. In effect, the two paths of blood from the heart are switched creating two parallel and thus useless circuits. Oxygenated blood from the lungs goes right back to the lungs and deoxygenated blood from the body returns to the body. The only way to survive is if you have another birth defect: a hole between the two sides of the heart.

WILTIMS #222: CLEAR!

Today was pretty awesome - we got our first crack at the super fancy medical mannequins that our school recently invested in. On monday I got to play around with "Harvey" the cardiovascular mannequin and, though he was indeed adept at making heart sounds and murmurs, he was lacking in both liveliness and limbs.

Today's nameless plastic patients had all their arms and legs (and pulses in each of them to boot!), dilatable eyes (that blink too!), breathing lungs and a beating heart. These are the sort of mechanical wonders that can be programmed on the fly from behind a mirrored window to behave as any sort of patient and get better or worse as we attempt to treat them.

A doctor lead our activity today by giving us the briefest of histories and then stepping back to see how we would do (rather poorly at this point, in case you were wondering). He would offer non-committal advice as we crowded around the mannequin listening with our stethoscopes, asking for test results, and trying to remember all that reading we haven't done yet. But I've never been more receptive to learn as when there is a dying (plastic) woman in front of me and we can (theoretically) save her.

Quote of the day: "If you can think and pee, your heart's working well enough to wait on getting a pacemaker." -our course clinical cardiologist when describing the most important organs that your heart perfuses.

TIL: Don't restart atria without anticoagulating first (if possible). When the atria are not contracting productively, as in atrial fibrillation, the blood can sit and clot. If you start up the atria right away, you will scatter these clots throughout the capillary beds of the body, notably in the lungs and brain, potentially causing a stroke if not killing the patient outright. That's why, if the afib is non-emergent (i.e. not already causing significant symptoms), you send the patient home on anticoagulants for a few weeks to dissolve any potential blood clots before trying to start the atria again.

And from yesterday's comments (yes, I do respond to questions in the comments! hint, hint, nudge nudge):

Q: What does it feel like to be defibrillated while awake? Is it terrible? 

A: We just learned this today actually! It really depends on the type of arrhythmia. If a person is in afib, you can reset the heartbeat with a relatively small shock - something that would make the person go "Ouch. That hurt!" If they are in v-tach, you may need to use 5- or even 10-times the power. Now, to be fair, if the person is in v-tach, they will almost definitely not be conscious. Regardless, this level of shock is the sort of thing you see portrayed on TV (although less dramatic): all the muscle cells in the heart are depolarized and will hopefully reboot, but with this level of shock, a bunch of the other muscle cells in the proximal body depolarize too, causing a fairly sizable full-body twitch. This would feel very much like being electrocuted... through your chest. So more of a "*#@$%!!!" than an "Ouch!"

WILTIMS #221: Physics - The Revenge!

The average med student regards physics is a necessary evil - a penance to placate the MCAT gods and then promptly forget. After all, most of us got into this business because we liked biology, not math. And yet as I've progressed through my first two years, I've noticed that hidden among the touchy-feely biologists are a handful of physics-heavy specialists who actually use those long forgotten equations to do their jobs.

Today we got a nice refresher on fluid dynamics from a cardiologist who specializes in echocardiography (using sound waves to image the heart, much like sonar in submarines). The following equations came up while discussing the flow of blood between the atria in a patient with an atrial septal defect:

P = Q × R   ∴   Q = P / R

A septal defect is when there is an abnormal hole in the heart connecting either the two atria or ventricles, neither of which are supposed to be connected. Generally, the left side of the heart is under more pressure than the right, so one might assume that blood would flow from the left to the right when there is gaping hole in the septum. With a big enough hole, the pressures equalize and you'd expect the flow through gap to stop... but it doesn't!

This is when the cardiologist coyly grinned as we all scratched our heads. Why would there be a flow of blood when there is no pressure difference? To the physics! Looking back at the equations above (or just remembering from physiology), flow (Q) is related to both pressure AND resistance. So, if the pressure is the same between the connected chambers and blood is still flowing, then the resistance must be different, and this, in fact, is the case.

TIL: Replacement valves last longer in place of the aortic valve than mitral valve. This is fairly counterintuitive because the aortic valve is generally dealing with bigger pressures. BUT, the mitral valve deals with a bigger change in pressure (AV: 120/80 vs MV: 120/12), and it's this that really causes the wear and tear.

Don't defibrillate people when they're awake. Generally not considered good bedside manner. If a shock would be good to reset their arrhythmic heart, knock them out first.

Rivaroxaban and apixaban have their mechanism in their names. What?! An intuitively named drug?! Crazy, I know! These anticoagulants counteract or ban Factor Xa. ban Xa → Xa ban → "-xaban". Tada!

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.