Chronic obstructive pulmonary disease: Clinical sciences

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Chronic obstructive pulmonary disease: Clinical sciences

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A 65-year-old man with a 40-pack-year smoking history presents to the primary care clinic with an 8-month history of progressively worsening shortness of breath, chronic productive cough, and wheezing. His past medical history is significant for hypertension. Temperature is 36.6°C (98.2°F), blood pressure is 109/72 mmHg, pulse is 98/min, respiratory rate is 22/min, and oxygen saturation is 90% on room air. On physical examination, he has diminished breath sounds and bilateral expiratory wheezing. Laboratory findings are unremarkable. Pulmonary function tests reveal an FEV1/FVC ratio of 0.55 with minimal reversibility after bronchodilator administration. Which of the following is most likely to decrease mortality in this patient?  

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Chronic Obstructive Pulmonary Disease or COPD, is a condition characterized by progressive airflow obstruction resulting in chronic respiratory symptoms. This can occur due to airway inflammation, like in chronic bronchitis, or because of alveolar wall destruction, as in emphysema.

Tobacco use is the leading cause of COPD, while less commonly it is due to secondhand smoke or environmental exposures, or hereditary causes like alpha-1 antitrypsin deficiency.

Based on history findings, some patients can present with a new diagnosis of COPD, while others can present with a positive history of COPD and clinical manifestations. The clinical manifestations can range from mild COPD exacerbation to complicated COPD, such as severe COPD exacerbation, bacterial pneumonia, pulmonary hypertension, and even acute respiratory failure.

Now, if you suspect COPD, perform an ABCDE assessment to determine if your patient is unstable or stable. If the patient is unstable look for alarm signs and symptoms, history might suggest worsening dyspnea and an increased production of purulent sputum, while physical exam typically reveals rapid shallow breathing, decreased breath sounds, use of accessory respiratory muscles like the scalenes and intercostals, and even cyanosis. Pulse oximetry may reveal hypoxemia. In this case you’ll need to begin acute management.

First stabilize the airway, breathing, and circulation, which may require noninvasive or invasive mechanical ventilation, as well as obtaining IV access and starting continuous vital sign monitoring.

Ok, let’s return to the ABCDE assessment. If the patient is stable, obtain a focused history and physical examination. These patients typically report symptoms like increased cough, change in sputum production, and shortness of breath, and will usually have a history of smoking, second hand smoke exposure, or exposure to another occupational or environmental irritant.

Physical exam often reveals wheezing, hypoxemia, tachypnea, tachycardia, prolonged expiration, and diffusely decreased breath sounds.

These findings are suggestive of COPD, so you should assess the history for an existing diagnosis of COPD.

If their history is negative, meaning there is no previous diagnosis of COPD, you should still suspect COPD, and perform spirometry tests including calculating the FEV1 to FVC ratio to confirm the diagnosis.

FVC, or forced vital capacity, is the maximum amount of air a person can forcibly exhale from their lungs after a maximum inhalation, while FEV1 is the volume of air exhaled during the first second of this forced exhalation.

Here’s a clinical pearl: Spirometry can be performed with a simple handheld spirometer. First, administer a bronchodilator, like albuterol, to your patient. Then, they’ll take a maximal breath in, then forcibly exhale into the spirometer until all of the air is emptied from their lungs.

This will help differentiate between restrictive and obstructive patterns of lung disease, as well as define key values used to grade disease severity and define treatment.

Now that you’ve completed spirometry, calculate the patient’s FEV1 to FVC ratio. If the ratio is greater than 0.7, consider an alternative diagnosis. On the other hand, if the ratio is less than 0.7, the diagnosis of COPD is confirmed.

Next, assess the FEV1 value to determine the Global Initiative for Obstructive Lung Disease or GOLD staging. If FEV1 is 80% of normal or more, your patient is at GOLD stage 1, the mildest stage of COPD.

This is treated with inhaled bronchodilators, starting with short acting beta-agonists, or SABAs for short, or short acting muscarinic antagonists, also known as SAMAs, as needed for dyspnea and wheezing. However, if the frequency of bronchodilator use is increasing, switch to or add a long-acting beta agonist, or LABA, or a long-aging muscarinic agonist, or LAMA to gain better control of symptoms.

In addition to pharmacologic therapy, all patients diagnosed with COPD should be counseled on lifestyle modifications like smoking cessation and increasing physical activity, and receive yearly influenza and pneumococcal vaccinations.

On the other hand, if FEV1 is less than 80% of predicted, then your patient has at least GOLD stage 2 disease, which indicates more advanced COPD. These patients should be started on a LABA or LAMA as initial therapy, or you may use both, depending on symptom severity, as well as a SABA as needed.

If the patient has GOLD stage 3 or 4 disease, or if respiratory symptoms persist despite their current regimen, then other agents, including inhaled corticosteroids, phosphodiesterase-4 or PDE-4 inhibitors, macrolide antibiotics, antioxidants, xanthines, and even biologics can be added to your patient's regimen on an individualized basis. In addition to pharmacologic therapy, counsel these patients on lifestyle modifications and yearly influenza and pneumococcal vaccinations.

As a clinical pearl, remember that patients with stable COPD should have formal assessment of GOLD grade and stage, which is based on their airflow obstruction, symptoms, and exacerbation risk; the specific classification has important treatment implications.

Sources

  1. "Clinical Aspects of Chronic Obstructive" Update
  2. "Chronic Obstructive Pulmonary Disease: An Overview" NCBI
  3. "Pathogenesis of chronic obstructive pulmonary disease (COPD) induced by cigarette smoke. Sep; 1(7): 34–42." J Pulm Respir Med. (2008)
  4. "Pathogenesis of chronic obstructive pulmonary disease (COPD) induced by cigarette smoke" JTD