Control of ventilation (physio) Flashcards
Does O2 bound to Hb in exert pressure in the blood?
No
What is hypoxaemia?
Decreased arterial pO2
What is hypoxia?
Decreased tissue pO2
What is hypercarbia/hypercapnia?
Increased arterial pCO2
How does ventilation change in response to low arterial pO2?
Increased ventilation -> restore pO2
- hypoxic drive
How does ventilation change in response to high arterial pCO2/H+?
Increase ventilation -> increased CO2 excreted and H+ lost -> restores pH
- hypercapnic drive
Fn of chemoreceptors
Detect changes in chemical composition of blood
Name of the chemoreceptors found in the brain and peripherals
Medulla
- medullary chemoreceptors
Peripherals
- carotid body chemoreceptors
- aortic body chemoreceptors
What do the chemoreceptors in the brain sense?
Mainly pCO2
What does the chemoreceptors in the peripherals sense?
Mainly pO2
pCO2
H+
Flow of info when chemoreceptors detect change
Change detected by chemoreceptors -> brainstem (pons+medulla) (central control) receives input
- medulla -> send info to respi muscles (effectors) -> normal quiet ventilation
- pons -> changes in ventilation
How does the pons affect ventilation?
Modify rate and depth of ventilation
How does the medulla affect ventilation?
Rhythmic discharge of neurons affect automatic ventilation
- inspiratory grp of neurons stimulate inspiration
- expiratory grp of neurons stimulate expiration
What is stimulated during quiet ventilation and exercise?
Quiet ventilation
- diaphragm and external intercostal muscles -> contract/relax
Exercise
- stimulate accessory muscles
Eg of input that modifies output of respi center
Brian above pons including cerebral cortex -> voluntary and involuntary control
Chemoreceptors
Lung stretch receptors
- lungs stretched -> vagus nerve discharge inhibits inspiration -> prevent overstretching of lung
Lung C-fibre receptors
- stimulated by irritation and abnormal states
Joint/muscle propioceptors
- movement of joints stimulate ventilation
What nerves does the input from carotid and aortic body chemoreceptors travel via?
Glossopharyngeal and vagal nerves
What changes in arterial blood would stimulate increased ventilation?
Decreased pO2
Increased CO2
Increased H+
What changes in arterial blood would stimulate decreased ventilation?
Decreased pCO2
Decreased H+
Potent stimulator of ventilation
Increase in arterial pCO2
How does ventilation change as arterial pCO2 increases?
pCO2 increase beyond normal range -> ventilation increases proportionately
What is the level of pCO2 that causes ventilation to change?
45-70mmHg
What is the level of pO2 that causes ventilation to change?
<60mmHg
How does CO2 stimulate response in medulla?
Increased pCO2 -> CO2 diffuses across BBB -> form H2CO3 in ECF of brain -> dissociate to release H+ -> free H+ stimulates medullary chemoreceptor -> relay info to medulla -> increase ventilation
Diff in body’s response to chronic vs acute increase in pCO2 and why
Ventilatory drive less sensitive to chronic increase compared to acute
- body’s capacity for buffering acid increases in chronic CO2 retention -> decrease free ions in blood (less H+) -> less stimulation to medullary chemoreceptors
COPD pt’s main drive to increase ventilation and precautions to take when giving O2
Hypoxic drive
Careful to monitor % supplemental O2 given
What is normal plasma pH?
7.35-7.45
What is acidosis and alkalosis?
Acidosis = pH <7.35
Alkalosis = pH > 7.45
What is respi acidosis?
Respi sys fails to get rid of CO2 normally generated by tissues
- decreased ventilation
What is respi alkalosis?
Resp sys removes too much CO2
- inappropriately increased ventilation
What is metabolic acidosis?
Tissues generate excess acids/kidneys fail to get rid of acids
What is metabolic alkalosis?
Body has lost acid/gained excess alkali (HCO3-) from other sys
Main mechanisms of regulation of pH
Buffers
Respi and renal responses
Compensatory measures for metabolic acidosis
Initial change = increase in arterial H+ -> increased ventilation -> decrease pCO2 and H+
Compensatory measure for metabolic alkalosis
Initial change = decrease in arterial H+ -> decreased ventilation -> increased pCO2 and H+
Changes in arterial blood during exercise
Arterial pO2 no change despite increase in O2 consumption by exercising muscles
No change in arterial pCO2
- increased CO2 produced but increased pCO2 not normally detected
Increase arterial H+ measures
- lactic acid in severe exercise due to increased metabolism
Compensatory measures during exercise
Ventilation increases -> normal H+ and normal/decreased pCO2
Bring more O2 to muscles
- reduced Hb affinity for O2 in exercising muscles
Increased CO
Vasodilate muscle arterioles
