Control of Respiration PDF

CONTROL OF RESPIRATION Breathing, like the heartbeat, is automatic. However, unlike the heart, the lungs don’t have a built-in pacemaker. Instead, they coordinate the complex skeletal muscle actions required to sustain ventilation. unconscious breathing cycle is controlled by r...

CONTROL OF RESPIRATION Breathing, like the heartbeat, is automatic. However, unlike the heart, the lungs don’t have a built-in pacemaker. Instead, they coordinate the complex skeletal muscle actions required to sustain ventilation. unconscious breathing cycle is controlled by respiratory centers in the brain, specifically in the medulla oblongata and pons. The thorax size is altered by the action of the breathing muscles, which contract as a result of nerve impulses transmitted from centers in the brain and relax in the absence of nerve impulses. respiratory center- divided into two principal areas based on location and function: (1) the medullary respiratory center in the medulla oblongata control the basic rhythm of respiration. two collections of neurons: dorsal respiratory group (DRG), formerly called the inspiratory area Normal quiet breathing, neurons of the DRG generate impulses to the diaphragm via the phrenic nerves and the external intercostal muscles via the intercostal nerves. These muscles contract and inhalation occurs.  ventral respiratory group (VRG), formerly called the expiratory area cluster of neurons called the pre-Bötzinger complex that is important in the generation of the rhythm of breathing. The remaining neurons of the VRG do not participate in normal quiet breathing. The VRG becomes activated when forceful breathing is required, such as during exercise, when playing a wind instrument, or at high altitudes. (2) Pontine respiratory group (PRG), formerly called the pneumotaxic area, is a collection of neurons in the pons. Active during inhalation and exhalation PRG transmits nerve impulses to the DRG in the medulla. The PRG may play a role in both inhalation and exhalation by modifying the basic rhythm of breathing generated by the VRG, as when exercising, speaking, or sleeping.  Activity of the respiratory center can be modified in response to inputs from: other brain regions, receptors in the peripheral nervous system, other factors in order to maintain the homeostasis of breathing. Cortical influences allow conscious control of respiration that may be needed to avoid inhaling noxious gases or water. Certain chemical stimuli modulate how quickly and how deeply we breathe. Central chemoreceptors are located in or near the medulla oblongata in the Central Nervous System. They respond to changes in H+ concentration or PCO2 or both, in cerebrospinal fluid. Peripheral chemoreceptors are located in the: aortic bodies, clusters of chemoreceptors located in the wall of the arch of the aorta The carotid bodies, which are oval nodules in the wall of the left and right common carotid arteries where they divide into the internal and external carotid arteries. Peripheral chemoreceptors respond to changes in H+ PCO2  Baroreceptors or stretch receptors are located in the walls of bronchi and bronchioles. When these receptors become stretched during over-inflation of the lungs, nerve impulses are sent along the vagus (X) nerves to the dorsal respiratory group (DRG) in the medullary respiratory center. In response, the DRG is inhibited and the diaphragm and external intercostals relax. As a result, further inhalation is stopped, and exhalation begins. As air leaves the lungs during exhalation, the lungs deflate, and the stretch receptors are no longer stimulated. Thus, the DRG is no longer inhibited, and a new inhalation begins. This reflex is referred to as the inflation reflex or Hering–Breuer reflex. The reflex in adults is a protective mechanism that prevents excessive inflation of the lungs. Other influences include blood pressure, limbic system, temperature, pain, stretching the anal sphincter, and irritation to the respiratory mucosa and blood pressure. BRONCHIAL ASTHMA AND EMPHYSEMA Allergic reaction to foreign antigens in the airways, such as from inhaled pollen or material on dust mites. Normally, cells of the larger airways secrete abundant mucus, which traps allergens. Ciliated columnar epithelial cells move the mucus up and out of the bronchi, then up and out of the trachea. However, in the smaller airways, mucus and edematous secretions resulting from the allergic response accumulate because fewer cells are ciliated. The allergens and secretions irritate airway smooth muscle, causing bronchoconstriction. Breathing becomes increasingly difficult, and inhalation produces a characteristic wheezing sound as air moves through narrowed and partially clogged passages. A person with asthma usually finds it harder to force air out of the lungs than to bring it in. this is because inspiration expands the lungs opening the air passages. Expiration, on the other hand, is due to elastic recoil of stretched tissues which compresses the airways, further impairing air movement through the narrowed air passages. Emphysema is a progressive, degenerative disease that destroys alveolar walls. air sacs merge into larger chambers, which greatly decreases the total surface area of the alveoli, reducing the volume of gases that can be exchanged across their walls. At the same time, the alveolar walls lose their elasticity, and the capillary networks associated with the alveoli diminish. A person with emphysema finds it increasingly difficult to exhale because of the loss of tissue elasticity. Abnormal muscular efforts are required to compensate for the lack of elastic recoil that normally contributes to expiration. Emphysema is caused by a deficiency of an enzyme, alpha-1 antitrypsin or due to smoking or exposure to other respiratory irritants. Emphysema is a type of chronic obstructive pulmonary disease (COPD). The other major form of COPD is chronic bronchitis.