Name:
Dyspnea
Description:
Dyspnea
Thumbnail URL:
/images/podcast-microphone-banner.jpg
Duration:
T00H22M19S
Embed URL:
https://stream.cadmore.media/player/0a3032f9-9fa6-4560-8ea3-f62daeb9323b
Content URL:
https://cadmoreoriginalmedia.blob.core.windows.net/0a3032f9-9fa6-4560-8ea3-f62daeb9323b/RTL- Ep 68- Approach to Dyspnea.mp3?sv=2019-02-02&sr=c&sig=tQx6u2d%2FWqv4ZtFsNzVeYhnLqBvm8TjSRKMXTCLcCTI%3D&st=2024-05-02T20%3A57%3A21Z&se=2024-05-02T23%3A02%3A21Z&sp=r
Upload Date:
2022-09-15T00:00:00.0000000
Transcript:
Language: EN.
Segment:0 .
[Dr. Smith] Welcome back to Run the List, a medical education podcast in partnership with McGraw Hill Medical. Our hosts are Dr. Navin Kumar, Dr. Walker Redd, Dr. Emily Gutowski, Dr. Joyce Zhou and myself, Blake Smith. As a quick disclaimer, this podcast is meant for informational and educational purposes only, and should not be understood as medical advice under any circumstances.
[intro music] [intro music] [intro music] [Dr. Zhou] Welcome back to another episode of Run the List. Today we'll be talking about an approach to dyspnea with Dr. Jeremy Richards, who's an assistant professor of medicine at the Beth Israel Hospital, who specializes in pulmonology and critical care.
He's super involved with medical education, teaching both first year Harvard medical students in a physiology course called Homeostasis I, as well as teaching upper-level students in a medical education longitudinal elective, which I have had the chance to take with him for the past two years. Dr. Richards is also the director of the Medical Education Research Lab at the BI.
Dr. Richards also has a great sense of humor, and I hope it comes out a little bit today as we chat. Dr. Richards, thank you for being here, it's great to have you today. [Dr. Richards] Thank you so much for having me, Joyce. It's exciting to be here. [Dr. Zhou] So today, as I said earlier, we're going to be talking about an approach to dyspnea. So dyspnea, or shortness of breath, is a super common chief complaint that you'll see in both the inpatient and outpatient settings.
So if you're ready, let's jump in and Run the List. So as usual, we'll start off with a case. So Ms. B is an 81-year-old female with a history of COPD on three liters of home oxygen. She also has hypertension, coronary artery disease and HFpEF. And she presents to urgent care clinic with three days of worsening shortness of breath. She endured several days of URI symptoms, which included rhinorrhea, hoarseness, and sputum that increased in quantity and changed in color from pink to green.
During this time, her visiting nurse also noticed that she had frequent desaturations to the 80s. Ms. B endorses some fatigue, but denies any leg swelling, orthopnea or any weight changes. At urgent care her vitals are a temperature of 98.2, heart rate of 79, BP of 106/91, a respiratory rate of 18 and O2 sat of 90% on three liters of oxygen.
On physical exam Ms. B looks fatigued, but can converse in full sentences, and her lung exam is notable for poor air movement and crackles bilaterally, left greater than right. We didn't hear any wheezes. In her cardiovascular exam she demonstrated a regular rate and rhythm without murmurs, gallops or rubs with a JVP that was not elevated, and there was no lower extremity edema.
Dr. Richards, let's just start out with what Ms. B initially presented with, so shortness of breath. Broadly, how do you approach this very common presenting symptom? [Dr. Richards] Great question. And I think that the first thing that we need to do is understand that even though there's a huge list of possible diagnoses that can result in shortness of breath, we can break things down into a physiologic framework to make this a lot easier, a lot more efficient in approaching this complaint.
So as we know, at baseline, the respiratory system can be divided into three different components. There's the ventilatory controller, or basically the brain; there's the ventilatory pump, which is the chest wall, the muscles, the lungs that move air in and out of the thoracic cavity; and then there's a gas exchanger, which we conceptualize as the alveolus and the capillary that oxygen and carbon dioxide pass across, taking oxygen up into the capillary and then into the arterial circulation and eliminating carbon dioxide from the body.
So these three different components, the brain, the ventilatory pump, and the gas exchanger, serve as a framework for approaching the respiratory system. When things go wrong in any of these three different components, that can result in a sense of unease, a sense of inadequate respiration, in a sense of dyspnea or shortness of breath. We can look at this a little more specifically and look at receptors that are involved in different parts of the respiratory system.
Specifically, you can look at receptors that are called stretch receptors that can be activated when the lung is stretched to a different degree than is expected by the brain. There can be a disconnect between the stretch that occurs in the lung and the stretch that the brain expects in a condition such as COPD or emphysema, when the lung is much more compliant and is overstretched for a given amount of effort.
So those stretch receptors can map to pathophysiology in the pulmonary system. There're irritant receptors that are located in the airways, and those can be activated when the airways are irritated. So in conditions like asthma, viral bronchitis, that can result in activation of these irritant receptors that can signal a lung or an airway problem and a sense of shortness of breath in the brain. The J-receptors, or the juxtacapillary receptors, live next to the capillaries or the blood vessels in the pulmonary circulation, and they can be stretched when the blood vessels are stretched themselves, when they're engorged.
That activation of the J-receptors can occur in conditions like congestive heart failure, that result in blood vessels being stretched, the J-receptors being activated and the brain sensing that something's not right in the lungs, and that's processed as a sense of dyspnea. And then finally, the fourth receptor that I'd like to mention is referred to as chest wall or mechanoreceptors, and this tells the brain how much stretch the chest wall is experiencing for a given effort or a given circumstance, clinically or pathologically.
When the mechanical receptor is activated because of inadequate or over-expected stretch, that can result in the brain sensing dyspnea as well in conditions like Myasthenia gravis, ALS, Guillain-Barré syndrome, can all activate the stretch receptors among many others. So really mapping this framework of the brain or the ventilatory controller, the ventilatory pump and the gas exchanger down to the receptor level of stretch receptors that map to pulmonary disease, irritant receptors that map to airway and/or pulmonary disease, J or juxtacapillary receptors that map to usually cardiovascular disease although other conditions can be in there as well, and then chest wall or mechanoreceptors that tell us more about neurologic or functional issues.
All of these are processed in the brain when they're activated and can be associated with the sense of shortness of breath or dyspnea. [Dr. Zhou] Great. This is super helpful. I think it's really useful for us to think about both systems but also connect it back to physiology, which I think is something we stop doing as we move through the years of training sometimes.
And so I think the next thing I want you to weigh in on is what you might ask about in a history to construct a differential for dyspnea. For instance, in COPD we've been taught to ask about things such as increased wheezing, changes in the quality or quantity of sputum and whether or not there is an infectious or environmental trigger. Can you talk about what you might ask about in some other causes of dyspnea?
[Dr. Richards] Absolutely. To briefly comment on other potential conditions, if we're concerned about heart failure or acute pulmonary edema being a component of her presentation, you know, we'd ask about congestive symptoms, right? Does she have edema peripherally, lower extremity edema? Has her weight been increasing?
Have there been potential precipitants in terms of dietary indiscretions? Not taking her furosemide, which she is scheduled to take every day. Does she have the paroxysmal nocturnal dyspnea or orthopnea? So there's a list of symptoms that we can ask about. But again, it's all founded on our foundational understanding of what causes heart failure and how that may manifest. We could ask about infectious symptoms, is she presenting with a potential pneumonia or an acute bronchitis?
It's 2021, so she certainly could have COVID as well. So we'd ask about fever, cough, other upper respiratory tract symptoms. She doesn't have asthma, but if we were concerned about that we could ask about episodic breathlessness that maybe exacerbated by a classic trigger such as cold air, exercise, exposure to, again, noxious inhalents such as tobacco smoke, et cetera.
And then finally, if we were concerned about a neuromuscular process such as ALS or Myasthenia gravis or Guillain-Barré, we could ask about peripheral or systemic weakness. And again, orthopnea could manifest in that manner if somebody with neuromuscular weakness lies flat, we take gravity out of the equation and their abdominal organs tend to move upwards, restricting the diaphragmatic excursion and causing again, supine or orthopneic shortness of breath.
[Dr. Zhou] So for Ms. B, how would you apply this approach and sort through her history, and what would be the next steps that you would take? [Dr. Richards] For sure. Yeah, and she certainly has potentially a lot of different things that could be going on with her, right? She has a history of COPD and we don't know the FEV1, as I said, but we do know that it's severe enough that she's on supplemental oxygen.
So that speaks to pretty bad obstructive disease. And she has a fair number of cardiocirculatory disorders with hypertension, coronary artery disease and chronic diastolic congestive heart failure. So those things, that context about what she already had before she started feeling sick over the past three days is really important. We then have the additional information that she has an asymmetric lung exam with crackles that are more on the left than the right.
She doesn't have wheezing but she does have poor air movement. She doesn't really have any symptoms that point us towards her having an exacerbation of her underlying heart failure, or her having an acute coronary syndrome with regard to her underlying coronary artery disease. So in that setting, I'd be thinking about again, you know, an acute COPD exacerbation is not unreasonable even in the absence of wheezing, but the left sided crackles more than the right would be pointing us towards and making us think about, could this be an actual consolidated bacterial pneumonia?
So in terms of thinking about how to evaluate this, we'd approach it broadly and pursue an infectious workup. She'd certainly undergo a chest X-ray. I think that in 2021, it's obligatory to get a COVID swab to assess, to see if that's contributing to her presentation, although left versus right-sided crackles would be a little inconsistent for acute viral pneumonia. And then depending on the season and her context, a respiratory viral panel looking for influenza, rhinovirus, coronavirus, human metapneumovirus would not be unreasonable.
From a cardiovascular perspective, I think that given the absence of symptoms that are really compelling for an acute cardiovascular issue, probably just starting with an EKG would be a reasonable first pass. I don't think people would fault you for getting a proBNP to look at left atrial stretch. But again, in the absence of orthopnea, lower extremity edema or other symptoms of congestion, I don't know that that's necessarily obligatory in this case.
With regard to basic labs, and by that I mean a complete blood count and a chemistry panel, I'm pretty sure that she would get these ordered, but I'm not sure how useful they would be. I think that a chest X-ray to look and see if there's an actual left lower lobe or left mid-lung consolidation, based on her physical exam, would be much more useful than finding out that she has, for example, an elevated white count.
Her white count could be elevated because she's having a COPD exacerbation, acute congestive heart failure with pulmonary edema or some other process we're not thinking about. Whereas the chest X-ray is a more focused way of looking specifically for pneumonia, which our physical exam is telling us is potentially, if not likely, the case here. So basic labs would probably be done.
I don't know if I would get them, and I certainly wouldn't prioritize them as compared to the other tests about which we'd spoke. [Dr. Zhou] Got it. Why don't I share a case update for you for Ms. B? So as a reminder, she came into urgent care with shortness of breath that was worse from baseline, and she had positive URI symptoms. And we're more concerned for COPD exacerbation, but potentially considering cardiac causes as well.
So in terms of her labs, they were notable for a white blood count that was elevated to 10.7. A BNP that was within normal range. And the nasal swab was negative for flu. Respiratory viral panel was negative and a rapid COVID-19 test was also negative. Her chest X-ray did report some consolidation in the left mid and lower lungs, which suggested possibly a pneumonia, though there was also pleural effusion and atelectasis mentioned in the note.
So how might this new information help you sort through what might be going on for Ms. B? [Dr. Richards] Yeah, so I think this is pretty confirmatory to what we spoke about previously, where her physical exam, her presentation with three days of worsening shortness of breath superimposed on her chronic conditions is concerning for, if not now really consistent with a left basal or mid-lung pneumonia.
I think that the suggestion of a possible pleural effusion and/or atelectasis are interesting, but the overall presentation is now quite consistent with pneumonia, potentially leading to an exacerbation of her COPD, but that precipitant of the lower respiratory tract bacterial infection is what we're going to focus on going forward. [Dr. Zhou] Wonderful. Okay.
So I didn't mention one other test that the urgent care providers acquired for Ms. B, which is the VBG. And so I'll just tell you what the VBG showed, which was a pH of 7.34, a PCO2 of 53 and a PO2 of 40. So I know there's confusion between what a VBG does, what an ABG does, when and how they're used. So can you share with us a little bit of this debate between VBGs and ABGs and how they might help us?
[Dr. Richards] For sure. Yeah. So I'm going to be blunt and say I think that in general, a VBG that's attained peripherally, so that is not from either a central venous line or from a PICC line, is pretty much, what's the medical term for it? Garbage. It's a test and it gives you numbers, but it may not be the most helpful thing in terms of assessing the patient in the moment.
Now, I'll caveat that a little bit and say that following serial VBGs and seeing if there are significant changes in a patient's PvCO2 may be helpful. This is a relatively data-free zone in terms of looking at this in a rigorous manner, but it's part of clinical practice, at least at some institutions. With that, I think if you're concerned about a patient's acid-base status and/or oxygenation, the test to get is an arterial blood gas.
And this can tell us more precisely, more specifically about what's going on systemically with the patient. How are the lungs taking up oxygen? How are the lungs eliminating carbon dioxide, and how is that reflected in the systemic arterial circulation? A VBG that you take from the left upper extremity with a tourniquet on, tells you about what's going on in the left upper extremity with a tourniquet on.
An arterial blood gas tells you what's going on systemically with the patient and reflects the patient's pulmonary function and their respiratory status. So with that, looking at this blood gas, her PCO2 on a venous gas is 53 and her pH is 7.34. her PCO2 on a venous gas is 53 and her pH is 7.34. And again, I'm sorry to do this again to you all, but going back to our first year of physiology and thinking about how to interpret that, we know that the pH is down, so she's acidemic, we know that the PvCO2 is up, so she has a respiratory acidosis.
And not to get too deep into the calculus, but her numbers are entirely consistent with chronic respiratory acidosis, acknowledging it's a VBG and not an ABG. [Dr. Zhou] Great. That's really helpful. So just to wrap up what happened to Mrs. B then, given this patient's H&P and her diagnostic testing, and specifically the fact that her VBG was reflecting more of a chronic respiratory acidosis, the team felt comfortable calling this a COPD exacerbation that was caused by a pneumonia, but didn't feel like she really needed to be admitted.
And so she ended up getting a course of antibiotics prescribed, was told how to use supplemental oxygen to support her oxygenation needs, and was given some instructions on when to return to the hospital in case her symptoms got worse. So that's Ms. B, but before we wrap up this episode, I wanted to step back and think about diagnostic modalities of dyspnea in more broad strokes.
So first let's start off with the D-dimer, which I think usually we think about in helping us diagnose DVTs and PEs. How do you think through the D-dimer and for what patients can it be useful? And what does it tell you? [Dr. Richards] Yeah, so interesting that we made it through this case without talking about a D-dimer at all. In terms of thinking about the D-dimer, the first thing that I think about is what is my pre-test probability that she has a pulmonary embolism?
And so we go back to our clinical stratification tools, and I like the Wells' criteria in terms of thinking about pulmonary embolism, and whether it's likely or unlikely. If you go through the seven different components of Wells' criteria, the likelihood that she has a PE is very low. It's unlikely. If however, we just got PE on our mind, and we couldn't stop thinking about it as a potential explanation for her presentation, then this would be the scenario to send a D-dimer.
If you're thinking a PE, but if you go through Wells' criteria and you stratify her as being low risk or unlikely to have a PE, this is the time to do it. So again in her case, I would not have sent a D-dimer, as indicated by I stopped talking about it at all, but if we're thinking about PE, you got to go through your risk stratification tool in terms of Wells' criteria, or using the PERC score or the Geneva scoring system, and then decide, do I do a D-dimer?
Or does it turn out that it's a likely enough possibility that we should go straight to CT angiogram? [Dr. Zhou] Great. So it sounds like it's probably most useful when you're in that intermediate suspicion range. If you've super high suspicion of a PE, you should just go straight to imaging, if you've super low suspicion of a PE, like in Ms. B, then you really shouldn't send it at all, but if it's in the middle, it can help stratify your patients a little further.
So let's turn to another diagnostic modality, which is the point-of-care ultrasound. So I've been spending some time in the ED doing POCUS, and I know that ultrasound is very valuable in providing some diagnostic information on patients whose, say, cause of shortness of breath is unclear. So, for what patients could POCUS be useful? And if you were to do an ultrasound, what areas would you focus on and what would you be looking for?
[Dr. Richards] Yeah, fantastic. I also am a fan of using, in a very focused way, point-of-care ultrasound, and I like that perspective of thinking about using ultrasonography in clinical practice, because when you talk about using focused ultrasonography, you can say the phrase focused POCUS and it sounds like you're casting a spell. [Dr. Zhou chuckles] [Dr. Richards] In terms of using POCUS for patients, I think that it would have been reasonable in this case just to stick a probe on her left chest, because the X-ray said maybe a pleural effusion, maybe consolidation, to sort out if there's actually fluid in the pleural space or not.
So I think that would be a very, very quick way to break down that X-ray, read and verify or refute whether or not there was actually an effusion or not in her case. Other things that we could certainly look at with ultrasound would be a quick cardiac ultrasound, taking a look at her cardiac structure and basic function in terms of, you know, is the LV, is the RV dilated and/or are they squeezing appropriately?
And then you can do very rough valvular assessments as well in terms of looking for regurgitation or stenosis with your point-of-care cardiac ultrasound. I think that looking for pulmonary edema on ultrasound is a little bit more advanced. We can try that and do that, but I think that the supplemental tests of the D-dimer, certainly the clinical exam, looking for lower extremity edema and other signs of congestion are important to add to the ultrasonographic approach.
So to summarize, I think the quick lung exam looking for effusions, consolidation, is reasonable, and then a quick cardiac ultrasound looking for a structure, a squeeze in valvular pathology is reasonable as well. [Dr. Zhou] Great. That's super helpful. Today we talked about a lot of things. We talked about how to sort through the causes of dyspnea, we've talked about VBGs and ABGs. We've talked about D-dimers as well as point-of-care ultrasound.
And so before we wrap up, I'd love to hear pearls from you that you want students or listeners to walk away with from today's episode. [Dr. Richards] Absolutely. Some things that I would really emphasize as potential take-home points would be, number one, don't forget your basic physiology. You went through first year of medical school for a reason, and those principles can be useful in the clinical setting.
So we broke it down at the beginning, but we'll review it right here. Thinking about the respiratory system as being comprised of the controller, your brain, telling your lungs what to do; the ventilatory pump, that's your neuromuscular system and the airways moving air in and out of the lungs; and the gas exchanger, where oxygen is taken up across the alveolar-capillary basement membrane, and where carbon dioxide is eliminated.
Keeping those component parts in mind can help us deal with and overcome the extensive list of potential differential diagnoses that we spoke about throughout this entire case. We can sort out what part of the respiratory system appears to be broken or having issues that can help focus our approach. In addition, I emphasize my somewhat provocative comments about VBG versus ABG.
If you have a patient who's sick and that you're concerned about, go for the Cadillac of tests in terms of assessing their acid-base status and their oxygenation, and get that ABG. And then finally, in terms of diagnostic assessments, we have so many tools, and using our clinical reasoning to apply those tools in a rational, focused, and patient-centered manner is really important.
And what I mean by that is we're not sending D-dimers capriciously, we're thinking about whether the patient is likely to have a PE or not, and then going through our risk stratification criteria such as the Wells' score to determine whether to send it or not. So I think those would be the big takeaways that I would have for this case.
And again, thank you so much, Joyce, for the opportunity to discuss this and to be here with you today. [Dr. Zhou] No, thank you so much for joining us today. I think our listeners really appreciated you breaking this down, and I hope to have you on the show again. Thanks so much. [Dr. Richards] I would love to be back.
Thanks for the opportunity. [outro music] [outro music]