Case Study: Structure and Function of the Respiratory System

Case Study: Structure and Function of the Respiratory System

Effective management of a chronic respiratory condition like Pneumoconiosis depends on one’s knowledge base about the disease. In essence, this discussion seeks to explain the predisposing factors and the associated pathophysiological changes of this disease. Central to the attainment of this purpose is the case study of Brad, a 45-year-old male client working in a coal mine. The likely diagnosis of Brad is Pneumoconiosis. Such is the case given his occupation and chronic coughing manifestation that is common among the coal workers(Linton, 2012).

Predisposing Factors

The severity and occurrence of this chronic respiratory condition are dependent on certain factors. Examples befitting of such factors that are central to this case study include gender and temporary factors such as the length of exposure to coal.

To begin with, the gender of Brad is crucial in the initiation of pneumoconiosis. According to Linton, (2012) the male gender is a risk factor for Pneumoconiosis. Such is the case given the increased likelihood of male individuals to engage in this type of occupation. The same applies to Brad whose is gender is that of the males.

On the other hand, the length of exposure and type of occupation is to blame for his current affliction. Brad has been working the coal mine for an extended period (25 years). As such is a risk candidate of the pneumoconiosis because he has had exposure for an extensive period. Furthermore, the occupation alone is a vital factor that can predispose the individual to this respiratory disorder (Linton, 2012). Thus, the presence of these two factors in this scenario puts it beyond doubt that Brad’s likely diagnosis is pneumoconiosis.

Pathophysiological Changes

Of significance to the comprehension of the pathophysiology of Pneumoconiosis are three aspects, which are under scrutiny in this section.

Ventilation and Perfusion (V/Q) Mismatch

Ventilation is the process of breathing in and out to facilitate gaseous exchange while perfusion refers to the blood entry into the tissues, in this case, the pulmonary tissues. Primarily, V/Q relates to the total amount of oxygen that reaches the alveoli divided by the total amount of blood flowing through the pulmonary capillaries of the lungs. In a normal healthy state, the ventilation and perfusion rates remain proportion. However, in unhealthy conditions, the ventilation and perfusion rates are subject to change.  V/Q mismatch is the term commonly used to refer to this change (Petersson & Glenny, 2014). Central to understanding the reason for the V/Q mismatch in this condition are two basic physiological adaptations, namely alveolar dead space and physiological shunt.

Alveolar dead space refers to all alveoli that participate in gaseous exchange but are devoid of blood flow (Petersson & Glenny, 2014). In disease conditions such the pneumoconiosis, alveolar dead space increases due to the fibrosis of the pulmonary capillaries and destruction of the alveoli. Consequently, this results in V/Q mismatch.

On the other hand, physiological shunting refers to the process in which there is redirection of blood flow away from a particular area of the lung that has inadequate ventilation. In this case, there is adequate perfusion with limited or no ventilation. A typical example of such a process is in lung disease where there is a destruction of the lung tissues. For instance, it is common in COPD and conditions like pneumoconiosis (Pinsky, 2012).

Concisely, the V/Q mismatch is because of the increased alveolar dead space and physiological shunting that are characteristic of this condition.

Difficulty in Exhaling than Inhaling in COPD

Critical to this difficulty when breathing out and not in inhalation are two factors. Primarily, in COPD, the individual finds it hard to exhale because he/she experiences narrowing of the airways, which results in airflow resistance causing a labored breathing. Typically, the lung parenchyma is essential for ensuring that the airway opens to allow exhalation. However, in this case, the lungs are not in the right shape to facilitate the process of opening the airways due to the emphysema. Moreover, the narrowing is also due to the chronic inflammation of the airways secondary to bronchitis. Thus, an individual has to put up with a forced expiration (Voelkel & MacNee, 2014).

Of the interest to the also to this subject is the loss of lung elastic recoil. Lung recoil refers to the ability of the lungs to assume their original shape soon after inhaling and exhaling. The elastin collagen fibers in the lungs are essential in the attainment of this purpose. However, in COPD, there is disruption of this function leading to the impairment of this equilibrium effect. Ultimately, the individual develops exertion dyspnea because of this disruption (Voelkel & MacNee, 2014).

Mechanisms affecting Diffusion Capacity across Alveolar Membranes

Diffusion property of a gas refers to the ability of the gas to cross across a membranous structure, in this case, alveolus, from regions of high concentration to areas of low concentration. In respiration, gaseous exchange utilizes this form of movement to reach the intended tissues. According to Fick’s law, the volume of a gas diffusing across the alveolar membrane in a fixed timeframe is directly proportional to its partial pressure, surface area and diffusion coefficient as well as inversely proportional to the membrane thickness. The thickness and surface area of the tissue are dependent on the anatomy of an individual (Rhoades & Bell, 2013).

Concerning this scenario, this means that the membrane thickness and surface area are among the crucial factors that are impairing the ventilation process of this patient. Such is the case since pneumoconiosis results to an in increase the thickness of the alveolar membrane through the destruction of the alveoli structure. Consequently, there is a massive reduction in the quantity of gas moving across the membrane because of the increased thickness (Rhoades & Bell, 2013).

Similarly, in pneumoconiosis, the surface area of the tissue membrane decreases due to the increased destruction of the alveoli and lung tissues. Ultimately, this significantly reduces the quantity of gas diffusing across the membrane because of the direct proportionality relationship that they share (Rhoades & Bell, 2013).


Indeed, from the above discussion, understanding a disease like pneumoconiosis is of the essence to its management since it entails a lot, which if left uncovered can lead to the formulation of an incorrect diagnosis. Thus, to avoid such instances, it is prudent to devote time to establishing such truths as they are of the essence in preventing, diagnosing and treating it. Failure to do so, however, will only lead to improper management of patients of this kind.

















Linton, A. (2012). Introduction to medical-surgical nursing (1st ed.). St. Louis, Mo.: Elsevier Saunders.

Petersson, J. & Glenny, R. (2014).Gas exchange and ventilation-perfusion relationships in the lung. European Respiratory Journal44(4), 1023-1041.

Pinsky, M. (2012). Applied physiology in intensive care medicine (1st ed.). Heidelberg: Springer.

Rhoades, R. & Bell, D. (2013). Medical physiology: Principles for clinical medicine (1st ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.

Voelkel, N. & MacNee, W. (2014). Chronic obstructive lung diseases (2nd ed.). Shelton: PMPH USA.



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