the physiology of carbon dioxide

CO₂

waste product of aerobic respiration

CO₂ is produced by the (?) cycle part of respiration

citric acid

oxidation of acetyl-Coa produces ATP and (?)

CO₂

mitochondria in cells use glucose and oxygen to produce:

CO₂, water and energy

transport of CO₂ to the (?) for removal from the body

lungs

CO₂ % distribution in the blood

• 90% diffuses into red blood cells

• 5% dissolved into blood plasma

• 5% binds to proteins (haemoglobin)

in red blood cells, CO₂ is rapidly converted to H+ and (?) by the enzyme:

converted to H+ and bicarbonate by the enzyme carbonic anhydrase

CO₂ is quickly converted into HCO3- which allows for the continued uptake of CO₂ into the blood down its:

concentration gradient

acidosis

occurs when there are too many H+ ions in the blood

what occurs chemically when HCO3- reaches the lungs? (refer to equation)

• HCO3- combines with H+ produced by the oxygenation of deoxyhemoglobin to produce water and CO2

• CO2 diffuses into the alveoli and is exhaled as a waste product

what is the normal partial pressure of arterial CO₂

35-45mmHg

hypercapnia

too much CO₂ in the blood

hypocapnia

too little CO₂ in the blood

what can occur to the pH of the blood when there is too much CO₂

pH can drop below normal levels

hypoventilation (not breathing enough) can result in (?) levels of CO₂ which leads to what type of acidosis?

high → leads to respiratory acidosis

examples of respiratory diseases/impairments that cause abnormally high levels of CO₂

• Chronic lung diseases (COPD, emphysema)

• Respiratory depression

• Severe asthma

• Hypoventilation

• Obstructive sleep apnoea -> problems with breathing when asleep

treatments that restore normal blood gas levels

1. Improving ventilation

• Mechanical ventilation

• Intubation

2. Treat underlying cause of hypoventilation

• Use of bronchodilators

• Antibiotics (if infection is the cause)

3. Oxygen therapy

• Oxygen tank

CO₂ excess can be caused by breathing CO₂ rich air (list 3 settings)

1. In unventilated indoor areas

• Classrooms

• Submarines

• Basements

2. Occupational setting (workplaces)

• Welders

• Firefighters

• Confined spaces

3. Natural environments

• Volcanic areas

• Caves

CO₂ levels (see more)

1. Very high levels of CO2

• In submarines and spacecrafts

• 3000-5000ppm

• Typically exposed for days to months

 

2. High levels of CO2

• In poorly ventilated classrooms/ offices/ public transport

• 1000-3000pm

• People typically exposed for hours

 

3. Elevated

• Our current atmosphere

• Level currently 425ppm

• 40% higher than pre-industrial levels

• People exposed to this throughout life

health effects of increasing levels of CO₂ exposure

• 400ppm → normal air

• 1000-2000ppm → drowsiness and difficulty concentrating

• 2000-5000ppm → confusion, headache, and dizziness

physiological response/mechanisms to high CO₂ (list 4)

1. Bicarbonate buffer system

2. Pulmonary compensation

3. Renal compensation

4. Osteological compensation

bicarbonate buffer system

• Maintains optimal pH of blood

• Neutralises excess acid or base

 

1. Too many H+

• HCO3- binds with excess H+ to form carbonic acid

• Carbonic acid can dissociate into CO2 and water

2. Too little H+

• Carbonic acid releases H+ (and HCO3-)

pulmonary compensation

• Central and peripheral chemoreceptors detect changes in the chemical composition of the blood

• Communicate to the respiratory centre in the medulla to increase or decrease ventilation

 

1. Central chemoreceptors

• Located in the brain

• Detect pH of cerebrospinal fluid

 

2. Peripheral chemoreceptors

• Located in the carotid and aortic bodies of the heart

• Detect pH of blood as well as O2, CO2, and H+ levels

peripheral vs central chemoreceptor response to elevated CO₂ levels

1. Central chemoreceptors

• Blood brain barrier is permeable to CO2

• Increase in CO2 will cause more CO2 to diffuse across blood brain barrier

• Drives increase in H+ which is sensed by central chemoreceptors

• Communicated to respiratory centres

• Promotes increase in ventilation

 

2. Peripheral chemoreceptors

• Increase in blood CO2 and H+ sensed by peripheral chemoreceptors

• Communicated to respiratory centres promoting increase in ventilation

renal compensation

• Adjusting excretion of H+ and HCO3- via kidneys

• Increase in CO2 in blood will increase H+

• This increases HCO3- reabsorption

• And increases H+ excretion 

renal compensation mechanism (explained)

1. H+ is excreted into the filtrate via Na+/H+ exchangers

2. Some H+ in filtrate combines with HCO3- to form CO2 and H2O

3. CO2 diffuses into tubule cell, combines with H2O to produce H+ and HCO3-

4. H+ produced from 3. is excreted into the filtrate via Na+/H+ exchangers

5. HCO3- produced from 3. is reabsorbed into the blood via Na+/HCO3- exchangers

6. NH3 combines with H+ to form NH4+ which is excreted into the filtrate

7. NH4+ and H+ is excreted via urine overall

osteological compensation

• Bones are made up of minerals that can help maintain normal blood pH

• Chronic acidosis causes bone reabsorption

• Osteoclasts break down and release CO32- and PO43-

• These ions act as buffers by binding to excess H+ ions and raising blood pH

• Long term this can lead to bone weakening (osteoporosis)

short term exposure to elevated CO₂ levels is easily (?)

reversible

long term exposure to elevated CO₂ levels can:

lead to renal and osteological impacts

Increasing levels of atmospheric CO2 (can/can’t) be withstood by our ventilatory, renal acid-base compensatory mechanisms and bicarbonate buffering system

can

can we cope with the increasing rise in CO₂ exposure?

summary

lecture outcomes