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MP - Lecture 29

Regulation of Breathing

Medical Physiology – Lecture 29 Regulation of Breathing
Short term regulation of breathing by: Breath to breath rhythmicity and coordination
Long term regulation of breathing by: Maintenance of alveolar and arterial PCO2 and PO2
Rhythm of breathing is generating in the: Brainstem
Unlike heart, muscles of breathing: Have no inherent rhythmicity
Apnea No breathing
Dyspnea Air hunger, not enough air
Apneustic Breathing Inspiratory gasps
Tachypnea Rapid breathing
Medullary respiratory center is located in the: Reticular formation
Dorsal respiratory group functions as: Main site of rhythm for breathing
Input to the dorsal respiratory group is from: Vagal and glossopharyngeal nerves
The vagal nerve relays information from: Peripheral chemoreceptors and mechanoreceptors
The glossopharyngeal nerve relays information from: Peripheral chemoreceptors
Output from the dorsal respiratory is carried by: Phrenic nerve to diaphragm
Ventral respiratory group outputs to: Both inspiratory and expiratory muscles
Function of ventral respiratory group is to: Modulate rhythmic breathing (modulate inspiration)
During normal quiet breathing the ventral respiratory group is: Inactive
Ventral respiratory group becomes active when: Expiration is an active process (i.e. exercise)
Pontine respiratory group is also called the: Pneumotaxic center
The pneumotaxic center is located in the: Upper pons
Function of pontine respiratory group is: Inhibit/terminate inspiration and increase breathing rate
During normal quiet breathing the pneumotaxic center is: Inactive
Apneustic center is located in: Lower pons
Function of apneustic center is: Prevent inspiration termination (stimulate inspiration) causing apneusis
Hering-Breuer Reflex Stimulation of bronchial stretch receptors signals vagal afferents to terminate inspiration and prevent overinflating
Bronchial stretch receptors are located in: Smooth muscles of airways
Bronchial stretch receptors adapt: Slowly
Irritant receptors are located: Between airway epithelial cells
Irritant receptor function is: Cause bronchoconstriction in response to noxious substances
Irritant receptors adapt: Rapidly
Juxtacapillary receptors are located in the: Alveolar walls close to the capillaries
Function of juxtacapillary receptor is: Detect fluid imbalance
Pulmonary capillary bronchial receptors detect: Injury, congestion, and large lung inflation
Joint and skeletal muscle receptors detect: Muscle stretch (during limb movement)
Function of joint and skeletal muscle receptors are: Regulate inflation, dyspnea of loaded breathing, and hyperpnoea of exercise
Central chemoreceptors are located in: Ventrolateral surface of the medulla
Direct stimulation of central chemoreceptors is by: pH (H+) in CSF
Decrease in CSF pH causes: Hyperventilation to decrease CO2 and directly increase pH
Central chemoreceptors are not stimulated by: Hypoxia
Changes in blood PCO2 strongly affects: CSF/ISF pH
H+/HCO3- cannot diffuse across the: Blood brain barrier
Changes in PCO2 produces a large pH change in CSF/ISF because: Low buffering capacity in CSF/ISF
Negative Feedback Regulation of PACO2 PACO2 > 40 increases CSF/ISF PCO2, decreasing pH which stimulates central chemoreceptors to increase ventilation to decrease PACO2 and PaCO2
Peripheral chemoreceptors are in the: Carotid and aortic bodies
Carotid bodies are located in the: Bifurcation of common carotid arteries
Aortic bodies are located: Above and below the aortic arch
Peripheral chemoreceptors are stimulated by: Low PaO2 (<60 mmHg), high PaCO2, and low arterial pH
Compared to central chemoreceptors, peripheral chemoreceptors: Respond faster
Peripheral chemoreceptors are more sensitive to PaO2 than arterial O2 content because: Very high blood flow
Acute response to decreased PaO2 is: Increased VE
If PaCO2 is held constant with decreased PaO2, VE: Increases rapidly
If PaCO2 is allowed to decrease with ventilation, VE: Increases slowly
Response to low O2: Decreased inspired PO2 causes decreased PAO2 and PaO2, stimulating peripheral chemoreceptors to increase VE, pushing PAO2 and PaO2 towards normal
Difference between inspired PO2 and alveolar PO2 is lowered by: Increased VE
Response to PaCO2 is steeper if: PaO2 is low (Hypoxia)
pH is returned to normal in CSF/ISF during chronic PaCO2 increase by: Slow transport of H+/HCO3-
Long term stimulation by elevated PCO2 results in: Reduced stimulation of central chemoreceptors
Supplemental O2 for hypoventilating COPD patients can: Increase PaCO2
Increase in PaCO2 in COPD patients is because: Long term hypoventilation increases PaCO2 and decreases PO2, CSF/ISF PaCO2 increases but pH is normal with no hyperventilation, low PaO2 increases ventilation but supplied O2 decreases ventilation drive, causing further CO2 retention
Cheyne-Stokes Breathing Increased time lag between alveoli and chemoreceptors
At high altitudes, VA is initially signaled to: Increase by peripheral chemoreceptor because decreased PaO2, but VA increase lowers PaCO2 which stimulates central chemoreceptors to decrease ventilation to decrease pH
After a few days at high altitudes: H+/HCO3- transport lowers CSF pH stopping VA inhibition, so only increase of VA by peripheral chemoreceptor
During first week at high altitudes, kidneys excrete: HCO3- to lower plasma pH towards normal
Long term at high altitudes increases: Erythropoietin release to increase Hb content, also 2,3-DPG increase
Created by: emyang



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