Mechanism of Breathing

During breathing, air moves into the lungs from the nose or mouth (called inspiration, or inhalation), and then moves out of the lungs during expiration, or exhalation. A free flow of air from the nose or mouth to the lungs and from the lungs to the nose or mouth is vitally important. Therefore, a technique has been developed that allows physicians to determine if there is a medical problem that prevents the lungs from filling with air upon inspiration and releasing air from the body upon expiration. An instrument called a spirometer records the volume of air exchanged during normal breathing and during deep breathing. A spirogram shows the measurements recorded by a spirometer when a person breathes as directed by a technician (Fig. 14.6).

Respiratory Volumes

Normally when we are relaxed, only a small amount of air moves in and out with each breath. This amount of air, called the tidal volume, is only about 500 ml.
It is possible to increase the amount of air inhaled, and therefore the amount exhaled, by deep breathing. The maximum volume of air that can be moved in plus the maximum volume that can be moved out during a single breath is the vital capacity. It is called vital capacity because your life depends on breathing, and the more air you can move, the better off you are. A number of different illnesses, can decrease vital capacity.

Vital capacity varies by how much we can increase inspiration and expiration over the tidal volume amount. We can increase inspiration by not only expanding the chest but also by lowering the diaphragm. Forced inspiration usually increases the volume of air beyond the tidal volume by 2,900 ml, and that amount is called the inspiratory reserve volume. We can increase the amount of air expired by contracting the abdominal and internal intercostal muscles. This so-called expiratory reserve volume is usually about 1,400 ml of air. You can see from Figure 14.6 that vital capacity is the sum of the tidal, inspiratory reserve, and expiratory reserve volumes.

Figure 14.6 Vital capacity. A spirometer measures the amount of air inhaled and exhaled with each breath. During inspiration, the pen moves up, and during expiration, the pen moves down. The volume of one normal breath (tidal volume) multiplied by the number of breaths per minute is called the minute ventilation. A lower-than-normal minute ventilation can be a sign of pulmonarymalfunction. Vital capacity (red) is the maximum amount of air a person can exhale after taking the deepest inhalation possible.

It’s a curious fact that some of the inhaled air never reaches the alveoli; instead, it fills the nasal cavities, trachea, bronchi, and bronchioles (see Fig. 14.1). In an average adult, some 70% of the tidal volume does reach the aveoli; but 30% remains in the airways. These passages are not used for gas exchange, and therefore they are said to contain dead-space air. To ensure that a large portion of inhaled air reaches the lungs, it is better to breathe slowly and deeply. Also, note in Figure 14.6 that even after a very deep exhalation, some air (about 1,000 ml) remains in the alveoli; this is called the residual volume. This air is not as useful for gas exchange because it has been depleted of oxygen. In some lung diseases, such as emphysema, the residual volume builds up because the individual has difficulty emptying the lungs. This means that the vital capacity is reduced because the lungs have more residual volume.

Ventilation

To understand ventilation, the manner in which air enters and exits the lungs, it is helpful to be aware of the following conditions:
     1. The lungs lie within the sealed-off thoracic cavity. The rib cage, consisting of the ribs joined to the vertebral column posteriorly and to the sternum anteriorly, forms the top and sides of the thoracic cavity. The intercostal muscles lie between the ribs. The diaphragm and connective tissue form the floor of the thoracic cavity.
     2. The lungs adhere to the thoracic wall by way of the pleura. (Any space between the two layers of the pleura is minimal due to the surface tension of the fluid between them).
     3. A continuous column of air extends from the pharynx to the alveoli of the lungs.

Inspiration

Inspiration is the active phase of ventilation because this is the phase in which the diaphragm and the external intercostal muscles contract (Fig. 14.7a). In its relaxed state, the diaphragm is dome-shaped; during deep inspiration, it contracts and lowers. Also, the external intercostal muscles contract, and the rib cage moves upward and outward.
Following contraction of the diaphragm and the external intercostal muscles, the volume of the thoracic cavity will be larger than it was before. As the thoracic volume increases, the lungs expand due to conditions 1 and 2. Now the air pressure within the alveoli (called intrapulmonary pressure) decreases, creating a partial vacuum. In other words, alveolar pressure is now less than atmospheric pressure (air pressure outside the lungs), and air will naturally flow from outside the body into the respiratory passages and into the alveoli due to condition 3.

Figure 14.7 Inspiration versus expiration. a. During inspiration, the thoracic cavity and lungs expand so that intrapleural pressure decreases. Now air flows into the lungs. b. During expiration, the thoracic wall and lungs recoil, assuming their original positions and pressures. Now air is forced out. The internal intercostal muscles only contract during forceful expiration.

It is important to realize that air comes into the lungs because they have already opened up; air does not force the lungs open. This is why it is sometimes said that humans breathe by negative pressure. The creation of a partial vacuum in the alveoli causes air to enter the lungs. While inspiration is the active phase of breathing, the actual flow of air into the alveoli is passive.

Expiration

Usually, expiration is the passive phase of ventilation, and no effort is required to bring it about. During expiration, the diaphragm and the intercostal muscles relax. Therefore, the diaphragm resumes its dome shape and the rib cage moves down and in (Fig. 14.7b). As the volume of the thoracic cavity decreases, the lungs are free to recoil due to conditions 1 and 2. Now the air pressure within the alveoli (called intrapulmonary pressure) increases above atmospheric pressure and air will naturally flow to outside the body due to condition 3.
What keeps the alveoli from collapsing as a part of expiration? The presence of surfactant lowers the surface tension within the alveoli. Also, as the lungs recoil, pressure between the two layers of pleura decreases, and this tends to make the alveoli stay open. The importance of a reduced intrapleural pressure is demonstrated when, by design or accident, air enters the intrapleural space. Now the lung collapses. While inspiration is the active phase of breathing, expiration is usually passive-that is, the diaphragm and external intercostal muscles are relaxed when expiration occurs. However, when breathing is deeper and/or more rapid, expiration can also be active. Contraction of the internal intercostal muscles can force the rib cage to move downward and inward. Also, when the abdominal wall muscles contract, they push on the viscera, which push against the diaphragm, and the increased pressure in the thoracic cavity helps expel air.

Figure 14.8 Nervous control of breathing. During inspiration, the respiratory center stimulates the external intercostal muscles to contract via the intercostal nerves and stimulates the diaphragm to contract via the phrenic nerve. Should the tidal volume increase above 1.5 liters, stretch receptors send inhibitory nerve impulses to the respiratory center via the vagus nerve. In any case, expiration occurs due to lack of stimulation from the respiratory center to the diaphragm and intercostal muscles.

Control of Ventilation

Normally, adults have a breathing rate of 12 to 20 ventilations per minute. The rhythm of ventilation is controlled by a respiratory center located in the medulla oblongata of the brain.
     The respiratory center automatically sends out impulses by way of nerves to the diaphragm and the external intercostal muscles of the rib cage (Fig. 14.8). When the respiratory center stops sending neuronal signals to the diaphragm and the rib cage, the diaphragm relaxes resuming its dome shape and the rib cage moves down and in. The respiratory center acts rhythmically to bring about breathing at a normal rate and volume. Although the respiratory center controls the rate and depth of breathing, its activity can be influenced by nervous input and chemical input.
     Nervous Input An example of nervous control of the respiratory center is the so-called Hering-Breuer reflex. During exercise, the depth of inspiration can increase due to recruitment of muscle fibers in the diaphragm and intercostal muscles. Then, stretch receptors in the alveolar walls are stimulated, and they initiate inhibitory nerve impulses that travel from the inflated lungs to the respiratory center. This causes the respiratory center to stop sending out nerve impulses. This reflex helps support rhythmic respiratory movements by limiting the extent of inspiration.
     Chemical Input The respiratory center is directly sensitive to the levels of carbon dioxide (CO2) and hydrogen ions (H⁺). When they rise, due to cellular respiration, the respiratory center increases the rate and depth of breathing. The center is not affected directly by low oxygen (O2) levels. However, chemoreceptors in the carotid bodies, located in the carotid arteries, and in the aortic bodies, located in the aorta, are sensitive to the level of oxygen in the blood. (Do not confuse the carotid and aortic bodies with the carotid and aortic sinuses, which monitor blood pressure.) When the concentration of oxygen decreases, these bodies communicate with the respiratory center, and the rate and depth of breathing increase.