Pressure in the Lungs and Pleural Cavity: Videos & Practice Problems

The lungs are elastic organs that change size in response to the thoracic cavity's movements. Despite their passive nature, they remain open due to a balance of inward and outward forces. The natural tendency of the lungs is to collapse, which can lead to conditions like a collapsed lung if these forces are not properly balanced.

Inward forces that contribute to lung collapse include elastic recoil and surface tension. The lungs contain collagen and elastin, proteins that provide structural support and elasticity. Collagen acts like a strong rope, while elastin behaves like a rubber band, always trying to return to its smallest size. Additionally, surface tension within the alveoli, caused by fluid covering their surfaces, tends to pull the alveoli together, further promoting lung collapse. This surface tension is mitigated by surfactant, a substance produced by the body that reduces surface tension, similar to how soap reduces tension in water.

On the other hand, outward forces help keep the lungs inflated. A key factor in this process is intrapleural pressure, which is the pressure within the pleural cavity surrounding the lungs. The pleural cavity consists of two membranes: the visceral pleura, which is attached to the lung, and the parietal pleura, which is attached to the chest wall. Between these membranes is a small amount of fluid that creates adhesion, allowing the lungs and chest wall to move smoothly against each other.

When the chest wall expands, it creates a negative pressure in the pleural cavity, akin to suction. This negative pressure resists the inward forces of elastic recoil and surface tension, preventing the lungs from collapsing. Essentially, as the chest wall pulls away from the lungs, the absence of air in the pleural cavity creates a vacuum effect, maintaining lung inflation. Thus, the balance of these forces is crucial for proper lung function and respiratory mechanics.

The lungs have a natural tendency to collapse due to various factors, and understanding these forces is crucial for grasping respiratory physiology. One significant contributor to this tendency is the surface tension in the alveoli. The alveoli are lined with a fluid, primarily water, which exhibits strong cohesive properties. This surface tension causes the alveolar walls to attract each other, thereby promoting lung collapse. Therefore, this factor is marked as c for contributing to the collapse of the lung.

In contrast, intrapleural pressure plays a vital role in resisting lung collapse. The pleural cavity, which surrounds the lungs, contains a negative pressure created by the visceral and parietal pleura being closely apposed. This negative pressure counteracts the natural tendency of the lungs to collapse, making it a significant factor in maintaining lung expansion. Thus, intrapleural pressure is marked as r for resisting collapse.

Another important factor is the pleural fluid found in the pleural cavity. This fluid helps keep the pleural membranes adhered to each other, similar to the effect of surface tension. By maintaining this adhesion, pleural fluid also contributes to resisting the tendency of the lungs to collapse, earning it an r designation.

The elastic recoil of the lungs is another factor that contributes to the collapse tendency. The lungs contain elastin, a protein that behaves like a rubber band, naturally wanting to return to a smaller size. This elastic recoil is a primary force driving the lungs toward collapse, thus it is marked as c.

Lastly, pulmonary surfactant is a substance that reduces the surface tension in the alveoli. By decreasing this tension, surfactant helps to prevent the alveoli from collapsing, making it a crucial factor in resisting lung collapse. Therefore, pulmonary surfactant is marked as r.

In summary, the interplay of these factors—surface tension in the alveoli and elastic recoil contribute to the lung's tendency to collapse, while intrapleural pressure, pleural fluid, and pulmonary surfactant work to resist this tendency. Understanding these dynamics is essential for comprehending how the lungs function effectively during respiration.

Understanding the pressures involved in lung function is crucial for grasping respiratory mechanics. There are three primary pressures to consider: atmospheric pressure, intrapulmonary pressure, and intrapleural pressure. Each of these pressures plays a significant role in the process of breathing and maintaining lung inflation.

Atmospheric pressure, denoted as P_ATM, refers to the pressure exerted by the weight of air in the atmosphere. At sea level, this pressure is approximately 760 millimeters of mercury (mmHg). This value serves as a standard reference point for comparing other pressures in the respiratory system. When discussing intrapulmonary and intrapleural pressures, we express their values relative to atmospheric pressure, using a scale where 0 indicates equality with atmospheric pressure, positive values indicate pressures above atmospheric, and negative values indicate pressures below it.

Intrapulmonary pressure, represented as P_PUL, is the pressure within the lungs, specifically in the alveoli. During normal breathing, at the end of inspiration and expiration, intrapulmonary pressure equals atmospheric pressure, thus it is typically expressed as 0. However, during the breathing cycle, this pressure can fluctuate slightly, varying by about ±2 mmHg. This fluctuation is essential for air movement into and out of the lungs.

In contrast, intrapleural pressure, denoted as P_IP, is the pressure within the pleural cavity surrounding the lungs. This pressure is always negative relative to intrapulmonary pressure, typically ranging from -4 to -6 mmHg. The negative pressure in the pleural cavity is crucial as it prevents lung collapse by counteracting the natural elastic recoil of the lungs. If intrapulmonary pressure were to equal intrapleural pressure, the lungs would begin to collapse, leading to inadequate ventilation.

In summary, the relationship between these pressures is vital for effective lung function. As long as intrapulmonary pressure remains greater than intrapleural pressure, the lungs will remain inflated, allowing for proper gas exchange and ventilation. Understanding these pressures and their interactions is fundamental for studying respiratory physiology and addressing potential respiratory issues.

Pneumothorax is a medical condition characterized by the presence of air in the pleural cavity, which can lead to the collapse of a lung. This can occur due to trauma, such as a stab wound, which compromises the pleural membrane and allows atmospheric air to enter the pleural space. Understanding the changes in pressure during this event is crucial for grasping the mechanics of respiration and lung function.

In a normal scenario, atmospheric pressure remains constant and does not change when a stab wound occurs. Therefore, the atmospheric pressure is categorized as no change. Intrapulmonary pressure, which is the pressure within the lungs and alveoli, typically equalizes with atmospheric pressure due to the open nature of the trachea. Consequently, intrapulmonary pressure also experiences no change when a stab wound occurs.

However, intrapleural pressure, which is the pressure within the pleural cavity, is normally negative. When air enters this cavity due to a stab wound, the pressure can equalize with atmospheric pressure, resulting in an increase in intrapleural pressure. This increase diminishes the negative pressure that normally helps keep the lung inflated, leading to lung collapse.

In summary, the presence of air in the pleural cavity disrupts the negative pressure that is essential for lung expansion. Without this negative pressure to counteract the natural recoil of the lung, the lung collapses. This phenomenon is sometimes referred to as a "sucking chest wound," as inhalation can draw air into the pleural cavity instead of the lungs, further exacerbating the collapse. Similar situations can arise from other injuries, such as broken ribs puncturing the lung, leading to pneumothorax.