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VentilationcontrolCJ
Control of Breathing, effect of altitude- CJ- 1/16/2013
| Question | Answer |
|---|---|
| Why is ventilation control necessary? | Because there are different O2 demands for different situations |
| Effectors in respiratory control | Muscles, especially diaphragm |
| Sensors in respiratory control | Chemoreceptors and stretch recepters in lungs |
| Sensor feedback in the respiratory control system | Respiratory control center in the medulla and pons |
| Respiratory control center is located in the | Medulla and pons |
| Role of respiratory control center | Generating a basic breathing pattern and integrating sensory and other information to modify breathing |
| Medullary respiratory center | Most important neurons, make basic breathing pattern |
| Apneustic neurons | Prolongs inspiration |
| Pneumotaxic neurons | Turns off inspiration to control tidal volume |
| Two divisions of the medullary respiratory center | Dorsal and Ventral |
| Dorsal respiratory group controls | Inspiration |
| Ventral respiratory group controls | Expiration but are normally quiescent because expiration is produced passively by simply turning off inspiration (normally) |
| When is the Hering-Breuer reflex activated? | In large tidal volumes |
| Hering-Breuer reflex | Stiulation occurs with lung inflation- Sends impulse via vagus to switch off neurons- Inhibits integrator neuron and inspiration turns off- receptors stop signal- inspiration |
| Lung irritant receptors stimulate | Rapid, shallow breathing and coughing |
| Stimulation of the J receptors and Bronchial C-fibers cause | Rapid and shallow breathing |
| Bronchial C fibers sense | Chemical composition of blood in the bronchial circulation |
| Where are J receptors found? | Alveaolar walls |
| What do J receptors sense | Engorgement of interstitial space (edema) |
| List the major groups of chemoreceptors in order of importance | 1. Central and 2. Peripheral |
| Where are central chemoreceptors located? | Medulla |
| Where are peripheral chemoreceptors located? | Aortic arch and Carotid split |
| Central chemoreceptors respond to the | pH in the CSF, which depends on arterial Pco2 |
| What makes the CSF more sensitive to H+ ions than the blood | The CSF lacks proteins so there is no buffer for the hydrogen ions |
| Explain how central chemoreceptors respond | The respond to H+ ions generated by the conversion of CO2 into carbonic acid in the CSF following diffusion of CO2 from blood to the CSF. |
| THE BBB IS IMPERMEABLE TO IONS | DON'T FORGET THIS OR YOU ARE SERIOUSLY STUPID |
| Peripheral chemoreceptors can respond to | Increased Pco2, Low pH, arterial hypoxemia |
| What is the most important parameter in controlling ventilation feedback? | Arterial Pco2 |
| An increase in 2mmHg of Pco2 will do what to ventilation | Double it! |
| What happens to chemoreceptors in COPD (why wouldn't you give a COPD patient pure O2) | Chronic hypoventilation causes the system to accept a new "set point" and central chemoreceptors become desensitized. Pure oxygen will cause the peripheral receptors to stop breathing and patient will die (<bad!) |
| Which chemoreceptors provide the main drive to breathe in COPD | Peripheral |
| Which chemoreceptors control 80% of the response | Central |
| Which chemoreceptors respond the fastest? | Peripheral |
| Explain breathing pattern often found in heart failure | Decreased O2 means central CR respond with a delay so hypoxia stimulates peripheral CR and cause hyperventilation. This decreases Paco2 but when the cetral CR finally detect decreased Pco2, they inhibit breathing and the Po2 falls again, causing hypoxia |
| Equation for Inspired O2 using barometric pressure | Pio2= (Pb-47) x .2093 |
| The higher the altitude, the __ inspired O2 | Less |
| O2 in atmosphere is always | 20.93% |
| List 4 acclimatizations to altitude | Hyperventilation, Polycythemia, O2 dissociation curve, Circulatory changes |
| Hyperventilation increases alveolar Po2 by | Decreasing Pco2, leaving more room for O2 |
| Describe the two stages of ventilation in alveolar hypoxia | 1. Hyperventilation causes respiratory alkalosis by removing CO2 and 2. Central CR slow hyperventilation once the pH is corrected with hyperventilation. After this, the limit of breathing is removed and ventilation increases again |
| Effects of acute mountain sickness | Headache, dizziness, palpitations,fatigue, insomnia, loss of appetite, nausea |
| Effects of acute mountain sickness are attributed to | Hypoxemia and alkalosis |
| Polycythemia | Increase in red blood cells that increases the O2 dissociation curve slope, helping to release O2 to the tissues more readily. Increased viscosity causes heart to work harder (bad!) |
| In moderate altitude, the O2 dissociation curve is shifted to the | Right |
| In high altitude, the O2 dissociation curve is shifted to the | Left |
| What positive changes occur in high altitude systemic circulation | Capillary formation and mitochondrial enzyme expression |
| What negative changes in Pulmonary circulation occur at high altitude? | Generalized hypoxic vasoconstriction leads to pulmonary arterial hypertension causing edema. This makes the heart work harder, leading to right side heart failure |
Created by:
mcasto
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