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Respiratory System

Pulmonary Ventilation

Pulmonary ventilation, or breathing, exchanges gases between the outside air and the alveoli of the lungs. Ventilation, which is mechanical in nature, depends on a difference between the atmospheric air pressure and the pressure in the alveoli. When we expand the lungs to inhale, we increase internal volume and reduce internal pressure. Lung expansion is brought about by two important muscles, the diaphragm and the intercostal muscles. The diaphragm is a dome-shaped sheet of muscle located below the lungs that separates the thoracic and abdominal cavities. When the diaphragm contracts, it moves down. The dome is flattened, and the size of the chest cavity is increased, lowering pressure on the lungs. When the intercostal muscles, which are located between the ribs, contract, the ribs move up and outward. Their action also increases the size of the chest cavity and lowers the pressure on the lungs. By contracting, the diaphragm and intercostal muscles reduce the internal pressure relative to the atmospheric pressure. As a consequence, air rushes into the lungs. When we exhale, the reverse occurs. The diaphragm relaxes, and its dome curves up into the chest cavity, while the intercostal muscles relax and bring the ribs down and inward. The diminished size of the chest cavity increases the pressure in the lungs, thereby forcing out the air.

Physicians use an instrument called a spirometer to measure the tidal volume, that is, the amount of air we exchange during a ventilation cycle. Under normal circumstances, we inhale and exhale about 500 ml, or about a pint, of air in each cycle. Only about 350 ml of the tidal volume reaches the alveoli. The rest of the air remains in the respiratory tract. With a deep breath, we can take in an additional 3,000 ml (3 liters or a little more than 6 pints) of air. The total lung capacity is about 6 liters on average. The largest volume of air that can be ventilated is referred to as the vital capacity. Trained athletes have a high vital capacity. Regardless of the volume of air ventilated, the lung always retains about 1,200 ml (3 pints) of air. This residual volume of air keeps the alveoli and bronchioles partially filled at all times.

A healthy adult ventilates about 12 times per minute, but this rate changes with exercise and other factors. The basic breathing rate is controlled by breathing centers in the medulla and the pons in the brain. Nerves from the breathing centers conduct impulses to the diaphragm and intercostal muscles, stimulating them to contract or relax. There is an inspiratory center for inhaling and an expiratory center for exhaling in the medulla. Before we inhale, the inspiratory center becomes activated. It sends impulses to the breathing muscles. The muscles contract and we inhale. Impulses from a breathing center in the pons turn off the inspiratory center before the lungs get too full. A second breathing center in the pons stimulates the inspiratory center to prolong inhaling when needed. During normal quiet breathing, we exhale passively as the lungs recoil and the muscles relax. For rapid and deep breathing, however, the expiratory center becomes active and sends impulses to the muscles to bring on forced exhalations.

The normal breathing rate changes to match the body's needs. We can consciously control how fast and deeply we breathe. We can even stop breathing for a short while. This occurs because the cerebral cortex has connections to the breathing centers and can override their control. Voluntary control of breathing allows us to avoid breathing in water or harmful chemicals for brief periods of time. We cannot, however, consciously stop breathing for a prolonged period. A buildup of carbon dioxide and hydrogen ions in the bloodstream stimulates the breathing centers to become active no matter what we want to do.

We are not in conscious control of all the factors that affect our breathing rate. For example, tension on the vessels of the bronchial tree affects the breathing rate. Specialized stretch receptors in the bronchi and bronchioles detect excessive stretching caused by too much air in the lungs. They transmit the information on nerves to the breathing centers, which in turn inhibit breathing. Certain chemical substances in the blood also help control the rate of breathing. Hydrogen ions, carbon dioxide, and oxygen are detected by specialized chemoreceptors. Inside cells, carbon dioxide (CO2) combines with water (H2O) to form carbonic acid (H2CO3). The carbonic acid breaks down rapidly into hydrogen ions and bicarbonate ions. Therefore, an increase in carbon dioxide results in an increase in hydrogen ions, while a decrease in carbon dioxide brings about a decrease in hydrogen ions. These substances diffuse into the blood. When we exercise, our cells use up oxygen and produce carbon dioxide at a higher than average rate. As a result, chemoreceptors in the medulla and in parts of the peripheral nervous system detect a raised level of carbon dioxide and hydrogen ions. They signal the inspiratory center, which in turn sends impulses to the breathing muscles to breathe faster and deeper. A lack of oxygen also stimulates increased breathing, but it is not as strong a stimulus as the carbon dioxide and hydrogen ion surpluses. A large decrease in oxygen stimulates the peripheral chemoreceptors to signal the inspiratory center to increase breathing rate.

In addition to chemoreceptors, there are receptors in the body that detect changes in movement and pressure. Receptors in joints detect movement and signal the inspiratory center to increase breathing rate. When receptors in the circulatory system detect a rise in blood pressure, they stimulate slower breathing. Lowered blood pressure stimulates more rapid breathing. Increased body temperature and prolonged pain also elevate the rate of pulmonary ventilation.


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