Chemical Control Of Breathing Flashcards
Normal parameters for serum: PACo2, PaO2, bicarbonate, ph
Packs: 4.7-6 KPa
PaO2: 9.3-13.3 KPa
Bicarbonate:22-26mmol/L
PH: 7.35-7.45
What happens to alveolar PO2 and PCO2 in hyperventilation? what could this lead to?
PO2 increases
PCO2 decreases
Could lead to respiratory alkalosis
What happens to alveolar PO2 and PCO2 in hypoventilation? What could this lead to?
PO2 decreases
Pco2 increases
Could lead to respiratory acidosis
How does hypocapnia occur? What can it lead to?
If PO2 changes without Change in PCO2, correction of Po2 will cause PCO2 to drop
Can lead to respiratory alkalosis
How are respiratory acidosis and alkalosis compensated for? How long does this take?
Ph depends on ratio of HCO3- to pCO2 so kidneys…
- increase HCO3- in resp acidosis
- decrease HCO3- in resp alkalosis
2-3 days
How does metabolic acidosis come about and how can it be compensated for?
Tissues -> acid -> + HCO3- -> fall in HCO3-> fall PH
Compensated for by increasing ventilation to lower PCO2
How does metabolic alkalosis come about? How can it be compensated for?
Plasma HCO3- increases e.g. after vomiting -> plasma Ph rises
Compensated for to a degree by decreasing ventilation (but limited as need O2 above 8kpa)
What sensors are part of the respiratory control pathway, where do they send Input to and where do these efferents reach?
Central chemoreceptors (H+), peripheral chemoreceptors (O2, CO2, H+), pulmonary receptors (stretch), joint/ muscle receptors (stretch/tension)
-> respiratory control centre
-> diaphragm
Inspiration -> external intercostal, accessory muscles
Exp -> internal ICM, abdo muscles
What makes up the peripheral chemoreceptors, what stimulates them and what effects do they have?
Carotid and aortic bodies
Large falls in pO2 stimulate these -> increase breathing, changes HR, changes blood flow distribution (increasing flow to brain & kidneys
What makes up the central chemoreceptors, what stimulates them and what effects do they have? Short and long term
In medulla of brain more sensitive to PCO2 changes. Acidification of CSF and ECF (separated from blood by BBB) from more PCO2 diffusing across stimulates neurones.
- > ventilation
- ve feedback control of breathing
Longer term control: choroid plexus cells control CSf [HCO3-]. This determines which PCO2 is associated with normal CSF PH.
What controls normal CSF PH?
CSF [HCO3-] sets the control system to a particular PCO2, can be reset by changing CSF [HCO3-]
What occurs in persisting hypoxia? Ph= 7.47
Hypoxia detected by peripheral chemoreceptors -> increases ventilation
But PcO2 will fall further -> decreased ventilation
So CSf composition compensates for altered PCo2 - choroid plexus cells selectively add H+ or HCO3- into CSF, central chemoreceptors accept the PCo2 as normal
What occurs in persisting hypercapnia?
Hypoxia and hypercapnia - respiratory acidosis - decreases Ph of CsF - peripheral and central chemoreceptors stimulates breathing but acidic Ph undesirable for neurones therefore choroid plexus needs to adjust PH of CsF by addition of HCO3-, central chemoreceptors accept high PcO2 as normal