Prof. J.P.N. Mishra
Physiology of respiration is combined of following steps:-
- Gaseous exchange in the lungs: The respiratory membrane through which gaseous exchange takes place consists of thin lining of the alveoli, the endothelium of the capillaries and the delicate interstitial connective layer. The uptake of CO2 and the release of CO2 by the blood of the alveolar capillaries can be explained by diffusion. The O2 diffuses from the alveolar air into the blood. By the time the blood leaves the capillaries its O2 pressure has been raised to about 100 mg of Hg, the same as alveolar O2. CO2 in the blood of the lung capillaries has a higher concentration than it has in the lung alveoli. This accounts for the diffusion of CO2 out of the blood to the alveoli. By the time the blood leaves the lungs its CO2 pressure has been lowered to approximately 40 mm. Thus in the diffusion of both these gases there is a marked diffusion gradient that determines the direction of their flow.
- Transport of gases by the blood: It is completed in two phases i.e. Transport of O2 and transport of CO2 (Details given earlier).
- Cellular respiration and Oxidation: The ultimate aim of all the respiration activities is the cellular oxidation i.e., the aerobic breakdown of the digestive food materials and the release of energy thereby. The breakdown of carbohydrates may be represented by: -
C6H12O6 + 6O2 -> 6CO2 + 6H2O + Energy (686 kcal/mol).
Within each cell glucose is first metabolized to pyruvic acid and then, if there is supply of O2, into CO2 and H2O. It is when hydrogen atoms are combined with O2 that most of the energy is released in the cell. By storing energy as ATP (Adenosine Tri Phosphate) molecules, the cell can utilize this energy for its various activities as needed.
Mechanism of respiration: Breathing process consists of two components -inspiration and expiration. Inspiration is performed by three distinct sets of muscles-those act upon the ribs, between the ribs and the diaphragm which is the floor of the thorax. In inspiration the chest cavity is made broader, longer and deeper. The sternum rises forward, thus the chest is made broader and deeper. It is made longer because, when at rest, the diaphragm muscle forms an arched floor that rises like a dome into the thorax, and on which the lungs rest. As this muscle contracts it flattens the floor, pulls the lungs down, and as a result makes them longer from top to bottom. Between each rib is a double layer of muscles called the intercostal muscles, because they are between the ribs. The top ribs being fixed as this contract, they tend to raise the lower rib, to which they are attached and thus, by acting together, all the ribs are elevated. This constitutes the movement of inspiration. In expiration, the chest returns to its original size without effort. This is mainly caused by elastic recoil. The lungs are full of elastic tissues, which is stretched when the lungs are expanded, and, as soon as muscular effort ceases, the elastic force is so great that the lungs pull the ribs down again, and pull up the floor of the diaphragm. During inspiration the abdomen swells out because of the contraction of the diaphragm, which presses all the digestive organs down and makes them bulge out the walls. In expiration the abdomen gets flat again, as the floor rises once more, and the abdominal muscles are contracted.
Nervous Involvement in respiration: The respiratory center situated at the posterior part of the brain and at its lower end. The center is responsible for controlling the activities of the muscles that cause inspiration and expiration. This central control is both voluntary and involuntary. Practically our breathing is under our own control up to the point where life is involved. We can also hold our breath up to a certain point. But when life is beginning to be threatened the voluntary control comes to an end, and in spite of the strongest effort of will, forces us to breathe. The involuntary control also acts continuously when we are not thinking of our breath at all. None of the vital processes require our constant attention, yet with some we are allowed to play up to the point of danger but not further (Fig 1-14).
Fig 1-14. Nervous regulation of respiration.
Mechanics of Ventilation
Inspiration : Pulmonary ventilation is achieved by rhythmically changing the pressure in the thoracic cavity. Air flows into the lungs when thoracic pressure falls below atmospheric pressure, then it's forced out when thoracic pressure rises above atmospheric pressure. The diaphragm does most of the work. It is dome-shaped at rest, but when stimulated by the phrenic nerves, it tenses and flattens somewhat, dropping about 1,5 cm in quiet respiration and as much as 7 cm in deep breathing.
This enlarges the thoracic cavity and thus reduces its internal pressure. Other muscles help. The scalene fix (immobilize) the first pair of ribs while the external intercostal muscles lift the remaining ribs like bucket handles, making them swing up and out. Deep inspiration is aided by the pectoralis minor, sternocleidomastoid, and erector spinae muscles.
As the rib cage expands, the parietal pleura clings to it. In the space between the parietal and visceral pleurae, the intrapleural pressure drops from a value of about -4mmHg at rest to -6 mmHg during inspiration. The visceral pleura clings to the parietal pleura like a sheet of wet paper, so it too is pulled outward. Since the visceral pleura forms the lung surface, the lung expands as well. Not all the pressure change in the pleural cavity is transferred to the interior of the lungs, but the intrapulmonary pressure drops to about -3mmHg. At an atmospheric pressure of 760 mmHg (latm), the intrapleural pressure 757 mmHg. The difference between these, 3 mmHg, is the trans pulmonary pressure. The trans pulmonary gradient of 757-754 mmHg helps the lungs expand in the thoracic cavity, and the gradient of 760-757 mmHg from atmospheric to intrapulmonary pressure makes air flow into the lungs,
When the respiratory muscles stop contracting, the inflowing air quickly achieves an intrapulmonary pressure equal to atmospheric pressure, and flow stops. The dimensions of the thoracic cage increase by only a few millimetres in each direction, but this is enough to increase its total volume by 500 ml. Thus, 500 ml of air flows into the respiratory tract during quiet breathing (Scanlon, 2007).
Expiration: Inspiration requires a muscular effort and therefore an expenditure of ATP and calories. By contrast, normal expiration during quiet breathing is an energy-saving passive process that requires little muscular contraction other than a breaking action explained shortly. Expiration is achieved by the elasticity of the lungs and thoracic cage-the tendency to return to their original dimensions when released from tension. The bronchial tree has a substantial amount of elastic connective tissue in its walls. The attachments of the ribs to the spine and sternum, and the tendons of the diaphragm and other respiratory muscles, also have a degree of elasticity that causes them to spring back when muscular contraction ceases. As these structures recoil, the thoracic cage diminishes in size. In accordance with Boyle's law, this raises the intrapulmonary pressure; it peaks at about +3 mmHg and expels air from the lungs (Scanlon, 2007).
Measurements of Ventilation: Four measurements are called respiratory volumes: tidal volume, inspiratory reserve volume, expiratory reserve volume, and residual volume. Four others, called respiratory capacities, are obtained by adding two or more of the respiratory volumes: vital capacity, inspiratory capacity, functional residual capacity, and total lung capacity. In general, respiratory volumes and capacities are proportional to body size; consequently, they are generally lower for women than for men.
The measurement of respiratory volumes and capacities is important in assessing the severity of a respiratory disease and monitoring improvement or deterioration is a patient's pulmonary function. Restrictive disorders of the respiratory system, such as pulmonary fibrosis, stiffen the lungs and thus reduce compliance and vital capacity. Obstructive disorders do not reduce respiratory volumes, but they narrow the airway and interfere with airflow; thus, expiration either requires more effort or is less complete than normal. Airflow is measured by having the subject exhale as rapidly as possible into a spirometer and measuring forced expiratory volume (FEV)-the percentage of the vital capacity that can be exhaled in a given time interval. A healthy adult should be able to expel 75% to 85% of the vital capacity in 1.0 second (a value called the FEV 1.0). Significantly lower values may indicate thoracic muscle weakness or obstruction of the airway by mucus, a tumor, or bronchoconstriction (as in asthma).
The amount of air inhaled per minute is called the minute respiratory volume (MRV). Its primary significance is that the MRV largely determines the alveolar ventilation rate. MRV can be measured directly with a spirometer or obtained by multiplying tidal volume by respiratory rate. For example, if a person has a tidal volume of 500 ml per breath and a rate of 12 breaths per minute, his or her MRV would be 500 x 12 = 6,000 ml/min. During heavy exercise, MRV may be as high as 125 to 170 L/min. This is called maximum voluntary ventilation (MW), formerly called maximum breathing capacity.
Respiration Control Centers in the Brainstem: The medulla oblongata contains inspiratory (I) neurons, which fire during inspiration, and expiratory (E) neurons, which fire during forced expiration (but not during eupnoea). Fibbers from these neurons travel down the spinal cord and synapse with lower motor neurons in the cervical to thoracic regions. From here, nerve fibres travel in the phrenic nerves to the diaphragm and intercostal nerves to the intercostal muscles. No pacemaker neurons have been found that are analogous to the autohythmic cells of the heart, and the exact mechanism for setting the rhythm of respiration remains unknown despite intensive research.
The medulla has two respiratory nuclei. One of them, called the inspiratory center, or dorsal respiratory group (DRG), is composed primarily of I neurons, which stimulate the muscles of inspiration. The more frequently they fire, the more motor units are recruited and the more deeply you inhale. If they fire longer than usual, each breath is prolonged and the respiratory rate is slower. When they stop firing, elastic recoil of the lungs and thoracic cage produces passive expiration.
The other nucleus is the expiratory center, or ventral respiratory group (VRG). It has I neurons in its midregion and E neurons at its rostral and caudal ends. It is not involved in eupnoea, but its E neurons inhibit the inspiratory center when center expiration is needed. Conversely, the inspiratory center inhibits the expiratory center when an unusually deep inspiration is needed.
The pons regulates ventilation by means of a pneumotaxic center in the upper pons and an amnestic (ap-NEW-stic) center in the lower pons. The role of the amnestic center is still unclear, but it seems to prolong inspiration. The pneumotaxic (NEW-mo-TAX-ic) center sends a continual stream of inhibitory impulses to the inspiratory center of the medulla. When impulse frequency rises, inspiration lasts as little as 0.5 second and the breathing becomes faster and shallower. Conversely, when impulse frequency declines, breathing is slower and deeper, with inspiration lasting as long as 5 seconds.
Chemoreceptors in the brainstem and arteries monitor blood pH, CO2, and O, levels. They transmit signals to the respiratory centers that adjust pulmonary ventilation to keep these variables within homeostatic limits. Chemoreceptors are later discussed more extensively.
The vagous nerves transmit sensory signals from the respiratory system to the inspiratory center. Irritants in the airway, such as smoke, dust, noxious fumes, or mucus, stimulate vagal afferent fibres. The medulla then returns signals that result in bronchoconstriction or coughing. Stretch receptors in the bronchial tree and visceral pleura monitor inflation of the lungs. Excessive inflation triggers the inflation (Hering-Breuer) reflex, a protective somatic reflex that strongly inhibits the I neurons and stops inspiration. In infants, this may be a normal mechanism of transition from inspiration to expiration, but after infancy it is activated only by extreme stretching of the lungs (Scanlon, 2007).
