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.
Treatment:
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.
1 comment:
As a person with chronic bronchitis, I carry an inhaler of Atrovent with me at all times. Due to a serious pharmaceutical mistake in the mid 1980s, I am very sensitive to Albuterol. If I am ever in an emergent situation, what would you use if Albuterol were off the table? Would it be my inhaler more often, or something in a nebulizer?
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