Respiratory System II Flashcards
(24 cards)
Where does the respiratory rhythm originate?
The dorsal (mostly inspiratory) and ventral (inspiratory and expiratory) respiratory groups of the medulla - groups of neurons discharging action potential corresponding to respiratory rhythm. Dorsal signal ventral as well as phrenic nerve. Ventral are upper respiratory motor neurons for phrenic and intercostal nerves.
What is the role of the pons in respiratory rhythm?
signals the dorsal and ventral respiratory groups to modulate respiration and other higher brain centres e.g. cerebral cortex via it.
How do the respiratory groups of the medulla coordinate breathing?
They receive inputs from the carotid and aortic bodies as well as the vagus nerve carrying afferent fibres from the lungs. Inspiration is initiated by dorsal RG neurons, this intrinsic activity sums with afferent activity from lung stretch receptors to inhibit inspiration and commence expiration.
Describe the reciprocal inhibition of respiratory control
The activity of inspiratory respiratory motorneurons in the spinal cord is inhibited during expiration and vice versa. This is not a local reflex but originates in the D&VRGs.
What is the Hering-Breuer reflex
The smooth muscle of the upper airways has slow adapting stretch receptors, which send impulses to the dorsal respiratory group and inhibit respiratory activity and limit inspiration. Lung inflation reflex not normally active during quiet respiration but may regulate rhythm during exercise.
How does the cough and sneeze reflex work
receptors on the upper airways or nasal mucosa respond to irritants with a cough or sneeze respectively. A deep inspiration precedes forced expiration against a closed glottis, pressure builds and the glottis opens - air is expelled at speed, dislodging some mucus on the epithelium and carrying with it irritants.
What is the pulmonary chemoreflex?
When smoke and noxious gases are inhaled, rapid adapting irritant receptors in the airways cause them to constrict and secrete more mucous. pulmonary tachypnea, shallow rapid breathing, occurs if the lungs become congested, due to C-fibre endings in the interstitial space of the alveolar walls.
Where are peripheral arterial chemoreceptors found?
AKA carotid bodies, located above the carotid bifurcation on each side of the body. Afferent fibres travel alongside those from the ipsilateral carotid sinus up the carotid sinus nerve, a branch of the glossopharyngeal.
What do the carotid bodies detect?
They respond to changes in PaCO2, PaO2 and arterial pH. Afferents increase rate of discharge significantly as PaO2 falls below about 8kPa.
What happens when you start breathing pure oxygen?
Breathing pure O2 reduces the respiratory drive from the peripheral chemoreceptors (carotid bodies), and so breathing rate slows. This lasts about ten minutes until PaCO2 rises so that central chemoreceptors cause breathing rate to return to normal.
What happens during hypoxia (in terms of respiratory reflexes)?
Breathing rate increasing significantly, as peripheral chemoreceptors detect falling PaO2 - not if aortic and carotid sinus nerves are cut. Increased CO2 still stimulates a response following this section, so hypercapnia is mediated by central chemoreceptors
Where are the central chemoreceptors located?
In the medulla near the glossopharyngeal and vagus nerves, and provide most of the chemical stimulus to respiration at rest.
Describe the function of the central chemoreceptors
Increased PaCO2 results in increased PCO2 of CSF (H+ can’t cross blood-brain barrier), resulting in increased carbonic acid formation and hydrogen ion concentration in the CSF. As CSF has little protein to buffer these ions, pH changes and this is detected by the chemoreceptors.
What happens if the PaCO2 is consistently abnormal?
the central chemoreceptors become less sensitive to changes - CSF bicarbonate concentration is regulated by exchange with Cl- ions derived from plasma. Individuals become more reliant on peripheral chemoreceptors and hypoxic drive to regulate respiratory rhythm
Why should you not give pure oxygen to a COPD patient?
chronic obstructive pulmonary disease causes chronically high levels of carbon dioxide and central chemoreceptor insensitivity. When pure oxygen is given to these patients:
1. Peripheral chemoreceptors are suppressed – High oxygen levels reduce the hypoxic drive, leading to a decrease in respiratory rate.
2. Ventilation decreases – With slower breathing, CO₂ is not adequately expelled, leading to CO₂ retention (hypercapnia).
3. Respiratory acidosis and CO₂ narcosis – Excessive CO₂ can cause confusion, drowsiness, and even coma.
Define hypercapnia, hypocapnia, hypoxaemia and anoxia.
Ain’t typing that its obvious
What is the principal chemical stimulus to respiration?
PCO2 of the alveolar air. Any change in PaCO2 quickly results in a proportional change in respiration to restore it to ~5.3kPa. Hypoxia doesn’t elicit increased ventilation strongly until alveolar PO2 falls below ~8kPa, below which any decrease causes steep increase in ventilation.
Why does change in alveolar PO2 have such a small effect on ventilation?
At a partial pressure of about 8kPa, the oxyhaemoglobin dissociation curve still shows about 90% saturation, but below this it begins to fall rapidly. At atmospheric pressure (101kPa), hypoxia is a weak stimulus.
How do respiratory influences of PO2 and PCO2 interact?
Increase in ventilation with increasing PaCO2 becomes steeper as PaO2 falls - sensitivity of respiratory drive to carbon dioxide is greater during hypoxia. Strong synergistic rather than additive interaction - important during breath holds.
What are some other influences on respiration?
Limbic system stimulation - anticipation of activity can increase ventilation. Breathing rate also correlates with body temperature and cold water exposure can cause temporary apnea. Severe pain -> brief apnea. Prolonged somatic pain -> increased breathing rate. Visceral pain may slow rate.
What is Ondine’s curse
Medically called congenital central hypoventilation syndrome, caused by bulbar poliomyelitis or certain brainstem lesions that result in loss of automatic regulation of respiration, keeping voluntary. Causes central sleep apnea syndrome
What are the two types of sleep apnea?
Obstructive sleep apnea is due to physical blocking of the airways during sleep - e.g. obesity. Central sleep apnea is due to CNS respiratory centres not responding to rising CO2, e.g. stroke, morphine.
What is Henry’s law?
At equilibrium, the amount of gas dissolved in a liquid (with which it does not chemically combine) is proportional to the partial pressure of the gas it is exposed to. V=sP or Amount dissolved = solubility coefficient × partial pressure.
