CNS Control of Breathing PDF

1 CNS CONTROL OF BREATHING Dr. Samantha Solecki, DC, MS Instructor, Biology Thinker. Learner. Motivator. Lover of Anatomy & Physiology [email protected] © 2019 Pearson Education, Inc. ...

1 CNS CONTROL OF BREATHING Dr. Samantha Solecki, DC, MS Instructor, Biology Thinker. Learner. Motivator. Lover of Anatomy & Physiology [email protected] © 2019 Pearson Education, Inc.  2 Learning Objectives *Acquired from the Human Anatomy and Physiology Society (HAPS) with personal additions Describe the locations and functions of the brainstem respiratory centers. List and describe the major chemical and neural stimuli to the respiratory centers. Compare and contrast the central and peripheral chemoreceptors. Define hyperventilation, hypoventilation, panting, eupnea, hypernea and apnea. Explain why it is possible to hold one’s breath longer after hyperventilating than after eupnea.  3 Neural Mechanisms Breathing has volitional and non-volitional influences Modified by higher brain regions, chemoreceptors and reflexes Mostly controlled by neurons/cell bodies within the reticular formation* Follows an on/off cycle 12-15 breaths/min on average Eupnea = normal breathing  4 Neural Mechanisms Medullary Respiratory Centers Ventral Respiratory Group (VRG) Located at the pontomedullary junction in the ventral brainstem (medulla) Receives input from: higher cortical areas, pontine respiratory centers, periphery sensory receptors, DRG Projects to: Spinal cord  inspiratory muscles Dorsal Respiratory Group (DRG) Located in the medullary portion of the brainstem, dorsally, near the root of cranial n IX Receives input from: Pontine respiratory centers Projects to: VRG  5 Ventral Respiratory Group Acts as an integrative center and a rhythm- generating center Acts through mutual inhibition Inspiratory neurons fire  motor neuronal pools in spinal cord segments  intercostal & phrenic nn  expansion of thorax  air enters lungs After inspiratory neurons fire,  output from the VRG stops and passive expiration begins as inspiratory mm relax  lungs recoil During moments of hypoxia VRG  gasping  increasing O2 flow (-) by morphine & excessive EtOH  6 Dorsal Respiratory Group Integration center Receives input from stretch receptors and chemoreceptors Projects impulses to VRG  7 Pontine Respiratory Centers Influences, controls and modifies respiration Acts to fine-tune rhythm at the medullary neuronal pools (transmit to the VRG of the medulla) Ensures a smooth transition from Inspiration  Expiration  Inspiration  Expiration Receives input from: higher cortical levels and sensory receptors Lesions to the pontine respiratory center produces apneustic breathing (slow, prolonged inspiration) Figure 22.23 Locations of respiratory centers and their postulated connections. 8 Pons Medulla Pontine respiratory centers interact with medullary respiratory centers to smooth the respiratory pattern. Ventral respiratory group (VRG) contains rhythm generators whose output drives respiration. Pons Medulla Dorsal respiratory group (DRG) integrates peripheral sensory input and modifies the rhythms generated by the VRG. To inspiratory muscles External intercostal muscles Diaphragm  9 Factors Influencing Breathing Rate and Depth Depth of inspiration is determined by the strength of stimulus to the motor neurons in the spinal cord to the respiratory mm Rate is determined by how long the respiratory center is active or how quickly it is shut off Body demands can change and therefore impact both depth and rate of breathing Chemical Factors Higher Brain Center Influence  10 Chemical Factors Arterial CO2, O2 and H+ levels are key here! 2 types of Chemoreceptors: Central Chemoreceptors Present in the brainstem (Ventrolateral medulla) Peripheral Chemoreceptors Located in aortic and carotid arches  11 PCO2 (40mmHg) Most important and most closely regulated! Regulated centrally by central chemoreceptors Hypercapnia = increased arterial CO2  increased cerebral CO2 Abundance of CO2 is hydrated from H2CO3   [H+] + H2O  drop in arterial pH   [H+]  central chemoreceptors  synapse with respiratory centers Result: rate & depth of respiration increases  ridding of CO2   arterial pH  12 HYPERVENTILATION Arterial CO2 (hypocapnia)  constriction of cerebral blood vessels   blood flow to the brain  ischemia  syncope  Arterial CO2  (-) rerpiratory centers  slow, shallow breathing   CO2 *Once homeostatic balance is reached, normal respiration occurs*  13 PO2 (60mmHg) Detected peripherally by peripheral chemoreceptors at the carotid * and aortic bodies Normally, a slight  in PO2 has limited effects on ventilation; this enhances peripheral receptors to PCO2 Arterial PO2 must drop substantially before O2 level drives ventilation Due to the built-up reserve of O2 bound to Hb  14 PO2 (60mmHg) Arterial PO2 