ILA4 - resp failure Flashcards
What is the order of air flow?
Nose, turbinates (sup., inf. and middle), pharynx, larynx, main bronchi, lobar bronchi, terminal bronchioles, respiratory bronchioles and alveoli
What is the function of the turbinates?
Increases surface area and slows down flow of air for more effective warming and humidifying
What are the three paired cartilages of the larynx?
arytenoid, corniculate, and cuneiform
What are the three single cartilages of the larynx
epiglottic, thyroid and cricoid
Where does the upper airway end?
Trachea
Where is the lower airway?
trachea onwards
Which part of the airway has the greatest resistance?
Trachea (long=increased resistance and less branching=decreased resistance)
Whats is the muscle covering the open posterior aspect of the c shaped cartilages in the trachea?
Trachealis muscle (smooth muscle)
What is the rough length of the left main bronchus?
5cm
What is the rough length of the right main bronchus?
1-2.5cm
Which main bronchus is more vertical?
Right
Name a cause of reduced perfusion to the pulmonary tisue?
Pulmonary embolism
What can cause reduced ventilation?
Blockage in airway
Chronic bronchitis: Blocks airways. Productive cough
(produces sputum)
Cystic fibrosis: Affects sodium channel resulting in thick
mucous secretions which block mucous ciliary
escalator
What is it when V/Q=0?
Shunt, no ventilation normal blood flow
What is it when V/Q=infinity?
Dead space, no perfusion normal ventilation
What does the respiratory centre do?
Control the pattern of breathing
Where is the respiratory centre located?
Medulla, it is a collection of neurons
Which neurons do the ventral lateral medulla contain?
Inspiratory and expiratory neurones
Which neurons do the dorsal medial medulla contain?
Inspiratory neurones
How does the primary centre work?
It consists of a collection of separately arranged neurones capable of altering their firing threshold so that activity oscillates between them during inspiration and expiration
Which areas of the pons stimulate the primary centre?
Apneustic (stimulates inspiration) and pneumotaxic (inhibits inspiration)
What can inhibit the drive for ventilation by depressing the respiratory neuons in the lungs?
Hypoxia, a range of therapeutic drugs and inhibition of blood supply
What do chemoreceptors do?
Detect changes in acidity of the blood and CSF
Where do central chemoreceptors lie?
Just below the anterolateral surfaces of the medulla, close to the origins of IX and X nerves (pontomedullary junction)
What do central chemorecpetors respond to?
Respond to change in pH in surrounding CSF
Rising pH inhibits ventilation and lowering pH stimulates it
How does the pH fall in the CSF
Blood brain barrier is impermeable to H+ so H2CO3 beaks into CO2 and H2O, CO2 then diffuses through the barrier and form bicarb in the CSF. H+ is then released, dropping pH. Stimulates chemoreceptors, stimulates ventilation.
Where are the peripheral chemoreceptors located?
Carotid bodies, found near the bifurcation of the common carotid artery on either side of the neck (glossopharyngeal afferents)
Aortic bodies in the aortic arch (vagus afferents)
How do peripheral chemoreceptors work?
- Surrounded by sinusoidal capillaries which allow cells within them to be bathed directly in blood
- Glomus cells respond to hypoxia by releasing dopamine on to afferent nerve of the carotid sinus which run to the glossopharyngeal nerve and thence the medullary respiratory centres
- Afferents of the aortic bodies run via aortic nerve to the vagus
- Rapid response
- Also baroreceptors
What receptors are in the lungs?
Pulmonary stretch receptors and J-receptors
Describe the pulmonary stretch receptors
- Lie in the smooth muscle of the bronchi and trachea. Localised chiefly at points of branching where smooth muscle is thickest
- Afferent fibres from receptors run in the vagus nerve to send impulses to the respiratory centre
- Inflating the lungs stimulates these receptors.
- Stimulation inhibits inspiration hence inspiration stimulates expiration
- Deep breathing rather than small shallow breaths
Describe J-receptors
- Lie in the alveolar walls close to the capillaries
- Impulses from these receptors travel along nerve fibres in vagus nerve
- Stimulated by fluid in the alveoli and by histamine and other inflammatory mediators
- Stimulation causes rapid, shallow breathing to clear lungs
How do muscle stretch receptors control breathing rate?
- Located in muscle spindles of diaphragm and intercostal muscles
- As muscle is stretched too far the rate of fire increases
- These receptors control the strength of muscle contraction to increase the depth of breathing
How do baroreceptors control breathing rate?
Rise in BP detected by carotid or aortic sinus baroreceptors tends to depress respiration
How is inspiration achieved?
- Diaphragm contracts, flattens and moves downwards.
- The diaphragm is attached to the parietal pleura and so movement downwards pulls the visceral pleura down so that airways and alveoli expand
- This increases the volume and so decreases pressure
- External intercostal muscles contract moving the ribcage upwards and outwards to increase lateral and anteroposterior diameter of the thorax
- This further increases volume and so decreases pressure
- If pressure in lungs is lower than that of the atmosphere then air is drawn into the lungs
What is Boyle’s Law?
P1 X V1 = P2 X V2. So pressure is inversely proportional to volume. So if volume increases, pressure decreases (below atmospheric) bringing air into the lungs.
Which way do external intercostals point?
Down and in (hands in pocket)
Which way do internal intercostals point?
Up and in
What is transpulmonary pressure?
The difference between the alveolar pressure and the intrapleural pressure in the pleural cavity
How is expiration achieved?
- Usually passive and results from the elastic recoil of the lungs and the chest wall and the inward pull of surface tension in the pleural space
- Muscles of diaphragm and intercostals relax
- Thoracic and intrapulmonary volumes decrease
- Intrapulmonary pressure increases to above atmos pressure
- Air is forced out of the lungs
What muscles are involved in forced expiration?
Abdominals, internal intercostals and accessory muscles
What is respiratory failure?
Inability of the respiratory system to adequately supply fresh O2 or remmove CO2. PaO2 falls below 8kPa, Pa CO2 can be normal or high depending on type
What is normal PaO2?
10-13 kPa
What is normal PaCO2
4.7-6 kPa
What is Type 1 resp failure?
Low O2 (<8kPa) (hypoxemia) Normal - slightly low CO2
What is the difference between restrictive and obstructive lung disease?
Obstructive lung disease is a narrowing of pulmonary airways, hindering a person’s ability to completely expel air from the lungs. Whereas restrictive causes increased difficukty fully expanding lungs during inhilation inhale.
Causes of type 1 resp failure?
Lung can still expel CO2, just problems with oxygenating the blood (damage to the tissue).
Restrictive lung disease, V/Q mismatch, pneumonia (infection and inflammation of alveoli), pulmonary oedema (fluid in lungs), ARDS (acute resp distress syndrome) ,pneumothorax (air in pleural cavity causing lung collapse), fibrosing alveolitis (idiopathic pulmonary fibrosis, fibrosis= scarring)
What is type 2 resp failure?
PaO2 low (<8 kPa) (hypoxia) PaCO2 high (>7 kPa) (hypercapnia)
Causes of type 2 resp failure?
Problem is woth mechanisms of breathing
Obstructive lung diseases, COPD, emphysema, asthma, chest wall deformity, resp muscle weakness, central repression of resp centre (eg heroin od), obesity
Clinical effects of hypoxia?
- Interferes with aerobic metabolism so that cellular function is disrupted
- Effects on brain lead to confusion and drowsiness, progressing to coma and death in severe cases
- To compensate for reduced PaO2, renal tubular cells increase erythropoietin production so that RBC numbers increase and resultant polycythaemia increases the O2-carrying capacity of the blood
- Pulmonary vasoconstriction to divert the blood from poorly ventilated parts of the lungs may lead to pulmonary hypertension and eventually cor pulmonade
Clinical effects of hypercapnia?
- Adds to the effects of hypoxia on the brain and also causes respiratory acidosis as a result of inadequate CO2 excretion
- In COPD the respiratory centre becomes desensitised to hypocapnia so that the centre ventilatory drive for elevated PaCO2 no longer operates
- Renal retention of bicarbonate can compensate for respiratory acidosis but is a slow process
- Combo of hypoxia and hypercapnia induced-respiratory acidosis can be fatal
