Differential Dx: Tachypnea Part 4

In part 1 I described the PH balance associated with the rapid breather. In part 2 we reviewed hyperventilation syndrome. In part 3 I gave a brief description of a chronic lunger, and how to treat them. In part 4 I am going to go over congestive heart failure(CHF). This happens to be one of my favorite topics.

Watch this video:

Congestive heart failure(CHF) is a global term, used to describe an inability of the heart's structure or function to provide adequate blood flow to supply the body's needs.
More specifically, the heart is unable to adequately perfuse the body.

Even though we treat CHF in the field commonly, we really can't be sure we are actually treating CHF. Physicians use a BNP(brain-type natriuretic peptide) and chest x-ray to diagnose CHF. We make an educated guess based on the patient's presentation.
More specifically, we treat what we think is left ventricular failure. This is
because failure of the left ventricle may cause blood to back up into the pulmonary system. This causes pulmonary edema.

Some things that might help us decide that the patient we are treating is suffering from CHF induced dyspnea:
  • Maybe the biggest clue would be a known history of CHF
  • Peripheral edema would indicate right ventricular failure, which could indicate left ventricular failure.
  • Crackles or rales both indicate pulmonary edema.
  • Hypertension
You may also suspect CHF based on patient's medications, some medications a CHF patient might be on include:
  • ACE Inhibitors (these are the drugs that end in "ril", lisinopril, benazepril, ramipril...)
  • Beta Blockers (these end in "lol", labetalol, atenolol, carevedilol, metoprolol...)
  • Diuretics (usually end in "ide" or "one", furosemide, hydrochlorothiazide, metolazone...)
Don't you hate it when the patient doesn't know that they have CHF and are on all these meds? Here are some findings to help your differential diagnosis. If one of these is present, consider other cause.
  • Hypotension (consider cardiogenic shock, or sepsis)
  • Fever (consider pneumonia, or sepsis)
  • Pleuritic chest pain (consider pulmonary embolism)
  • Palpitations, irregular pulse (consider arrhythmia)
  • For a complete differential diagnosis click here
Some treatments could be pretty harmful given to the wrong patient with similar presentation. You don't want to give diuretics to a septic patient, and nitrates for cardiogenic shock might be detrimental.

Before we talk about the treatment for CHF, I'd like to review some of the pathophysiology.

If you watched the video up top, you heard the narrator mention left-sided and right-sided heart failure. These are more commonly termed left ventricular or right ventricular failure. There is a third type, biventricular failure.

Left Ventricular Failure(LVF) - This is the most common type of unilateral heart failure. This may be caused by a number of things. Most commonly HTN, AMI, RVF, or valvular abnormalities. Since this means that the left ventricle isn't pumping out good enough, the blood backs up. The only place the blood has to go, is the lungs. This is why CPAP(continuous positive airway pressure) and nitrates do so much for these patients. By reducing preload and afterload and using PEEP(positive end expiratory pressure) to assist the patient's own ventilations, you can greatly improve the condition of a CHF patient.

Right Ventricular Failure(RVF) - This almost always accompanies LVF, since LVF is the main cause of RVF. There is a small percentage of people that have RVF alone, and this will usually lead to biventricular failure anyhow. RVF could be a result of pulmonary HTN in a COPD patient, this is called cor pulmonale. RVF usually displays with peripheral edema. Isolated RVF is not treated by us paramedics because it doesn't present with an acute emergency. By "treated", I mean with invasive procedures, of coarse supportive care is always appropriate.

Before I start, take a look at this:

McKinney, Brywczynski, Slovis "Med under scrutiny: the declining roles of furosemide, morphine & beta blockers in prehospital care." Journal of Emergency Medicine, (January 2009)

One of the mistakes in the use of furosemide in acute pulmonary edema is the assumption that the patient is "fluid overloaded." Studies have shown that many patients with pulmonary edema are actually euvolemic, or even hypovolemic, in the acute setting and that furosemide can cause rapid deleterious fluid shifts. Despite these facts, many medical providers continue to believe that patients with acute heart failure syndromes are volume overloaded, thus necessitating a diuretic.
Studies have also shown that when patients in heart failure are acutely given furosemide, preload and blood pressure are paradoxically increased in the initial 15–20 minutes. Conversely, in 1987, Hoffman demonstrated that the administration of furosemide alone, or in combination with morphine, added no benefit in the acute management of pulmonary edema and led to deleterious side effects, such as hypotension, and worsened clinical outcomes.
In addition to the established fact that some patients with pulmonary edema are not volume overloaded and that furosemide may cause worsening hemodynamics in the acute setting, evidence also suggests that we may be doing harm to patients because of incorrectly identifying pulmonary edema. Patients may have other medical conditions that can lead to acute shortness of breath, such as congestive heart failure (CHF), pneumonia, chronic bronchitis and emphysema. Many patients also have co-existing medical conditions.
In 2006, Jaronik et al studied the appropriateness of prehospital furosemide. They retrospectively identified all patients given this medication in the prehospital environment. The results were substantial. Of the 144 patients included in the study, 60 patients (42%) did not have any evidence of CHF during their hospital stay and 33 patients (23%) needed IV fluid administration from the dehydrating effects of furosemide.
That's right, in case you haven't heard, Lasix is not improving the outcome of your CHF, or presumed CHF, patients. In fact, Lasix is responsible for increased morbidity and mortality amongst these patients. That's not all, here's more from the same article.

[...]However, multiple studies demonstrate morphine’s potential dangers when used in patients with pulmonary edema. In 1987, Hoffman and Reynolds compared Lasix, nitroglycerin and morphine for the treatment of presumed pulmonary edema. Not only did this study demonstrate the potential for misdiagnosis of heart failure in the prehospital setting, as only 77% of patients received an emergency department (ED) or in-hospital diagnosis of CHF, it also demonstrated the potential for harm. They found adverse effects in the first hour of treatment only in patients who received morphine.Sacchetti et al also demonstrated a trend toward higher intubation rates and ICU admissions in patients receiving morphine.
In a recent study reported in the Emergency Medicine Journal in 2008, Peacock et al reviewed the ADHERE (Acute Decompensated Heart Failure National Registry) database in an attempt to compare the outcomes of patients who did and did not receive morphine during hospitalization for acute decompensated heart failure. This retrospective analysis demonstrated a higher rate of inotrope usage, longer hospitalization, higher need for mechanical ventilation, more ICU admissions and a greater mortality in the morphine group.
Although many studies evaluating morphine efficacy are often retrospective, the trend toward increased morbidity and mortality in patients receiving morphine for acute decompensated heart failure is fairly consistent. There’s no debate that the early aggressive treatment of patients presenting with acute decompensated heart failure can reduce morbidity and mortality; however, morphine does not appear to be the right medication.
Yep, Morphine seems to be a culprit too. Morphine and Lasix have remained in prehospital protocols based on theory. The research has shown that these theories were wrong. This is pretty hard for the old-timers to grasp, and the drugs are still being administered routinely. I predict they will fall in the way of stacked shocks, and MAST pants. The article also slams Lopressor, but I'll save that for a different discussion. By the way, I have done the research on this, and these aren't new statements, just finally being recognized.

So, does this leave you wondering what's left? If not, just pretend that's what you're wondering.


Since the implementation of CPAP in the prehospital environment, it has become an asset. We no longer have to watch a CHF patient in severe respiratory distress decompensate into a state where we can intubate them; unless you had RSI. If you have used CPAP you have probably seen the magic it can do right before your eyes. But you don't have to rely on anecdotal evidence. Read this:

Sullivan R. "Prehospital use of CPAP: Positive pressure = positive patient outcomes." Emergency Medical Services 34, no. 8 (August 2005)

When used correctly, CPAP has been shown to alleviate symptoms and decrease the need for intubation for patients with CHF, COPD and asthma. It is safe, portable and easy to apply. CPAP does not replace intubation, but rather is a less-invasive means of providing respiratory support while medications work to correct the underlying cause of distress.
Nitrates(sublingual nitroglycerine, and Tridil drip) have also shown to be a great treatment for the emergent treatment of cardiac induced pulmonary edema. Like I stated before, these patients are having a preload problem along with increased afterload(resistance). The nitro relieves both of these problems pretty well along with managing hypertension. Here are some exerts from a study on the use of nitrates for the prehospital treatment of pulmonary edema.

Bertini G et al. "Intravenous nitrates in the prehospital management of acute pulmonary edema." Annals Of Emergency Medicine 30, no. 4 (October 1997)
STUDY OBJECTIVE: We sought to assess the effect of nitrates on prehospital mortality among patients with acute pulmonary edema (APE).[...] RESULTS: Overall prehospital mortality rate for APE in all patients was 7.8% (50 of of 640 patients). Mortality after 1984 was significantly lower than before (5.3% versus 13%, P < .01). Nitrates were effective in reducing mortality, even in hypotensive patients.[...]CONCLUSION: Our findings suggest that the use of intravenous nitrates improves short-term prognosis in APE.
So that's pretty much it. If you have nitro for infusion(Tridil), it is much easier to administer nitro while they are on CPAP. It is also much easier to titrate a nitro drip, than a sublingual spray.


Shaggy said...

I just wanted to add a little note about CPAP and PEEP in the treatment of Acute Decompensated Heart Failure in relation to preload and afterload.
As we know, when alveolar pressure is above atmosmospheric pressure, air flows out, and with the inverse, with negative alveolar pressure, air flows from higher pressure outside to the lungs. The negative pressure draws it in. The same premise holds true for the negative pressure of the right ventricle. The right ventricle is very reliant on Intrathoracic Pressure (ITP). With negative pressure, such as at the beginning of the inspiratory phase, causes a vacuum in the right side of the heart, drawing more blood in and subsequently increasing right ventricular (RV)filling.
Now with the opposite effect, with increased ITP, there is a DECREASED RV preload. CPAP and PEEP increase the ICP, thus decreasing RV preload and by impairing systemic vascular return. It also increases RV afterload for many reasons that cannot be explained by the consensus of physiologists.

We know that increasing ICP reduces PVR by counteracting hypoxic pulmonary vasoconstriction. PEEP and CPAP "opens" collapsed alveoli, increasing alveolar pO2, therefore, hypoxic pulmonary vasoconstriction will be reduced. This then increases RV ejection (to the lungs).

Now with the return to the heart from the lungs: A decrease in systemic venous return and, thus, right preload, will result in decreased pulmonary venous return, and left preload because the two ventricles pump together. Not only that, blood flow returning from the lungs is regulated by ITP as well as its stress on the flow. Though PEEP/CPAp increases the intravascular hydrostatic pressure in the alveolar vessels, it increases the interstitial space pressure and forces much of the fluid out through the lymphatic system.

Left ventricular (LV) pumping is dependant on LV preload, LV contractility and the pressure against which the left ventricle ejects (afterload), as we know. And yet, cardiac output is better, for many reasons most cannot agree on. One thing that is agreed upon is the elevated ITP from PEEP or CPAP puts a higher pressure than the rest of the circulation (which is at atm), decreasing the force necessary to eject the blood from the LV. This all leads to a slight decrease in BP while maintaining CO. Can we see why now hypotension and relative hypovolemia can be contra-indications to PEEP and CPAP?

So, in a nutshell, CPAP and PEEP when the patient is on a vent, can decrease preload as well as the Nitrates and ACE inhibitors. If this was too detailed, in which it actually was not, remember that as medics, we are healthcare professionals and should understand a moderate amount of pathophysiology and the physiological affects of our treatments.

Adam Thompson, EMT-P said...

I think you accidently stated "ICP" instead of ITP a few times. No biggy. Good comment though. This is also an important thing to remember in consideration of AMI patients. If your patient shows increased ST elevation or a sudden and unstable drop in BP, you may want to consider removing the CPAP.

If they are having a RV infarct, their condition may deteriorate with the use of CPAP.

Shaggy said...

Thanks for pointing out the "ICP". I am so used to discussing ICP when teaching about TBIs and Cushing's Triad, that when I rant on in the middle of the night discussing ITP, I write ICP instead. Yes, you would think even subconsciously I should be able to differentiate the brain from the chest. But not all of us are blessed with an above average IQ like some other folks (ahem-like you, Tom, and others).

I did not consider to mention the effects of CPAP/PEEP on RV infarct when discussing treatment of respiratory distress from ADHF, but it is a great point to bring up. The effects are very similar to giving NTG. In fact we had a crew bottom out a BP the other day with CPAP. I suspect the patient was suffering from pneumonia and was initially normotensive, but the medic thought the patient was in CHF because she had a history of it.

Anyway, yes, if there is ST elevation in the inferior leads, and the pressure is even normotensive, I would be carefull to use CPAP unless I checked RV4 and R/O an RCA occlusion. Very good point, but I think it would be unlikely for a patient to develop pulmonary edema from RV infarct, and cardiogenic shock is usually not something commonly seen by EMS as it is in a CCU.

Adam Thompson, EMT-P said...

It's okay shaggy, you should see my posts before I proof-read them.

"I think it would be unlikely for a patient to develop pulmonary edema from RV infarct"

Correct, but most RVIs are not isolated to the RV. I have had one patient in cardiogenic shock in my short career. You're right, it's not very common at all.

Craig said...

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can any tell me if this is a little risky ?

Rogue Medic said...


You are asking about a generic version of Viagra. Probably just to drop some spam into the comments. This is not really an emergency drug, although the emergency may be in the eye of the beholder.

If you take this, or any other erectile dysfunction drug, it would not be a good idea to follow it with NTG. NTG is a very effective drug for pulmonary edema.

The drugs appear to have a combined effect that is dramatic and may cause you blood pressure to drop to dangerous levels, perhaps as low as zero.

Most important - Do not buy drugs on the internet. You have no real oversight of the manufacture of what you buy. The ingredients might not be what you are trying to buy.

Anonymous said...

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