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Writer's pictureJason Hewitt

COPD

COPD


COPD is an umbrella term used to describe patients with the 2 most common obstructive lung diseases; Emphysema, and Chronic Bronchitis. Both of these illnesses are primarily attributed to exposure to tobacco smoke. Other causes can exist, such as toxic exposures, or the rare alpha-1 anti-trypsin disorder, however most patients with COPD are either active smokers, or former ones. In cases where a patient does not have a formal diagnosis of COPD, but has hallmark signs and symptoms, a 20 pack-year history of smoking is often sufficient to treat them as having COPD.


COPD Pathophysiology:


Emphysema:

In the case of emphysema, exposure to cigarette smoke causes damage to the bronchial walls and the walls of the alveolar septa. There is destruction of the elastic tissue in the alveolar walls, leading to loss of surface area for gas exchange, hyper-inflated alveoli, and collapse of the small airways during exhalation. Air trapping becomes a major problem for these patients, as exhalation becomes an active process, requiring accessory muscle use. As a result of increased energy expenditure during respiration, these patients frequently have a higher caloric expenditure and trouble maintaining their weight. Impaired gas exchange means they also retain higher levels of CO2 in the bloodstream.


Chronic Bronchitis:

Exposure to cigarette smoke over a prolonged period leads to hyperplasia (increase in the size and number) of mucous producing goblet cells in the bronchial tree. There is also significant inflammation of the airways themselves, similar to that seen in asthma. These patients also have difficulty getting air out, and tend to retain higher than normal levels of CO2 in the bloodstream.


COPD patients have a chronic issue with gas exchange, as they are able to move air into the lungs, but cannot easily get it out. This causes chronically elevated CO2 levels in the blood, and may lead to a hypoxic drive. Hypoxic drive occurs when the medulla, which usually triggers respiration in response to elevated PaCO2, raises the threshold. Meaning that blowing off excess CO2 can actually cause respiratory depression. The ideal target SPO2 for a COPD patient is 88-92%. This helps avoid this phenomena. Most COPD patients call 911 due to sudden worsening of symptoms in response to an infection. As infection triggers a fever, body temp rises. This rise in core temperature leads to increased metabolic oxygen demand. A healthy person could compensate, but a COPD patient is unable to do so and may be in respiratory distress. This is known as a COPD exacerbation. Other common causes include: abnormal amounts of exercise, hot environments, and exposure to allergens or irritants.


Common pharmacological treatments include:

 -Beta 2 agonists: Trigger bronchodilation by stimulating beta 2 adrenergic receptors.


 -Epinephrine: Stimulates rapid bronchodilation in severe asthma. Also mediates the

inflammatory effect of histamines, and overrides parasympathetic bronchoconstriction caused

by stimulation of cholinergic receptors.

-Anticholinergic medications: Block parasympathetic bronchoconstriction, and inhibit mucous

production in the bronchioles.


-Corticosteroids: Act to inhibit the inflammatory process and reduce swelling in the airways.


Prehospital treatment:


In the case of COPD exacerbations, we generally treat as follows:


-Ensure a patent and protected airway

-Provide supplemental O2 if indicated, or initiate PPV based on patient presentation

-Ensure pulses, cap refill, and skin colour/condition do not indicate a circulatory issue

-Provide Beta 2 agonist if indicated

-Provide corticosteroid if indicated

-Initiate CPAP/BIPAP if indicated

- Perform a 12 lead ECG to rule out cardiac issues associated with the patient’s dyspnea

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