Friday, December 12, 2014

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%.

Wednesday, December 10, 2014

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.

Tuesday, December 9, 2014

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.

Friday, December 5, 2014

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.

Thursday, December 4, 2014

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.

Wednesday, December 3, 2014

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!"

Tuesday, December 2, 2014

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!