1. CHAPTER 41 DR FARZANA

2. Learning Objectives Regulation of ventilation by the CNS and PNS. Know the basic anatomy of the CNS respiratory center. Know how the dorsal respiratory group, ventral respiratory group and the pneumotaxic center control respiration. 3. Understand how chemical changes in the CNS and PNS influence the respiratory changes. Know how respiration is regulated during exercise. Understand the changes in the pulmonary system that cause Cheyne-Stokes breathing and sleep apnea. 4. Control of breathing Automatic control and Voluntary control AUTOMATIC CONTROL This is achieved by group of pacemaker cells in medulla Activate motor neurons of cervical spinal cord (innervates diaphragm via phrenic nerve) and thoracic spinal cord (innervates external intercostal muscles and expiratory muscles) 5. There is reciprocal innervation of respiratory muscles This is due to shared innervation of muscles in descending pathways which excites agonists and inhibit antagonists and vice versa 6. VOLUNTARY CONTROL Modulate the activity of the more primitive controlling centers in the medulla and pons. Allow the rate and depth of respiration to be controlled voluntarily. During speaking, laughing, crying, eating, defecating, coug hing, and sneezing. . Adaptations to changes in environmental temperature --Panting 7. 9 8. Control systems of respiration Nervous regulatory systems and Chemical regulatory system Nervous regulation (respiratory centers) Medullary system * Pre Botzinger complex (Pre BOT-C) * Dorsal group of neurons * Ventral group of neurons Pontine system * Pneumotaxic centre * Apneustic centre 9. Control systems Chemical Regulation (PO2, PCO2 and pH) CO2 via CSFcentral chemoreceptors O2 via blood.peripheral chemoreceptors H+ via blood peripheral chemoreceptors 10. Respiratory Centers of the CNS The primary portions of the brainstem that control ventilation are the medulla oblongata and the pons. 11. Respiratory Center Following groups of neurons in the respiratory center. Pre BOT-C (medulla) Dorsal respiratory group (medulla). Ventral respiratory group (medulla). Pneumotaxic center (pons). Apneustic center 12. Pre- botzinger complex Present on either side of medulla between nucleus ambiguous and lateral reticular nucleus Consists of network of neurons which display pace maker activity Undergoes self induced action potentials similar to those in SA node It is now believed that rate at which the DRG inspiratory neurons rhythmically fire is driven by synaptic input from this complex 13. Dorsal Respiratory Group Sets the basic respiratory rate. Stimulates the inspiratory muscles to contract (diaphragm). The signals it sends for inspiration start weakly and steadily increase for ~ 2 sec. This is called a ramp and produces a gradual inspiration. The ramp then stops abruptly for ~ 3 sec and the diaphragm relaxes. 14. Stimulation of receptors Peripheral chemoreceptors Baroreceptors Several pulmonary receptors 9th and 10th cranial nerve (glossopharyngeal & vagus) Sensory input can change 2 qualities of the ramp: The rate of increase (e.g., increase during heavy breathing to fill lungs more rapidly). The timing of the stop (e.g., stopping the ramp sooner Shortens the rate of inspiration and expiration, thus increasing the frequency of respiration) 15. Ventral Respiratory Group Inactive during normal, quiet respiration. At times of increased ventilation, signals from the dorsal group stimulate the ventral group. The ventral group then stimulates both inspiratory and expiratory muscles. E.g., the abdominal muscles are stimulated to contract and help force expiration. 16. Pneumotaxic Center Controls stopping point of the dorsal group ramp. Strong pneumotaxic stimulation shortens the duration of inspiration and expiration. This increases the breathing rate. rate of breathing increases upto 30-40 breaths/min and weak pneuomotaxic stimulation can decrease the breathing rate to 3-5 breaths/min. 17. Apneustic center Prevents inspiratory neurons from being switched off but this is dominated by pneumotaxic center Stimulation causes apneusis (prolonged inspiratory gasps with shortened expiration) Occurs in severe types of brain damage. 18. Chemical Control of Respiratory Center Objective To maintain proper concentrations of H+, O2 and CO2 in blood and tissue fluids This is achieved by chemoreceptors Two types of chemoreceptors Central Peripheral 19. Chemoreceptors Monitor changes in blood PC02, P02, and pH. Central: Medulla. Peripheral: Carotid and aortic bodies. Control breathing indirectly. Insert fig. 16.27 Figure 16.27 20. Central Chemoreceptors More sensitive to changes in arterial PC02. H20 + CO2 H+ cannot cross the blood brain barrier. C02 can cross the blood brain barrier and will form H2C03. Lowers pH of CSF Directly stimulates central chemoreceptors. H+H2C03 21. 27 Central Chemoreceptor Stimulation Arterial CSF CO2 CO H O HCO H 2 2 3 Central Chemoreceptor H+ H+ slow ??? ?? BBB 22. Peripheral Chemoreceptors Are not stimulated directly by changes in arterial PC02 H20 + C02 H2C03 H+ Stimulated by rise in [H+] of arterial blood. Increased [H+] stimulates peripheral chemoreceptors. 23. 29 Peripheral Chemoreceptor Pathways 24. Chemoreceptor Control of Breathing Insert fig. 16.29 Figure 16.20 25. Chemical Signals in the CNS In the CNS, CO2 and H+ are particularly important O2 has a greater effect in the PNS. 26. 32 Peripheral Chemoreceptors Carotid bodies Sensitive to: PaO2, PaCO2, and pH Afferents in glossopharyngeal nerve. Aortic bodies Sensitive to: PaO2, PaCO2, but not pH Afferents in vagus nerve 27. 33 28. H+ is the Main Stimulus (in the CNS) In the chemosensitive areas of the respiratory center, increased H+ is the main stimulus. Activation of the central chemoreceptors by H+ excites the dorsal respiratory group of neurons (inspiratory area) and thus increase the respiration rate. 29. CO2 and H+ are Linked The blood-brain barrier is not very permeable to H+; however, CO2 easily diffuses across the BBB As we have discussed, increases in CO2 cause increases in H+. So, once CO2 diffuses into the chemosensitive regions of the CNS, H+ is formed and stimulates the dorsal group. 30. Acute and Chronic Elevation of CO2 and H+ An acute increase in CO2/H+ stimulates respiration, which helps remove the excess CO2/H+. What system regulates the long-term levels of H+? 31. Renal Control of Acid- Base Balance Bicarbonate must react with H+ before it can be reabsorbed. If H+ is high, the kidneys reabsorb nearly all the bicarbonate. The excess H+ in the tubular lumen combines with phosphate and ammonia and is excreted as salts. The extra bicarbonate will then slowly diffuse into the CNS and bind the excess H+. 32. Sensing PO2 in the CNS Why does the CNS directly monitor levels of CO2 or H+ ions more than O2? Remember the O2-hemoglobin dissociation curve. Hemoglobin buffers O2 delivery to the tissues even with large changes in PO2. Also remember, the brain receives a very steady supply of blood under normal conditions. So, O2 delivery in the brain is fairly stable under normal conditions and there is no as much of a need to directly monitor PO2. 33. Peripheral Chemoreceptors Peripheral chemoreceptors are located in carotid and aortic bodies and sense the level of O2 (PO2). Blood flow to the receptors is very high; so very little deoxygenated (venous) blood accumulates. Thus, they sense arterial O2 levels. 34. Low PO2 levels stimulates the dorsal respiratory group. The signal is sent to the respiratory center via the vagus or glossopharyngeal 35. Effect of CO2 and H+ on Peripheral Chemoreceptors Elevated CO2 and H+ also stimulate peripheral chemoreceptors. This effect is less powerful than the effect on CNS chemoreceptors, but it occurs ~ 5 x faster than occurs in the CNS. 36. Hering-Breuer Inflation Reflex When the lungs become overinflated, stretch receptors in the muscle portions of bronchi and bronchioles send a signal through a branch of the vagus nerve to the dorsal respiratory group of neurons. This signal switches off the inspiratory ramp sooner. This decreases the amount of filling during inspiration, but increases the rate of respiration. 37. Respiration During Exercise During exercise, O2 consumption and CO2 formation can increase 20-folds The partial pressures do not change much. This can occur if the ventilation increases in proportion to the increase in O2 consumption and CO2 production.