This or That: COPD and CHF

If there is one thing that can set you apart from your peers as a prehospital clinician, it is the ability to think outside of the box. I’m am not using that cliché in the traditional sense, but in the nearly literal sense. Technicians have to have a clear set of symptoms and “cardinal signs” in order to be able to “see” what they are dealing with and be able to select the “right” protocol. A clinician on the other hand, they know that very few patients fit neatly and snugly inside of those little protocol boxes.   CHF vs. COPD is perhaps a perfect example of trying to force a patient to “fit” into a protocol. These two diseases often present together, which leads one to begin thinking like: “which one do I treat?” or “which one is the problem?” They are reaching desperately for one of the nursery rhyme heuristics they were taught in school about blue bloaters and pink puffers.   In actuality, the bloater and puffer thing is a throwback to the last half of the 20th century when we lacked some of the tools and technology that have only become mainstream in the last decade. Prehospital clinicians have a plethora of technology and evidence based practice to support their field diagnoses and treatment plans.  

Let’s graduate beyond wheezes = COPD and rales = CHF. Mostly because our patients have graduated to having COPD and CHF. This combination confounds our heuristics and the rote application of protocol.  

The Mindset

HF is not treated differently because the patient has COPD. COPD is not treated differently because the patient has HF. Are there some precautions and "stop and think" moments? Sure. But for the most part one treatment is not contraindicated because of the presence of another disease (unless your local medical direction deems it so). In fact, they both benefit from some of the same treatments, but the fear that treating one makes the other worse is largely not supported in the literature.  

The Problems

The patient who has both HF and COPD has both an obstructive pathology (COPD) AND a restrictive pathology (CHF).  Both of which make it difficult to move volume in and out of the lungs, move oxygen into the blood, and remove carbon dioxide. The patient has both a forward flow (CO) problem and an oxygen content problem. The result is a fragile oxygen delivery process that can be overwhelmed by something a simple as a set of stairs or a bucket of chicken.  

It may be helpful to remember that COPD can cause HF, but HF does not cause COPD. COPD can become complicated by pulmonary hypertension, and that pulmonary hypertension leads to a higher afterload for the RV to pump against. The patient eventually loses normal function of the right ventricle (RV). As the LV makes a valiant attempt to cover the load for both ventricles, it too fails. This is one way COPD leads to heart failure. There is also a hypothesis that chronic inflammation and the heart's constant exposure to inflammatory mediators and cytokines leads to ischemic heart disease, and eventually, heart failure.                  

Assessment Pearls

Assessment is where the newer folks can get into some trouble. They will invariably be looking for a single set of symptoms that relates to the heuristic they have created (wheezes = COPD / rales = CHF). The reality is that when both diseases are present, the heuristics don't fit anymore. The "pink this" and "blue that" presentations are distorted to the degree that they are not so helpful. There are no qualitative assessment findings that are unique to either disease. You may or may not hear rales. You may or may not hear wheezing. You may hear wheezes when the patient has CHF due to pulmonary congestion that narrows the airways. You may not hear any air movement in the hyper-inflated chest. They may be so obese that you cannot appreciate a "barrel chested" appearance. These heuristics we are taught to rely on in paramedic school are useless if another disease makes the picture a little more cloudy. I will concede that they can be helpful on a static exam to clue you in on where the question is heading but are of little use beyond that.  

ETCO2 waveform may help with differentiation, but don't rely so much on the numbers (quantitative data) to do that. The shark fin appearance of the waveform is not easily confounded by CHF, which should lead to a primary bronchoconstriction problem when this is seen on the monitor. There really is no ETco2 waveform that indicates CHF. The patient with both diseases can be hypercapneic or hypocapneic depending on how the primary problem is impacting their ability to ventilate adequately.  

Of course, any discussion of physical assessment of a respiratory distress patient in 2025 is not complete without mentioning the use of ultrasound. Ultrasound assessment can show b-lines, which can confirm the presence of pulmonary edema (and thereby CHF). The downside to it is that the absence of b-lines does not confirm the presence of COPD. However, if you are on the fence about what primary treatment pathway you want to go down, it can be helpful information to help you move one direction or the other.  

Treatment Plans

Treating these patients is not as complicated as it may seem. Remember, we don't treat CHF differently if they also COPD and vice versa. Do a good assessment and try to get your head around what may be the primary problem.  

CPAP improves outcomes in both patients and could be a great place to start if they do not experience relief from more basic maneuvers. It reduces the instances of intubation and improves the resolution of respiratory distress. The questions start to come after that is initiated.  

Inhaled beta agonists have a place in the treatment of these patients. Over the years I have heard from other instructors, and even at one point in my career repeated the guidance that these should be avoided in CHF patients due to the risks of over stimulating the heart and speeding up the process of decompensation (to the point that they "flash"). What we know now is that this is not great guidance. The other downside is that the data we have on these types of treatment dilemmas is really weak and heavily weighted on observational data and anecdotal evidence. Neither of which should be a cornerstone that dictates clinical practice.  

If they are in distress, start working with the things we know can help with it. If they are hemodynamically unstable (dangerously hypertensive and tachycardic), then perhaps adrenergnic stimulation is a bad idea. If you started with an albuterol neb and they appear to have gotten worse afterwards, then it is an easy decision to discontinue that therapy. The inhaled beta agonists we use are short acting and the untoward effects should be limited, should they manifest. At that point the addition of NTG to assist with afterload reduction and improving the LV's ability to unload will be beneficial as well.

Close Out

Hopefully this helps unpack some of these concepts and add some weight to the discussion you may be having with a fellow clinician who may need a hand with teasing these two problems apart.  

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