0901 - Respiratory Regulation Flashcards
Outline the central organisation of breathing
Consists 3 areas (sensors, controller, effectors)
Arterial CO2 is the primary driver - small changes in CO2 drive big changes in ventilation.
Sensors (central - CO2 and peripheral O2/H+) provide negative feedback to a control centre (CPG) in the brain (pons, medulla - rostral, intermediate, and caudal, and higher centres).
Afferents then go to the respiratory muscles to affect the feedback. CN’s 5, 7, 9, 11, 12 innervate in a particular order (upper airways, diaphragm and rib cage, glottis).
There are also tracheo-bronchial receptors (stretch and irritant) which respond to lung hyperinflation via CN X)
Where and how are CO2 and central pH sensed? How do these regulate respiration?
CO2 is sensed in the ventrolateral medulla, within the blood brain barrier. CO2 can easily penetrate the BBB, but H+ and HCO3- cannot. As a result, a rise in PaCO2 leads to a rapid decrease in CSF pH. It is actually the change in pH that is detected by the central chemoreceptor. Central chemoreceptor then alters respiratory drive - very good for acute situations, but lose sensitivity in COPD. This is overwhelmingly the primary sensor for respiratory drive.
Where and how are O2 and peripheral pH sensed? How do these regulate respiration?
PaO2 is sensed by glomus cells in carotid body (glomus caroticum), relayed by CN IX to the central pattern generator. Fast response to changing PaO2 (via O2-sensitive K+ channel). The response is potentiated (heightened) if high PaCO2 and low pH. While this sensor is only responsible for <20% of ventilatory drive, it is responsible for all increases in ventilation due to lower PaO2.
How do pulmonary mechanoreceptors regulate respiration?
3 types: Smooth muscle stretch - detects large inspiration, relays Hering Breuer reflex via CN X to shorten inspiration, bronchodilate, tachycardia, hyperpnoea (why?)
Airway epithelial irritant - detects hyperinflation, exo/endogenous irritants. Relays Hering Breuer via CN X, as well as cough, bronchoconstriction and mucus production.
Pulmonary interstitial (chest wall) - detect large hyperinflation, or exo/endogenous irritants. Relays apnoea followed by tachypnoea via unmyelinated C fibres in CN X. Also bronchoconstriction, bradycardia, hypotension, and mucus secretion.
How does the respiratory CPG work?
Has both CNS (CN/spinal neves) and ANS (vagal and SY) components, because it is linking blood vessels with skeletal muscles. It does not consist of a single ‘respiratory centre’ but rather control is distributed between the spinal cord, brainstem (medulla with CPG), Pons and other areas.
Different areas of the medulla correspond to inspiratory and expiratory control - consider it a rostral to caudal ‘inspiratory sandwich’ (expiratory nuclei as the bread). The CPG itself is based on tonic inspiration (constant) and occasional phasic expiratory. 3 pools of muscles:
A - dorsal group (NTS inputs from chemoreceptors), continuously drive inspiration (tonic), and to drive pool B.
B - Ventral group (NA, NPA) inputs from A and stretch receptors, drive later inspiration, and drive pool C.
C - Expiratory Group (NRF, NRA) Inputs from Pool B, and inhibits pool A. Thus, when B undertakes sufficient activity, C inhibits A, and you get phasic expiratory output.
Essentially, you’re stuck in inspiration (A) until you hit a certain level where A drives B to drive C to inhibit A and you get expiration.
How is respiration controlled during exercise?
Increased ventilation is matched by increased O2 uptake and CO2 output, keeping PaO2 and PaCO2 stable up to anaerobic threshold (90 L/min). Above this, lower pH drives ventilation very strongly, decreasing PaCO2 and increasing PaO2. Maximum ventilation is 120L/min (15x normal). PaCO2 will only ever stay stable or drop during exercise (unknown driver).
How is respiration controlled at high altitude?
Cheyne-stokes respiration (see diagram) - characterised by periods of apnoea followed by hyperventilation. Unknown mechanism, but suggested to be delay between peripheral and central chemoreceptors..
What are some abnormalities in respiratory control?
–Cheyne-Stokes: periods of apnoea followed by hyperventilation; seen at high altitude and during sleep, severe heart disease and brain damage. Mechanism ? (delay between peripheral and central chemoreceptors).
–Ataxic breathing: brain damage
–Apneustic breathing: after head trauma with damage to pons: inspiratory breathholds of many seconds followed by brief exhalations.
–Sleep apnoea: see other lectures.
