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MP - Lecture 29
Regulation of Breathing
| Question | Answer |
|---|---|
| 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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