Properties of Lung Tissue

Physical Factors Influencing Pulmonary Ventilation

As we have seen, the lungs are stretched during inspiration and recoil passively during expiration. The inspiratory muscles consume energy to enlarge the thorax. Energy is also used to overcome various factors that hinder air passage and pulmonary ventilation. These factors are listed below.

1. Airway Resistance

The major nonelastic source of resistance to gas flow is friction, or drag, encountered in the respiratory passageways. The relationship between gas flow (F), pressure (P), and resistance (R) is given by the following equation:  

Flow = P/R

Notice that the factors determine gas flow in the respiratory passages and blood flow in the cardiovascular system are equivalent. The amount of gas flowing into and out of the alveoli is directly proportional to ΔP, the difference in pressure, or the pressure gradient, between the external atmosphere and the alveoli. Normally, very small differences in pressure produce large changes in the volume of gas flow. The average pressure gradient during normal quiet breathing is 2 mm Hg or less, and yet it is sufficient to move 500 ml of air in and out of the lungs with each breath.

But, as the equation also indicates, gas flow changes inversely with resistance. That is, gas flow decreases as resistance increases. As with the cardiovascular system, resistance in the respiratory tree is determined mostly by the diameters of the conducting tubes. However, as a rule, airway resistance is insignificant for two reasons:

1.   Airway diameters in the first part of the conducting zone are huge, relative to the low viscosity of air.

2.   As the airways get progressively smaller, there are progressively more branches. As a result, although individual bronchioles are tiny, there are an enormous number of them in parallel, so the total cross-sectional area is huge.

Hence, as shown in the greatest resistance to gas flow occurs in the medium-sized bronchi. At the terminal bronchioles, gas flow stops and diffusion takes over as the main force driving gas movement, so resistance is no longer an issue.

HOMEOSTATIC IMBALANCE

Smooth muscle of the bronchiolar walls is exquisitely sensitive to neural controls and certain chemicals. For example, inhaled irritants activate a reflex of the parasympathetic division of the nervous system that causes vigorous constriction of the bronchioles and dramatically reduces air passage. During an acute asthma attack, histamine and other inflammatory chemicals can cause such strong bronchoconstriction that pulmonary ventilation almost completely stops, regardless of the pressure gradient. Conversely, epinephrine released during sympathetic nervous system activation or administered as a drug dilates bronchioles and reduces airway resistance. Local accumulations of mucus, infectious material, or solid tumors in the passageways are important sources of airway resistance in those with respiratory disease.

Whenever airway resistance rises, breathing movements become more strenuous, but such compensation has its limits. When the bronchioles are severely constricted or obstructed, even the most magnificent respiratory efforts cannot restore ventilation to life-sustaining levels.  

Alveolar Surface Tension

At any gas-liquid boundary, the molecules of the liquid are more strongly attracted to each other than to the gas molecules. This unequal attraction produces a state of tension at the liquid surface, called surface tension, that (1) draws the liquid molecules closer together and reduces their contact with the dissimilar gas molecules, and (2) resists any force that tends to increase the surface area of the liquid.

Water is composed of highly polar molecules and has a very high surface tension. Because water is the major component of the liquid film that coats the alveolar walls, it is always acting to reduce the alveoli to their smallest possible size. If the film was pure water, the alveoli would collapse between breaths. But the alveolar film contains surfactant (ser-fak′tant), a detergent-like complex of lipids and proteins produced by the type II alveolar cells. Surfactant decreases the cohesiveness of water molecules, much the way a laundry detergent reduces the attraction of water for water, allowing water to interact with and pass through fabric. As a result, the surface tension of alveolar fluid is reduced, and less energy is needed to overcome those forces to expand the lungs and discourage alveolar collapse. Breaths that are deeper than normal stimulate type II cells to secrete more surfactant.

When too little surfactant is present, surface tension forces can collapse the alveoli. Once this happens, the alveoli must be completely reinflated during each inspiration, an effort that uses tremendous amounts of energy. This is the problem faced by newborns with infant respiratory distress syndrome (IRDS), a condition peculiar to premature babies. Since inadequate pulmonary surfactant is produced until the last two months of fetal development, babies born prematurely often are unable to keep their alveoli inflated between breaths. IRDS is treated with positive-pressure respirators that force air into the alveoli, keeping them open between breaths. Spraying natural or synthetic surfactant into the newborn’s respiratory passageways also helps.

Many IRDS survivors suffer from bronchopulmonary dysplasia, a chronic lung disease, during childhood and beyond. This condition is believed to result from inflammatory injury to respiratory zone structures caused by use of the respirator on the newborn’s delicate lungs.  

Lung Compliance

Healthy lungs are unbelievably stretchy, and this distensibility is referred to as lung compliance. Specifically, lung compliance (CL) is a measure of the change in lung volume (ΔVL) that occurs with a given change in the transpulmonary pressure [Δ (Ppul – Pip)]. This is stated as 

The more a lung expands for a given rise in transpulmonary pressure, the greater its compliance. Said another way, the higher the lung compliance, the easier it is to expand the lungs at any given transpulmonary pressure.

Lung compliance is determined largely by two factors: 
(1) distensibility of the lung tissue, and
(2) alveolar surface tension. 
Because lung distensibility is generally high and alveolar surface tension is kept low by surfactant, the lungs of healthy people tend to have high compliance, which favors efficient ventilation.

Lung compliance is diminished by a decrease in the natural resilience of the lungs. Chronic inflammation, or infections such as tuberculosis, can cause non-elastic scar tissue to replace normal lung tissue (fibrosis). Another factor that can decrease lung compliance is a decrease in production of surfactant. The lower the lung compliance, the more energy is needed just to breathe.

Since the lungs are contained within the thoracic cavity, we also need to consider the compliance (distensibility) of the thoracic wall. Factors that decrease the compliance of the thoracic wall hinder the expansion of the lungs. The total compliance of the respiratory system is comprised of lung compliance and thoracic wall compliance.

Deformities of the thorax, ossification of the costal cartilages (common during old age), and paralysis of the intercostal muscles all reduce total respiratory compliance by hindering thoracic expansion.

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