Lecture 3, neural and chemical control of breathing
Page 1: Overview
Key structures involved in respiration: Hypothalamus, Midbrain, Cerebellum, Pituitary Gland, Pneumotaxic Area, Apneustic Area, Dorsal Respiratory Group (DRG), Medulla, and Ventral Respiratory Group (VRG).
Presented by Dr. Lucy Privitera.
Page 2: Learning Objectives
Brainstem Role: Discuss the organization and function of respiratory centers in controlling ventilation.
Sensors and Effectors: Explain the sensors and effectors involved in neural and chemical control of ventilation.
CO2-HCO3 Buffer System: Describe its role in chemical control of breathing and pH homeostasis.
Chemoreceptors: Compare the location, function, innervation, and differences between peripheral and central chemoreceptors.
Graph Interpretation: Analyze how changes in arterial oxygen (PaO2) and carbon dioxide (PaCO2) levels affect ventilation.
Page 3: Homeostatic Control of Breathing
Major components include the Medulla, Pons, Spinal Cord.
Control System: Utilizes Peripheral and Central Chemoreceptors for sensing, and involves respiratory muscles, including the diaphragm.
Receptor/Effectors: Mechanoreceptors and chemoreceptors help maintain balance in breathing.
Page 4: Nervous System Control Overview
Ventilation Control: Managed by groups of neurons in the brainstem (Medulla and Pons).
Neuronal Groups:
Dorsal Respiratory Group (DRG)
Ventral Respiratory Group (VRG)
Apneustic Center
Pneumotaxic Center
Page 5: Nervous System Control of Ventilation (Continued)
Reiterates neuron groups affecting breathing control.
Emphasizes the divisions within the brainstem affecting respiratory regulation.
Page 6: Pattern Generator in Ventilation Control
Basic Respiratory Rhythm: Set by the central pattern generator in the VRG (pre-Bötzinger complex).
DRG: Receives inputs from sensors through cranial nerves, activates diaphragm and intercostal muscles for inspiration.
Function of DRG: Coordinates respiratory signals; integrates information from chemoreceptors and mechanoreceptors.
Page 7: VRG Functionality
Primary Roles: Coordinating accessory muscles for inspiration and expiration.
Ventilation Adjustment: More active during physical exertion or respiratory distress.
Page 8: Fine Tuning Ventilation Control
Pontine Respiratory Center: Includes Pneumotaxic and Apneustic centers; regulate transition between inhalation and exhalation, influence breathing rate.
Page 9: Chemical Control of Ventilation
Respiratory centers automatically regulate breathing rhythms subconsciously, adjusting based on PO2, PCO2, and pH levels.
Chemoreceptors in peripheral and central locations sense varying gas levels to modulate ventilation.
Page 10: Chemical Control Overview
Key centers: Medulla, Pons, Spinal Cord; highlighting the roles of peripheral and central chemoreceptors in breathing control.
Page 11: Peripheral Chemoreceptors
Carotid Bodies: Located at the bifurcation of common carotid arteries; respond to changes in arterial PO2, PCO2, and pH.
Aortic Bodies: Located in the thoracic aortic arch; similarly responsive to arterial gas levels.
Page 12: Glomus Cells and Hypoxaemia
Mechanism: Hypoxaemia causes potassium channel closure in glomus cells, leading to depolarization and release of neurotransmitters, signaling respiratory control centers.
Page 13: Nerve Supply to Chemoreceptors
The carotid body is influenced by parasympathetic and sympathetic nervous systems, modulating sensitivity to oxygen levels.
Page 14: Carotid Body Functionality
Nerve impulse firing rate correlates with arterial PO2 levels; significant increases in firing are noted below PO2 of 60 mmHg.
Page 15: Responses to Inhaled CO2
Increased sensitivity to CO2 in conditions of low oxygen; higher ventilation at lower levels of oxygen in blood.
Page 16: Responses to Inhaled O2
Little respiratory system response to low oxygen without CO2 elevation; hypercapnia enhances sensitivity to hypoxaemia.
Page 17: Summary of Graph Interpretations
Main Drive: Hypercapnia (increase in CO2) is the primary driver for ventilation under normal oxygen conditions.
Highlighted importance of PO2 levels in determining respiratory effort.
Page 18: Peripheral Chemoreceptor Responses
Low levels of PO2 and/or high PCO2 increase ventilation; this also relates to acidosis, where ventilation helps to restore pH balance.
Page 19: Blood pH Homeostasis
Normal blood pH maintained by various buffers, critical for physiological functions; both acidosis and alkalosis can disrupt cellular functions.
Page 20: Bicarbonate Buffer System
The major extracellular buffer within the body; described through reversible reaction of CO2 and water forming bicarbonate and protons.
Page 21: Kidney and Lung Responses in pH Homeostasis
Kidneys regulate bicarbonate levels over days; lungs can quickly adjust CO2 levels to correct pH disturbances in minutes.
Page 22: pH Compensation via Ventilation
Relationship between CO2, bicarbonate, and protons illustrated; ventilation can adjust rapidly to correct metabolic acidosis.
Page 23: Summary of Peripheral Chemoreceptors
Carotid and aortic bodies respond chiefly to arterial PO2; greater sensitivity noted in hypoxaemic conditions.
Page 24: Central Chemoreceptors
Located in the ventral medulla, monitor changes in arterial PCO2 and reflect changes in pH indirectly, but not PO2 directly.
Page 25: Mechanism of Central Chemoreceptor Response
CC respond to pH changes in CSF due to CO2 levels; rapid diffusion of CO2 through the blood-brain barrier is critical in their function.
Page 26: Sensing Mechanisms of Central Chemoreceptors
CO2 enters the CSF freely, altering pH and thus increasing ventilation; chronic conditions require compensation by the kidneys.
Page 27: CNS Compensation for Chronic Conditions
Choroid plexus aids in regulating CSF composition; crucial for understanding respiratory responses.
Page 28: Choroid Plexus Functionality
Specialized tissue facilitates the regulated passage of substances into CSF; lacking protein means lower buffering capacity than blood.
Page 29: Compensation in Chronic Hypercapnia
Chronic high CO2 leads to increased bicarbonate reabsorption and synthesis over time, gradually normalizing pH levels.
Page 30: Chronic Hypocapnia and Buffers
Rare condition with hyperventilation; compensation mechanisms adjust bicarbonate transport to normalize pH levels over days.
Page 31: Timeframe for Compensation
Defining the timeline for bicarbonate adjustments in CSF and kidneys demonstrates the chronic nature of acid-base disturbances.
Page 32: Pulmonary Receptors in Breathing Control
Stretch Receptors: Protect against over-inflation; inhibited when lungs are fully inflated.
Irritant Receptors: Trigger cough reflex to clear large objects from airways.
J-receptors: Response to pulmonary pathologies; stimulate increased ventilation.
Page 33: Responses to pCO2 and pO2
Arterial PCO2 is the primary trigger for respiratory changes; peripheral receptors mainly respond to hypoxaemia.
Page 34: Inputs Affecting Respiratory Control
Multiple inputs from higher brain centers and various receptors signal to the respiratory centers.
Page 35: Summary of Respiratory Control Components
Integrates mechanoreceptors, chemoreceptors, and muscle proprioceptors in coordinating breathing.
Page 36: Conclusion
Review of respiratory control mechanisms and their importance in maintaining homeostasis.