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.

Differential Dx: Tachypnea Part 3

Ok, in part 1 I explained the many causes of rapid breathing, and in part 2 we went over one of them, hyperventilation syndrome. In part 3 I am going to briefly go over some other causes of rapid breathing.

Remember how I said I like to categorize these patients as either patients that need O2, or patients that need CO2? Well, all of the following patients are going to fall in the need O2 category.

To get a complete differential diagnosis for tachypnea check out Diagnosis Pro.

I am going to stay away from the traumatic causes of tachypnea because it doesn't really apply to the discussion. Just keep in mind that they exist and if there is the possibility of a traumatic injury, you should consider a traumatic cause.

Now within the medical causes, you can break these down in to two types. Acute(new onset) and chronic(old disease). If it is a patient with a chronic respiratory ailment, your presence probably means they are having an exacerbation of symptoms. The onset of their current condition may be acute, but their condition is chronic. Your acute/new onset patients are having a completely new onset of symptoms. These patients may have no medical history.

In this part I am going to go over the patients with chronic respiratory conditions and exacerbation of symptoms. I like to call these patients chronic lungers, a term I stole from my paramedic instructor. These patients may be simple to diagnose and they could respond to an easy fix, or they could take additional treatment and may be having a status episode.

The first of these is going to be one we are all very familiar with, Chronic Obstructive Pulmonary Disease/Disorder (COPD).
Emphysema and Chronic Bronchitis are both considered to be the diseases of COPD. Depending on where you read, asthma may also be considered a disease of COPD. I am going to talk about asthma separately because it has some more specific factors. I do realize asthma is chronic, it is obstructive, and it is a pulmonary disease. This picture to the right is a pretty pathetic way to explain how COPD effects the alveoli. It's what you find if you Google COPD. I guess it does make a simple point, but we are going to get a little more in depth.

Please watch the video on COPD below...

I plan on using quite a few images and videos in my blog to assist the visual learner. I hope this helps.

Most COPD patients have chronic bronchitis so lets start by explaining chronic bronchitis. As Dr. Fink stated, this condition occurs when the bronchial tubes become inflamed, hints the term bronchitis. This is different from the common respiratory infection, also termed bronchitis, that may accompany cold symptoms. This condition is more associated with smokers. Check out this video for a pretty cool look at the effect of smoking on the alveoli.

Chronic bronchitis is defined clinically as a persistent cough that produces sputum(phlegm) and mucus, for at least three months in two consecutive years.
- Wikipedia
Chronic bronchitis and emphysema are almost exclusively caused by smoking. Asthma isn't, that is one of the reasons I personally categorize it differently. Continued exposure to air pollution, dust, asbestos, or toxic fumes may also cause COPD.

You may have heard the terms "blue bloater" or "pink puffer" used when describing COPD patients. I love the image to the right from MAC.edu that depicts a chronic bronchitis patient. Blue bloater is used to describe the clinical manifestations of a chronic bronchitis patient. Excess body fluids, barrel chest, and cyanosis(late sign). These patients are usually bigger than emphysema patients. Your treatment will probably not change based on what type of COPD patient is in your care. Being able to differentiate them will only help you in predicting if signs and symptoms correlate with their history. The barrel chest I mentioned is a result of prolonged pursed-lip breathing. This technique is used by chronic lungers to create their own PEEP(positive end expiratory pressure). This helps them get the air through their clogged, inflamed, constricted pipes(bronchi).

To the left here you can see a barrel chest. This condition is also present in some patients with asthma, dysplasia, cockayne syndrome, and silicosis. Emphysema patients, pink puffers, are the more commonly known barrel chested patients.

Emphysema is characterized by a loss of elasticity of the lung tissue, caused by destruction of the structures feeding alveoli. The smaller airways end up collapsing during exhalation. About 1/3 of COPD patients have emphysema. You end up with pathological destruction of the alveolar walls without fibrosis. The clinical manifestations of emphysema include pursed-lip breathing, use of accessory muscles to breath, minimal or absent cough, leaning forward to breath, and dyspnea on exertion(late sign). The absence of a productive cough may help to differentiate these patients from the chronic bronchitis patient. Emphysema patients are using that pursed lip breathing to keep their alveoli open, so they can get more air out.

Some other distinguishing features:
  • Emphysema leads to weight loss, Chronic bronchitis leads to weight gain
  • Edema is usually absent with emphysema and present with chronic bronchitis
  • Central cyanosis is particular to advanced chronic bronchitis
  • Emphysema patients are usually thin waisted.
  • Hyperresonance is more commonly percussed on emphysema patients
  • JVD may be more present in chronic bronchitis patients(sign of pulmonary HTN)
  • Right axis deviation, RVH, and atrial arrhythmias are more associated with chronic bronchitis.

Above, to the left is a "pink puffer" and to the right is a "blue bloater". Both images courtesy of bronchitis.com

The next type of patient I am going to describe is the asthma patient. Then, since asthma and COPD patients require similar treatment, I will go over treatment strategies.

Asthma is defined by the National Heart, Lung, and Blood institute as a common chronic disorder of the airways that is complex and characterized by variable and recurring symptoms, airflow obstruction, bronchial hyperresponsiveness(bronchospasm), and an underlying inflammation. While COPD usually effects people over the age of 40, asthma can be present in all age groups.

In terms of symptoms, asthma is defined by paroxysms of diffuse wheezing, dyspnea, and cough, resulting from spasmodic contractions of the bronchi. Airway obstruction is reversible(but not completely in some patients). The increased responsiveness is due to a variety of stimuli. Here is another video

The biggest indicator that you are dealing with an asthma or COPD patient will be a medical history. These patients will usually know that they have one of these conditions. Usually when these patients are having an exacerbation of symptoms they won't even need us.
This is a significant thing to remember, because if they called us it could be bad.

Status asthmaticus is an acute exacerbation of symptoms that does not respond
bronchodilation or other primary treatments. These patients may be in tripod position, using accessory muscles, they may have chest tightness, and a dry cough. Extreme wheezing and labored breathing will be present. These patients are at high risk for hypoxic induced cardiac arrest. The picture to the right is of tripod position.


Department of Emergency Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA. delbridget@msx.upmc.edu

The treatment of acute asthma exacerbation consumes a significant portion of emergency medical services (EMS) system resources. Because few studies have addressed EMS treatment of asthma, most EMS providers model their approach to treatment on strategies thought to be effective in the emergency department. During the treatment of asthma, a patient's history and current airway and respiratory status are important components of the initial assessment. Although the general evaluation may address a patient's appearance, vital signs, mental status, level of fatigue, and ability to speak normally, the initial assessment of an asthmatic patient must focus specifically on his or her respiratory effort and quality and on objective measurement of the patient's blood oxygenation. Inhaled beta-agonist therapy is the widely recommended first choice of treatment, but anticholinergic agents and steroids may also have roles. Although not routine treatments, parenteral magnesium and epinephrine may also be beneficial for certain patients. Endotracheal intubation is a procedure of last resort and should be reserved for patients at immediate risk of respiratory arrest. Finally, EMS providers must be alert to the danger of using a "treat and release" approach, as recommended by some protocols, in the treatment of acute asthma. The quick results and benefit that short-acting treatments provide can easily and erroneously lead a provider to believe that an attack has been adequately controlled when, in fact, a more serious exacerbation may be imminent. Treatment protocols, therefore, should discourage EMS personnel from this practice and advise them to always transport asthmatic patients they have treated to the hospital to undergo more extended care and monitoring.

Your treatment should be based on the severity of your patient's condition. The following are treatments for COPD and asthma.

Mild respiratory distress with mild hypoxia - Use a calm and reassuring voice, provide increased supplemental O2. Nebulized Albuterol, if refractory. Remember, these patients may have chronic mild hypoxia.

Moderate respiratory distress and hypoxia - Albuterol(proventil) updraft, add ipratropium(atrovent) if the patient has been using their inhaler or nebulizer. Consider corticosteroids (Solumedrol). If refractory, consider magnesium sulfate or epinephrine.

Severe respiratory distress - Consider immediate endotracheal intubation and/or epinephrine if the patient is pre-arrest. If possible, administer nebulized Albuterol/Atrovent, and magnesium sulfate before resulting to intubation.

*If you have a CPAP with adjustable PEEP, it may be possible to improve the outcome of your patient using a low PEEP setting. Higher PEEP settings run a high risk of causing a pneumothorax due to the increased intrathoracic pressure.

New Castle County EMS, DE, USA. R.Sullivan@co.newcastle.de.us

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.

Intensive Care Unit, State University of Campinas, Brazil.

BACKGROUND AND OBJECTIVE: Hyperinflation with a decrease in inspiratory capacity (IC) is a common presentation for both unstable and stable COPD patients. As CPAP can reduce inspiratory load, possibly secondary to a reduction in hyperinflation, this study examined whether CPAP would increase IC in stable COPD patients. METHODS: Twenty-one stable COPD patients (nine emphysema, 12 chronic bronchitis) received a trial of CPAP for 5 min at 4, 7 and 11 cmH(2)O. Fast and slow VC (SVC) were measured before and after each CPAP trial. In patients in whom all three CPAP levels resulted in a decreased IC, an additional trial of CPAP at 2 cmH(2)O was conducted. For each patient, a 'best CPAP' level was defined as the one associated with the greatest IC. This pressure was then applied for an additional 10 min followed by spirometry. RESULTS: Following application of the 'best CPAP', the IC and SVC increased in 15 patients (nine emphysema, six chronic bronchitis). The mean change in IC was 159 mL (95% CI: 80-237 mL) and the mean change in SVC was 240 mL (95% CI: 97-386 mL). Among these patients, those with emphysema demonstrated a mean increase in IC of 216 mL (95% CI: 94-337 mL). Six patients (all with chronic bronchitis) did not demonstrate any improvement in IC. CONCLUSIONS: The best individualized CPAP can increase inspiratory capacity in patients with stable COPD, especially in those with emphysema.

I don't really need to explain these treatments. If you have been a paramedic for any period of time, you have probably created your own treatment routine for these patients. That's fine, this blog isn't trying to change that. I'm just giving you some tools to better understand each patient's physiological situation. This may assist you in making a better clinical decision in the future.

One thing I haven't mentioned yet is hypoxic drive. I will leave it to this great link, "The death of the hypoxic drive theory".

Ok, so that's all I have to say about the chronic lungers. In part 4 I am going to go over the main cardiac cause of rapid respirations, congestive heart failure.

Differential Dx: Tachypnea Part 2

In part 1 I discussed the possible causes of rapid respirations and the physiological need for CO2 to maintain acid-base balance. In this part, I plan to explain hyperventilation syndrome in detail and how to develop a differential diagnosis for these patients.

Developing a differential diagnosis for these patients is important. This isn't very hard to do but it may be something that was never taught to you in paramedic school. It is important because treating a patient with hypoxia as if they had hyperventilation syndrome could absolutely be causing more harm than good. Don't go into these calls just guessing as so many do.

So what is hyperventilation syndrome?

As classically defined, hyperventilation syndrome is a condition in which minute ventilation exceeds metabolic demands, resulting in hemodynamic and chemical changes that produce characteristic dysphoric symptoms. Inducing a drop in arterial pCO2 through voluntary hyperventilation reproduces these symptoms. Recently, however, this model has been challenged with the observation that many patients with hyperventilation syndrome do not manifest low arterial pCO2 levels during attacks. In some cases, patients with this syndrome have demonstrated altered respiratory physiology that is manifest as a slower return to baseline of the pCO2 after voluntary hyperventilation to a defined level of pCO2.
- eMedicine

Wow, okay now that we got through that I am going to explain what I am talking about a little better(well maybe not better, but definitely easier to understand).

Hyperventilation syndrome is a stress induced form of tachypnea. The rapid respirations are generally brought on by a stressful event or chronic stress that has just become too much. These rapid respirations cause the body to blow off too much CO2, and don't allow for adequate cellular respiration. This situation may be termed a "panic attack", and is most common, as you may have guessed, in people with a history of anxiety.

These patients tend to breath using their upper thorax and subsequently have hyperinflated lungs. This interferes with their tidal volume increasing dyspnea.

Here's the problem:

Although these rapid breathers will feel like they can't get enough air, the opposite is true. These patients will be retaining too much O2, and will have too little CO2 in their blood. This leads to respiratory alkalosis.

Fortunately, this problem usually doesn't kill people. In fact, I have never heard of a case where a patient died as a result of a panic attack. I guess they could be driving and end up in a deadly traumatic event, but you know what I mean. The reason they don't die is that they will usually end up passing out before their condition becomes deadly.

*The image above was borrowed from a stress treatment website.

I remember a call that I ran involving a more severe case of hyperventilation syndrome. The patient was a 19 year old female with a history of panic attacks. She was breathing about 40-50 times per minute upon arrival. I attempted to talk her down, which usually works for me, but to no avail. She ended up passing out. I figured this would be a good thing and she had just fixed herself. While she was unconscious her respirations returned to normal but the second she awoke, her rate was sky high once again. Her mother was contacted and she told us that the patient usually receives Ativan at the ER. I administered 5mg of Versed intranasal which helped us get her to the ambulance, and I received orders for 1mg of Ativan during transport.

So how did I know that she was having a hyperventilation crisis?

First, obtain a SAMPLE history(Hx):
S (signs/symptoms) - This will obviously include rapid respirations and possibly any of the following: Dizziness, parasthesia (tingling in hands and mouth), stiffness in fingers and hands, cold hands/feet, palpitations, or anxiety.

A(allergies) - Not relevant for inclusion criteria, but a good way to rule out anaphylaxis.
M (medications) - anxiety meds (ex. Xanax) will help for inclusion criteria, and lack of repiratory meds would help to rule out a chronic lunger(COPD/asthma patient).
P (past medical Hx) - Obviously anxiety or agorophobia would be inclusive, and the lack of chronic respiratory problems, recent surgeries, smoking, etc. would help rule out other issues.
L (last oral intake) - Another way to rule out possible allergic reaction and/or dehydration.
E (events leading up to) - Any stress induced event would be inclusive, usually emotional stress but physical stressors are a possibility.

Next, conduct an assessment:

Skin - pink, warm, & dry skin indicates hyperventilation syndrome. Cyanosis would indicate a more severe hypoxic situation.
Vitals - HR usually increased with hyperventilation syndrome. Initially increased with hypoxia then it may rapidly decrease. *SPO2 should be about 100%.

*The SPO2 finding is pretty important when differentiating hypoxia-induced tachypnea from hyperventilation syndrome. Because we are retaining too much O2 and not enough CO2, our O2 saturation should be 100% while our ETCO2 will decrease. This may be your most conclusive finding.

Above is an image from capnography.com which shows how hyperventilation will appear on wave form capnography. As respirations increase, CO2 output decreases. This results in smaller wave forms. Your readings will drop well below 35 mmHg.

So obviously it is not necessary to do all this just to decide if your patient is just hyperventilating. These are just some tools to assist you if you are having one of those tough cases. If your patient has a history of anxiety, 100% SaO2, and has clear breath sounds, they are probably just hyperventilating. Time to treat them, and this is another way to help you make your differential diagnosis. If they are refractory to your treatment, they may be having another issue. If they respond, abracadabra!

The best way to treat the majority of these patients will be firm instruction. I say firm, but that doesn't mean to be hostile. Be calm and explain the situation. It helps to have the patient rub their tingling/stiff hands on their legs while you instruct their breathing. Have them take a deep breath and hold it. Then have them exhale on your command and breath when you tell them to. It is also helpful if you tell them to breath from the belly. This may help them use their diaphragm more effectively. Stay away from deflated non-rebreathers and paper bags. We don't do that!

If the patient is in hyperventilation syndrome and does not respond to the above treatment, pharmaceutical therapy may be indicated. My protocol allows me to administer Versed for these patients. Any prehospital benzodiazepine would probably do pretty well.

More from eMedicine:

Because respiratory distress or chest pain has many potentially serious causes, this diagnosis should never be made in the field. Even when a patient carries a prior diagnosis of hyperventilation syndrome (HVS), it is still necessary to transport patients with these complaints to a hospital for a more complete evaluation. Rebreathing into a paper bag is not recommended in the field. Deaths have occurred in patients with acute myocardial infarction (MI), pneumothorax, and pulmonary embolism who were initially misdiagnosed with HVS and treated with paper bag rebreathing.

Okay, the talk down method and benzodiazepines will probably not harm these patients. I think eMedicine is stretching with the first statement. Putting them in the ambulance and driving is not a solution. We are clinicians and we have the ability to help these people. Treating paramedics like cab drivers is a result from the few bad apples in our field. We need to raise the bar for ourselves if we want the respect we deserve. I'm starting to rant here, so I am going to stop myself before I get too far off topic. Anyhow, treat these patients, please.

So that is hyperventilation syndrome. In part 3 I will explain other causes of rapid respirations.

Check out this video for simple treatment methods of hyperventilation.

Some other sources:

Differential Dx: Tachypnea Part 1

In the wide world of EMS calls we encounter a lot. The intent of this posting will be to differentiate and treat patient's with rapid respirations appropriately. This doesn't sound like a hard thing to do, but why not make it easier? If we treat the wrong patient the wrong way, we are effectively doing nothing to improve the patient's outcome.

As you read through these blog posts, you will notice quotes, videos, links, and research abstracts. This is just a way to let you know that the information is factual and not based on my own anecdotal evidence. It is my intention to spread the practice of evidence-based medicine amongst the world of prehospital clinicians. So lets get started...

You are dispatched to a 17 year old female complaining of difficulty breathing. Upon arrival you find a conscious patient with respirations at about 40 per minute. No audible wheezing or stridor. What do you do next?

This is a very frequent call type. A few things that stand out are the patient's young age and sex. This age coupled with the female gender may alert many that this could be something stress induced. This demographic is highly sensitive to relationship-induced stress. This is not a conclusive finding however, and we should always consider the worst. This patient also fits into a category of patient's that may take birth control. If she is on birth control and is a smoker, than she would be at increased risk of developing a pulmonary embolism.

To create a differential diagnosis, and treat this patient effectively, we need a clear understanding of what conditions may be causing her signs and symptoms. With this we can develop an adequate assessment to figure out what exactly is going on.

Causes of rapid respirations: there are tons but I'm going to list the most common
source: wrongdiagnosis.com, In a page: Signs & Symptoms, 2004
  • Cardiovascular etiologies (pulmonary embolism, CHF, AMI, HTN)
  • Pulmonary etiologies (COPD, asthma, pneumothorax, restrictive lung disease)
  • Metabolic/Toxicologic etiologies (DKA, dehydration, salicylate toxicity, acidosis)
  • Neurologic etiologies (CVA, head trauma)
  • Anxiety/Hyperventilation (panic attack)
  • Sepsis
  • Hyperthyroidism
  • Medications/Drugs

I like to place these patients in two, very basic categories:

Patient's that need O2
Patient's that need CO2

Now, I know that we don't give patient's CO2. That isn't what I am implying. Instead, I am referring to the body's physiological need to maintain a PH balance. CO2 is an essential ingredient to maintain homeostasis. I'll explain:

The image above describes where certain elements lie on the PH scale. It also explains that the lower the number, below 7, the more acidic something is. The higher the number, above 7, the more alkaline (basic) something is. Don't ask why the higher numbers are always on the bottom, maybe because that is considered the base, I dunno.

Normal PH for human blood is around 7.4. The common range used is 7.35 to 7.45.

Not on there is oxygen & carbon dioxide. It is important to know that
CO2 is acidic, and O2 is alkaline.

The healthy body will react according to the PH(depending on the amount) of what enters the body. The body uses it's metabolic and respiratory systems to assist in maintaing a normal acid-bas balance. Consequently, respiratory alkalosis will not appropriately fix metabolic acidosis, and visa versa; even though the body will sometimes try to attempt this type of regulation, it's a feeble attempt.

CO2 + H2O → H2CO3 → H+ + HCO3

When CO2 is disolved in water(H2O), carbonic acid (H2CO3) is formed. This prcoess is regulated by the respiratory and metabolic systems. Bicarobonate(HCO3-) and hydrogen (H+) can cause this effect in reverse. Take a look at this image.

It's not going to be the end of your career or anything if you don't memorize the equation. It is important, however, to remember that CO2 is a vital ingrediant to maintain homeostasis. This image describes how the buffering system works. The most basic thing we usually remember is that O2 is used by the body and CO2 is the waste product. Well, the hyperventilating patient teaches us something else. Some of that CO2 is needed!!

We have all seen the paper bag breathers. These people are attempting to rebreath their expired CO2 to self-regulate their CO2 level. This sounds like a good treatment and may even work.

In Part 2 I will describe why this isn't the best course of action. I will also give a detailed description of hyperventilation syndrome and how to develop a differential diagnosis.

If you have any questions or find something incorrect with the information I provide, please let me know.

GSW TO HEAD: To save or not to save

First let me explain why I even got this call. My lieutenant was having me meet him at our dispatch center, way out of our zone, so he could fix my key ring. Our narc keys are on a special ring which was damaged, and they have a special tool to fix it. So I was subject to calls out of our zone while on the way.

Medic 8 respond to possible suicide attempt.

Dispatch Notes
65 y/o male unconscious, breathing. GSW(gunshot wound) to the head.

We wait for the scene to be secured by law enforcement and head in. Of coarse the address we have is a little off, but we eventually locate the patient indicator lights (cop cars).

Scene Size Up
The patient is located supine, on the ground, just outside the driver-side door of his pickup truck. The police officer stated that he found a 0.22 caliber rifle about 5 feet away from the patient. The patient was found by a friend of his, and by our arrival the patient's adult son and daughter were both on scene. This road is on the patient's property.

Obvious hemorrhaging from the patient's head; unsure exactly where from. The patient was breathing about 8 to 10 times per minute with blood in his oropharynx. My first impression was to control the patient's airway. I have heard of the calls where the bullet misses the brain somehow. I do, however inspect for brain matter. The patient had an obvious skull fracture indicated by bilateral periorbital ecchymosis. The patient had a good radial pulse and HR of about 70. I called trauma alert.

Control the bleeding, get the patient packaged and into the ambulance. We needed room to work, and I didn't want to work this patient right in front of his family. As we are placing the patient on to a backboard I notice it, the wound was proximal to his frontal lobe, dead center of the forehead. We were assisting ventilations at the time via bag-valve mask. I noticed what appeared to be brain matter oozing from the wound. I had never seen brain matter before, and always thought it to be grey, but this was yellow. It was like slime, what else could it be?

At this point I had made the decision that this patient was obviously not going to make it. Our protocol states that if a patient has injuries incompatible with life, resuscitation is unnecessary. In addition, as we were rolling the stretcher towards our truck, the daughter stated that the patient has a DNR. I told her to get it, because we were going to need it.

This patient subsided rather quickly, leaving me with an uneasy feeling as I watched him die. I know the patient's outcome wasn't going to change. I took into consideration that the patient obviously didn't want to live, and this helped me cope with my decision.


By moving the patient to my ambulance, I successfully turned my rig into a crime scene. We had to await the medical examiner's arrival. Once there, he did in fact confirm the presence of brain matter.

Here's the unusual part. He identified the wound on the forehead as an entrance wound. I presumed that the blood in the mouth possibly indicated an entrance wound with the exit wound on the forehead. This meant possible homicide. Fortunately, with further examination, this was a confirmed suicide.

When the ME checked the patient's wallet, he identified the label "organ donor" on the patient's driver's license. This thought never entered my head. He was an old guy, and I didn't think anything would be viable. The ME explained how his kidneys and liver could have been used.

I will never forget this call. I think I did the right thing. I believe this is what the patient wanted, and I don't feel organ harvesting would have been appropriate. Guess that is a matter of opinion. What do you think?

*****Update May 4, 2009*****

A related study by American Surgery, Mar 2009
Gunshot wounds to the head are associated with poor outcome. We reviewed data to identify prognostic factors. We performed a retrospective study of all patients admitted to a Level 1 trauma center with isolated gunshot injury to the head during 6 1/2 years. Data collected included demographics, mechanism of injury, prehospital and resuscitation room data, and initial CT scan characteristics. The primary outcome measure was the Glasgow Outcome Scale. Seventy-two patients with isolated gunshot wounds to the head were admitted. Overall mortality was 58 per cent. The mortality for patients with an initial Glasgow Coma Scale score of < or =" 8"> 8 (P < or =" 0.0001)." p =" 0.06).">
*****End Update*****