S4: CO2 transport & neural + chemical control of ventilation Flashcards
List the reactions of CO2 in blood
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)
State the normal range of blood pH
Between 7.35 – 7.45
State the equation of the bicarbonate buffer system
CO2 + H2O -> H2CO3 -> H+ + HCO3-
Describe bicarbonate production of red blood cells
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
State the proportion of CO2 travelling in various forms
60% - bicarbonate
30% - carbamino compounds
10% - dissolved CO2
Describe how bicarbonate buffers extra acid
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
Describe the buffering action of haemoglobin in red blood cells
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
Describe the process of transport of CO2 from tissues to lungs
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
What happens when venous blood arrives at the lungs?
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
Describe the formation of carbamino compounds
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
Describe ABG analysis for acidosis
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
Describe ABG analysis for alkalosis
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
Define hypoxia
Reduced level of tissue oxygenation
Can be due to either defective delivery or defective utilisation of oxygen by the tissues
Define hypoxaemia
Decrease in the partial pressure of oxygen in the blood
Define hypercapnia
A rise in alveolar, and hence arterial pCO2
Define hypocapnia
A fall in alveolar, and hence arterial pCO2
Define hyperventilation
Removal of CO2 from alveoli is more rapid than its production
Define hypoventilation
Removal of CO2 from lungs is less rapid than its production
Describe the respiratory pattern generator
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)
Describe the neural control of breathing
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
What is ondine’s curse?
A stroke which destroys the brainstem
Patient loses their ability to regulate their breathing involuntarily -> constantly have to tell their muscles what to do
Describe chemical control of ventilation
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
Where are peripheral chemoreceptors located?
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)
Describe the action of peripheral chemoreceptors
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
Where are central chemoreceptors located?
Specialised neurons located on the brain side of the blood brain barrier – bathed in CSF
Describe the action of central chemoreceptors
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
How do the central chemoreceptors sense changes in pCO2 and pH?
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
Describe the effect of chronic hypercapnia on central chemoreceptors
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
Describe the main causes of respiratory alkalosis
Breathe too fast/too deep and CO2 levels drop too low (hyperventilation)
Heart attack
Drug use
Panic attack
Describe the main causes of respiratory acidosis
Asthma
COPD
Acute pulmonary oedema
Severe obesity (can interfere with expansion of the lungs)
What acid-base change are you likely to get at increased amplitudes?
Respiratory alkalosis
Low partial pressure of oxygen results in hypoxia
Stimulates peripheral chemoreceptors
Resulting hyperventilation causes a reduction in pCO2
