¶ Intro / Opening
From Kerkow media coming up on the show, the first patient I saw when I was an intern, I was at Duke University, I went down to the E.R. to admit my patient. She was twenty five. She'd come in the a couple of weeks before pregnant. She was second trimester tachycardic and short of breath, fast heart rate. Couldn't breathe. Well, she was told she was anxious from her first pregnancy, was sent home, came back. I was there to admit her, but by the time I got it, she'd already had
a cardiac arrest and died. I went to her autopsy. I have pictures of it to this day. And she had huge blood clots. One, I never forgot that. You know, we've both seen a lot of interesting things in medicine, but that really got my eye that something like this not only takes the lives of older patients, but can take the lives of young people who seem to have no particular risk factors. Dr..
Having trouble catching your breath, slightly dizzy, maybe battling a small cough, perhaps, that it's probably nothing, right, for the patients or doctors listening, we're not trying to make you nuts, but these seemingly benign symptoms might be something that require a second look. And apparently part of this diagnosis process comes from perspectives that only come from doctors with years
of experience. A pulmonary embolism has been deemed a silent killer because most often than not, it's diagnosed only in an autopsy. Yep, when it's too late. Well, today we're joined by a renowned doctor from Cedar Sinai whose research helps lift the curtain behind a disease that plays hide and seek. It's used to hiding and will only present itself if you seek it out. It's a sobering lesson, but it's highlighted with hope. This is medicine we're still practicing.
I'm Bill Kurtis. So first, my co-host, the quadruple board certified doctor of internal medicine, pulmonary disease, critical care and neuro critical care, and my very best friend, Dr. Stephen Tayback. How are you doing, Steve Cable.
Good to see you.
We've got a special guest today that I know you're going to like because it's just right up your alley. That's a fact. Our special guest, Dr. Victor Tapson, he's a professor of medicine and director of clinical research at the Women's Guild Lung Institute. He's also associate director of the Pulmonary and Critical Care Division at Cedars Sinai Medical Center. He's authored more than two hundred peer reviewed manuscripts and a whole bunch of books and book chapters. We're lucky
to have him here. Vic, I imagine this past year
¶ How has COVID played a role in blood clots?
with covid has been quite a challenge. And I understand covid creates all kinds of blood clot issues in your patients. Has it been for the last year?
It's been such a bill as it has for everyone, but because a lot of problems, a lot of them involve the lung, of course, and many of them actually involve specifically a blood clotting in the lung and blood clotting in other places, too. So we've been trying to figure out how to deal with how to treat it, how to diagnose it. It's been a trying, but I think we've made a lot of progress.
Why does it cause blood clots? How does the virus do that?
Well, it's interesting, but there's something that go into thulium cells that line your blood vessels. These are the cells that line the blood vessels, become very inflamed and irritated by this virus. And we get something called an endothelial IDUs, sort of. So these viruses get in there, they inflame the lining of the cell. And when that happens, it releases substances from inside the cells. One of them is called Tissue Factor. It can really get clotting going and
it's more complicated than that. But we certainly learned that in many blood vessel linings, not just the lungs, this develops blood clots in their legs called gvt, and they break off and go to the lungs. We call that pulmonary embolism. And we've seen a lot of this and it's been difficult to try to decide who we should look for that because a fairly high percentage of patients with Koban do get it.
¶ Dealing with the social devastation of COVID as a physician.
Back in January, we had 10 deaths a day, and which is just unprecedented and morale was at an all time low and just the human tragedy of it. And the staff was just reeling every day from the terrible emotional trauma. What did you guys do over the hill? Over the hill? Because Cedars is over the hill from where we're at. How did you folks deal with the social devastation both to the patient's family and also to your staff?
I can tell you, Stephen, I'm sure you did the same thing. It was very difficult, especially early in the pandemic when we weren't putting patients in the room. No one was coming in. And later the same thing Jan came along. It was much worse than over the summer for us to we didn't really notice a really high death rate the whole first year until that surge after the holidays. Then we noticed something a little different. I don't know if that was a variant California variant. We
were getting some of the one one seven Bériot. I don't know the reason we didn't sequence everything right away. I could just tell you, though, we saw what looked like a difference to us and to handle those problems that you're mentioning, the emotional social issues, me was a lot of phone calls and we enrolled patients in clinical trials. And normally we would talk to them and say, well, Mrs. Jones, we wouldn't like to enroll in this trial. And I
know your husband's on the phone. Let's tell you a little bit about the study. And it was not just like a usual study where we would fill them in on some details. We had tons of questions about Kojm therapy, everything from other members of our family, how they could prevent it. So it was a lot of communication, a lot of phone calls. And I think that's really important treatment during this kind of thing. And it was family members,
the patients themselves, isolated patients, the rooms. You know, Steve, it was terrible. It was terrible. A lot of communication, a lot of handholding.
So I probably can't say the name, but I have
¶ Are blood clots in COVID patients different than those who get clots without COVID?
a friend of mine who spent 59 days in your ICU and was on the ventilator for a long, long time. And nobody was really too positive about how that was going to turn out. And you guys sent him home and he had to relearn to walk. And he lost all kinds of weight, of course, but you had to put him back home among his wife and all of us who love them. And we really appreciate it.
I'm glad he did. Well, boy, I'll tell you and I'm sure Steve took care of some of the same kind of folks. We just had some very, very long hospitalizations that were complicated by subsequent to see someone in the ICU for a long time or whatever they have covered or whatever. And then they get a urinary tract infection, they get a bloodstream infection, they get another kind of pneumonia. So, yeah, just like you're saying, Bill, these were complicated patients in many cases.
No question for you. The general public, I think, is very familiar with the idea that if you've had a knee replacement, you're going to need to be put on blood thinners. People have heard they've been on a long plane flight. They've heard of cases of people developing a blood clot.
And I think it's
it's just general knowledge that when you're on an airplane, you should get up and walk around the mechanism for blood clotting in the covid patients pathologically. Is it? Exactly. The same as those people who undergo a surgical procedure or those people who are on a long plane flight is a blood clot, a blood clot, or is there something, a nuance to covid patients that we've identified during this past year?
I think it's a little bit different. I think people do form clots in their legs. They break off and go to the lungs. But we're seeing patients that came in the hospital, as you suggested earlier, are nurse coordinators drawing blood from cold patients. The two clot it off and this doesn't happen by the two keeps falling off. I can't get it quite literally easily. We're seeing something called micro thrombosis, small clots in blood vessels, blood clots
in the lungs don't start in the lung. They start in the legs and they go to the lung where some of these patients getting clots in their lungs. It might even be building up inside to do some I don't think know blood clots for forming and veins that niobium that usually would stay open. And so I think
it was different. Steve, I think this very pro thrombotic, as we call it, tendency Cauvin was causing problems and a little different way, not just big macroscopic clots in the leg veins breaking off and going to the lungs, but small clots even causing strokes, causing heart problems, causing
kidney problems. So we're seeing multi organ problems and what we call micro thrombosis, because this organism seems to be much more pro thrombotic than the flu, more than nerves or SARS or some of the past infections we've seen,
in addition to the treatment, I should say, of blood thinning anticoagulation. Have you folks done any research on antiinflammatory agents, immunotherapy that may have some impact on either prevention or treatment of blood clots?
We haven't actually done some of the studies on some of the antivirals. In the early stages, the desert disappear. We completed a study on a drug called Burset NIB.
¶ Does anti-inflammatory agents or immunotherapy have any effect on blood clots?
There's something called a jack inhibitor. One thing we learn, as you know, in the Soviet era is that steroids seem to help. And why do they help? To help is cytokine storm. These patients get such immune responses and tremendous inflammation that steroids can tend to kind of shut that down and calm things down. It put them on steroids for a long time to early and then they get covered. Then they're in trouble because their immune system shut down, can fight the virus. Once they get covered.
Steroids may help. And I think steroids probably help with thrombosis. But right now, the data don't prove that. One study published in February suggested that there's no real proof right now that steroids reduce the chance of getting a clot. But it's hard to ignore the fact that if you do the right study, they might because inflammation and coagulation
or clotting are so intimately linked. One way we know that if look at obesity, obesity, we don't think of it as an inflammatory disease, but it is obesity is chronic inflammation. The more we see, the more information there is. A heavier you are, the more likely you are to be hospitalized if you got covid and the more likely you were to get a blood clot. So I think there's really something to that.
Personally speaking to you and I, we live and breathe this type of issue in the ICU. Naturally, it's interesting to us. But was there something in particular that caused you to pull your focus and to dedicate your life to dangerous blood clots and pulmonary hypertension?
¶ What got Dr. Tapson originally interested in studying Pulmonary Embolism?
I could see the first patient. I saw it with my arm. I was an intern. I was a Duke University. I went down to the E.R. to admit my patient. She was twenty five. She'd come in the last couple of weeks before pregnant. She was second trimester tachycardic and short of breath. Fast heart rate. Couldn't breathe well. She was told she was anxious from her first pregnancy, was sent home, came back. I was there to admit her, but by the time I got it, she'd already had
a cardiac arrest and died. I went to her autopsy. I have pictures of it to this day and she had huge blood clots. I never forgot that. You know, we've both seen a lot of interesting things in medicine that really got my eye that something like this not only takes the lives of older patients, but can take the lives of young people who seem to have no particular risk factors sometimes. So it's always been fascinating to me. I've maintained my interest.
It's one of the most misdiagnosed syndromes in medicine and one of the most highly litigated syndromes and pulmonary embolism. Why is it so hard to diagnose? Why is it that the general population of physicians out there, why is it that we're still missing so many of these cases?
I think a couple of reasons are I can see
¶ Why do DBT and PE consistently get missed on diagnosis?
the symptoms, as you know, are very nonspecific. But you're short of breath. You rarely have coffee. You might have a cough. You might, in rare cases, cough up blood not nearly as common with people. You're short of breath. You listen to the lungs, you don't hear anything. They sound normal. You don't hear wheezing like you do in your crackles, like a pneumonia or fibros. You don't hear decreased breath. Sounds like there's fluid in the lungs. Look
at the chest x ray, chest x rays. Clear, clear x ray with a big polymorphism, you don't see pneumonia, heart failure. So people looking at your lungs, they look your arteries and maybe got a little asthma. Some I'm not sure what this is. And you're sent home. And we've learned from four or five autopsy studies, if you die from pulmonary embolism, more likely than not, you're not diagnosed until you're dead. And more likely than not, you're not even suspected until you're dead. So see that that's
right on target and it's still a problem. So I think we I think we've raised awareness and I. We have, but we still see this still litigated and it still poses a huge problem. So you're absolutely right.
So what is the best test at this point to diagnose this?
One of the best tests off the bat? I'd say,
¶ What are the best tests to diagnosis PE?
Bill and I kind of see a tongue in cheek is using good clinical gestalt. And there's been a study that's been shown by one of my colleagues over in Belgium. She did a nice study that showed that you have these scoring systems as well as well score the revised. You need to score the perks for to maybe help you if you're suspecting whether you should do a test or not. And what Dr. Peñaloza showed was good stock is better, better even than any of these scoring system.
If you think someone might have P.E. and there's a reasonable chance they do, you've got to go for a simple blood test called a dimer. You can do dimer test is negative. It's very unlikely to have a clot if it's positive. You can't be sure it's nonspecific, but you've got to have a low threshold to go ahead and do a CT scan of the chest. And sure, you're going to maybe do too many CT scans expected.
Too often you don't want to miss this diagnosis. So a good gestalt, I think, about the diagnosis and think about simple things like we've got an unexplained fast heart rate. Why is your heart rate 110 or 120? Maybe you are anxious, but maybe it's something else. Maybe it's your asthma inhaler, but maybe it's pulmonary embolism. So unexplained fast heart rate, unexplained shortness of breath, even someone's kind of anxious, a little bit shorter, but I've got to think about it.
So once it comes to your consciousness, I think you're in better shape.
So let me bring this into the mix, because this is the era of cost containment and you want to minimize testing. That's not necessary. And so using a score like the well
score, which
is supposed to help delineate who's the low risk, mid risk and high risk, and obviously, if it's a high risk, you're going to treat the patient. If it's a low risk, maybe you're going to let the patient leave your E.R. and certainly a seasoned practitioner such as yourself, your gestalt
means a lot. But for a young practitioner who's making an assessment, who's relying heavily on a well score, and who feels pressure to minimize the amount of testing that they're ordering, what kind of a conundrum is that and where do we go with that?
¶ Young physicians and the conundrum of minimizing the amount of testing with a disease that's diagnosis relies mostly on "suspicion."
It is a conundrum and we do have to think about that for sure. And in the end, I think you should use these new scoring systems. I think the catch is use a scoring system together with a dimer in a body dimer is negative. You're almost always off the hook. If your suspicion is somewhat lower moderate, you're off the hook. If it's very high suspicion, probably nothing should supersede a very high suspicion. So I think what
you do is you use those things together. And again, just don't ever second guess a really strong start feeling. But it's a problem. I think the tests testing make it better, make it easier. We're using artificial intelligence now, machine learning. We've done a couple of protocols. Now we've done with it. Are we able to predict code with a group we worked with coming up with an AI program without doing a COBA test? We were ninety nine
point something percent accurate predicting covid. I think the same thing could be done with pulmonary embolism. And now now we've got A.I. artificial reading of CT scans, too. But I think that's going to come into the you may have seen something on TV using a robot who is taking histories from people. In the end, it was amazing. I think using machine learning, artificial intelligence, together with Gestalt, we're going to do a better job at saving money.
But again, when it gets down to see I've been really lucky. No one's ever pressured me to save money. But we do want to use our common sense and try.
But wait a minute. We're the patient here talking. Are you saying that there are considerations, perhaps with your relationship with some doctor's relationship with insurance companies that could affect whether or not you CT scan my dad if you have a well, let's say a minor suspicion that he might have a clot.
Part of it is money and part of his resources. And for example, if you've got a busy day, there's one hundred people in there being seen. The CT scan is being used for all kinds of things. And so it's money and it's also using your resources carefully. But no, I would never think about money when I really thought someone that I think in general makes a good point.
You've got to take that into consideration. But when it gets down to an individual patient to me, I will never, ever not get a test because I think it might cost me a little more if I have some doubt.
¶ Minimizing CT scans because of the dye/contrast's effects on kidneys.
But there is another consideration, and that is, if so, the public may say, well, if I'm a little short of breath, I'm having some chest pain. Everybody should just get a CT angiogram and and delineate. Is this a pulmonary embolism? Is it not? But the reality is the dye, the contrast that are being given with CT scans actually can have a deleterious effect. It can cause some kidney damage.
And you don't want to, in a cavalier fashion, start scanning everybody that comes in because you don't want to miss a pulmonary embolism and wind up causing a certain percentage of patients to have serious kidney damage. That may or may not be reversible because you wanted to be super meticulous about making sure you're scanning everybody. So so medicine granted should not be it. Certainly in this country, we should not be thinking resources first by any means.
But we do want to be judicious in our testing because some of the testing can have some negative impact on our patients well-being as well.
You've got a screen. You've got you're absolutely right. You've got to look at that and look at the kidney test. If it's too high, we can't do the CD. There is another test you can do called the BQE and the ventilation perfusion scan. Very good test. Not as accurate as a CT scan, especially if the X-ray is already abnormal or the patient has other kinds of lung problems. But still a good test. But you got. Yeah, you're right.
But look, the lab tests make sure that that's normal or near normal or you can't do this and you may have to empirically treat someone you think they might have until you can do a scan. You may have to wait a day sometimes to get the kidneys better.
So can I just ask you guys about the treatment for just a second,
because logic tells
me that if you guys treat a blood clot with a blood thinner, it would seem that that is going to reduce the size of the blood clot. Right. Kind of thin it out. And it would seem that it could then get dislodged and actually move into a more destructive location.
¶ How do blood thinners work?
They do a couple of things. They don't actually break the clot down themselves, at least the ones we usually use. They prevent the body from forming more clot, which is helpful. They allow the clock to stabilize by keeping it from growing. It sticks to the wall and is less likely to break off as it stabilizes like this. The other thing it does is by thinning the blood, it allows the blood to flow better. So these remaining channels you have open,
you get blood through better. You've got a blocked off artery. The heart can't pump the blood as well. If you can open up some channels by making the blood thinner, it gets through better so it can help even without affecting the clot directly. But it takes time for your own body's fiber optic system or clot busting system to kind of break down these clots in the blood thinners will give you a time for that to happen. But it does happen. You can treat someone and they may
still have another blood clot or form one. But generally speaking, once they get on, that clot stabilizes and size doesn't get bigger. And one thing we've learned is blood thinners save lives. It's one of the dogmatic things we can say about blood clots is as soon as you get someone on the blood thinner, their chance of dying gets lower. It's been shown in one nice research study by a colleague published in Chest, one of our journals in 2010.
If you're on a blood thinner with an at an adequate level within twenty four hours, your chances of dying are far, far lower than if you're not.
And once you're on a blood thinner, very often my dad and his case, I think warfarin. Was that excessive? Yeah.
We didn't have the docs at the time that your father was first placed on uncommitted.
OK, but basically once you're on blood thinners, you kind of stay on blood thinners. Is that the case?
We're doing that more and more nowadays. Why don't we try to divide clots into what we call promote and unprovoked? That's a little bit simplified. But the bottom line is, if you have a really good reason for a clot, you have a hip replacement and you get a blood clot, usually will treat you for three months, sometimes six, unless you have other risk factors. If you fly from Paris to L.A., actually get a clot. We know the plane flights increase the risk of clotting, but to me, that's
a minimal increased risk. I've flown my four million miles of American Airlines. I've never had a clot, I think. But people are more susceptible, increase their risk, lower the threshold. They may get a clot, someone that's the only reason they get a clot because they're flying. I'd be inclined to treat them long term. I wouldn't say forever, but
I'd say indefinitely. Forever's a long time. And what we can do now that we've learned with these new drugs that Steve mentioned, called the Doakes, is we can drop the dose at six months and reduce the risk of bleeding dramatically and still offer protection. So no kind of a new paradigm is to consider many patients treat them longer. If someone comes in, they have a plot and their only risk factors, they're obese. We might say, well, we'll keep you on this drug. We'll drop the dose in
six months. If you lose weight, we'll take you off. But if you don't want to keep you on the slopes, there's a lot more versatility nowadays with these new drugs.
OK, well, we're going to take about a 30 second break here, and when we come back, I'd like to talk a little about pulmonary hypertension. We'll be right back.
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All right, Vic, pulmonary hypertension. I'm assuming that is high blood pressure specifically in the lungs. How is that different than plain old high blood pressure?
So high blood pressure. You measure your blood pressure, your arm,
¶ Pulmonary hypertension vs. high blood pressure.
it's it's 120 over 80 when the heart's squeezing. It's 120 when it's relaxed, it's eighty. And in the lungs, you have a separate circulation. Normally in the lungs, the pressure's much lower because the blood vessels are very dispensable. They can open up, they can handle more flow. The pressure might be twenty over ten, much lower pressure. Different things can make this pressure go up and we call that pulmonary hypertension.
Now, I had a patient of mine who's become actually a very good friend of the
family, and
she had a pregnancy and right after she delivered suddenly became short of breath and she was diagnosed as pulmonary hypertension. One of my competitors at the hospital said, you know, you have two years to live and you better get your affairs in order. And then I walked into the room and I said, OK, well, things have changed now. And we obviously put her on some of our newer medications.
It's been ten years and she's doing great. So maybe give a little bit of history about the earlier prognosis and where we are today in terms of
the hope and the better
outcomes that we're seeing relative to pulmonary
hypertension. Well, Steve, I'm glad you were there to reassure her,
¶ What are the 5 classes of pulmonary hypertension?
because you're absolutely right. Things have really changed. Mortality actually dropped over the years. Just in a very brief nutshell, kind of five classes of permanent protection once called pulmonary arterial hypertension. It's the kind of young women tend to get more commonly than men unknown cause Group two is from chronic heart disease. That's much more common in older folks. Gets to FART'S and get heart has more trouble pumping attention.
Group three, you have emphysema, lung fibrosis, scarring in the lungs. You destroy many of these millions of blood vessels in your lungs and the pressure goes up. You have to just treat the underlying disease. Group four is blood clots. About one in one hundred patients with pulmonary embolism, like we were talking about, will go on and get chronic pulmonary embolism. And that's got to be treated differently in the group. Five is kind of the muscle group. One
is the one I suspect your patient had. It can be what we call idiopathic pulmonary hypertension, young women probably for women, for every man it gets it unknown cause sometimes brought out by pregnancy. And in the old days, we had no treatments. First patient I saw in nineteen eighty two, his name was Gary. There's a minister for South Carolina again. I was an intern. He had severe
pulmonary hypertension of unknown cause. Our attending physician very insightfully sent them to Berkeley Griffith in Pittsburgh who had already done about a seven or eight heart lung transplant. Gary got a heart lung transplant and survived a good three or four more years after that. Now, we rarely have to do heart lung transplants, my judgment. And if we do, patients do much better nowadays. The idea is we have medications we've studied for the years. It was nineteen ninety six.
We published the first paper on using prostacyclin drug IVI pulmonary hypertension to be published in England Journal. We studied eighty patients and 40 of those patients didn't get the drug. Eight of them died within 12 weeks. The patients that did get the drug all survive. We learned a lot. We started doing more and more treatment with that drug IV with a pump twenty the two we came up with another drug pill and so on. Over the years.
Now we've got about fourteen pulmonary hypertension drugs. We combine them. We often have people on one or two or three at a time and we've just done so much better than we used to do. So just like you told your patient, nowadays we can tell people that they can do well, have a normal life. We don't really like getting pregnant again if we try to talk them out of it. But patients can live a much more normal life now than they used to.
Doctors, how do you test for this? I mean, you can't put a cuff around the lung, so how do you know that someone has hypertension specifically in their lungs?
¶ How do you test for PH?
It is harder. And it's it reminds me a lot of a more chronic form of something like pulmonary embolism, where you often come in the emergency department suddenly short of breath, something just happened with pulmonary hypertension. It's often slowly over months, someone notices I can't walk. My dog is for a little short of breath walking up the steps. So you see almost uniformly chronic shortness of breath is worsened over time, usually at least months. And again, there's
a failure to diagnose. And a lot of cases you're told you gain weight, you're just you're deconditioned, et cetera. But what you do, one of the key tests while you examine someone and if you carefully listen, your loud heart sounds, you hear this blood's being pumped into the lungs. The pulmonic valve, one of the heart valves, is slammed shut by this high pressure. You're allowed second heart stop.
You can pick that up. You do more tests. If you don't hear that, you still think about doing echocardiogram. And echocardiogram is the kind of the pivotal test that gives you a really good clue. If you've got it, then we do a heart catheterization to prove it. But you're right. But you got to suspect it first. Then do consider doing an echocardiogram and you'll be most of the way there.
Are there any thoughts about what predisposes one individual to this disease versus another?
Well, I think there's truly some genetics with this group.
¶ What predisposes one to pulmonary hypertension?
One pulmonary hypertension. It's often undiagnosed unknown cause it can be due to certain connective tissue diseases, lupus, scleroderma, things like this. It can be from a hole in the heart. Congenital heart disease, HIV, we learned, can cause from hypertension. But again, in terms of predispositions, the classic patient that gets pulmonary hypertension is unknown. Cause probably has genetic some genetic abnormalities, bumper to gene mutation, one mutation, certain mutations
that some people have, we don't completely penetrate. You might get this mutation. Not yet. We're still understanding, learning more about the genetics. But certainly what I can say is just because someone gets it doesn't mean other people in the family will. I've taken care of many families with pulmonary hypertension. One was notably a young woman, forty years old, that got pulmonary hypertension. And two years later, we diagnosed her eighty year old grandfather with the same kind of
pull my hypertension. So it's fascinating. But what we can tell our patients and reassure them is the vast majority of them will not get it. If they have a family member that has so well, it may be genetic. It doesn't mean everyone going to actually get the disease itself.
So because it's on your radar, probably more than everybody else's, are you seeing more pulmonary hypertension in covid and post covid Long Pollaers or is there not that association?
It's a great question, Steve. You know, I think it's
¶ Has PH risen with COVID "long-haulers?"
a little early to know. So far, we haven't seen much of it. We've seen patients who have chronic scarring, lung problems that could easily get pulmonary potentially if this keeps progressing. So far, though, we haven't seen we've seen this blood clotting problem we talked about, but so far we haven't seen or proven that patients are going to get chronic pulmonary embolism with pulmonary retention or getting any
other form of, like Group three from chronic scarring. But I think it might be too soon to know that maybe the next six months or year we'll learn more about this. If it takes longer to evolve.
I can't help but bring my dad back into this. And I know both of you guys have had to deal with this quite a bit. And that's the balancing act between the treatment that you would like to administer for a variety of these diseases and someone's kidney function and whether or not they're capable of withstanding the treatment that would be best for dealing with pulmonary hypertension or
any other lung issues. Have there been any advancements in the last number of years that helps you navigate those
¶ The balancing act of 'best-treatment' for a disease and kidney/liver function.
balancing act?
Yeah, I think the idea of of kidney function and liver function, too, is a balancing act because the kidneys and liver are so important for metabolizing certain drugs. Some drugs are tablas almost exclusively by the kidney, some of the liver, some by both. What we don't want is a beneficial drug to build up in the bloodstream and cause problems because you got too much of it. And we usually fine tune these drugs and we try treat them up to a certain dose. For example, for Pulman hypertension,
but not beyond that. So a careful physician is going to check a patient's blood test periodically every three to six months, making sure that kidney functions OK, liver function is OK, and we don't have to make adjustments, but we do have new drugs. Now, for example, the proximally drug that I've inhaled, oral subcutaneous, one of the strongest medicines we have for Pulman hypertension. And that drug, fortunately, is not metabolized by the kidneys and you can use
it indiscriminately in patients that have kidney problems. So in the blood clotting world, we learn you have to be a little careful. The docs, these newer drugs that Steve alluded to earlier, one of them, you have got to stop if the kidney function gets too severe, the other one, you're probably OK even with severe renal failure if you dose it carefully.
So, Vic, before we leave, I just wanted to ask you, over the course of the last, let's say. Three or four years, what are the biggest breakthroughs that have helped you with your specialty? And as a warning, I'm going to ask you for the next three or five years, what are your expectations?
I think in the past, if you want to go
¶ Dr. Tapson shares the biggest breakthroughs and exceptions in his field.
ten years, the Doakes, we used to use this drug called Coolman, you mentioned earlier, difficult drug. I mean, we used it for 50 years. Good drug. But you give someone an extra dose of Tylenol every day for three days. Their blood gets way too thin. You put them on a different drug, it gets too thick. They eat too much greens, their blood gets too thick. The dough acts a very few drug and a few critical drug interactions, you know, but but very few. They're much easier to
use than we used to. And we don't need to monitor. We don't need a blood test. We don't get INR every week, every two weeks or every month with these new drugs. So these drugs have really revolutionized practice, made them much easier in the blood clotting around another area. And pulmonary embolism has been we're learning how to treat blood clots that are really big ones, causing big problems without using high doses of dangerous drugs that can cause
bleeding without using clot busters or TPA. We can use lower doses by putting an I.V. or catheter in the lung and putting low doses in the lung or even just putting a Katharyn in suctioning the clot out. We're still learning when that's necessary. We don't want to overdo it. So those have been big advances, too. And the blood clotting work in pulmonary hypertension. We've had new drugs. We have three classes of drugs. Now, the prostate annoys the
endothelium receptor antagonist and the PD five inhibitors. And a nice paper was just published in the journal. The new drug called Aricept even has a little bit different mechanisms. And we've got several other drugs like this that may be coming soon. So I think that we've just kept pace. I kind of feel like we're surfing and just staying on the edge of the wave, just able to kind of keep up with some of these diseases.
Vic, thank you so much for joining us today. We certainly appreciated it. How can our listeners follow you if they want to connect?
I'm on Twitter, Tapson. I don't get a chance to get on it as often as I like to, but I try to say something profound every once in a while. My email address, the typical Cedar's email address. Victor Don Tapscott Xpress, Doug
Vick, thank you for joining us. And of course, Dr. Tayback, my good friend. Thank you for doing these shows. We're Still Practicing is produced and edited by AJ Mosley music, but we're still practicing as composed and performed by Celeste Anorectic. Don't forget the hit that follow button so you don't have to hunt around for a next episode. We'll catch you next time, everybody. From Kerkow media media for your mind.