Air in and out of the lungs: pressure causes the movement of air

2021-02-08 12:00 AM

Pleural pressure is the pressure of fluid in the thin cavity between the visceral pleura and the parietal pleura. This pressure is normally slightly aspirated or slightly negative.

The lungs are a ball-like elastic structure that expels all the air through the trachea where there is no force to keep it from expanding. Lungs and chest wall are not joined together, except for the hilum with the mediastinum, the middle segment of the thoracic cavity. The lungs are surrounded by a thin layer of pleural fluid, which helps the lungs move smoothly in the chest.

In addition, the continuous suction of excess fluid into the lymphatic canal maintains a slight suction between the visceral leaf of the pleura and the parietal leaf of the thoracic cavity. From there, the lungs are stored in the chest wall as if there were glue there, except that they are well lubricated and can slide freely when stretching or contracting the chest wall.

Pleural pressure and its changes in respiration

Pleural pressure is the pressure of fluid in the thin cavity between the visceral pleura and the parietal pleura. This pressure is normally slightly aspirated or slightly negative.

Normally the pleural pressure at the beginning of the inhalation is about -5cmH2O, which is the amount needed to keep the lungs open. In the normal inhalation test, the chest cavity expands the lungs with greater force and creates negative pressure, averaging about -7.5 cmH2O. The relationship between pleural pressure and the change in lung volume is shown in Figure 38-2. the negative pressure in the pleural space decreases from -5 to -7.5 cmH2O during inhalation and lung volume increases by 0.5 litres. Then, while breathing out is the opposite.

Alveolar pressure - The air pressure inside the alveoli

When the glottis is open and there is no air entering or leaving the lungs, the pressure in all parts of the respiratory tree, all alveoli, is in equilibrium with atmospheric pressure, equal to 0 cmH2O.

Figure. Changes in lung volume, alveolar pressure, pleural pressure, and trans-pulmonary pressure during normal breathing.

Air can flow into the inner alveoli on inhalation because the pressure in the alveoli has to drop to a value below atmospheric pressure (below 0). Curve 2 (label “alveolar pressure”) Figure shows that with normal inhalation, alveolar pressure drops to -1cmH2O. This gentle negative pressure was enough to pull 0.5 litres of air into the lungs for 2 seconds during gentle normal inhalation. During exhalation, alveolar pressure is raised to approximately + 1cmH2O.

Spreads air out of the lungs for 2-3 seconds with each exhalation.

Pulmonary pressure - The difference between alveolar and pleural pressure

The figure shows the pleural pressure as the differential pressure between the alveoli and the outer surface of the lung (pleural pressure) and it is measured by the elastic force of the lung towards the hilum during each respiration, called elastic pressure.

Lung suitability

The dilatation of the lungs causes each unit of the lung to expand, increasing the trans-pulmonary pressure (if enough time is allowed to reach equilibrium) is known as lung dilation. The sum of all pulmonary dilation in the normal adult averages approximately 200 ml air / cmH2O of transpulmonary pressure. That means each time the pulmonary pressure increases by 1 cmH2O, the lung volume after 10-20s will expand by 200ml.

The proper expansion of the lung

The figure shows the relationship between the change in lung volume and the change in pleural pressure. Note that this association is different in inhalation and exhalation. Each curve is recorded by a small incremental change in pleural pressure and allows the lung volume to change step by step between successive steps. Two separate curves, the curvature of the expansion of the lungs, are inhaled and exhaled. And the total graph is called the expansion graph of the lung. The characteristic of this plot is determined by the elasticity of the lung. This elasticity can be divided into 2 parts:

(1) Lung elasticity.

(2) Pulmonary elasticity is caused by the surface tension of the fluid inside the alveolar wall and the air space.

Figure. Adaptation scheme of the lungs in a healthy person. This diagram shows the changes in lung volume during a change in pressure in the lung (alveolar pressure minus pleural pressure).

The elastic force of lung tissue is determined mainly by elastin and collagen fibres intertwined in the lung parenchyma. When the lungs collapse, these fibres contract and curl. Then, as the lungs relax, these fibres become tense and non-curl, elongating, and creating elastic force.

Elastic force is caused by surface tension. The significance of the elastic force is shown in the figure, compared with the graph of the expansion of the lungs when filled with saline and when filled with air. When the lungs are filled with air, there is a common surface between the alveolar fluid and the air in the alveoli. But with the lungs filled with saline, there is no common surface, so there is no presence of surface tension. Note that the pressure through the lungs requires the lungs dilated by air 3 times greater than lungs filled with saline solution. Therefore, this force of tissue elasticity towards the collapse of the air lung corresponds to about 1/3 of the total elasticity of the lung, the surface tension between the fluid-gas in the alveoli accounts for 2/3. The fluid-gas surface tension increases greatly if no substance known as surfactant is present in the alveolar fluid.

Figure. Compare the adaptive scheme of fluid-filled and air-filled lungs when alveolar pressure is maintained at atmospheric pressure (0 cm H2O) and pleural pressure is changed for pressure changes in the lungs.

Surfactant, surface tension and collapse of the alveoli

When water is in contact with air, the water molecules on its surface are strongly attracted to each other. As a result, the surface of the water shrinks, squeezing together like a drop of water

The membrane shrinks slightly of water molecules like the surface of the water droplet. Now let's reverse this and see what the inner surface of the alveoli plays out.

Here, the water surface also tries to shrink. This results in the force to push air from the alveoli to the bronchi, causing atelectasis. This network exerts the elastic force of the entire lung, called the elastic force of the surface tension.

Surfactant and its effect on surface tension

Surfactant is a surfactant in water, ie it reduces the surface tension of the water. It is secreted by type II alveolar epithelial cells, which occupy 10% of the alveolar surface area. These small cells contain lipids. Surfactants are complex blends of different phospholipids, proteins, and ions. The most important components of are phospholipid dipalmitoylphosphatidylcholine, surfactant apoprotein and Ca ion. Dipalmitoyl phosphatidylcholine and other important phospholipids are important roles in reducing surface tension. They do this by not dissolving in the alveolar lining. Instead, part of the molecules decomposes while the remainder spreads into the surface of the water in the alveoli. This surface accounts for between 1/12 and of the surface tension of pure water. Surface tension varies between different types of water:

Surface tension causes pressure in the alveoli

If the air leading from the alveoli is blocked, the surface tension in the alveoli is directed toward atelectasis. This collapse causes positive pressure in the alveoli, which expels air. The amount of pressure generated in the alveoli in this way can be calculated using the formula:

Pressure = 2 x surface tension / alveolar radius

The average size of the alveoli is about 100micrometers in diameter and lined with a normal surfactant, calculating a pressure of about 4cmH20 (3mmHg). If the alveoli are lined with purified water without any surfactant, the total pressure can be about 18cmH2O, with pressure 4.5 times. Thereby we see the importance of reducing the alveolar surface tension of surfactant and reducing the support of respiratory muscles to relax the lungs.

The effect of the alveolar radius on pressure caused by surface tension

Note from the formula, the pressure generated from the surface tension in the alveoli acts inversely to the alveolar radius, meaning that if the alveoli are smaller than the alveolar pressure caused by the surface tension is greater. Therefore, when the alveoli are reduced in radius to half as usual (50 instead of 100micrometers), the pressure doubles. This phenomenon is a special signal in preterm infants, many of whom have an alveolar radius of only compared with adults. In addition, surfactant does not secrete normally until between 6 and 7 months of pregnancy, in some cases even later. Consequently, premature infants have little or no surfactant in the alveoli while they live, and their lungs are extremely prone to collapse. What causes this condition is respiratory distress syndrome in newborn babies. It is pregnant if left untreated, especially with continuous positive pressure breathing.


Pathophysiology of cardiogenic shock

Urine formation: Reabsorbed glomerular filtration

Mechanism of urine concentration: osmotic pressure changes in different segments of the renal tubule

Absorption and excretion of potassium through the kidneys

Prothrombin activation: initiates blood clotting

Pulmonary capillary dynamics: capillary fluid exchange and pulmonary interstitial fluid dynamics

Graphical analysis of high-volume heart failure

Calculate the glomerular filtration rate (GFR): the forces that cause the filtration process

Estimated renal plasma flow: PAH clearance

Nephron: The functional unit of the kidney

Reduced sodium chloride, dilates arterioles, increases Renin release.

Ammonia buffering system: excretes excess H + and creates new HCO3

Red blood cells: differentiation and synthesis

Concentrated urine formation: urea contributes to increased osmotic pressure in the renal medullary

Extracellular fluid distribution between interstitial space and blood vessels

The proximal tubule reabsorption: active and passive reabsorption

Origin of lymphocytes: the body's resistance to infection

The endocrine regulates tubular reabsorption

Acidosis causes a decrease in HCO3- / H + in renal tubular fluid: compensation mechanism of the kidney

Sodium channel blockers: decrease the reabsorption of sodium in the manifold

Physiological anatomy of the kidneys and urinary system

Self-regulation of glomerular filtration rate and renal blood flow

Pathophysiology of fever

The kidneys excrete sodium and fluid: feedback regulates body fluids and arterial pressure

Iron metabolism: haemoglobin synthesis