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Phys2 Cont of Vent
| Question | Answer |
|---|---|
| Why is ventilation control necessary? | To maintain BL PO2 and PCO2 levels. B/c O2 demand and CO2 production vary depending on what we are doing. **Hypoventilation can cause Dec PO2, Inc PCO2, and Dec pH. |
| What type of control system is ventilatory control? | NEGATIVE feedback |
| Ventilatory control system: Effector | Repiratory muscles (diaphragm, ext intercostals) |
| Ventilatory control system: Sensor | 1.Chemoreceptors (regulate arterial PO2 and PCO2). 2.Lung receptors: respond to inflation and irritants. |
| Ventilatory control system: Controller | Respiratory center in the Medulla and pons (brainstem). |
| Ventilatory control system: variables | Arterial PO2 and PCO2. |
| Location of respiratory control center? | Medulla and Pons |
| 2 basic types of neurons in the respiratory control center? | 1.Pattern generator: responsible for generating basic pattern breathing. 2.Integrators: integrate sensory feedback from chemorecep, lung recep, hypothalamus/Limbic system, cortex (emotions). |
| 3 main groups of neurons controlling inspiration and expiration and their functions | 1.Medullary respiratory center (most important). 2.Pneumotaxic center (upper pons): Turns off inspiration, tweeks Vt and RR. 3.Apneustic center (lower pons): Prolongs inspiration. |
| 2 types of neurons in the medullary respiratory center | 1.Dorsal respiratory group (dorsal medulla): trigger inspiration. 2.Ventral respiratory group (ventral medulla): involved with expiration, so they are inactive at rest. |
| What activates the inspiratory neurons? | Integrator neurons. They synch up inspiration and expiration. Get EXCITATORY input from chemorecep and lung irritant recep and IHIBITORY input from "switch off" neurons. Net input determines action. |
| What controls the "off switch" neurons that send inhibitory signals to the Integrator neurons? | Activated by: 1.Lung stretch receptors, 2.Pneumotaxic center in the upper pons. Inhibited by: 1.Apneustic area of lower pons. |
| Hering-Breuer reflex | 1.Inflation stim lung stretch receptors. 2.CN X carries impulses to activate "off switch" n. 3.Off-swith n. inhibit intergratory n. (turning off inspir). 4.deflation of lungs leads to loss of stim of stretch recep and inh of intergrator n. |
| How much stretch during inhalation must occur to activate the Hering-Breuer reflex? | Tidal Volume (Vt) >1L. |
| Hering-Breuer reflex: What affects does cigarrette smoke and cold air have on lung irritant receptors? | Promoting inspiration and coughing. they accomplish this by directly activating integrator neurons. |
| Lung receptors: J-receptors | 1.Location: Alveolar wall. 2.Stimuli: Inc interstitial fluid (Edema). 3.Neuronal pathway: CN X. 4.Effects: Rapid shallow breathing |
| Lung receptors: C-receptors | 1.Location: Bronchioles. 2.Stimuli: chemical composition of bronchiole BL, Inflammatory mediators. 3.Neuronal pathway: 4.Effects: Bronchoconstriction and rapid shallow breathing. |
| What are the most important receptors in ventilation control? | CHEMORECEPTORS (central and peripheral) |
| Central chemoreceptors | Location: ventral medulla close to medullary respiratory center. Stimuli: H+ (indirectly, PCO2) in CSF, CO2 creates more H+ here than interstitially b/c of the lack of proteins. Effect: Inc Ventilation **more important for minute by minute chages. |
| Peripheral chemoreceptors | Location: Carotid sinus, Aortic bodies. Stimuli: Dec PO2/hypoxia (ex: COPD and altitude), Inc PCO2 & H+ |
| Can H+ ions in the BL stimulate central chemorecpetors? | NO, their ionic charge wont allow them to cross the BBB |
| Why does CO2 have a greater H+ production effect in CSF than BL? | Lower protein content in CSF to buffer the H+ (Hb does this in BL). Effect: Increased ventilation. |
| Which parameter is most important for control of breathing under normal conditions? | Arterial PCO2 **b/c relationship b/w PCO2 and ventilation is very steep (2mmHg PCO2 Inc DOUBLES ventilaion) |
| Are peripheral chemoreceptors sensative to O2? why or why not? | Not really, arterial PO2 must be reduced to <50mmHg in order to significantly Inc ventilation. |
| Why does pure O2 decrease ventilation in COPD patients? | B/c they have no central chemorecep (due to body's adjustment to chronic Inc PCO2), they must rely only on peripheral chemorecep. Chronic Inc O2 will cause those receptors to dec activation & the drive to breathe is diminshed (hypoventilation, Inc PCO2) |
| Peripheral Vs Central Chemoreceptor's response to PCO2 | Peripheral respond faster but only contribute 20% of total response to CO2. **May be due to closeness to lungs. |
| What chemoreceptors will be activated: Inc PCO2 | 1.Central 80%. 2.Peripheral 20%. |
| What chemoreceptors will be activated: Dec PO2 | **Peripheral ONLY** |
| What is a typical Cheyne-stokes breathing pattern? | rapid increases and then decreases in ventilation followed by prolonged apnea. |
| When is Cheyne-stokes commonly seen? | 1.End of Life (goodbye). 2.HF. |
| Mechanism behind Cheyne-stokes | 1.Dec CO causes slowed circulation. 2.This Dec central response time to PCO2 change. 3.Hypoxemia stimulates peripheral. 4.J-receptors cause hypervent. 5.Dec PCO2. 6.Delayed central detection of dec PCO2, then they inhibit breathing. 7.Starts over |
Created by:
WeeG
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