# Air Trapping?



## jaksasquatch (Feb 25, 2015)

Hey guys,

   Had this pt that absolutely stumped me yesterday. I'm currently in medic school and evaluating this pt was difficult. Dispatched as "breathing problems", arrive on scene to find one elderly male pt sitting in his recliner on home oxygen in no apparent distress. Pt is on home oxygen at 2 lpm and has a Hx of COPD. Pt has an inhaler laying next to him which he hasn't used. Pt reports that the "finger thing has been reading really low lately". His SpO2 was reading 84% at the time. This was confirmed with our machine as we ran baseline vitals: BP 120/80, HR manually palpated at 75 bpm regular and strong. Respiratory rate 30 per min. with heavy "belly breathing" rapid and deep. When asked if he has any difficulty breathing he replies "no not at all". Wife says he usually doesn't breath that fast. Breath sounds reveal diminished in all fields. 12 lead reveals no abnormalities but when watching the monitor screen he throws PVC's every 15 seconds or so with a run of V-tach at one point (uncaptured on the LP15). When we put him on capnography he had a slight shark fin waveform with a reading of 18-22 mmHg consistently. Pt's hands felt cold to the touch although his environment was very warm. Once we move the pt over to the stretcher he has some audible wheezes and difficulty breathing. This all goes away after 1 min of laying on the stretcher semi-fowlers. When lung sounds were reassessed I heard air movement in all fields with no wheezing. 

   A few questions. Could this be air trapping? I noticed no pursed lip breathing but heavy belly breathing at 30 times per min is obviously not normal. The diminished lung sounds are normal in COPD why go to wheezing and then back to good airflow? My differential was vague but more of a cardiac etiology possibly the start of left sided heart failure. What are your thoughts?


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## Brandon O (Feb 25, 2015)

Sounds like pretty classic COPD exacerbated by something.

Nice assessment.


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## sdadam (Mar 1, 2015)

Ehhh, that's a tough question to answer beyond theoretically. I mean, with that level of disease, yes there is certainly air trapping.

Not everyone compensates the same. Compensitory mechanisms like pursed lip breathing are in response to a specific thing, not just "aspects of a disease" if you will. Meaning that someone who is pursed lipped breathing is trying to create a PEEP to help artificially keep airways open. This generally is the result in COPD of a long and chronic breakdown of the elastic tissue of the lung by the immune system in response to the inhaled and trapped toxins in cigarettes resulting in emphysima. Or a result of chronic inflamation bronchorrhea and bronchoconstriction in response to the same. This PT had Emphysema, which is characterized more by structural changes of the lungs and not bronchorrhea or bronchoconstriction. That's why you only really had positional or exertional wheezing. Wheezing is a result of whistling, so just like your lips it is the result of wetting and constricting your airways and then forcing air through.

This guy has more of a diseased lunch than reactive airway. This is why the term COPD is really no longer correct. They used to group Asthma, Emphasyma, and Chronic Bronchitis under COPD, as they ended up being treated the same in acute illness. They dropped asthma into the Reactive Airway Disease category years ago, but the idea that emphysima and bronichtis are COPD is still out there a lot. Truthfully, they could be more different.

This PT is compensating with hyperventilation to increase the alveolar min. volume. This works best for him because his issue is decreased gass disolving and diffusing into the blood stream because of how thick and scarred the alveoli have become. So by increasing the alveolar min. volume he can artificially increas the rate of gass exchange. Since his problem is emphysema PEEP wouldn't help him as much as a chronic bronchitis patient. (Not that you don't see patients with emphysima that purse lipped breath and vice versa with chronic bronchitis, medicine is all grey area).

What wrong here is that he thinks he's ok. He doesn't have an air hunger because of a decreased response to hypercarbia. I know his CO2 read low, but in reality he has a V/Q mismatch from the level of lung disease, hence the hyperventilation. Remember to not treat the capno number. In his case a few things could be going on from massive respiratory acidity, to a PE. The increase in respiratory rate is a very early sign that he has had a major change in his disease state. It could have been a temporary excitation, or something more serious.

It sounds to me like you should read up on the pathophysiology of emphysima and chronic bronchitis outside of the context of COPD, in five years that term will be depreciated out of use.

Let me know if you have any questions about the patho above!


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## Brandon O (Mar 1, 2015)

sdadam said:


> It sounds to me like you should read up on the pathophysiology of emphysima and chronic bronchitis outside of the context of COPD, in five years that term will be depreciated out of use.



Not sure about that. Few patients really embody the classic version of either isolated emphysema or chronic bronchitis. A mixed picture is the norm, which is why "COPD" is a useful term. I would say that describing each condition individually is mostly a teaching tool.


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## sdadam (Mar 1, 2015)

Brandon O said:


> Not sure about that. Few patients really embody the classic version of either isolated emphysema or chronic bronchitis. A mixed picture is the norm, which is why "COPD" is a useful term. I would say that describing each condition individually is mostly a teaching tool.



I have to disagree. Brandon, what you are talking about is very old thinking in medicine and there are very few similarities between the two. Although PT's with emphysema are at risk for bouts of bronchitis the disease process of chronic bronchitis and emphysema are completely different and result in entirely different pathophysiology. Hence the classic textbook description of "Pink Puffer" vs. "Blue Bloater".

For a great source check out "Emergency Pathophysiology: Clinical Applications For Prehopital Care.

You're last statement is completely false however. In fact COPD is a confounding term that resulted in the OP's confusion in the first place. I understand that it's commonly taught but I gave a thorough description of the pathophysiology involved and you replied with "no that's not true." I don't mean to be a ****, but could you explain in equal detail in what way those disease processes are the same? I understand that this is contrary to what is in the EMT and Paramedic Text books, but in this case the EMT and Paramedic textbooks are hopelessly oversimplified.


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## Brandon O (Mar 1, 2015)

There are discrete pathophysiological processes, but since they tend to occur in the same people, from similar etiologies, and run together in the clinical picture, trying to put a wall between them in actual practice has somewhat limited validity. I find it very useful to teach them separately (well, for learners at a level where they might care), and sometimes useful to look at a COPD patient and say that they're predominantly an emphysematous or bronchitic picture (or with an asthmatic component for that matter). But even the guy in the textbook under the "pink puffer" caption most likely has some degree of the changes we associate with chronic bronchitis and vice versa, so there's only so much mileage to get from the distinction. It's a spectrum.

(An appropriate comparison might be to conflating auscultatory "crackles," as is currently recommended and which I agree with, rather than trying to distinguish "rales" or "ronchi." Although it makes sense on paper, in practice there's so much overlap and confusion that it ends up failing to touch down with reality more often than it helps.)

Have you come across many patients who truly, distinctly resemble the classic gestalt of solely emphysema or chronic bronchitis?


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## sdadam (Mar 1, 2015)

Yes, I have. I do not agree with you at all. These disease processes are in actuality drastically different processes and rarely overlap. In fact some of the changes are rather mutually exclusive. I'm going to go in to detail below.

In "COPD" over a long period of time, and nearly all of the time with smoking as the cause, toxins and non-self material are deposited in the lungs. In normal healthy people regular bronchorrhea and epithelial cilliary movement would remove those things, along with the lymph and immune systems. Over a long period of time this cilliate facilitated removal is destroyed as the delicate epithelial linings of the lungs literally scar over from the chronic exposure to smoke or another irritant. That's where any similarity between emphysema and chronic bronchitis ends.

So, now the patients body responds to the toxins and foreign material with an immune response, which of these two distinct diseases the patient ends up with has everything to do with the nature of that immune response, and again some of the changes are mutually exclusive.

In emphysema the immune system responds with adaptive immunity, actively attacking and destroying molecules of foreign material. This all out war with T-Cell Mediated killing and massive B-Cell mediated antibody response results in major damage to the non-self material AND the incredibly delicate environment. That environment is the lung parenchymal tissue, and alveolar membranes. As these areas are destroyed the lung loses elasticity increasing over workload and respiratory effort. The Patients airway diameter is only effected slightly and the scarred lung tissue has a hard time producing mucous as the goblet cells are now scarred over. This leads to the compensatory process of tachypnea because the only way left in lungs damaged this way to increase gas exchange is by increasing the alveolar minute volume.

In contrast chronic bronchitis patients have an immune response to the same group of toxins with the older, simpler innate immune system. This results is widespread and non-specific inflamation and bronchorrhea, bronchoconstriction, etc. In a chronic bronchitis patient the tissue of the lung is much less diseased and in a way it's a more active disease process. These patients need to compensate positionally, and with things like extended expiratory phases (something that would be bad for emphysema which is why we don't see it with those patients), and artificial pressure (pursed lipped breathing).

As you can see these are distinct disease processes that have significant clinical implications. A chronic bronchitis PT is much more likely to respond to adrenergic rescue drugs than and emphysema PT for instance.

I agree with you that many things exist on a spectrum but this is not one of them. You are talking about the state of medical knowledge about ten years ago, it's no longer true. Please provide physiologic examples to support your case.

I don't mean this in an offensive way but this seems like a case of you having trouble discerning between the two and deciding that it's because they can't be differentiated, but that's not the case.


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## NomadicMedic (Mar 1, 2015)

Interesting discussion. Where's Vent Medic when we need her. 

While the differentiation in COPD disease process makes for a good discussion, does any of this significantly change the typical paramedic PREHOSPITAL emergent treatment? Inhaled beta agonists, perhaps CPAP, steroids and hopefully not an intubation.

Reactive airway disease has a limited prehospital treatment pathway. Like I mentioned, while a good academic discussion, it's virtually useless in the field, which is why COPD is a fair catchall of these processes.


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## Brandon O (Mar 1, 2015)

I disagree with some of your points there, but that's not really the crux of this, since I think our main point of disagreement is whether the distinction typically has clinical relevance at the bedside. I have no axe to grind here (I have pet topics but this is not one of them), and I'm sure there are smart pulmonologists and other authorities who see things differently, but the general contemporary theme is to conflate the two. Here are a few references:

Harrison's Principles of Internal Medicine (18e):

"Although traditional teaching is that patients with predominant emphysema, termed "pink puffers," are thin and noncyanotic at rest and have prominent use of accessory muscles, and patients with chronic bronchitis are more likely to be heavy and cyanotic ("blue bloaters"), current evidence demonstrates that most patients have elements of both bronchitis and emphysema and that the physical examination does not reliably differentiate the two entities."

UpToDate ("Chronic obstructive pulmonary disease: Definition, clinical manifestations, diagnosis, and staging"): "Interrelationships among asthma, chronic bronchitis, and emphysema — Early definitions of COPD distinguished different types (ie, chronic bronchitis, emphysema, asthma), a distinction that is not included in the current definition [the GOLD criteria]..."

Sapira's Art and Science of Bedside Diagnosis: "Two forms of chronic obstructive lung disease, each supposedly antipodal to the other, have been popularized. Ectomorphs with emphysema were called "pink puffers" because they were able to maintain oxygenation, and they also puffed against pursed lips to keep their intrabronchial expiratory airway pressures high. The group with chronic bronchitis was often cyanotic and tended to be mesomorphs or endomorphic and edematous, hence the term "blue bloaters." While the pink puffers had small hearts, the blue bloaters were often suffering from right-sided heart failure.

... When one actually tries to categorize each patient into one or the other of these two stereotypes, it is discovered that the largest single group is a third consisting of patients who do not clearly fit into either category."

Additionally, none of these sources makes any mention of modifying the treatment of acute exacerbations according to the specific phenotype.


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## sdadam (Mar 1, 2015)

DEmedic said:


> While the differentiation in COPD disease process makes for a good discussion, does any of this significantly change the typical paramedic PREHOSPITAL emergent treatment? Inhaled beta agonists, perhaps CPAP, steroids and hopefully not an intubation.



I have to say that's a really disappointing anti-intellectual argument DEmedic. If you will excuse me for answering a question with a question. Can you imagine a scenario where a deeper and better understanding of this wouldn't help a prehospital provider? I HATE the "well, I don't need to know it if it doesn't change my treatment".

That attitude means that you think that's the only place you could possibly make a mistake. This understanding will help you diagnosis. We all miss-diagnose things, we aren't 100% all the time. This knowledge will help you get closer to that. Additionally it will change your treatment. I'm much more likely to move early to CPAP on chronic bronchitis patient. I have a better understanding and can notice subtle changes in vital signs in order to recognize and intervene early so that you don't have to get to the point of CPAP. 

If you really feel like you don't know how yo apply the above knowledge to your clinical practice to positive outcome I don't know what to say, but I've seen your other posts and I think your smarter than that and more creative than that and you might just be repeating what others say about "I don't need to know that". I see medics and have failed interns over their inability to understand and describe respiratory pathophysiology. If you want the responsibility to diagnose and treat something in a stranger it's your responsibility to know everything about it possible.


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## sdadam (Mar 1, 2015)

Let me try to describe this in a different way. I'm not trying to argue that these diseases only exist in a vacuum, although yes, some aspects of them are mutually exclusive. But they are also well differentiated enough that they should be easily discernible to a skilled clinician for instance I have above given a logical pathophysiologic explanation of how my thinking describes the patient in the original post. You've said I'm wrong but then claim it's to confounding a topic to figure out. Of course the disease processes are similar that doesn't prove your point though.

COPD is like Paroxsysmal Supraventricular Tachycardia. It is not a rhythm. Likewise COPD is not really a disease in the truest sense of the word. PSVT is any one of 20 rhythms, but if the ECG tracing we are looking at is too nonspecific to say which rhythm we are actually looking at we call it PSVT.

Same with COPD, and in the same way it is incorrect to label a patient as a COPD patient if you can identify them further. I go on to say that they are very different disease processes and give a detailed physiologic description of how they are different. I agree that the classic textbook example of pink puffer and blue bloater are false or at least simplified examples, but what in the EMT textbook isn't? That doesn't mean they are undifferentiateable processes. What they are, is an example of how we have known there are major differences in these disease processes but were failing to understand that.

You are now swinging to the far side of the spectrum claiming they are nearly inseparable but the truth is we were much closer to being right originally than a pan-pathophysiologic COPD disease.

Clinically it is absolutely important, it gives me an advanced ability to understand a details prognosis of my patient for the time I'm with them as I understand the specifics of their disease processes. The skills involved in monitoring the decline of critical respiratory patients declining from chronic bronchitis are different than those of emphysema, the treatment protocols don't drastically change, but that argument makes no sense they don't drastically change for asthma either, however that is an incredibly different pathophysiology. The argument that "I'll treat them both the same" is not an excuse for not understanding the detailed and different pathophysiologys not only academically but in a clinically applicable way. Saying your patient is a COPD patient is saying you don't know any more specifically what's going on. You seem to be arguing that you belie we CAN'T differentiate. But I've been doing and teaching Paramedics to do just that successfully for a decade, so I just don't see the weight of your argument.

I would really appreciate it if you would describe your understanding of the pathophysiology of this and how you see it happening and a description of what is happening to confound the diagnosis. I took the time to show you how they have significant mutually exclusive pathophysiologies, but you have yet to explain anything physiologically. If you are only repeating what you have been told, I'm sorry but I'm not willing to be convinced of your point of view. I need you to explain in detail how you believe the disease process works, and in what way I am mistaken about differentiating them or the manner in which they overlap clinically in my physiologic description.  I'm sorry but you are avoiding the topic by focusing on the "Pink Puffer" / "Blue Bloater" thing, that isn't significant.

EDIT TO ADD: I would point to my clinical proof being the understanding I have of the OP's patient. Versus your response of "eh, COPD, whatchya goona do." I have to say I would have failed my internship if I couldn't differentiate to more specific than COPD.


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## Brandon O (Mar 1, 2015)

I would rather not dive into the underlying pathophysiology here if it's not necessary. If that's actually our point of disagreement, then we can talk about that, but you seem to be saying more that the mechanistic differences are important _because_ they inform clinically relevant distinctions, which I'm not sure is true. I love chatting pathophys more than anyone, but the question is whether it bears upon emergency treatment. (I am not sure about your suggestion that the catch-all term COPD is an older view, whereas distinguishing the two entities is a more modern approach. My understanding is that the opposite is true.)

Toward that end, I provided a few authoritative references that do not indicate that differentiating emphysema-dominant versus bronchitis-dominant COPD has clinical relevance in managing their exacerbations. (I've just checked Tintinalli as well and it says the same.) If you have a different view -- e.g. that bronchitis responds better to NIPPV and similar points -- I'm eager to see any references or studies in support of that.

It's not that I don't WANT to connect the underlying physiology to the care we provide, but sometimes it turns out the connection is not as strong as we thought. "We thought it mattered, but it doesn't" is not an uncommon trend in the whims of modern medicine.


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## sdadam (Mar 1, 2015)

I'm saying that there is more to clinical relevance than what treatment protocol you follow. That's the definition of cook book medicine. I agree that they have many similarities, that's why I made the PSVT analogy. The point is arguing against a deeper understanind of the pathophysiology and refusing to talk about it because "it won't effect my treatment" is not the same thing as adhering to evidence based medicine. Your links are not comprehensive, two sentences in an internal medicine book do not inform emergency medical treatment. I really didn't want to say this but you are not approaching this from an ALS or critical care perspective. I understand that you are an EMT-Basic, but you have to understand that your perspective is one that is not compatible with advanced medicine. "I don't need to know if it won't effect my treatment" is not a meaning full response.

I have flat out described how this WILL effect your clinical thinking. How they are blatantly different. Your talking about evidence based medicine, great the first and most important evidence is your personal understanding. The "sources" you provided are nonsensical in this discussion.

"Although traditional teaching is that patients with predominant emphysema, termed "pink puffers," are thin and noncyanotic at rest and have prominent use of accessory muscles, and patients with chronic bronchitis are more likely to be heavy and cyanotic ("blue bloaters"), current evidence demonstrates that most patients have elements of both bronchitis and emphysema and that the physical examination does not reliably differentiate the two entities."

This may very well be difficult in internal medicine dealing with long term and progressive early and mid stage disease, that's not my area of expertise.

You can't look at two sentences from and internal medical textbook and say see I'm right. According to ACEP Comprehensive Study Guide of Emergency Medicine:

"Chronic bronchitis is defined as the presence of chronic productive cough for 3 months in each of 2 successive years in a patient in whom other causes of chronic cough have been excluded."

"Emphysema is defined as abnormal, permanent enlargement of the airspace distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis."

The definition of these diseases are not even close to each other.

The definition of COPD is "...characterized by airflow limitation that is not fully reversible." The airflow obstruction is generally progressive and associated with an abnormal inflammatory response to noxious gas or particles.

That's out of the latest edition of the standard emergency room clinical reference. Nothing about them is spoken about together because they have so little to do with each other. Just because they both fall into the same TREATMENT algorithm does not mean the information isn't clinically valuable in your assessment, monitoring and anticipation of the patient. You don't seem to understand what evidence based practice is as you have not provided sources that anyone would even imagine practice should be changed based off of. It's no just about finding a sentence that supports what you say in a book, it has to be applicable.

There is a huge difference in a declining emphysema patient (about 15% or "COPD" or chronic bronchitis (~85%) and what I'm anticipating next with them, what my priorities of treatment and assessment are, the point at which I consider them inevitably in failure, the exact point to consider or prepare for intubation. How much do you want me to list?

"UpToDate ("Chronic obstructive pulmonary disease: Definition, clinical manifestations, diagnosis, and staging"): "Interrelationships among asthma, chronic bronchitis, and emphysema — Early definitions of COPD distinguished different types (ie, chronic bronchitis, emphysema, asthma), a distinction that is not included in the current definition [the GOLD criteria]...""

Asthma has not been even joked about being part of COPD for ten years. It is a Reactive Airway Disease (RAD) this information is so out of date it's irrelevant.

"... When one actually tries to categorize each patient into one or the other of these two stereotypes, it is discovered that the largest single group is a third consisting of patients who do not clearly fit into either category.""

Finally this doesn't prove anything either, of course there is overlap but no one is saying that it's not beneficial to continue to investigat until you can say your patient has more than "airflow limitation that is not fully reversible". That's what COPD is. No medic I know would be comfortable pushing drugs based off that differential. Just like settling for PSVT instead of AVNRT or AVNRTj or MAFT, or any other more specific rhythm is better than saying PSVT. Even if it doesn't change your treatment the more you understand about your patient the better you can treat them. Please drop the attitude that if it doesn't effect your treatment directly it must be useless information.

I want you to get into the pathophysiology because it's clear you don't understand it at the molecular level but you are verry adamant about your viewpoints. You have yet to speak physiologically about any of this. We don't live in a pure evidence based world, this is an applied science and we practice science based medicine not evidence based medicine. There are few places in the world that try to practice solely evidence based medicine because you need a balance and you can't skip physiologic knowledge in favor of random internal medicine textbooks. What would even make you think that was applicable to emergency care?

At the end of the day my understanding let me give a detailed description of the OP's PT's pathophysiology based off his description explaining every question he asked in detail. You sad "lol COPD from something". I'm trying to tell you that's not acceptable and I don't understand why you are defending it. You can't just say "this PT has airflow limitation that is not fully reversible." case closed, diagnosed! Come on.

You literally didn't answer one question the OP asked, but feel comfortable telling me I'm wrong when you either refuse to talk about or have no understanding of the pathophysiology involved. Where exactly did you learn about this in this way?


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## sdadam (Mar 1, 2015)

This was an accidental post but I want to add:

Chronic Bronchitis is a disease that is diagnosed based of the patients history only.

Emphysema is diagnosed by observing structural changes in the anatomy of the lung they are literally completely different physical things caused by a common origin.


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## sdadam (Mar 1, 2015)

I found the article that led me to researching this, sorry I've been looking for it for a while and just found it! It's called Chronic Obstructive Pulmonary Disease: Knowing What We Mean, Meaning What We Say J.M. Joshi Department of Respiratory Medicine, T.N. Medical College and B.Y.L. Nair Hospital, Mumbai, India.

It clearly outlines the clinical significance of the 10+ things that fall under "COPD" and why COPD is not an adequate clinical term.

http://medind.nic.in/iae/t08/i1/iaet08i1p89.pdf

The conclusion of the paper states:

The importance of uniform usage of medical terminology is obvious. “COPD” when used as a broad descriptive term is an annoyance to those who want to maintain diagnostic clarity. Clinical discussions rely on a shared language so that we do not have to re-define everything in every discussion.82 The various disorders that cause chronic airway obstruction have a different natural history, response to treatment and prognosis. Therfore, it is important to recognise them as distinct entities not only for the purpose of discussion but also for clinical management and research. Chronic obstructive pulmonary disease (COPD) should, therefore, be defined exclusively as tobacco smoking related chronic progressive airway disease and must be diagnosed using the criteria that support this definition.

Based of of this research preformed on the specific topic we are talking about I feel it's clear we should be using the more specific terms in clinical care.


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## Brandon O (Mar 1, 2015)

Okay! I'm still not totally sure if you feel that the two entities should be approached differently in the emergency setting; you seem to be going both ways. But it sounds like you primarily want to talk about the pathophys, which I'm happy to do.

We'd better agree on what sources you would consider acceptable, though. You didn't seem interested in Tintinalli, probably the most widely-accepted provider-level emergency medicine textbook, or Harrison's, which I'd say is the most authoritative provider-level general medicine textbook, or UpToDate, which is far and away the most relied-upon provider-level point-of-care reference. You cited a peer-reviewed narrative review article, so is that the sort of thing you're looking for? Or primary research? Or do you want to focus on personal experience? If you've done clinical or bench research yourself on this topic, I'll have to cede to that, as I certainly have not.


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## sdadam (Mar 1, 2015)

" The various disorders that cause chronic airway obstruction have a different natural history, response to treatment and prognosis. Therfore, it is important to recognise them as distinct entities not only for the purpose of discussion but also for clinical management and research. "

OK am I missing something. This is research on the exact topic we are talking about.b http://medind.nic.in/iae/t08/i1/iaet08i1p89.pdf


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## Brandon O (Mar 2, 2015)

All righty, here goes. Great topic by the way, good way to force some board review...

Both chronic bronchitis and emphysema fall into the category of "obstructive" lung disease, which is a broad group set in distinction to "restrictive" diseases. The short definition is that restrictive diseases (which are generally uncommon and include sad and weird things like interstitial pulmonary fibrosis) involve difficulty inflating the lungs and hence getting air *in,* whereas obstructive diseases introduce difficulty deflating the lungs and getting air *out.* (In asthma, for instance, an obstructive disease, this difficulty is caused by bronchoconstriction.) In the case of COPD and particularly emphysema, this is largely influenced by the loss of elastin, which normally provides some radial "recoil" to brace the airways open; without this support they tend to collapse during expiration (as the increase in intrathoracic pressure bears down upon the lungs, there needs to be structure in the airways to prevent them from shrinking in the same manner as the alveoli). Airways collapse, air is retained. This is seen in increased expiratory times (a feature of all of these obstructive diseases), breath stacking, and a so-called "obstructive" pattern on pulmonary function tests (i.e. the greatest change is in the loss of expiratory ability).

The etiology is certainly toxins in most cases, with smoking being the distant leader. The glamorous runner-up is probably alpha-1 antitrypsin deficiency, a hereditary deficiency of a protective enzyme which essentially leads to smoking-like damage even when you don't (not exactly the same damage -- classically a1-antitrypsin deficiency produces panacinar changes, versus centriacinar disease from smoking -- but that's mostly a pathological subtlety).

The predominant changes of emphysema are destruction of elastin (as above) and obliteration of the alveolar walls, causing loss of surface area for gas exchange. One of the keys is that these occur in the distal terminal bronchioles and beyond, i.e. primarily in the respiratory bronchioles and alveoli -- in other words in the most distant branches of the tree, in the "twigs and berries" rather than higher in the branches. This is the explanation I've usually heard for why emphysema is a less "cyanotic" disease than bronchitis (i.e. more work of breathing, but less difficulty oxygenating per se). Although there is damage to the lungs, it's very distal, meaning other areas may be preserved; in contrast, the changes of bronchitis are more proximal and may "knock out" entire segments of lung parenchyma via mucus plugging. An analogy might be made to the increased dead space of a PE (which is not primarily a hypoxic disease except when very large -- you can compensate okay with the unaffected lung tissue) versus the increased shunting of pneumonia (which can easily cause hypoxia). This explanation always seemed somewhat incomplete to me, but hey, I just do what they tell me.

As you might imagine, on exam these people have diminished lung sounds (less air is moving, and there's less lung tissue to move it through anyway), big barrel chests (from hyperinflation and from hypertrophy of the respiratory muscles, plus probably a "relative" increase alongside the peripheral wasting we typically see), and perhaps pursed-lip breathing. This last should make sense in the context of the physiology -- to help brace open those airways that want so badly to collapse, as well as to increase the time for exchange of the small volume of air they're moving, they exhale against a constricted outlet to create PEEP. Hence "pink puffers."

(It may help to understand that although this is an obstructive disease -- expiration is the main problem -- it ends up having a restrictive component, in this sense: due to the constant hyperinflation, the end-expiratory state of the lungs remains very enlarged. This means when you're ready to take a breath, the diaphragm is already fairly low, the thorax is already fairly expanded, and your next breath won't have much volume because there's no ROOM for it. Thus they're not getting much air in either direction.)

On the other side of the coin is bronchitis. The causes are similar, although I don't think there's much association with a1-antritrypsin. I have also never heard the specific distinctions in immune response you describe, although it wouldn't blow my mind if it were so. Rather, the main pathological feature is an increase in mucus production within the airways (via both hypertrophy, hyperplasia, and metaplasia of the goblet cells). There is also some actual hypertrophic thickening and fibrosis of the bronchial walls. Both result in narrowed airways. As I said, these changes are characteristically more proximal, within the larger airways, although there is certainly more mucus produced in bronchi and bronchioles as well. (Sidebar: having now typed "mucus" this many times, I think I've finally figured out which one is the adjective and which one is the noun. My life is making great strides today.) This of course causes obstruction, both to expiration and to inspiration, hence the cyanosis as discussed (and hence some chronic crackles on auscultation). The abundant mucus in combination with absent or dysfunctional ciliary clearance also creates a tendency for infection, which as we all know is a feature of COPD.

What about muscular bronchoconstriction, a la asthma? It's not a primary feature of either category, which is why failure of your numbers to greatly improve after a hit of bronchodilators during PFTs is helpful for diagnosing COPD versus asthma. On the other hand, there is typically SOME dynamic activity of the bronchial tree, and probably more so during exacerbations, which is why wheezing -- and at least some improvement from puffing an inhaler -- is still seen.

The cardiac effects are worth remarking upon. Emphysema may contribute to right-heart strain to a certain extent due to destruction of the alveolar capillaries (if you lose the alveolar walls, you're losing the circulation that ran through them too), but this usually isn't considered a primary feature. But pulmonary hypertension is associated with bronchitis, because when you lose oxygenation to the alveoli from that shunting we discussed, the alveolar capillaries vasoconstrict -- remember, the lungs are just about the only place where LOW oxygen causes vessels to CONSTRICT, in order to improve V/Q efficiency -- and when this is widespread, overall resistance goes up in the pulmonary circulation, causing strain and eventual right heart failure. This isn't helped by the compensatory polycythemia we often see (chronic hypoxia -> more red cell production to improve carrying capacity -> thicker, more sluggish blood -> even more heart strain). Hence the peripheral edema of the "blue bloater."

Following these chains along, it should make sense that neither process excludes the other. In fact, since they often both arise from similar triggers, they frequently coexist, although individual patients may demonstrate one morphology predominantly. A couple more quotes:

"Persons with COPD often have overlapping features of both emphysema and chronic bronchitis... In practice, differentiation between the two types of COPD is often difficult." (Porth)

"The major risk factor for both conditions is cigarette smoking, and many patients share characteristics of each condition. Therefore, guidelines have moved away from using these subsets and instead focus on chronic airflow limitation." (Chisholm-Burns)

I find no reference suggesting that bronchitis responds better to NIPPV, emphysema better to bronchodilators, or prognosis differs greatly between them. Again, none of the above would blow my mind, but I would love to see any evidence in support of these, as they would obviously have relevance for all of us. The aforementioned challenges sorting individual patients into one pile or the other would certainly make studying this difficult, but if you have found personal success, share your methods and maybe publish them! Spread the wealth.

The paper you linked seems to be making the point that use of the broad COPD umbrella, along with the strict definitions currently in use, may capture some heterogeneous diseases that don't clinically belong there. This is no doubt true. On the other hand, I don't know any competent clinician who would refer to bronchiectasis as "COPD," even if it technically met the definition -- that would be like calling appendicitis "constipation" -- or bronchiolitis obliterans, or lupus-induced lung disease, etc. So I take the author's point but am not sure if the definitional vagueness has much importance in clinical practice. He makes little mention of bronchitis versus emphysema, you may note; he focuses on the other diseases and on staging.

Sources for the above: in addition to the aforementioned, sources include in-person lectures, Goljan's pathophys material, Porth's "Essentials of Pathophysiology 3e", and Chisholm-Burns's "Pharmacology: Principles and Practice 3e."


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## Brandon O (Mar 2, 2015)

If that bored anybody, feel free to click on "dead space," which the autoparser has apparently turned into an Amazon link to the PlayStation game.


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## sdadam (Mar 11, 2015)

Hey Brandon, great discussion for sure!

I'm sorry but I fail to see the point in your post. You keep coming back to this idea of if it doesn't change your treatment it must be useless.

I don't know how else to explain to you what I consider the value of the knowledge in the pathophysiology. I don't believe that just because something isn't going to change my treatment it's useless. That's not how real differential diagnosis works.

You act like it's a simple matter to even be 100% sure in the field that you are dealing with COPD. Sure, 8 out of 10 times it is. 8 out of 10 patients are simple no matter what. But a small part of the time they aren't. I'm not arguing that differentiating between the two will necessarily change my treatment. These patients may be minor and I'm not going to treat them at all, but that doesn't mean it's not by job to diagnose them to the best of my ability.

Have you ever heard the term aim small miss small? Well, if I'm busy trying to figure out if my patient has Chronic Bronchitis or Emphysema, I'm not trying to figure out if they have COPD or CHF, asthma, pulmonary emboli, or something else. I feel like we are on the same page that the diseases are drastically different and your saying, sure but the presentation and clinical care are hopelessly intertwined so working with them together is simpler, and more effective. From a student point of view, or studying for the boards I get that. However I disagree that they can't be differentiated, or that it's not clinically valuable.

These are unarguably different diseases, caused by and sharing some factors. But the pathophysiology that in-between the cause and presentation, and the altered mechanics, and physics of gas exchange in the new environment are entirely different. The long term effects of the diseases are different on the body, and reactions to treatments are effected by the different changes in those dynamics in each disease. Here is one example about oxygen utilization but there are many studies. In a sample size of only 20 drastic physiologic differences were found: http://www.ncbi.nlm.nih.gov/pubmed/8520795

_ Thus, in emphysematous patients, the oxygen available for tissues other than respiratory muscles was significantly reduced (emphysema: 124 +/- 51 ml/min/m2; chronic bronchitis: 207 +/- 78 ml/min/m2; p < 0.02). This could explain nutritional differences observed between patients with emphysema and those with chronic bronchitis._​
This is the kind of information that makes you a better clinician. You have to practice science based medicine rather than evidence based medicine. The above study shows me that in emphysema patients it's likely that we are dealing with an entirely different physiologic oxygen delivery situation than chronic bronchitis patients. This affects every decision I make from O2 management, to how quickly I will consider bicarb in a prolonged resuscitation. Information like that makes me think more about affecting the offload affinity of oxygen in an emphysema patient and the on-load affinity of oxygen in a bronchitis patient. Does it make a difference? I don't know it would be impossible to gather data on such a specific subset of patients in a meaningful way, for me at least, but I do know that calling all those patients COPD and treating them the same means that those few that would benefit from tailored care don't get it. We are taught that evidence is the most important thing, it's not. Evidenced based medicine is giving way to science based medicine, where we understand that because data collection isn't perfect and ubiquitous we should use evidence to inform scientific theory and base practice on that. I'm not changing treatment protocols, I'm changing how I utilize them based on the specific patient.

This doesn't even touch on the idea of concurrent pathology that muddies the waters. These patients often have confounding and unrelated physiologic process going on. A more complete understanding of the different pathophysiologies under the umbrella "COPD", in my opinon, can ONLY lead to better clinical care. I don't think you are arguing that they aren't different, we just have different outlooks on what that means. If someone has advanced CHF, Emphysima, PNE and Diabetes related pathology, looking for COPD among significant amounts of signs and symptoms from those diseases is difficult, looking for something more specific will help you determine what S/S are being caused by what process.

I spent the last five years or so working in critical care and flight medicine so, my perspective isn't of a textbook stand alone COPD patient. In that case, you're right, I doubt any of this knowledge would come in handy. But I really don't care about a standalone COPD patient, I can care for that person without significant thought. It's the one out of ten, one out of a hundred, patients that this sort of specialized knowledge comes into play. If it were up to me we would teach Paramedics the specifics of A-type, B-type and centrilobular and panlobular emphysema.

That being said it is my opinion that we are going to continue to see how different these diseases are and, as we removed asthma from the spectrum we will realize that other than initial causes and overlapping S/S the two have little to do with each other, but are often concurrently present. One study in Feb. 2013 in .... (Chronic Bronchitis and COPD)found that:

_"It is known now that many patients with severe emphysema can develop CB, and small airway pathology has been linked to worse clinical outcomes..."
_
and goes on to state:

_"However, in recent years, a greater understanding of the importance of CB as a phenotype to identify patients with a beneficial response to therapy has been described"_​
That's far from the only place making progress on this, but I've never hear anyone argue that they are prognostic-ally the same. Since that's your statement it falls on you to provide proof that they are. Just because we reported COPD statistics together for a long time doesn't mean that the morbidity and mortality is the same for everything in that category, just that we averaged them all together.

All THAT being said. It doesn't matter. If you really are an EMT and you have the level of knowledge to engage in this conversation, you're fine, I'm fine, we're giving better medical care with a deeper understanding of these things than most practicing emergency physicians could still remember from school. These are the kinds of disagreements that I'm totally ok with having because I know you understand this better than 99% of people out there. We're really just arguing semantics, who cares what we call it. 

​


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## Nova1300 (Mar 11, 2015)

sdadam said:


> Hey Brandon, great discussion for sure!
> 
> I'm sorry but I fail to see the point in your post. You keep coming back to this idea of if it doesn't change your treatment it must be useless.
> 
> ...





Why?


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## sdadam (Mar 11, 2015)

I don't follow your question.


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## Nova1300 (Mar 11, 2015)

Ok.

Why would you include that it their curriculum?

You gonna throw antitrypsin in there too?


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## sdadam (Mar 11, 2015)

Nova1300 said:


> Ok.
> 
> Why would you include that it their curriculum?
> 
> You gonna throw antitrypsin in there too?



You expected me to know that "why" was in reference to that one statement in my multi-paragraph post. And then reply "Ok." as if I'm stupid for asking what "why" meant. Give me a break with your disingenuous games.

If you have a point, feel free to make it... I don't have time to play games. You pretty obviously disagree, and I feel like most rational people can clearly see that my response would be similar to the several previous posts about the value of information itself.


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## sdadam (Mar 11, 2015)

I just saw that you underlined that line in your quote of my entire post, I didn't re-read my own post....

Regardless, my point above stands, what's your point?


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## Nova1300 (Mar 11, 2015)

Well, I certainly didn't mean to take so much of your time with my games.  

I guess I'm asking your opinion...
What major management shift in the prehospital treatment period do you foresee that would necessitate differentiating this level of pathology for the management of respiratory failure? 

Do you believe this is important enough to fit into what is already a high-paced, information-dense curriculum in emergency life support?  

I am, of course, referring to the part of your statement which I bolded in my reply. I'm sorry if that was unclear from the outset.


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## Brandon O (Mar 11, 2015)

sdadam said:


> All THAT being said. It doesn't matter. If you really are an EMT and you have the level of knowledge to engage in this conversation, you're fine, I'm fine, we're giving better medical care with a deeper understanding of these things than most practicing emergency physicians could still remember from school. These are the kinds of disagreements that I'm totally ok with having because I know you understand this better than 99% of people out there. We're really just arguing semantics, who cares what we call it.



I agree! And I think -- for all intents and purposes worth lighting a candle over -- that we're on the same page.

And I didn't mean to be misleading. I'm currently finishing up PA school. But I am a Basic at heart and that's how I came up.


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## Brandon O (Mar 11, 2015)

Nova1300 said:


> What major management shift in the prehospital treatment period do you foresee that would necessitate differentiating this level of pathology for the management of respiratory failure?



Not to get involved in this when I just escaped, but I would say that at least a general understanding of alpha-1-antitrypsin deficiency is worth having. Otherwise you might be very confused by a younger patient who appears to have COPD, discount it as implausible, and go down a (wrong) alternate pathway.


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## Nova1300 (Mar 11, 2015)

Brandon O said:


> Not to get involved in this when I just escaped, but I would say that at least a general understanding of alpha-1-antitrypsin deficiency is worth having. Otherwise you might be very confused by a younger patient who appears to have COPD, discount it as implausible, and go down a (wrong) alternate pathway.




I said the same thing after I went back home to work one weekend during my first year of school.  

Patient with ankylosing spondylitis had a car wreck.  

My thought "well hell.  Why aren't medics taught about this?  Everyone should know about this disease!!  People have wrecks all the time!!  Paramedics must all be educated on ankylosing spondylitis!!!" 

And then the patient got backboarded and sent to the hospital.

Just like a 30 yo with alpha-1 will get bronchodilators for resp distress and sent to the hospital.  

Yes, understanding pathology is great.  But paramedic courses aren't 4 years long.  And there is still a lot of very important material to cover.  Far more important, I think, than alpha-1 or AS.  


Only my opinion.


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## Brandon O (Mar 11, 2015)

Well, a 30 year old with respiratory distress might end up getting his chest darted or some other nonsense if a medic is really confused. Similarly (and if peer review favors me and some other nice folks, you'll be able to read about this in a couple months), AS may be enough of a risk factor for spinal instability that it should indeed favor into field decision-making.

But all of that being said, I agree that time is limited, and I'm glad I'm not the one who has to decide what goes into a certification curriculum.


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## sdadam (Mar 11, 2015)

Nova1300:

I don't mean to be short with you but I just feel like you are asking redundant questions that have been the topic of this entire thread.

I feel like you think I have a specific reason for thinking that we should include this issue with these pathology's into the Paramedic curriculum, that's not it at all. I think that the curriculum should be expanded, significantly longer, and with significantly more basic science pre-requisites. We should then teach all pathology's to this level.

Why? It makes people better clinicians, see my previous posts.

Brandon;

For sure, we're square! I'm bummed to hear your completing advanced education to be honest, I want to find more EMT-B's who have taken the time to learn things to this level! But, I'm glad you made it through, all the best Doctors and PA's I know started in EMS. I think the way you learn to think as a basic, and the feeling of helplessness that your limited scope gives you in emergencies teaches you lessons that you literally can't get anywhere else.


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## Nova1300 (Mar 11, 2015)

sdadam said:


> Nova1300:
> 
> I don't mean to be short with you but I just feel like you are asking redundant questions that have been the topic of this entire thread.
> 
> ...



I don't disagree with you, in an ideal world.  Education is great.  

But I still think you are talking about medical school level pathology for paramedics.  I'm just not sure the cost of the classroom time would be of tangible benefit in the real world.  

The goal is to prepare judicious emergency clinicians.  But does a judiciois emergency clinician need to know the disease process to the cellular level?  

That just sounds expensive to me.

But I'm tight.


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## Nova1300 (Mar 11, 2015)

i just want to clarify, I think a bachelors of paramedicine focused on hard sciences is a fantastic idea, if it were feasible.

I think a EMS is a great stepping stone to other healthcare careers.  And, a bachelors degree would make that much easier.

PA school, AA school, med school, etc.  They are all natural transitions for smart folks with an EMS background.

But the financial implications, the collapse of volunteer services, the time commitments, and many other obstacles lay between here and that kind of change for the EMS world. 

I do respect your ideal, albeit rather lofty.


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## Carlos Danger (Mar 12, 2015)

More education is always a good thing. But time is finite and at some point you just have to decide where to draw the line. We can argue over whether that line should come before or after covering a1at and the subtypes of emphysema, but the reality is that line has to be drawn somewhere and wherever it falls, there will be plenty of patho and pharm on the other side of it. 

I complain as much about the state of paramedic education as anyone else, but honestly I think we do a pretty good job of covering the what is relevant to paramedic practice and forgoing things that aren't clinically important. it's not perfect, but for the most part it works pretty well.


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