Respiratory Flashcards
Define Boyle’s law.
Pressure is inversely proportional to volume.
Define Charles’ law.
Pressure is inversely proportional to temperature.
What is meant by the partial pressure of oxygen?
The pressure exerted by oxygen as a proportion of the total pressure.
It is the same proportion as the volume of O2.
So po2/ total pressure = volume O2/ total volume
How can the partial pressure of oxygen be calculated?
Volume O2/ total volume x total pressure
Give 5 places for an upper respiratory tract infection in the nose to spread to? How would they get there?
Paranasal sinuses - through openings in the meati
Eye - through nasolacrimal duct
Ear - through Eustachian tube
Pharynx and larynx - directly
How many lobes are in each lung?
3 on right
2 on left - need space for the heart
At what point along the respiratory tract does gas exchange start to occur?
Terminal bronchioles
What is the classic description of respiratory epithelia?
Pseudostratified, columnar with cilia and goblet cells
What type of epithelia are required for gas exchange to occur? Where are these found?
Simple cuboidal or squamous. No cilia or goblet cells - Clara cells secrete serous fluid instead.
Below the terminal bronchioles - respiratory bronchioles, alveolar ducts and alveolar sacs
Most of the mucosa in the nose has respiratory epithelia. What other type of epithelia are there? Where? Why?
Olfactory around the olfactory bulb.
Contains olfactory nerve fibres and no goblet cells to aid sense of smell.
Where is the angle of Louis? What can be found there?
Manubriosternal joint between the manubrium and the body of the sternum.
Forms a notch which makes it easy to find the second rib.
What are the boundaries of the mediastinum?
Anterior - pericardium (thymus in children)
Posterior - pericardium
Lateral - mediastinal pleura
Inferior - diaphragm
Superior - imaginary line between sternal angle and T4
Where are the three openings in the diaphragm? What passes through them?
T8 - vena cava
T10 - oesophagus
T12 - aortic hiatus
(Count letters)
Name the anatomical structures that could cause problems during a thoracostomy?
- Intercostal neurovascular bundle running in the costal groove at the bottom of each rib
- Liver and spleen
Where is the appropriate location for a thoracostomy? Why?
In the triangle of safety.
Above the 5th intercostal space in the mid axillary line.
Because the liver is found below the 5th rib.
What is the costodiaphragmatic recess?
Pleural gutter around the perimeter of rib 8. Allows expansion of the lungs.
What is the pleural seal? What is its function?
Force of attraction between molecules in the two layers of pleura due to low pressure in the intrapleural space.
Keeps the lungs inflated.
What is the relative pressure in the intrapleural space? Why?
Negative - always less than atmospheric pressure due to opposing forces of intercostal muscles and lungs.
What would happen to the lungs if they were removed from the body?
Deflate
What happens to the volume of the thorax when the diaphragm contracts?
Increases
When a person chokes, the foreign body tends to fall down the right main bronchus. Why?
Shorter, wider and more horizontal than the left.
Where is the carina of the respiratory tract? What can cause it to widen?
Bifurcation of the trachea into the two main bronchi.
Enlarged tracheobronchial lymph nodes - malignancy.
Describe the blood supply that supports the respiratory tissue (not gas exchange).
Bronchial arteries and azygous vein.
If a thrombus forms in the lung, why is there a low risk of necrosis?
Pulmonary arteries (usually for gas exchange) anastomose with the bronchial arteries and provide some oxygen.
Describe type 1 and type 2 alveolar cells.
Type 1 - simple squamous. Most common.
Type 2 - simple cuboidal with Clara cells and lots of macrophages.
Which muscles are involved in quiet inspiration?
Diaphragm and external intercostals.
Which muscles are involved in forced inspiration?
Accessory muscles - Sternocleidomastoid, scalene, serrated anterior and pec major.
Which muscles are involved in quiet expiration?
None. Elastic recoil.
Which muscles are involved in forced expiration?
Internal intercostals and abdominals (internal and external oblique and rectus abdominalis)
What is the tidal volume?
Volume of air that moves in or out of the lungs during quiet breathing.
What is the inspiratory reserve volume? Why is it greater than the expiratory reserve volume?
Volume of air that is breathed in beyond the tidal volume.
Greater than expiratory reserve because in forced expiration the pressure becomes so high that some of the smaller bronchioles are compressed and not all the air can be breathed out. It leaves a “residual volume.”
Why is expiration more difficult than inspiration in obstructive pulmonary disease?
In obstructive pulmonary disease pressure is increased in bronchioles and so resistance increases. This means more force is required for the air to get through.
Resistance increases even more in expiration because the volume is decreased.
What is compliance of the lung? Give an example of a disease process that increases and decreases compliance.
Stretchiness. Change in volume for a given change in pressure.
Increases - emphysema
Decreases - fibrosis
What two factors affect compliance of the lung?
Elastin content (increases compliance) Surface tension (decreases compliance)
What is surface tension in the lung?
Surface molecules in the alveoli attract each other and resist inflation.
At what volume is lung compliance greatest?
Low volume.
Because surfactant works best at low volume, where there is less surface area for it to cover.
What are the 2 functions of surfactant.
- Decrease surface tension - by disrupting attractive forces between molecules.
- Equalise pressure between different sized alveoli - by being less effective at larger volumes.
At what lung volume is surface tension greatest?
High volume. Because surfactant becomes less effective at high volumes.
How does surfactant equalise pressure between different sized alveoli?
Should be that big bubbles eat little bubbles due to Laplace’s law.
Because high pressure little bubbles collapse into low pressure big ones.
But surfactant acts to lower pressure. And it only works on little bubbles. So in the end they all have the same pressure.
Why are small breaths easy and big breaths hard?
At high volumes (big breaths) surfactant is less effective, so surface tension is greater and compliance is decreased.
At what stage in embryonic development do lungs become viable? Why?
Terminal sac stage at 28 weeks. When surfactant starts to be produced
Give 5 factors affecting diffusion of gas into a fluid
Molecular weight Solubility of gas Pressure gradient Surface area of fluid Distance of diffusion
Why does co2 diffuse more easily than O2?
Even though O2 is lighter and faster, co2 is much more soluble in blood.
Why does the pressure gradient across the alveolar wall have to be steeper for O2 than for co2?
Even though O2 is smaller, co2 is much more soluble in blood so diffuses much more easily. It therefore requires less of a pressure gradient.
What are the partial pressures of O2 and co2 in the alveoli and in the veins?
O2 - alveoli 13.3kPa —-veins 5.3kPa
Co2 - veins 6.1kPa —- alveoli 5.3kPa
What happens to the partial pressure of O2 in the alveoli if there is a decrease in v/q?
Decrease in ventilation - decrease in O2 and increase in co2.
What might cause a decrease in v/q?
Lobar pneumonia, TB (affects apex where pao2 is higher)
What happens to the partial pressure of O2 in the alveoli if there is a increase in v/q?
Decrease in perfusion - blood does not exchange. Increase in O2 and decrease in co2.
What might cause an increase in v/q?
Pulmonary embolism
What mechanism aims to maintain the v/q?
Ventilation perfusion coupling. In areas of high po2 - vasodilation and low po2 vasoconstriction. Maximises flow through the effective alveoli.
What disorder can cause an increase in the surface area of the lungs? What effect will this have?
Emphysema
Leads to decreased levels of diffusion
What disorders can cause an increase in the distance of diffusion in the lungs? What effect will this have?
Fibrosis and oedema.
Decreased rate of diffusion
What is physiological dead space? What is it made up of?
Serial - volume of airways that are not used in gas exchange
Distributive - volume of damaged/ incapacitated airways
Wha type of breathing minimises waste through dead space ventilation?
Slow, deep, through the mouth.
Mouth - minimises dead space volume
Slow - minimises dead space ventilation
Deep - maximises non dead space ventilation
What is the alveolar ventilation rate? What does it take into account?
Actual levels of ventilation in the alveoli, taking into account the ventilation of dead space.
If pulmonary ventilation rate is doubled by doubling resp rate (with all other factors kept the same) will alveolar ventilation rate double?
No!
Because dead space ventilation rate also doubles and this must be taken away from the total. Slow breaths minimise dead space waste.
What happens to the functional residual capacity in asthma?
Increases.
Because increased expiratory resistance means lungs can’t empty - barrel chest.
What happens to the functional residual capacity in fibrosis?
Decreases.
Because decrease in compliance means the lungs can’t fill properly
What happens to the functional residual capacity in fetal respiratory distress syndrome?
Decreases.
Because no surfactant, compliance decreases and lungs can’t fill.
What happens to the functional residual capacity in emphysema?
Increases.
Because increased compliance means lungs can’t fill.
Describe the vitalograph curve in obstructive lung disease.
Flatter and slower.
Total forced vital capacity is normal.
But forced expiratory volume in the first second is greatly reduced.
Describe the vitalograph curve in restrictive lung disease.
Same initial rate but reaches a lower total capacity.
Describe the flow-volume curve in obstructive lung disease.
Decreased rate especially as lungs compress and resistance increases.
Scooped out curve.
Can reach normal peak
Why is the peak flow measurement not very sensitive?
Because peak flow may be normal and only becomes abnormal later in expiration when resistance increases. But used as a screen for severe asthma.
How is dead space volume measured?
Nitrogen washout. Inhale oxygen and see how long it takes for nitrogen to come back. Because last in is first out.
How is residual volume measured?
Helium dilution
Why is myoglobin a good store of oxygen in the muscles?
It binds well to oxygen at the lungs but doesn’t give it up at the tissue until it reaches a very low partial pressure. Therefore it waits until there is high demand.
How many O2 molecules can bind to myoglobin?
1
How many O2 molecules can bind to haemoglobin?
4
What is different about fetal haemoglobin? What effect does this have?
Instead of 2 alpha 2 beta it is 2 alpha 2 gamma.
Binds with greater affinity to oxygen so can compete with maternal haemoglobin and steal O2 at the placenta.
What is cooperative binding? What effect does it have on haemoglobin?
Once one 02 binds it increases affinity, and turns to relaxed state.
Means that at low pao2 there is low affinity which takes a while to increase. When paO2 increases, affinity increases rapidly. Creates sigmoidal shape. Means that O2 can be given up at the tissue
Give 3 factors that can shift an 02 binding curve to the right? What effects do they have?
Low ph - give more O2 to tissue in exercise (lactic acid)
High co2 - give more O2 to tissue in exercise (co2)
2-3 bpg - give more O2 to tissue in altitude (low pao2)
Why is the oxygen binding curve not always shifted right?
So there is an O2 reserve and resp rate does not have to increase too much in exercise.
How does carbon monoxide affect oxygen binding?
Binds with haemoglobin so decreases available binding sites and therefore decreases sats
But also increases unaffected subunits affinity for O2 so makes them unable to give up O2 at tissues. Curve looks like myoglobin.
How does anaemia affect O2 binding?
Decrease in available binding sites.
Why might pao2 and sats both be normal in severe anaemia?
Sats measure percentage saturation so might be 100% of very few hb molecules
Pao2 only measures dissolved O2 (as a proportion of total gas.) Reflects exposure at alveoli which will be normal.
What happens to alveolar pao2 and pco2 when v/q > 1?
V/q > 1 means decrease in perfusion eg pe
Less O2 binding means pao2 increase and less co2 dumping means paco2 decrease
What determines paco2 in blood?
Paco2 in alveoli so resp rate.
What determines HCO3 in blood?
Kidney excretion.
When blood becomes acidic, how is it buffered?
Rbcs mop up a H+ and drive reaction towards HCO3 production.
Name 3 ways that CO2 can travel through the blood.
- Dissolved
- As HCO3, converted by buffering reaction.
- Bound to carbamino compounds in rbcs (similar to O2 transport, bind at tissue and released at lungs)
What are the two types of respiratory failure? Which can be more serious?
Type 1 - decrease pao2
Type 2 - decrease pao2 plus increase paCO2
Type 2 can be more serious because it can lead to hypercapnia and respiratory acidosis on top of O2 issues.
Why should O2 therapy be delayed as long as possible in COPD?
- Chronic type 2 respiratory failure means chronic hypercapnia which has been reset as the new normal by the choroid plexus.
Now the central chemoreceptors will only be activated by a very high paCO2. So the peripheral O2 alarm system is the driver. If we give O2 then sats return to normal and neither the peripheral or the central respiratory controls want to make any effort. Hypoventilation and eventual death.
- Also ventilation of dead areas gets rid of ventilation-perfusion coupling mechanism but it is still dead space. Now more perfusion of dead space.
Give 5 causes of type 2 respiratory failure
(Pump failure)
COPD exacerbation Opiate OD Pneumothorax Myopathy - muscular dystrophy (duchenne) Neuropathy - myasthenia gravis
What are diffusion defects? What type of respiratory failure will be caused by diffusion defects?
Increase diffusion time eg fibrosis, oedema, emphysema
Type 1 because CO2 is more soluble than O2 and does not struggle as much to diffuse. Peripheral alarm activated so increased ventilation will keep it low.
What type of respiratory failure is caused by a V/Q mismatch that is not compensated by vasoconstriction coupling?
Decrease in pao2 leads to peripheral alarm being activated. Increase ventilation blows off co2 but can’t increase pao2 because already 100% in healthy areas.
Type 1
What are the 3 main features of asthma?
- Reversible obstruction by contraction of smooth muscle in the bronchioles
- Inflammation and remodelling (thick sm, damaged epithelia, increased eosinophils, neutrophils and mast cells, increased cytokines
- Hyper responsive ( eg to histamine, amplified by PGe and exercise)
Why does asthma mostly affect the bronchioles?
Above bronchioles cartilage keeps airway open. Below bronchioles there is minimal sm.
What are the 2 respiratory control systems that maintain pao2 and paco2?
Central - chemoreceptors in the medulla indirectly sense paCO2 by the amount that diffuses into CSF. Sensitive.
Peripheral - carotid and aortic bodies sense drastically low pao2. Insensitive.
Why are the central chemoreceptors that control ventilation unaffected by pH? Why is this important?
H+ and HCO3 don’t diffuse across into the CSF
This means that the chemoreceptors are unaffected by blood pH.
How does the central respiratory chemoreceptor reset itself to a chronic hypercapnia?
Choroid plexus allows some hco3 to cross into CSF
How do you interpret a blood gas result?
- pH - high or low?
- pCO2 - does it explain the pH? High for acid, low for alkali. If yes - respiratory acidosis/alkalosis
If not .. - HCO3 - does it explain the pH? Low for acid, high for alkali. If yes - metabolic acidosis/alkalosis
Give 3 risk factors for COPD
Smoking
Occupational exposure eg asbestos
Alpha 1 anti trypsin deficiency
Which 2 conditions are included under the umbrella of copd?
Chronic bronchitis
Emphysema
What is cor pulmonale?
Lung disease causes right heart failure
What is an ideal FEV1 and FEV1/FVC to aim for?
FEV1 - over 80% of expected
FEV1/FVC - over 70% of expected
How do you differentiate between asthma and copd?
COPD - productive, persistent, progressive. Old, smoker.
Asthma - none of above plus night time waking and diurnal variation
Give four infection defences in the respiratory tract.
- Ciliary escalator
- Coughing and sneezing reflex
- Lymphoid tissue in pharynx and tonsils
- Alveolar macrophages
Give 3 mechanisms which might cause someone to be infected by pneumonia.
- Aspiration due to dysphagia
- Damaged cilia due to smoking/cystic fibrosis
- Immunosuppression
How can you differentiate between acute bronchitis and pneumonia?
Acute bronchitis affects the medium sized bronchioles and does not include the parenchyma. Usually viral.
Pneumonia affects alveoli and lung parenchyma. Can be viral or usually bacterial. Pneumonia shows consolidation on the X-ray
Where would you listen to hear the middle lobe of the right lung?
4th intercostal space
2,4,6 for superior, middle, inferior
Which virus is usually implicated in viral pneumonia?
Influenza
Which bacteria is usually implicated in aspiration pneumonia?
Mixed from normal mouth/throat flora
How would you assess severity of pneumonia?
CURB 65 Confusion Urea over 7 Resp rate over 30 BP under 90/60
Over 65?
Score 2-5 consider admission
What bacteria is usually implicated in community acquired pneumonia?
Streptococcus pneumoniae
What bacteria is usually implicated in hospital acquired pneumonia?
Staphylococcus aureus
What are the symptoms of lung cancer?
Common - no symptoms
Cough Dysphagia - oesophageal compression Dyspnoea Hoarseness - vagus Bloated face - svc compression
Which 2 types of cancer have lowest 5 year survival?
Lung and pancreatic
Where does lung cancer metastasise to?
Local - pericardium, pleura, liver, lymph
Systemic - adrenals, bone, brain
What are the two types of lung cancer and their subdivisions? Which is most common?
Small cell
Non small cell (most common)
Includes squamous cell carcinoma and adenocarcinoma
What type of lung cancer is most common in non smokers?
Adenocarcinoma - because no damage to ciliary lining of squamous cells.
Why is TB found in the apex of the lung?
It is an obligate aerobe and prefers the apex where the pao2 is higher.
Where does TB lie dormant in the body? How is this possible?
Alveolar macrophages.
Long chain fatty acids in the cell wall allow them to survive and multiply inside macrophages.
How long does it take to culture TB?
At least 2 weeks due to long reproduction time of about 15hours.
Name some risk factors for TB transmission.
Overcrowded environment eg prison or school
Family member with TB
Most people who are infected with TB can clear it out of their own system or at least send it latent. What are the risk factors for primary disease?
T cells send it dormant
Therefore HIV, corticosteroids and TNF alpha antagonists weaken this system.
Is active primary or active secondary TB more likely to be symptomatic?
Active secondary.
It has had time to multiply and become more powerful.
Is latent TB infectious or not?
Non infectious.
How would you know you had latent TB?
You wouldn’t unless you were tested with TST or IGRA (interferon gamma releasing assay). Tests would be positive.
What is the pathology of TB under a microscope and in radiology?
Caseous necrosis and Langhans giant cells
Patchy consolidation with cavities
What tests would you order for suspected TB?
Chest x Ray Full blood count for wbc Rapid sputum smear (3 Samples) IGRA sputum culture HIV test Notify public health
Sepsis 6 if required
How would you treat confirmed TB? Why?
4 different antibiotics at first to avoid development of resistance.
RIPE: Rifampicin Isoniazid Pyrazinamide Ethambutol
What is interstitial lung disease? How does it commonly present?
Restrictive pattern lung disease caused by inflammation and fibrosis.
Shortness of breath and dry cough only.
Insidious onset and gradual decline
What signs would you find on examination of interstitial lung disease?
Fine crackles
What signs would you find on examination of obstructive pulmonary disease?
Coarse crackles
What would you see on a chest X-ray of interstitial lung disease?
Honey combing
Reticular (lines) and nodular (circles) shadowing
Give 4 common causes of interstitial lung disease.
Infection - TB Drugs - methotrexate, Bleomycin, nitrofurantoin, Amiodarone Sarcoidosis Connective tissue disease Asbestos Idiopathic
What is the difference between a tension pneumothorax and a normal pneumothorax? What is the difference in their treatment?
Tension - ‘valvular’ mechanism which means it grows each time the patient takes a breath. Tracheal deviation/mediastinal shift. Very unwell patient. High hr and low bp. Aspirate immediately then chest drain later.
Normal - stable area of air that does not grow with each breath. Chest drain only if greater than 2cm.
Where would you aspirate a pneumothorax?
2nd intercostal space, mid clavicular line
Give two transudative causes of pleural effusion.
Heart failure, cirrhosis
Give three exudative causes of pleural effusion.
Infection
Cancer
PE
What is the name of the type of cancer caused by asbestos exposure? Where is it found?
Mesothelioma in the pleura.
What hormone is commonly secreted by a bronchial squamous cell carcinoma? What about a small cell carcinoma?
Squamous - PTH
Small cell - ADH and ACTH (cortisol)
