COPD CXR with Bullae Emphysema

Emphysema is a subtype of chronic obstructive pulmonary disease (COPD). Along with chronic bronchitis and chronic obstructive asthma, these lung conditions typically present with airflow limitations.1 COPD is the fourth leading cause of death in the United States, killing more than 120,000 people each year. The World Health Organization (WHO) estimates suggest that emphysema will become the third most common cause of death worldwide this year.2

Emphysema can be diagnosed when the lungs have abnormal enlargement of the air spaces distal to the terminal bronchioles with destruction of their walls and a lack of signs of fibrosis.3 This alveolar level is where the gas exchange takes place. Obvious clinical findings are hypoxemia and hypercapnia. Less obvious discoveries include uneven distribution of ventilation throughout the lung, referred to as heterogeneous spatial distribution of emphysema. This uneven distribution is of great concern when applying any form of positive pressure ventilation (PPV) to this patient population.

Typically, patients with emphysema have good lung compliance but exhibit poor lung elastance. In short, compliance is the measurement of the lungs’ ability to expand, while elastance is the ease at which the lungs return to its starting point of inflation. The increase in compliance is because of the lungs’ parenchymal destruction and decrease in their elastic nature. Elastance is the reciprocal of compliance. Some examples of patients with poor lung compliance would be Acute Respiratory Distress Syndrome, pulmonary fibrosis, asthma exacerbation. The important thing the remember is that applying CPAP or BiPap to the patient with emphysema to improve his hypoxemia could quite possibly cause harm because of this uneven distribution of positive pressure. The flow/pressure delivered to the patient is going to find the areas of the lung with better compliance and, quite possibly, over-distend those areas of the lung.

Emphysema is usually the result of long-term smoking, but it’s important to note that not everyone with emphysema has a smoking history. People with a disorder called Alpha-1 antitrypsin deficiency may exhibit signs of emphysema. The deficiency comes from mutations of the gene SERPINA1. Alpha-1 antitrypsin protects the body from a powerful enzyme called neutrophil elastase, which helps fight infection but can also attack the body’s tissue if it is not controlled by Alpha-1 antitrypsin. Other names for this form of emphysema are genetic emphysema, hereditary pulmonary emphysema, and Alpha-1 protease inhibitor deficiency.

CT scan showing signs of Bullae emphysema

The typical picture of emphysema includes shortness of breath, chronic cough, mucous production, wheezing, diminished or absent breath sounds, ongoing fatigue, cyanosis, barrel chest, accessory muscle use, tripoding, cor pulmonale, jugular vein distention, elevated pulmonary artery pressures, peripheral edema, and chronic lung infections. Further evaluation and diagnostic testing include chest x-ray, and pulmonary function testing to evaluate the disease as restrictive (decreased airflow) or obstructive (disruption of airflow) and to determine the severity of the process. Arterial blood gases may be drawn to determine any imbalance in pH because of hypercarbia as well as to assess the actual degree of hypoxemia. High-resolution computed tomography can identify emphysema-related changes. An echocardiogram may be warranted to further evaluate cardiac involvement.

It is important to gather as much information as possible when formulating a plan of care for this patient population. Smoking history is a good place to start; it is typically measured in packs/years. For example, if the patient states he smokes a pack a day for 50 years, he is a 50- pack/year smoker. In one study, the best variable for predicting airflow obstruction was people who classified as 40 pack/year smokers or greater. Other data suggest that the duration of smoking may be a greater risk for COPD than the number of packs smoked per day.4 A person who never smoked but lived or worked in an environment with second-hand smoke or heavy air pollution may end up with emphysema damage to the lungs.

Another important assessment detail is use of oxygen at home. Typically, home oxygen concentrators can provide up to 6 liters per minute (lpm). If more is required, he can be operated on in tandem setups. Also, it helps to determine what medications the patient is using and how often. The majority of these people will be on long- and short-acting beta agonists for bronchodilation along with some form of inhaled corticosteroid for the inflammation process. More often, when transporting these patients, we may have to administer a cocktail of a beta-2 agonist and an anticholinergic through a nebulizer (DuoNeb). Intravenous magnesium sulfate has shown positive results in the patient with asthma exacerbation, but studies of IV magnesium sulfate in the COPD population are relatively small and routine use is not recommended. One study showed nebulized ipratropium bromide as clearly effective and superior to magnesium sulfate.5

If a patient you are transporting requires PPV, it is important to remember the potential damaging effects this may have on a patient with severe COPD. I learned a valuable lesson a few years back on a hospital rapid response team that was called to a patient’s room who was in respiratory distress 20 minutes after receiving his scheduled nebulizer treatment. I walked in the room and he immediately failed the “look test”; he was on a 6-lpm nasal cannula and his pulse oximetry read 82 percent with a good waveform. He was tachycardic and tachypneic and had BiPap written all over his face.

My first reaction was to grab a BiPap machine and place him on it while titrating pressures and FiO2 as needed. Fortunately, I paused long enough to pull up his chart and investigate his history. In digging through the massive amount of information I found, he had end-stage COPD with severe emphysema and was on 6-lpm nasal cannula at home with a baseline saturation of 90 percent (with the oxygen). His CT scan showed bullae emphysema, which is characterized by large air spaces in the lung formed from damaged alveoli. If I had applied too much positive pressure to this patient, it would have created deleterious effects. I quickly placed the patient on a NRB mask and decided to go get a high-flow nasal cannula to supplement his increased work of breathing and his oxygen requirement.

When caring for the patient with suspected COPD, obtain as much information as possible before formulating a plan of action. History and physical exam should precede any form of PPV. We should always “tune up” the lungs in concert with our strategy. Patient safety comes first, followed by patient comfort and synchrony with any device applied to help supplement ventilation and oxygenation. When caring for the emphysema patient population, I often refer to the much-misunderstood phrase “primum non nocere.”

References

  1. Chronic obstructive pulmonary disease: Definition, clinical manifestations, diagnosing, and staging up to date (2020).
  2. NCBI emphysema.
  3. Hess, DR. “Respiratory care principles and practice.” Jones and Bartlett. pg. 802
  4. Chronic obstructive pulmonary disease: Definition, clinical manifestations, diagnosing, and staging up to date (2020).
  5. Ann Thorac Med. 2014 Apr-Jun; 9(2): 77–80.

About the Author(s)

Michael Schauf, RRT-NPS, has been a Registered Respiratory Therapist at Albany Medical Center Hospital in New York since 1994. He covers all in-patient units, ICUs, the adult and pediatric Emergency Departments and is a member of the neonatal/pediatric transport team at this Level I Trauma and Level 3 NICU Center. Michael is the founder of Vent-Pro Training, teaching medics and nurses around the world how to manage mechanically ventilated patients during ground, rotor, and fixed-wing transports. He has been a flight respiratory therapist since 1998, currently working for AirMed and as a Clinical Education Specialist for AMR. Michael authored the respiratory chapter of, “Critical Care Transport, 2nd edition,” published by Jones & Bartlett and is an adjunct instructor in the Respiratory Care Program at Hudson Valley Community College.