Introduction
This paper aims at evaluating concepts of alteration in homeostatic state, secondary to temporal variables. It analyses the case study of Brad, a 45-year old coal cutter who has held the job for 25 years. Brad is experiencing a chronic cough due to prolonged exposure to coal. Importantly, he has not been attending yearly checkups because he fears that his lung is “black.” The disease leads to fibrosis, reduced diffusing ability, and dilation of the small airways. In the final stage, the airways, alveoli, and pulmonary capillaries become damaged.
How the disease described in the case study creates incongruous between ventilation and perfusion
Chronic lung disease may induce mismatch in ventilation and perfusion if the alveolar and circulatory tissues are damaged. The imbalance between the perfusion and ventilation impacts the concentration of CO2 and O2 in the blood and alveoli during inhalation and exhalation. Importantly, the mismatch causes depression in the arterial PO2 since blood flow is affected at the apical parts of the lung.
Dead space is the amount of air which is inhaled, but not utilized in gas exchange due to poorly perfused alveoli or nonfunctional capillaries. There is anatomical and physiological dead space. The anatomical dead space is the part of airways which supplies gas to the alveoli including the trachea. Notably, the gaseous exchange does not take place in this part. The anatomical dead space traps gas during each inspiration, but the air is exhaled in the same state. Hence, if the tidal volume is approximately 500ml, close to 30 percent of the inhaled gas does not take part in gaseous exchange (Kim, Jung, and An, 2012). Even though the trachea is relatively flexible, the anatomical dead space remains unchanged. Physiological dead space comprises both the anatomical and alveolar dead space. In healthy persons, the alveolar dead space is small due to sufficient perfusion, but the dead space tends to increase due to conditions such as chronic lung disease. An increase in the dead space decreases the gas exchange surfaces, which consequently results in a reduction of O2 and increase in CO2 in the body (Smolka, Borkowski, and Zaton, 2014). The chronic lung disease causes a physiological shunt. Ideally, the physiological shunt reduces ventilation but has no effect on perfusion. The result is incongruous between ventilation and perfusion and impact on gas exchange.
Why people with Chronic Obstructive Pulmonary Disease (COPD) have difficulties exhaling than inhaling
Airway obstruction is low when one is inhaling due to the elastic characteristics of the lung. During the process of inhalation, the elastic fibers continually pull airways open with the expansion of the thoracic cage. On the other hand, during the process of exhalation, the natural contraction of the lung tissues causes the passages to narrow.
According to Grossman and Mattason (2013), COPD is characterized by persistent obstruction of air flow in the pulmonary airways. Most individuals who suffer from COPD may have damaged air sacs, which limits the amount of oxygen in the body. Other breathing problems associated with COPD include a chronic cough and coughing mucus.
Chronic bronchitis and emphysema are the two major breathing conditions related to COPD. These two diseases primarily occur together, and their primary cause is smoke such as exposure to coal cutting as described in the case study. Notably, it is challenging to differentiate the diseases, but both have similar treatment approaches.
Emphysema
Emphysema is a condition whereby the alveoli get damaged. This disease occurs in several steps. First, the walls of the alveoli get inflamed and defaced (Eugenio, 2014). With time, the alveoli lose their elastic nature (shrink and stretch) and bullae develop in the injured parts. Next, bullae obstruct the natural functions of the lungs by contracting the airways, snaring air, and causing difficulties in breathing. Evidently, Emphysema does not impact the breathing process during the initial stages. However, the disease affects the breathing system adversely during its late stages.
Chronic bronchitis
Chronic bronchitis manifests itself through excessive mucus and coughing (Jindal and Vijayan, 2013). The disease exhibits the following features. The bronchial tubes get inflamed resulting in the production of mucus. The mucus consequently blocks the airways leading to difficulties in breathing. Ideally, when a patient who has chronic bronchitis coughs, they remove the mucus. Persistent inflammation and coughs may destroy the bronchial tubes. Importantly, the airways bulge and condense, reducing the space for air flow.
Most importantly, COPD is associated with Emphysema and Chronic Bronchitis that contracts the size of the airways increasing resistance. The result is difficulties in exhalation and easy inhaling.
The mechanism in lung disease that can impact the diffusing ability across alveolar membranes – Fick law
The Fick law holds that the amount of air passing athwart the alveolar membranes at a particular time is proportionate to the negative pressure variance of the subject air, the diffusion coefficient and the surface area of the membranes (Mark, 2012). Importantly, air transmission is inversely proportionate to membranes thickness. Lung diseases like chronic bronchitis expand the alveoli walls. As the thickness of the membranes increase, the diffusing ability across the alveolar membranes declines. The mechanisms of lung disease that impact diffusing ability through the alveolar membranes include
Thickening of the alveoli membranes
Lung disease increases the thickness of the alveoli membranes which decreases the diffusing ability of air. A condition such as an edema fluid in alveolar is a critical condition that increases the membrane's thickness. Increased thickness also increases resistance in the airways.
Decreasing the surface area of the alveolar membranes
Notably, some lung diseases may damage the alveolar. For instance, Emphysema causes the alveoli to condense consequently reducing the surface area. A reduction in the surface area will limit the size of the membrane that is in direct contact with gas resulting to reduced gas diffusion.
Conclusion
Chronic lung disease is a primary cause of mismatch between ventilation and perfusion. The mismatch happens due to damage of the alveolar whereby the concentration of CO2 and O2 in the body is impacted. Lung disease also affects both the anatomical and physiological dead space. In a healthy individual, the dead space is negligible; however, in persons with lung disease, the size is relatively large. Physiological shunt also develops due to lung disease, and it decreases ventilation. These factors increase the amount of CO2 in the body.
Individuals who suffer from COPD have more challenges exhaling than inhaling since the disease blocks the airways. Chronic bronchitis and emphysema (conditions associated with COPD) increase difficulties in breathing. These diseases damage the alveoli by causing inflammation, bullae and other defects that result in breathing problems.
The Fick law holds that air diffusion is inversely proportionate to membranes thickness. Lung disease mainly thickens the alveolar membranes impacting the ability of air diffusion. Other lung disease mechanisms that affect capacity to diffuse across the alveolar membrane include reduced surface area and formation of bullae in the alveoli.
References
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Jindal, S. K., & Vijayan, V. K. (2013). World clinics: Pulmonary & critical care medicine - chronic obstructive pulmonary disease: Volume 2. India: Jaypee Brothers Medical Publishers.
Mark, H. H. (2012). Armand Imbert, Adolf Fick, and their tonometry law. Eye, 26(1), 13-16.
Kim, S., Jung, K., & An, T. (2012). Effects of tidal volume and PEEP on arterial blood gases and pulmonary mechanics during one-lung ventilation. Journal Of Anesthesia, 26(4), 568-573.
Smolka, L., Borkowski, J., & Zaton, M. (2014). The Effect of Additional Dead Space on Respiratory Exchange Ratio and Carbon Dioxide Production Due to Training. Journal Of Sports Science & Medicine, 13(1), 36-43.
