Respiratory Areas in the Brainstem

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Respiratory Areas in the Brainstem Medullary respiratory center Dorsal groups stimulate the diaphragm Ventral groups stimulate the intercostal and abdominal muscles This section is especially sensitive during infancy, and the neurons can be destroyed if the infant is dropped and/or shaken violently. The result can be death due to "shaken baby syndrome” Pontine (pneumotaxic) respiratory group Involved with switching between inspiration and expiration (fine tunes the breathing pattern-----there is a connection with medullary resp. center but precise function unknown)

Rhythmic Ventilation Starting inspiration Increasing inspiration Medullary respiratory center neurons are continuously active Center receives stimulation from receptors (that monitor blood gas levels) and simulation from parts of brain concerned with voluntary respiratory movements and emotion Combined input from all sources causes action potentials to stimulate respiratory muscles Increasing inspiration More and more neurons are activated (to stimulate respiratory muscles) Stopping inspiration Neurons stimulating the muscles of respiration also stimulate the neurons in the medullary respiratory center that are responsible stopping inspiration. They also receive input from pontine group and stretch receptors in lungs. Inhibitory neurons activated and relaxation of respiratory muscles results in expiration. Note: although the medullary neurons establish the basic rate & depth of breathing, their activities can be influenced by input from other parts of the brain & by input from peripherally located receptors.

Rhythmic Ventilation Chemical control Carbon dioxide is major regulator, but indirectly through p H change Increase or decrease in pH can stimulate chemo-sensitive area, causing a greater rate and depth of respiration Oxygen levels in blood affect respiration when a 50% or greater decrease from normal levels exists CO2. Hypercapnia: too much CO2 Hypocapnia: lower than normal CO2 Apnea. Cessation of breathing. Can be conscious decision, but eventually PCO2 levels increase to point that respiratory center overrides Hyperventilation. Causes decrease in blood PCO2 level, which causes respiratory alkalosis (high blood pH). Fainting, leads to changes in the nervous system fires and leads to the paresthesia (pins & needles) Cerebral (cerebral cortex)and limbic system. Respiration can be voluntarily controlled and modified by emotions (ex: strong emotions can cause hyperventilation or produce the sobs & gasps of crying)

Modifying Respiration

Chemical Control of Ventilation Chemoreceptors: specialized neurons that respond to changes in chemicals in solution Central chemoreceptors: chemosensitive area of the medulla oblongata; connected to respiratory center Peripheral chemoreceptors: carotid and aortic bodies. Connected to respiratory center by cranial nerves IX and X (9 & 10) Effect of pH : chemosensitive area of medulla oblongata and carotid and aortic bodies respond to blood pH changes Chemosensitive areas respond indirectly through changes in carbon dioxide Carotid and aortic bodies respond directly to p H changes

Chemical Control of Ventilation Effect of carbon dioxide: small change in carbon dioxide in blood triggers a large increase in rate and depth of respiration - ex: an increase PCO2 of 5 mm Hg causes an increase in ventilation of 100%. Hypercapnia: greater-than-normal amount of carbon dioxide Hypocapnia: lower-than-normal amount of carbon dioxide Chemosensitive area in medulla oblongata is more important for regulation of PCO2 and pH than the carotid & aortic bodies (responsible for 15% - 20% of response) During intense exercise, carotid & aortic bodies respond more rapidly to changes in blood pH than does the chemosensitive area of medulla

Chemical Control of Ventilation Effect of oxygen: carotid and aortic body chemoreceptors respond to decreased PO2 by increased stimulation of respiratory center to keep it active despite decreasing oxygen levels (50% or greater decrease----------bec. of oxygen-hemoglobin dissociation curve-------at any PO2 above 80 mm Hg nearly all of hemoglobin is saturated with oxygen) Hypoxia: decrease in oxygen levels below normal values

Regulation of Blood pH and Gases

Hering-Breuer Reflex Limits the degree of inspiration and prevents overinflation of the lungs Depends on stretch receptors in the walls of bronchi & bronchioles of the lung. It is an inhibitory influence on the respiratory center & results in expiration. (as expiration proceeds, stretch receptors no longer stimulated) Infants Reflex plays a role in regulating basic rhythm of breathing and preventing overinflation of lungs Adults Reflex important only when tidal volume large as in exercise

Effect of Exercise on Ventilation Ventilation increases abruptly At onset of exercise Movement of limbs has strong influence (body movements stimulate proprioceptors in joints of the limbs) Learned component (after a period of training, the brain “learns” to match ventilation with the intensity of exercise) Ventilation increases gradually After immediate increase, gradual increase occurs (4-6 minutes it levels off) Anaerobic threshold: highest level of exercise without causing significant change in blood pH. If exercise intensity is high enough to exceeded anaerobic threshold, lactic acid produced by skeletal muscles

Other Modifications of Ventilation Activation of touch, thermal and pain receptors affect respiratory center Sneeze reflex (initiated by irritants in the nasal cavity), cough reflex (initiated by irritants in the lungs) Increase in body temperature yields increase in ventilation

Respiratory Adaptations to Exercise Athletic training Vital capacity increases slightly; residual volume decreases slightly At maximal exercise, tidal volume and minute ventilation increases Gas exchange between alveoli and blood increases at maximal exercise Alveolar ventilation increases Increased cardiovascular efficiency leads to greater blood flow through the lungs

Effects of Aging Vital capacity and maximum minute ventilation decrease (these changes are related to weakening of respiratory muscles & decreased compliance of thoracic cage caused by stiffening of cartilage & ribs) Residual volume and dead space increase Ability to remove mucus from respiratory passageways decreases Gas exchange across respiratory membrane is reduced