S4: CO2 transport & neural + chemical control of ventilation Flashcards

1
Q

List the reactions of CO2 in blood

A

1) Dissolved CO2
2) CO2 reacts chemically with water to form bicarbonate – HCO3-
3) CO2 reacts with Hb to form a carbamino-haemoglobin compound (carbamino)

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2
Q

State the normal range of blood pH

A

Between 7.35 – 7.45

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3
Q

State the equation of the bicarbonate buffer system

A

CO2 + H2O -> H2CO3 -> H+ + HCO3-

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4
Q

Describe bicarbonate production of red blood cells

A

Enzyme carbonic anhydrase present in RBCs but not present in plasma
In tissues: reaction in RBC proceeds in forwards direction and hence produces HCO3-
HCO3- is transported out of the RBC chloride:bicarbonate exchanger
H+ is bound to haemoglobin
RBC makes HCO3-, but does not control the concentration of it – this is done by the kidney

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5
Q

State the proportion of CO2 travelling in various forms

A

60% - bicarbonate
30% - carbamino compounds
10% - dissolved CO2

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6
Q

Describe how bicarbonate buffers extra acid

A

Acids react with HCO3- to produce CO2
Pushes reaction to the left
CO2 levels increase – removed by breathing & pH changes are minimised
More HCO3- needs to be produced to replenish buffers

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7
Q

Describe the buffering action of haemoglobin in red blood cells

A

Buffering depends on level of oxygenation
If more O2 binds Hb -> R-state & less H+ ions bind = at the lungs
If less O2 binds Hb -> T-state & more H+ ions bind = at the tissues

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8
Q

Describe the process of transport of CO2 from tissues to lungs

A

Hb binds more H+ in RBCs in venous blood -> more HCO3- can be produced as decreased H+ drives reaction to the right
More HCO3- transported out of RBCs into plasma in venous blood = increased the amount transported of CO2 in the form of HCO3-
Increased dissolved CO2 in blood as well

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9
Q

What happens when venous blood arrives at the lungs?

A
Hb picks up O2 & goes into R-state
Causes Hb to give up the extra H+ it took on at the tissues
H+ reacts with HCO3- to form CO2
Reaction is pushed to the left 
CO2 is breathed out
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10
Q

Describe the formation of carbamino compounds

A

Binds directly to amine groups on globin of Hb
More carbamino compounds are formed at the tissues – pCO2 is higher & unloading of O2 from Hb facilitates binding of CO2 to Hb (T-state binds CO2 better)
This CO2 is given up at the lungs as Hb becomes oxygen rich
Oxygenated Hb unloading CO2 = Haldane effect

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11
Q

Describe ABG analysis for acidosis

A

pH < 7.35 = acidosis
If pCO2 raised = respiratory acidosis (if normal/low, not respiratory acidosis)
If HCO3- decreased = metabolic acidosis
If respiratory acidosis: HCO3- elevated = compensation, if pH 7.35-7.39 = full compensation, if pH < 7.35 = partial compensation
If metabolic acidosis: pCO2 decreased = compensation, if pH 7.35-7.39 = full compensation, if pH < 7.35 partial compensation

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12
Q

Describe ABG analysis for alkalosis

A

pH > 7.45 = alkalosis
If pCO2 low = respiratory alkalosis (if normal/elevated, not respiratory alkalosis)
If HCO3- increased = metabolic alkalosis
If respiratory alkalosis: HCO3- decreased = compensation, if pH 7.4-7.45 = full compensation, if pH > 7.45 = partial compensation
If metabolic alkalosis: CO2 increased = compensation, if pH 7.4-7.45 = full compensation, if pH > partial compensation

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13
Q

Define hypoxia

A

Reduced level of tissue oxygenation

Can be due to either defective delivery or defective utilisation of oxygen by the tissues

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14
Q

Define hypoxaemia

A

Decrease in the partial pressure of oxygen in the blood

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15
Q

Define hypercapnia

A

A rise in alveolar, and hence arterial pCO2

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16
Q

Define hypocapnia

A

A fall in alveolar, and hence arterial pCO2

17
Q

Define hyperventilation

A

Removal of CO2 from alveoli is more rapid than its production

18
Q

Define hypoventilation

A

Removal of CO2 from lungs is less rapid than its production

19
Q

Describe the respiratory pattern generator

A

Centres in the CNS which produce certain patterns
Specialised circuit which facilitates some type of stereotyped behaviour – respiratory rate typically 12 times a minute
Located in the brainstem (medulla and pons)

20
Q

Describe the neural control of breathing

A

RPG has four different inputs: pO2, pCO2, pH & lung stretch (vagus nerve gives info about this)
Basic rhythm of respiration set by the inspiratory neurons -> muscles of inspiration; expiratory neurons -> muscles of expiration (quiet as it is a passive process, unless exercising)
Both groups of neurons can inhibit each other to ensure we are either inspiring or expiring (system of mutual inhibition)
Able to override the pattern generator – voluntary connection from the cerebral cortex which can regulate activity of the motor neurone in the spinal cord

21
Q

What is ondine’s curse?

A

A stroke which destroys the brainstem
Patient loses their ability to regulate their breathing involuntarily -> constantly have to tell their muscles what to do

22
Q

Describe chemical control of ventilation

A

Peripheral chemoreceptors – sense pO2, pCO2 and pH levels
Central chemoreceptors – sense pH and pCO2 levels
Send information to the brain respiratory centres -> results in adjustments both in depth and frequency of ventilation as needed

23
Q

Where are peripheral chemoreceptors located?

A

Carotid bodies – located in the bifurcation of the common carotid arteries (sensory innervation = CN IX)
Aortic bodies – located in the aortic arch (sensory innervation = CN X)

24
Q

Describe the action of peripheral chemoreceptors

A

Both bodies primarily sensitive to decreases in arterial pO2, although high pCO2 and low pH can also stimulate
Sense hypoxaemia & signal cells in the medulla to increase ventilation
Rapid responders – first chemoreceptor to respond

25
Q

Where are central chemoreceptors located?

A

Specialised neurons located on the brain side of the blood brain barrier – bathed in CSF

26
Q

Describe the action of central chemoreceptors

A

Sense increases in arterial pCO2 and (much more slowly) decreases in arterial pH, but NOT pO2
When blood-gas parameters nearly normal, central chemoreceptors are the primary source of feedback to the brainstem for needed adjustments

27
Q

How do the central chemoreceptors sense changes in pCO2 and pH?

A

BBB has a high permeability to small molecules like CO2
CO2 diffuses into CSF, bathing the brain cells, including the central chemoreceptor neuron cells
Very limited HCO3- buffering capacity, so acidosis develops
Small decreases in pH -> raise firing rate of central chemoreceptors -> increasing ventilation

28
Q

Describe the effect of chronic hypercapnia on central chemoreceptors

A

If CO2 remains elevated, pH of CSF slowly recovers -> choroid plexus increases active transport of HCO3- into CSF
Bicarbonate buffers protons generated by increased CO2
Represents CNS metabolic compensation to respiratory acidosis
This adjustment means that a higher level of CO2 is needed to cause acidosis and thereby increase ventilation -> CO2 drive for ventilation has been reset at a higher level

29
Q

Describe the main causes of respiratory alkalosis

A

Breathe too fast/too deep and CO2 levels drop too low (hyperventilation)
Heart attack
Drug use
Panic attack

30
Q

Describe the main causes of respiratory acidosis

A

Asthma
COPD
Acute pulmonary oedema
Severe obesity (can interfere with expansion of the lungs)

31
Q

What acid-base change are you likely to get at increased amplitudes?

A

Respiratory alkalosis
Low partial pressure of oxygen results in hypoxia
Stimulates peripheral chemoreceptors
Resulting hyperventilation causes a reduction in pCO2