Respiratory Physiology II PDF
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Jordan University of Science and Technology
Rawan Asrawi, Yanal Shafagoj
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Summary
This document discusses the regulation of respiration, covering topics such as the control of breathing, feedback systems, and the role of the respiratory centers in the brain. It also details the functions of carotid and aortic bodies. The respiratory system, its components, and the physiological processes involved in gas exchange are explained.
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9 Dental student Rawan Asrawi + Dental student Yanal Shafagoj Regulation of Respiration We are going to talk about the controller system (control of breathing ) →The purpose of control breathing is to maintain normal ABGs (Homeostasis of O2 , CO2 , H+) (PaO2=100 , PaCO2= 40 , PH= 7.4) → What are the...
9 Dental student Rawan Asrawi + Dental student Yanal Shafagoj Regulation of Respiration We are going to talk about the controller system (control of breathing ) →The purpose of control breathing is to maintain normal ABGs (Homeostasis of O2 , CO2 , H+) (PaO2=100 , PaCO2= 40 , PH= 7.4) → What are the tools? ↑ventilation or ↓ventilation *What is the feedback system…(nature of the receptor)? ↓ PaCO2 , ↑PaCO2 , ↓ PaO2 (below 60 mmHg, if it was more than 60 there would be no effect because respiratory centers in medulla oblongata will not work), ↓ H+, and finally ↑H+ Note: increasing in We mean by feedback system: if there PaO2 has no effect on is a problem how it will be corrected controller or feedback →This is the brain stem → consists of mid-brain + pons + medulla oblongata (connected with spinal cord). -In Medulla oblongata we have respiratory center -In medulla 2 collections of neurons: 1 is located Dorsally (DRS) and 1 is located ventrally (VRN) DRN → inspiratory:I neurons VRN → inspiratory and expiratory.: I +E neurons systems Center: collection of neurons having related functions, ex: cardiac center and the vascular center DRN= dorsal respiratory neurons VRN: ventral respiratory neurons →These neurons will send signals to phrenic neurons located At (C3-C5) SPINALNEVES (the origin of phrenic nerve) then the signal will be transmitted to the diaphragm through phrenic n ( also called diaphragmatic n ) and this will cause contraction of diaphragm. The upper 1/3 of the pons (called Pneumotaxic center) switches off DRN ,and the Lower 1/3 (Apneustic center) switches on DRN →There are signals from periphery (as another feedback) from lung and arterial system acts on DRN -Diaphragm is skeletal muscle it is voluntary (needs motor neuron..no automaticity as in the heart),so can you stop breathing?? Yes, but up to certain limit. -In medulla there is other center which sensitive to H+ called chemo-sensitive area it is sensitive to change in [H+], ex: when there is acidosis (↑H+) that activates through chemosensitive area which stimulate DRN → PHRENIC N → contraction of diaphragm → more ventilation →In aortic arch and in the carotid artery there is aortic bodies and carotid bodies, respectively (carotid bodies are more important, they are very small and they send impulses to DRN about PaO2 Aortic body → through vagus n, carotid body → through glossopharyngeal n *let's revise things from previous sheets: O2 uptake from alveoli = 350 ml (1/7 from FRC) and PAO2 = 100 (should O2 (intake)= O2 (uptake)) but if ventilation increases (O2 intake > uptake) So PAO2> 100, specifically it will be 150 (not 160 due to H2O vapor) PACO2 becomes 0, Here we have Hyper ventilation. Hyper ventilation is when you try to make the composition of air inside alveoli closer to Note: PaO2 is as composition of outside air by definition when same as PAO2 PaCO2 decreases below 40 mmHg How can we make PAO2 more than 150? PaO2 or We make the percentage of O2 more than PAO2 The dot means liter/min V 21% When we reverse axis (PO2 on the x axis → independent): →If we increased PaO2 above 60 the ventilation will not be affected →if we decreased PaO2 below 60 there will be Hyperventilation 1= 4.2 L → For CO2 the opposite will occur since when we increase the alveolar ventilation Pco2 will decrease until 0 When we reverse axis: If PaCO2 becomes more than 40 there will be hyperventilation to wash it out (linear relation ) PaCO2 If someone decided to hold his breath, (the signal come out from the cortex of the brain)→ this (negative or decreasing) signal goes to the phrenic neurons → to the diaphragm →the ventilation stops, but you can’t hold your breath for ever, So: If ventilation decreases→ PaCO2 will increase→ then CO2 will cross the arterial blood to the BBB (blood brain barrier/CSF barrier) →CO2 will bind with H2O to produce H2CO3 that will dissociate into H+ and HCO3- →THEN H+ will go to chemo-sensitive area in medulla that will activate DRN → PHRENIC N → contraction of diaphragm → more ventilation. H+ can't cross BBB but CO2 can cross any membrane as if CO2 works indirectly here it is not exist H+ can cross but slowly. (through the H+) → This negative feedback happen by the H+ increment (acidosis), as example: after taking one pack of aspirin, the H+ takes time to enter the CSF (slow, because it is a charged molecule). We mentioned before carotid and aortic bodies, but how are they going to be able to tell the DRN about the levels of arterial PO2? Arterial PO2 is 100, interstitial PO2 is 40 and inside cells