Category: Airway

Topic: Respiratory Ilnesses and Disease

Level: EMR

32 minute read

Quick and Dirty Guide to Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease is a major health issue in the US, affecting as many as 1 in 4 Americans; initiating hundreds of thousands of 911 calls, annually. Predisposing factors contributing to the disease include smoking, environmental pollutants, industrial exposure, and other pulmonary infectious processes. The triad of chronic obstructive pulmonary diseases simply called COPD, includes asthma, bronchitis, and emphysema. Even though it is so commonly treated by EMS, there have been misconceptions created over the years concerning the initial treatment of COPD patients in the prehospital environment. Our failure to understand the different disease concepts involved can reduce our ability to identify and treat these patients, safely and effectively. It is important to know COPD inside and out; you will see it often.


Chronic Bronchitis "The Blue Bloater

Chronic bronchitis involves inflammatory changes with excessive mucus production in the bronchial tree. This disease is characterized by an increase in the number as well, as the size of the mucus producing glands resulting from prolonged exposure to inhalation irritants, mainly cigarette smoke. Most patients with bronchitis are aware of the disease and have been diagnosed previously. The patient's alveoli are not seriously affected and diffusion remains relatively normal. Patients with severe chronic bronchitis have low oxygen pressure (Po2), because of the changes in the ventilation-perfusion relationship in the alveoli. During a crisis, hypoventilation ensues, leading to high levels of carbon dioxide (CO2), known as hypercapnia and a low level of oxygen (O2), known as hypoxemia. There is also, a rise in arterial carbon dioxide pressure (Pco2). Patients with chronic bronchitis have frequent respiratory infections that eventually cause lung tissue scarring. In time, the scarring and other chronic changes cause irreversible damage to the lungs, leading to emphysema or bronchiectasis, an abnormal dilation of the bronchi, caused by pus producing infection of the bronchial wall.

medictests.com Q&D guide to COPD


Emphysema "The Pink Puffer"

Emphysema results from pathological changes in the lungs. It is the end stage of a degenerative process that progresses over the course of several years. The disease is characterized by permanent abnormal enlargement of the air spaces beyond the terminal bronchioles and the eventual collapse/destruction of the alveoli. The active disease process reduces the number and elasticity of the remaining functional alveoli, reducing the overall area for adequate gaseous exchange, leading to air trapping in the damaged alveoli. Therefore, the residual volume increases while the vital capacity remains somewhat normal.

The reduction in Po2 leads to an increased production of red blood cells; called Polycythemia. This elevation in hematocrit is much more common in the "Blue Bloater" than in the "Pink Puffer". This is mainly because patients with chronic bronchitis are more chronically hypoxemic. Decreases in alveolar surface area as well as, a significant decrease in pulmonary capillaries in the lungs, reduces the area available for adequate gas exchange. This, in turn, increases the resistance to pulmonary blood flow.

Patients with emphysema have some resistance to airflow in and out of the lungs. Yet, most of the hyperexpansion of the lungs is caused by air trapping, as previously mentioned. Patients with bronchitis have increased airway resistance during both the inspiration and expiration phase of respiration. The emphysemic patient will have increased airway resistance mainly on exhalation. In other words, they can get the air in but, have a significantly harder time getting it out.

Breathing is normally a passive, involuntary act but, with emphysema patients, expiration becomes a muscular act. Over time, the "Pink Puffer", will develop a rigid barrel-chested appearance and depend on muscles of the neck, chest, and abdomen to carry out the work of respiration. Full deflation of the lungs becomes more and more difficult, finally becoming impossible. Therefore, emphysemic patients will not only appear barrel-chested, but they are also often thin due to poor dietary intake and with the added work of respiration, they burn more calories than a non-COPD patient. Patients with emphysema often develop bullae (thin-walled cystic lesions in the lungs) from the destruction of the alveolar walls. When the bullae burst it increases the problems associated with air exchange and may cause spontaneous pneumothorax to develop.

A request for EMS assistance means that something has changed in the chronic condition. Don't underestimate patients with COPD, they will usually have an episode of acute dyspnea manifested at rest, an increase in mucus production, or an increase in the general malaise that accompanies the disease. These patients are already tired so, any worsening dyspnea can cause exhaustion and impending respiratory arrest, quickly! These patients will often give the EMS professional clues at first sight. They are often in severe respiratory distress, found sitting upright in a leaning forward in a tripoding position in an unconscious attempt to increase the ease of respirations. They may also be breathing through pursed lips; the bodies attempt to keep the collapsing alveoli open at the end of respiration.



Asthma also is known as a reactive airway disease, is a very common condition that is mostly seen in children, but many adults are affected as well. Children often outgrow the condition by early adulthood. While adults with asthma are normally afflicted for life. Asthma attacks generally occur in acute episodes of variable duration. The patients are symptom-free between episodes. The acute exacerbations are characterized by reversible airflow obstruction caused by bronchial smooth muscle contraction (bronchospasm); hypersecretion of mucus, resulting in bronchial plugging, and inflammatory changes in the bronchial walls. The increased resistance to airflow leads to alveolar hypoventilation, marked ventilation-perfusion mismatching (leads to hypoxemia) and carbon dioxide retention, which stimulates the body to increase respirations (hyperventilation). During an acute asthma attack, the combination of increased airway resistance, increased respiratory drive, and air trapping creates excessive demand on the muscles of respiration. This leads to greater use of the accessory muscles increasing the chance of respiratory fatigue and possible failure. If labored breathing continues, high pressure in the thorax can reduce the amount of blood returning to the left ventricle of the heart. This leads to a decrease in cardiac output and systolic blood pressure known as near-fatal asthma.
Most asthma-related deaths occur outside of the hospital. In the prehospital setting, cardiac arrest in patients with severe asthma has been linked to the following factors:

  • Severe bronchospasm and mucous plugging leading to asphyxia
  • Cardiac dysrhythmias caused by hypoxia
  • Tension pneumothorax, often bilateral

The severity of wheezing does not correlate with the degree of airway obstruction. The absence of wheezing may actually indicate a critical airway obstruction; whereas increased wheezing may indicate a positive response to therapy.

The asthma patients mental status is a good indicator of their respiratory efficiency. Lethargy, exhaustion, agitation, and confusion are all serious signs of impending respiratory failure. An initial history containing OPQRST/SAMPLE questions is crucial as well as, past episode outcomes (i.e., hospital stays, intubation, CPAP).
On auscultation of the asthmatic lungs, a prolonged expiratory phase may be noted. Wheezing is normally heard from the movement of air through the narrowed airways. Inspiratory wheezing does not indicate upper airway occlusion. It suggests that the large and midsized muscular airways are obstructed, indicating a worse obstruction than if only expiratory wheezes are heard. Inspiratory wheezes also indicate the large airways are filled with mucus.
A silent chest (i.e., no wheezes or air movement noted) may indicate a severe obstruction to the point of not being able to auscultate any breath sounds. Other significant signs and symptoms of asthma include:

  • Reduced level of consciousness
  • Diaphoresis/pallor
  • Sternal/intercostal retractions
  • 1 or 2 word sentences from dyspnea
  • Poor, flabby muscle tone
  • Pulse > 130 bpm
  • Respirations > 30 bpm
  • Pulsus Paradoxus > 20 mmHg
  • End-tidal CO2 > 45 mmHg


Asthma, Bronchitis, and Emphysema Management

All patients experiencing shortness of breath will receive oxygen. Much has been said over the years, and much misinformation exists, in reference to hypoxic drive and COPD patients. The axiom "All patients who need oxygen should receive it in the field" remains both accurate and a standard of care. 

  • Patients suffering from asthma should be treated quickly and aggressively with bronchodilating medications and oxygen. With known COPD history. 4-6 lpm O2 and monitor SpO2. If not or severe dyspnea administer 10 -15 lpm NRB to maintain a SpO2 >90
  • EMS should ask the patient or the patient’s family what medications the patient is prescribed, so that the patient is not over medicated or given a medication that his asthma is resisting.
  • Begin an IV of normal saline at a KVO rate mainly for medication administration. Fluid bolus is usually not indicated with asthma.
  • If the patient is moving an adequate volume of air:  Start a handheld nebulizer treatment using albuterol 2.5 mg with 6-10 lpm oxygen.
    If the patient is too tired to hold the nebulizer it can be connected to a non-rebreather mask with 12 -15 lpm oxygen. (check local protocol).
    (In the event the patient is not able to breathe deep enough to get the medication into the bronchioles then the patient’s respirations should be assisted with a BVM that has a nebulizer connected).
    It is important to note that the paramedic and the patient will have to work together since a breath must given by the medic at the same time that a breath is taken by the patient.
  • It is tempting in such situations to sedate and intubate the patient. If assisting respirations is not successful then Rapid Sequence Intubation (RSI) should be done but, if possible the patient should be allowed to remain conscious.
  • Non-invasive positive pressure ventilation (NPPV) is a way to provide a patient airway support without intubation.CPAP and BI-PAP are both forms of NPPV, that are being used to ventilate patients with COPD. NPPV is especially successful in cases of acute asthma. (check local protocol).
  • Since the patient is still conscious they are able to exhale with as much force as possible. This allows more of the inhaled medication to get into the lungs with deeper penetration into the lower airway where the medication may be needed most.
  • In patients who have been intubated, emptying of lungs is dependent on the elasticity of the lungs and ribcage.
  • In the event that the patient’s level of consciousness becomes decreased then intubation should be performed in order to improve the patient’s tidal volume and to protect the airway from aspiration. An intubated asthma patient should be given slow deep breaths.
  • The lungs should be kept inflated longer than normal to give oxygen and medication time to penetrate the mucus. A long expiration time should also be given to allow the lungs to empty. End-tidal monitoring is especially useful because you can see when the patient has stopped exhaling.
  • Caution should be used with patients who are intubated. Pneumothorax can occur whenever a PEEP valve is being used or when the patient is being aggressively ventilated. This is a particular concern when the lungs are already hyper distended and the treatment being given results in more distention then the pleural lining of the lungs can tolerate.
  • Keep in mind that “all that wheezes is not asthma”. In a patient with CHF and asthma, wheezing may just as easily be related to CHF as it is asthma.
  • In almost all cases the best treatment for the patient is prompt transport to the emergency department. More time spent in the field results in the options running out before you reach definitive care.
  • In severe cases where a long transport time is expected air transport should be considered.

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