00:00 / 00:00
Apnea of prematurity
Acute respiratory distress syndrome
Pulmonary changes at high altitude and altitude sickness
Congenital pulmonary airway malformation
Superior vena cava syndrome
Meconium aspiration syndrome
Neonatal respiratory distress syndrome
Sudden infant death syndrome
Transient tachypnea of the newborn
Alpha 1-antitrypsin deficiency
Idiopathic pulmonary fibrosis
Restrictive lung diseases
Retropharyngeal and peritonsillar abscesses
Upper respiratory tract infection
Apnea, hypoventilation and pulmonary hypertension: Pathology review
Cystic fibrosis: Pathology review
Deep vein thrombosis and pulmonary embolism: Pathology review
Lung cancer and mesothelioma: Pathology review
Obstructive lung diseases: Pathology review
Pleural effusion, pneumothorax, hemothorax and atelectasis: Pathology review
Pneumonia: Pathology review
Respiratory distress syndrome: Pathology review
Restrictive lung diseases: Pathology review
Tuberculosis: Pathology review
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Part 2 - Living with Emphysema
COPD & Emphysema
emphysema p. 694
emphysema p. 728
activity in emphysema p. 694
α1 -antitrypsin deficiency p. 399
compliance in p. 685
diffusion in p. 686
diffusion-limited gas exchange p. 686
elastin in p. 50
panacinar p. 400
presentation p. 728
emphysema p. 694, 728
Emphysema means “inflate or swell”, which makes sense because in the lungs of people with emphysema, the alveolar air sacs, which are the thin walled air spaces at the ends of the airways where oxygen and carbon dioxide are exchanged, become damaged or destroyed.
The alveoli permanently enlarge and lose elasticity, and as a result, individuals with emphysema typically have difficulty with exhaling, which depends heavily on the ability of lungs to recoil like elastic bands.
Emphysema’s actually lumped under the umbrella of chronic obstructive pulmonary disease (or COPD), along with chronic bronchitis.
The two differ in that chronic bronchitis is defined by clinical features, like the productive cough, whereas emphysema is defined by structural changes, mainly enlargement of the air spaces.
That being said, they almost always coexist, probably because they share the same major cause—smoking.
With COPD, the airways become obstructed, the lungs don’t empty properly, and that leaves air trapped inside the lungs.
For that reason, the maximum amount of air people with COPD can breath out in a single breath, known as the FVC, or forced vital capacity, is lower.
This reduction is especially noticeable in the first second of air breathed out in a single breath, called FEV1—forced expiratory volume (in one second), which typically is reduced even more than the FVC.
A useful metric therefore is the FEV1 to FVC ratio, which, since the FEV1 goes down even more than FVC, causes the FEV1 to FVC ratio to go down as well.
Alright so say normally your FVC is 5 L, and your FEV1 is 4 L, your FEV1 to FVC ratio would end up being 80%.
Now, someone with COPD’s FVC might be 4 L instead, which is lower than normal, but the volume of air that he or she can expire in the first second is only 2 L, so not only are both these values lower, but their ratio is lower as well—and this is a hallmark of COPD.
All that had to do with air breathed out right? Conversely, for air going in, the TLC, or total lung capacity, which is the maximum volume of air that can be taken in or inspired into the lungs, is actually often often higher because of the air trapping.
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