4. Respiratory failure Flashcards
Q Anatomy – describe the anatomical structures air will pass through as it travels from the
nose to the alveoli
Nasopharynx, oropharynx, laryngopharynx, trachea (bifurcates at the carina – sternal angle, T4), left and right main bronchi, then lobar bronchi, then segmental bronchi, bronchioles (several branches), terminal bronchioles, respiratory bronchioles, alveolar duct, alveolus (type 1 pneumocytes)
Resistance greatest in the 5th-7th division – narrow radius, hasn’t yet got a great enough surface area to balance out this (not enough of them), and you still have turbulent flow. Once you reach the smaller bronchioles, there is only laminar flow and there are so many of them that surface area is much higher.
10 bronchopulmonary segments in the right lung, 9 in the left. Bronchopulmonary segment – an area with its own bronchus, pulmonary artery and bronchial artery. The venous drainage is more general so each segment doesn’t necessarily have its own vein.
Significant for infection – infections can be contained within segments, blood flow can be diverted away from certain segments if they’re blocked, and needed for drainage in cystic fibrosis.
Q
Upper airway =
Lower airway =
Q where is the greatest reisistance to airflow
- all the structures above the bottom of the larynx (including paranasal sinuses)
- starts at the level of the origin of the trachea (C6)
***highest total resistance is actually in the trachea and larger bronchi
Q Control of ventilation - Describe how the body detects O2 levels to adjust respiration
- O2 conc. are only detected by peripheral chemoreceptors, not central
- Peripheral chemoreceptors are located in carotid sinus and aortic arch
- Project to the inspiration centres (dorsal respiratory group in the medulla)
- Control by oxygen is not really important, until you are really severely hypoxaemic (not a good control because it requires very large drops in oxygen – below partial pressure of 60, because of the shape of the oxygen haemoglobin curve)
- Hb is still fully saturated until partial pressure of around 80
Q Control of ventilation - Describe how the body detects CO2 levels to adjust respiration.
Central chemoreceptors in the medulla take a long time to act upon because H+ and
bicarbonate cannot cross the blood-brain barrier
- Therefore it has to cross the blood brain barrier as carbon dioxide and THEN break down into
H+ and bicarb in the brain to be detected by the chemoreceptors
- These receptors detect a change in H+ in the CSF in response to increased carbon dioxide
levels
- To compensate for this slow response time of central chemoreceptors, there are also
peripheral chemoreceptors to detect changes in both H+ and CO2
***bicarbonate
cannot cross the blood-brain barrier
Control of ventilation -
Control by pH
Changes in pH occur due to either increases in CO2 levels or as a by-product of anaerobic respiration
- Detected by peripheral chemoreceptors
- On increased H+ levels, impulses sent to the DRG in the medulla (inspiratory centre) to cause
inspiration to occur
- the strongest drive for inspiration comes from increased CO2 levels because the low pH is the
most harmful thing to the body
Q. Describe how a decrease in INTRA thoracic pressure is achieved during inspiration. What
happens during expiration to force air out of the lung?
- Diaphragm and external intercostal muscles contract
- Diaphragm – contracts and flattens to increase the size of the thoracic cavity. External
intercostals contract to pull the rib cage up and outward to increase the size of the thoracic cavity - The expansion of the ribcage pulls with it the parietal pleura, which increases the size of the
intrapleural cavity, decreasing its pressure - This causes a increase in transpulmonary pressure, to allow passive expansion of the
lungs - Which causes an increase in alveolar volume as they are now stretched
- Increase in alveolar volume causes decrease in alveolar pressure
- This means that Palv is now less than Patm – meaning air moves from the atmosphere into
the lungs
At rest, alveoli are being kept open by the transpulmonary pressure opposing their recoil
Q What happens during expiration to force air out of the lung?
External intercostals and diaphragm relaxes
- Intrapleural pressure increases
- Transpulmonary pressure therefore decrease
- This allows for the elastic recoil, rapidly decreasing the volume of the alveoli which then
increases the pressure to rapidly expel the air
How do alveoli stay expanded at rest?
Surfactant – decreases surface tension to stop the alveoli adhering together
Chest wall compliance – the chest wall expands outwards to pull some of the pleura outwards to increase the expansion of the pleural cavity. This keeps the pleural cavity open enough to generate a transpulmonary pressure. (elastin involved)
CW pressure = Pip – Patm = -4mmHg
With age, this decreases, meaning that chest wall compliance decreases, meaning that the lungs are not as well expanded at rest
for inspiration Thoracic pressure has to?
Expiration it must… so..
TP pressure has to increase
And for expiration, it has to decrease to allow some elastic recoil
a increase in transpulmonary pressure,
to allow passive expansion of the
lungs
Surfactant –
decreases surface tension to stop the alveoli adhering together
Chest wall
- compliance
- pressure equation
- with age ….
Chest wall compliance – the chest wall expands outwards to pull some of the pleura outwards to increase the expansion of the pleural cavity. This keeps the pleural cavity open enough to generate a transpulmonary pressure. (elastin involved)
CW pressure = Pip – Patm = -4mmHg
With age, this decreases, meaning that chest wall compliance decreases, meaning that the lungs are not as well expanded at rest
Q Define type 1 respiratory failure and its causes.
Type 1 – low oxygen and normal carbon dioxide (hypoxia and hypercapnia)
Causes of type 1 - VQ mismatch, acute asthma (asthma – restriction, so you are still breathing CO2 but struggling to breath in oxygen), altitude sickness, pulmonary embolism
In altitude – your body thinks there is a lung obstruction due to the low pO2 available. This means the arterioles constrict to divert the blood flow away from the “blocked area” – but because everywhere is blocked, this causes overall vasoconstriction in the blood
Carbon monoxide – shifts the haemoglobin curve to the left because it binds to haemoglobin (irreversibly) and then has a really high oxygen binding affinity – it binds to it and then never lets go again
Q Define type 2 respiratory failure and its
causes.
Type 2 – low oxygen and high carbon dioxide (hypoxia and hypercapnia)
Causes of type 2 – chronic asthma, COPD, drug overdose, muscle wasting disorders (eg. Muscular dystrophy, because the muscles of respiration will waste and have a massively reduced capacity to contract)
Hypoxic drive – someone gets used to having
F Which nerve supplies motor function to the diaphragm?
e) phrenic
