Respiratory Control Of Breathing Flashcards
Define hypercapnia
Abnormally high carbon dioxide concentration in the blood
Define hypoxia
Deficiency of oxygen in tissues
Define hypocapnia
Abnormally low concentration of carbon dioxide in the blood
Define hyperventilation
Breathing at an abnormally rapid rate at rest
Ventilation changes with no change in metabolism
Define Hypoventilation
Breathing at an abnormally shallow and slow rate
What is the effect of hypo and hyperventilation on carbon dioxide concentration in the blood?
Hypoventilation - increases carbon dioxide concentration, decreases pH
Hyperventilation - decreases carbon dioxide concentration, increases pH
What is respiratory failure?
When not enough oxygen enters the blood
When not enough carbon dioxide leaves the blood
Don’t necessarily have to occur together
What is type I respiratory failure?
Not enough oxygen enters the blood but carbon dioxide removal is normal
Low oxygen, normal or low carbon dioxide
What is type II respiratory failure?
When not enough oxygen enters the blood and not enough carbon dioxide leaves the blood
pO2 in arterial blood is low
pCO2 is high
What happens to carbon dioxide and oxygen in hyperventilation?
pCO2 will fall
pO2 will rise
What can severe hyperventilation lead to?
Rise in pH
Respiratory alkalosis
Lethal tetany because free calcium concentration falls
Why does an increase in pH cause tetany?
Calcium is only soluble in acid
Leaves blood when pH rises
Nerves become hyperexcitable
What happens in hypoventilation?
pCO2 rises and pO2 falls
If pH falls below 7.0, enzymes become lethally denatured
Define respiratory acidosis
When lungs cannot remove enough carbon dioxide produced by the body, causing a fall in pH
Define respiratory alkalosis
Wher hyperventilation raises blood pH
Associated with hypocapnia
Define compensated respiratory acidosis
When respiratory acidosis persists, kidneys respond to low pH by reducing excretion of HCO3-, thus restoring ratio of CO2:HCO3
Define compensated respiratory alkalosis
When respiratory alkalosis persists, kidneys respond to high pH by excreting HCO3 and restoring ratio of CO2:HCO3
Takes 2-3 days
What are the values for it to be classed as metabolic acidosis?
pH < 7.35 and
Plasma [HCO3-] < 22mmol/L
What normally occurs with metabolic acidosis?
Respiratory compensation - hyperventilation
What is metabolic alkalosis?
When plasma pH rises and [HCO3-] rises
What value does pO2 need to be kept above?
8kPa
Which gas needs to be controlled precisely? Why?
Carbon dioxide
To avoid acid-base problems
Where are peripheral chemoreceptors located and what do they respond to?
Carotid and aortic bodies
Changes in carbon dioxide by a rise of 1.3kPa
Fall in pO2
Change in H+ concentration of blood
Pros and cons of peripheral chemoreceptors?
Not particularly sensitive
Respond quickly to large pCO2 changes
If pCO2 rises, what is the chemoreceptors response?
Send impulses to medulla oblongata
This sends nervous impulses to external intercostal muscles and diaphragm via intercostal nerve and phrenic nerves
This increases tidal volume and rate of respiration
Changes circulation, directing more blood to brain and kidneys
Increases pumping of blood by heart
Where are central chemoreceptors located?
Medulla of the brain
What do central chemoreceptors do?
Detect changes in pH a of cerebrospinal fluid
If there is an increase in carbon dioxide, what do central chemoreceptors do?
Stimulate breathing
What controls the concentration of HCO3 in CSF and why?
Choroid plexus cells
HCO3- cannot diffuse across the blood brain barrier so cannot be controlled by the kidneys
What controls the CSF pCO2?
Arterial CO2
Why are central chemoreceptors more sensitive?
[HCO3-] of CSF is fixed in the short term because it cannot diffuse across the BBB
Change in pCO2 will change the pH (increase in CO2, fall in pH)
What is the feedback control for central chemoreceptors?
Elevated pCO2 drives CO2 into CSF across BBB
CSF pH falls, detected by central chemoreceptors
Drives increased ventilation, lowers pCO2, restores CSF pH
Role of choroid plexus in setting pH?
CSF [HCO3-] determines which pCO2 is associated with a ‘normal’ CSF pH
Therefore CSF [HCO3-] sets control system to a pCO2
Can reset by changing [HCO3-]
Symptoms of type 1 respiratory failure?
Exercise intolerance
Breathlessness
Central cyanosis
What can cause type I respiratory failure?
(Reduced transfer of oxygen to blood from alveoli)
Poorly perfused alveoli due to a pulmonary embolism
Poorly ventilated alveoli due to pneumonia, consolidation, early stages of acute asthma
When, in type I respiratory failure, is ventilation and perfusion not matched?
Poor oxygen uptake in some alveoli cannot be compensated by increased uptake in others
What problems can lengthen the diffusion pathway?
Pulmonary oedema Asbestosis Fibrosis alveolitis Extrinsic allergic alveolitis Pneumoconiosis
What is type 2 respiratory failure due to? (Oxygen not getting in)
A ventilation failure
What can cause type II respiratory failure? (Oxygen not getting in and Co2 not getting out)
Respiratory depression due to narcotics - opioid analgesics
Muscle weakness (upper/lower motor neurones)
Chest wall problems
- scoliosis/kyphosis
- trauma
- pneumothorax
Difficulty ventilating lungs due to
- high airway resistance
- COPD
- asthma
Acute effects of type II resp failure?
Increased pCO2 and decreased pO2
Breathlessness
Chronic effects of type II resp failure where there is CO2 retention?
Co2 retention
- CSF acidity corrected by choroid plexus (produce more HCO3-)
- central chemoreceptors reset to higher CO2 level
- persisting hypoxia
- reduction of respiratory drive, now driven by hypoxia via peripheral chemoreceptors
What are the chronic effects of the pulmonary circulation with type II respiratory failure?
Effects of hypoxia on pulmonary arterioles
- pulmonary hypertension
- right heart failure
- cor pulmonale
What are other effects of hypoxia?
Increased oxygen transport capacity
Increased haemoglobin (polycythaemia)
2,3-BPG
What can cause a barrel shaped chest?
Narrowing of small airways.
Makes it difficult to force air through them during forced expiration