Doctoring Reflection

Changing the mind of a doctor — Not an easy matter

Changing one’s mind is hard. Changing the mind of doctors is even harder.

Doctors are supposed to be the medical experts. Often we are. But sometimes I wonder whether our attachments to old ideas gets in the way of seeing the obvious.

I am reading Michael Lewis’s book The Undoing Project. Learning how Kahneman and Tversky made their discoveries gets me thinking about how our minds trick us into missing important clues.

The information age levels the degree of expertise. Of course an internet connection and a smartphone does not transform people into skilled and experienced clinicians. What connectivity does do, however, is it allows anyone to look up the current evidence for or against a medical intervention.

In some cases, people without preconceived notions may be better judges of medical evidence.

Davide Epstein is a reporter for ProPublica and author of the Sports Gene. He’s written an important article on how tough if it is for doctors to incorporate new medical evidence into decision-making.

It’s called When Evidence Says No, but Doctors Say Yes.  It’s worth your time.

I am quoted in it. So are lots of other giants in the field of common-sense medicine.


6 replies on “Changing the mind of a doctor — Not an easy matter”

A good example is the way EECP is such a well-kept secret — at least in the US. NOW, after I told my cardiologist i was going to try it he said, “Great idea!” But with the warning that EECP is not known to increase LVEF. False! What is frustrating is that after my SCA 2+ years ago, I made it very clear to him that I wanted to take every possible pro-active approach possible for my cardiac health and fitness. So I got a generic lecture about Mediterranean diet, your weight is pretty good, you get plenty of exercise, we have you on the right meds, cholesterol, etc. etc. Not a word about EECP and he knows we have a facility right here in Austin, Tx. My internet “research” found that EECP CAN increase LVEF and is, in fact, Medicare approved for shortness of breath, and heart failure — not only for angina symptoms. Multiple echos for two years came back at 37.5% LVEF, but right after EECP 45%. So not only could I feel the difference, (and my cycling friends say “What has got into you Don? You are kicking ass!”) but objective measurement confirmed significant benefit.

I don’t tend to be a conspiracy theorist but is hard not to wonder if the fact that there is nothing in EECP for hi-tech cardiac surgeons is a factor. Had I done EECP two years ago I would not have qualified for the buzz-box that was put in my chest — not that I mind having it, but was it needed? And, of course, the surgery entailed risk as did the 3x bypass right after SCA.

Searches all over the internet for “improve ejection fraction” produced no references to EECP. I only know about it because it worked very well for an acquaintance. Now that I know how to find references to EECP, I am appalled with the near universal recommendation: “It works, so try it when all else fails and bypass or stents are not an option.” WTH?? Why not try it first? Cost is a pittance compared with any surgery, risk and side effects are essentially none.

When my general cardiologist and cardiac surgeon were asked “Why didn’t you tell me about this?” I got evasive double-talk. I try to be charitable and say they are stuck in conventional thinking and not consciously thinking only of revenue, but I wonder.

Don — (Going back for another round of sessions in a couple of months and hoping to break 50% LVEF!)

Are we starting to see a pattern here? Prior to a mitral valve repair, 12 or so years ago, that I had to suggest myself after being sold hard on the idea of a artificial valve and Coumadin for life, I went to work for 24 HOUR FITNESS and became their top-selling fitness trainer in the world. In the early 1960s, I had the first Italian bike (ATALA) in my Northern Virginia neighborhood. Then I had the surgery and the syncope began but nobody warned me, suggesting instead a “seizure disorder” and I had a fall, striking my head, and had emergency surgery for a bilateral subdural hematoma and subsequently lost my ability to think clearly, find the words to say, and finally lost my ability to speak for a season. Not long ago, I had to suggest to my cardiologist that my new pacemaker record led me to believe that I might be a candidate for ablation. Two procedures later and I certainly feel, think, and speak like a new man.

My mother had a similar experience. And my 23-year-old daughter who played college soccer was, I’m told, wearing a Holter monitor recently and is diagnosed with A-fib at what I’d think is a pretty young age. I’m awaiting new posts on these subjects, including whether this is a pandemic, with bated breath.

I’m not convinced that my cardiologist has a sufficiently open mind, not to mention respect for me, to be a resource for me any longer. Sound familiar to anyone?

Dr. John, my question/comment is off topic, if you have time will you please answer this. In sinus rhythm is the signal that is sent from the SA node equal to the signal coming from the AV node? From your book when the heart is in flutter the signal coming from the SA node can be 200-300 bpm and is reduced at a 2:1 ration leaving the AV node. Is the signal from the SA node always higher/faster than what leaves the AV node.

Thank you,

Paul Fuller

I will take a response from any or all with this information.

The signal from the SA node is usually
the same as the signal from, the AV node. However the AV node acts as a kind of buffer in that if the SA node signal is very slow the AV node can pick up the rate and send faster signals than the SA node ( to keep the heart beating enough to keep you alive) and when the SA node is too fast, the AV node can block some of the signals to keep the heart rate from getting too fast. (If the heart rate gets too fast, it can paradoxically limit the
amount of blood that gets pumped out of the heart. SO this breaking action is beneficial with very fast SA node beats

The benefit of stenting in stable coronary disease is not settled.

See BMJ 348:g3859 and
AmJ Cardiol 2015 May 1 1194-9

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