PHYSIOLOGY OF BREATHING

BIOMECHANICS OF RESPIRATORY ACT.

Lungs ventilation

I. Common characteristic of breathing. The respiratory system is divided into a respiratory zone, which is the site of gas exchange between air and blood, and a conducting zone, which conducts the air to the respiratory zone. The exchange of gases between air and blood occurs across the walls of tiny air sacs called alveoli, which are only a single cell layer thick to permit very rapid rates of gas diffusion.

The term respiration includes three separate but related functions: (1) ventilation (breathing); (2) gas exchange, which occurs between the air and blood in the lungs and between the blood and other tissues of the body; and (3) oxygen utilization by the tissues in the energy – liberating reactions of cell respiration. Ventilation and the exchange of gases (oxygen and carbon dioxide) between the air and blood are collectively called external respiration. Gas exchange between the blood and other tissues and oxygen utilization by the tissues are collectively known as internal respiration.

Ventilation is the mechanical process that moves air into and out of the lungs. Since the oxygen concentration of air is higher in the lungs than in the blood, oxygen diffuses from air to blood. Carbon dioxide conversely moves from the blood to the air within the lungs by diffusing down its concentration gradient. As a result of this gas exchange, the inspired air contains more oxygen and less carbon dioxide than the expired air. More importantly blood leaving the lungs (in the pulmonary veins) has a higher oxygen and lower carbon dioxide concentration than the blood delivered to the lungs in the pulmonary arteries. This result bring the fact that lungs function is to give gaseous equilibrium between blood and the air.

 

Main process of the external respiration. The passage air respiratory systems are divided into two functional zones. The respiratory zone is the region where gas exchange occurs, it includes the respiratory bronchioles (which contain separate outpouchings of alveoli) and the terminal cluster of alveolar sacs.

Gas exchange between the air and blood occurs entirely by diffusion through lung tissue. This diffusion occurs very rapid because there is a large surface area within the lungs and a very short diffusion distance between blood and air.

Phases of respiratory act. Inspiration & Expiration

Pulmonary ventilation consists of two phases: inspiration and expiration. Inspiration (inhalation) and expiration (exhalation) are accomplished by alternately increasing and decreasing the volume of the thorax and lungs.

The thorax must be sufficiently rigid so that it can protect vital organs and provide attachments for many short and powerful muscles. Breathing, or pulmonary ventilation, requires the flexibility of the thorax to function as a bellow during the ventilation cycle. The rigidity and the surfaces for muscle attachment are provided by the bony composition of the rib cage. The rib cage is pliable, because the ribs are separate from one another and most of the ribs (upper ten of the twelve pairs) are attached to the sternum by resilient costal cartilages. The vertebral attachments also provide considerable mobility. The structure of the rib cage and associated cartilages provides continuous elastic tension, so that after stretched by muscle contraction during inspiration, the rib cage can return passively to its resting dimension when the muscles relax. This elastic recoil is greatly aided by the elasticity of the lungs.

Respiratory muscles cause passage of air into the Lung. Between the bony portions of the rib cage are two layers of intercostals muscles: the external intercostal muscles and internal intercostal muscles. Between the costal cartilages, there is only one muscle layer, which its fibers oriented in the same manner to those of the internal intercostal muscle. These muscles may called as the interchondral part of the internal intercostal muscle or parasternal intercostal muscle..

 

An unforced, or quiet, inspiration primarily results from contraction of the dome– shaped diaphragm, which become lowered and flattened. This increases thoracic volume in a vertical direction. Inspiration is also aided by the parasternal and external intercostal muscles, which raise the ribs when they contract and increase thoracic volume laterally. Other thoracic muscles involved in forced (deep) inspiration. The most important of these is the scalenus muscle, followed by the pectoralis minor muscle, and in extreme cases the sternocleidomastoid muscle. Contraction of these muscles elevates the ribs in an anteroposterior direction; simultaneously, the upper rib cage is stabilized so that the intercostal muscles become more effective.

Mechanism of normal quiet inspiration and expiration. Quiet inspiration is an active process. The contraction of the inspiratory muscles and diaphragm increases intrathoracic volume. This stretch the thorax and lungs. Quiet expiration is a passive process. The thorax and lungs recoil when the respiratory muscles relax. due to their elastic tension

 

Control of Bronchial Tone

The walls of bronchi and bronchioles contain smooth muscle and they are innervated by the autonomic nervous system. In general, sympathetic discharge via Beta-2-adrenergic receptors causes the bronchi to dilate and parasympathetic discharge via the vagus nerves causes them to constrict.. It may be similar to the intrinsic enteric nervous system in the gastrointestinal tract and there is evidence that VIP (Vasoactive intestinal polypeptide) is the mediator secreted by its neurons.

The function of the bronchial muscles is still a matter of debate, but in general, they probably help to maintain an even distribution of ventilation. They also protect the bronchi during coughing. There is a circadian rhythm in bronchial tone, with maximal constriction at about 6 A.M and maximal dilatation at about 6 P.M. Thats why the asthma attacks are more severe in the late night and early morning hours, pi–stimulants such as isoproterenol are effective in asthma because they mimic the effects of sympathetic stimulation. Cooling the airways causes bronchoconstriction, and exercise triggers asthmatic attacks because it lowers airway temperature.

Lung Volumes. The amount of air that moves into the lungs with each inspiration (or the amount that moves out, with each expiration) is called the tidal volume. The air inspired with a maximal inspiratory effort in excess of the tidal volume is the inspiratory reserve volume. The volume expelled by an active expiration effort after passive expiration is the expiratory reserve volume, and the air left in the lungs after a maximal expiratory effort is the residual volume. Normal values for these lung volumes, and names applied to combinations of them, are shown in Fig. 43-1.

 

1. Tidal volume (TV), 2. Inspiratory reserve volume (IRV). 3. Expiratory reserve volume (ERV). 4. Vital capacity (VC).

Figure. Lung volume and some measurements related to the mechanics of breathing. The diagram at the upper right represent the excursions of a spirometer plotted against time.

The space in the conducting zone of the airways occupied by gas that does not exchange with blood in the pulmonary vessels is the respiratory dead space. The vital capacity, the greatest amount of air that can be expired after a maximal inspiratory effort, is frequently measured clinically as an index of pulmonary function. The fraction of the vital capacity expired in 1 second (timed vital capacity; also called forced expired volume in 1 second, or FEV I”) gives additional valuable information. The vital capacity may be normal but the timed vital capacity can be greatly reduced in diseases such as asthma, in which the resistance of the airways is increased due to bronchial constriction. The amount of air inspired per minute (pulmonary ventilation, respiratory minute volume) is normally about 6 L (500 ml/breath x 12 breaths/min). The maximal voluntary ventilation (MVV), or, as it was formerly called, the maximal breathing capacity, is the largest volume of gas that can be moved into and out of the lungs in 1 minute by voluntary effort. The normal MVV is 125-170 L/min.

Effects of Gravity on the Lung. Because of gravitational forces,the pressure gradient present. Intrapleural pressure at the bases of the lungs is 5 mm Hg greater than at the apexes. Consequently, the transmural pressure (the difference between intrapulmonary and intrapleural pressure) may become negative at the end of forced expiration, causing airways to close. For the same reason, more of the gas inspired during the first part of inspiration goes to the apexes than to the bases.

Gravity also affects the pressure in the pulmonary blood vessels.Dead Space &Uneven Ventilation. Since gaseous exchange in the respiratory system occurs only in the terminal portions of the airways, the gas that occupies the rest of the respiratory system is not available for gas exchange with pulmonary capillary blood. Thus, in a man who weighs 68 kg, only the first 350 ml of the 500 ml inspired with each breath at rest goes through gaseous exchange in the alveoli. Conversely, with each expiration, the first 150 ml expired is the gas that occupied the dead space, and only the last 350 ml is from the alveoli.

It is wise to distinguish between the anatomic dead space (respiratory system volume exclusive of Alveoli) and the total (physiologic) dead space (volume of gas which do not equilibrate with blood and air, e.g waste ventilation). In health, the 2 dead spaces are identical. In disease states that may be no exchange of gas between the alveoli and the blood, and some of the alveoli may be overventilated. The volume of gas in nonperfused alveoli and any volume of air in the alveoli in excess of that necessary to arterialize the b1ood in the alveolar capillaries is part of the dead space (no equilibrating) gas volume. The anatomy dead space can be measured by analysis of the single breath N₂ curves. From mid inspiration,the subject take a deep breath as possible of pure O₂, then exhales steadily while the N₂ content of the expired gas is continuously measured. The initial gas exhaled (phase I) is the gas that filled the dead space and that consequently contains no N₂.

Alveolar Ventilation. Because of the dead space, the amount of air reaching the alveoli (alveolar ventilation) at a respiratory minute volume of 6 L/min is 500 minus 150 ml times 12 breath/min, or 4.2 L/min. because of the dead space, rapid, shallow respiration produces much less alveolar ventilation than slow, deep respiration at the same respiratory minute volume (Table 43-2).

Table 43-2. Effect of variations in respiratory rate and depth on alveolar ventilation.

 

 

 

During quiet breathing, the intrapleural pressure, which is about – 2.5 mm Hg (relative to atmospheric) at the start of inspiration, decreases to about — 6 mm Hg, the lungs are pulled into a more expanded position. and the pressure in the airway becomes slightly negative, which cause the  air flows into the lungs. At the end of inspiration, the lung recoil pulls the chest back to the expiratory position, where the recoil pressures of the lungs and chest wall become balance. At this time, the pressure in the airway becomes slightly positive, and air flows out of the lungs. Expiration during quiet breathing is passive because no muscles contract which decrease intrathoracic volume. However, there is some contraction of the inspiratory muscles in the early part of expiration. This contraction exerts a braking action on the recoil forces and slows expiration.

Mechanism forced ventilation. Strong inspiratory efforts reduce the intrapleural pressure value as low as —30 mm Hg, producing correspondingly greater degrees of lung inflation. When forced ventilation is increased, the extent of lung deflation is also increased by active contraction of expiratory muscles that decrease intrathoracic volume.

Movement of the diaphragm accounts for 75% of the change in intrathoracic volume during quiet inspiration. This muscle attached around the bottom of the thoracic cage, and it arches over the liver and moves downward like a piston when it contracts.

The other important inspiratory muscles are the external intercostals muscles, which run obliquely downward and forward from rib to rib. The ribs pivot as if hinged at the back, so that when the external intercostals contract they elevate the lower ribs. This pushes the sternum outward and increases the anteroposterior diameter of the chest. The transverse diameter is actually changed little if at all. Either the diaphragm or the external intercostals muscles alone can maintain adequate ventilation at rest. Transaction of the spinal cord above the third cervical segment cause fatal without artificial respiration, but transaction below the origin of the phrenic nerves that innervate the diaphragm (third to fifth cervical segments) is not fatal; conversely, in patients with bilateral phrenic nerve palsy, respiration is somewhat labored, but adequate to maintain life. The scalene and sternocleidomastoid muscles in the neck are accessory inspiratory muscles that they help to elevate the thoracic cage during deep labored respiration.

A decrease in intrathoracic volume and forced expiration result when the expiratory muscles contract. The internal intercostals have this action because they pass obliquely downward and posterior from rib to rib and therefore pull the rib cage downward when they contract. Contractions of the muscles of the anterior abdominal wall also aid expiration by pulling the rib cage downward and inward and by increasing the intraabdominal pressure, which pushes the diaphragm upward.

Change of pressure in pleural cavity in correlation from phases of respiratory act. The lungs and the chest wall are elastic structures. Normally, there is no more than a thin layer of fluid between the lungs and the chest wall. The lungs slide easily on the chest wall but resist being pulled away from it in the same way as 2 moist pieces of glass slide on each other but resist separation. The pressure in the “space” between the lungs and chest wall (intrapleural pressure) is sub atmospheric. The lungs are stretched when they are expanded at birth, and at the end of quiet expiration their tendency to recoil from the chest wall is just balanced by the tendency of the chest wall to recoil in the opposite direction. If the chest wall is opened, the lungs will collapse; and if the lungs lose their elasticity, the chest expands and becomes barrel-shaped.

Movement of blood on venous in correlation from phases of respiratory act.

Contraction of the diaphragm during inhalation also improves venous return. As the diaphragm contracts, it lowers to increase the thoracic volume and decrease the abdominal volume. This creates a partial vacuum in the thoracic cavity (negative intrathoracic pressure) and a higher pressure in the abdominal cavity. The pressure difference thus produced favors blood flow from abdominal to thoracic veins. 

Change of pressure in alveoli. The respiratory muscles cause pulmonary ventilation by alternatively compressing and distending the lungs, which in turn causes the pressure in the alveoli to rise and fall. During inspiration the intra-alveolar pressure becomes slightly negative with respect to atmospheric pressure, normally slightly less than -1 mm Hg, and this causes air to flow inward through the respiratory passageways. During normal expiration, on the other hand, the intra-alveolar pressure rises to slightly less than +1 mm Hg, which causes air to flow outward through the respiratory passageways. Note that, how little pressure is required to move the air into and out of the normal lung, though in most of the time, much pressure is required in some types of lung diseases.

During maximum expiratory effort (with the glottis closed )the intra-alveolar pressure can be increased to as much as 140 mm Hg in the strong, healthy man, and during maximum inspiratory effort it can be reduced to as low as -100 mm Hg.

Recoil Tendency of the Lungs, and the Intrapleural Pressure. The lungs have a continual elastic tendency to collapse and therefore to pull away from the chest wall. This is called the recoil tendency of the lungs, and it is caused by two different factors. First, throughout the lungs are many elastic fibers that are stretched by lung inflation and therefore attempt to shorten. Second, and even more important, the surface tension of the fluid lining the alveoli also causes a continual elastic tendency for the alveoli to collapse. This effect is caused by intermolecular attraction between the surface molecules of the alveolar fluid. That is, each molecule pulls on the next one so that the whole lining sheet of fluid on the alveolar surfaces acts like many small elastic balloons continuously trying to collapse the lung.

Ordinarily, the elastic fibers in the lungs account for about one third of the recoil tendency, and the surface tension phenomenon accounts for about two thirds.

The total recoil tendency of the lungs can be measured by the amount of negative pressure in the pleural space required to prevent collapse of the lungs; this pressure is called the pleural pressure or, occasionally, the lung recoil pressure. It is normally about – 4 mm Hg. This negative pressure (-4 mm Hg) on the outer surfaces of the lungs is required to keep them expanded to normal size. When the lungs are stretched to very large size, such as at the end of deep inspiration, then the pleural pressure required may be as great as -12 to -18 mm Hg.

“Surfactant” in the alveoli, and its effect on the collapse tendency.

A lipoprotein mixture called “surfactant” is secreted by special surfactant-secreting cells (the “type II granular pneumocytes“) which are the component parts of the alveolar epithelium. This mixture, containing especially the phospholipids dipalmitoyl lecithin, decreases the surface tension of the alveolar fluid lining. In the absence of surfactant, lung expansion is extremely difficult, which often requires negative pleural pressures as low as – 20 to – 30 mm Hg to overcome the collapse tendency of the alveoli. This illustrates that surfactant is exceedingly important for minimizing the effect of surface tension which cause the collapse of the lungs.