Resp Flashcards
Describe how the structure of the nose is conducive to warming, humidifying and filtering/trapping particles in inspired air
Warming:
- Good blood supply close to the mucosal membrane
- Conchae cause turbulence and slow down airflow.
Humidifying:
- Mucous and blood keeps the area warm
- Conchae cause turbulence and slow down airflow.
Filtering/ trapping particles:
- Hairs
- Mucous
Describe how the structure of the paranasal sinuses are conducive to warming, humidifying and filtering/trapping particles in inspired air
Warming:
-Good blood supply
Humidifying:
-Goblet cells produce mucous
Filtering/trapping particles:
-Mucous traps particles
Name the paranasal sinuses?
Maxillary
Ethmoidal
Frontal
Sphenoidal
What is the name of the muscle that connects the two cartilaginous rings together of the trachea and what is the function?
Trachealis muscle
Pull the rings together to constrict the trachea to increase the air pressure in the lungs for example during a cough
The airways are separated into two areas, what are they called?
Conducting airway and respiratory airways
What is included in the conducting airways?
Trachea Primary Bronchi Secondary Bronchi - lobar bronchi Tertiary bronchi - segmental bronchi Bronchioles Terminal bronchioles
What is included in the respiratory airways?
Respiratory bronchioles
Alveolar ducts
Alveoli
What part of the respiratory system is extrapulmonary and intrapulmonary?
Extrapulmonary: Nasal Cavity Pharynx Larynx Trachea Primary bronchi
Intrapulmonary: Secondary bronchi - lobar bronchi Tertiary bronchi - segmental bronchi Bronchioles Terminal bronchioles Respiratory bronchioles Alveolar ducts Alveoli
Explain why hoarseness of voice/ voice change may be a sign of intra-thoracic disease?
Left recurrent laryngeal nerve innervates the intrinsic laryngeal muscles except cricothyroid.
The route of the recurrent laryngeal nerve is:
Originates from the left vagus nerve as it passes over the arch of the aorta inferior to the left superior intercostal vein. It passes medially and posteriorly deep to the ligamentum arteriosum before curving inferior to the arch of the aorta. It then passes superiorly over the left main bronchus to ascend in the groove between the left side of the trachea and the anterior of the oesophagus.
Branches: mucosa of upper oesophagus, inferior thyroid artery, inferior thyroid veins. Paratracheal lymph nodes, parathyroid glands, lateral lobe of thyroid gland, cardiac and tracheal branches.
At the level of the thyroid gland it passes beneath the inf border of cricopharyngeus to run deep to it and sup towards the pharynx and larynx.
If there is pathology in any of the areas of the route of travel then there could be effects seen in the terminal branches of the larynx.
Describe the structure of the bony thorax?
12 Thoracic vertebrae 12 ribs:1-7 attached ribs 8-12 false ribs 11-12 floating ribs 1 sternum
Superior thoracic aperture is where the lungs stick out of the top of the ribs.
Inf thoracic aperture is the location of the diaphragm
Sternum:
Manubrium
Body
Xiphoid process
Costal cartilage connect the rib bones to the sternum.
Parts of the rib post to ant:
Head -> Neck
Costal groove on the inside separate the sup and inf part of the rib.
Crest separates the facet joints of the head of the rib.
Joints: Thoracic vertebrae: Demifacets on each. Sup demifacet of T2 and Inf demifacet of T1 will articulate with Rib 1 etc. Articular facet of rib articulates with transverse costal facet of the vertebrae.
Thoracic vertebrae is connected with a rib by superior costotransverse ligament and lateral costotransverse ligament.
Describe rib movements during respiration?
Bucket handle movement.
During inspiration:
Ribs move up and out to increase thoracic volume and decrease pressure. Lateral and anterior dimensions increase.
During expiration:
Ribs move down and in to decrease thoracic volume
Describe the intercostal muscles, their nerve supply and actions in respiration?
3 layers of intercostal muscles:
External intercostal membrane above the muscles.
External m. - direction of fibres: obliquely, inferiorly, post to ant
Action: inspiration - contraction brings ribs up and out. Expiration - relaxed.
Internal m. - direction of fibres: Obliquely, inferior, ant to post
Action: forced expiration they will contract bringing ribs down and in
Innermost m. - direction of fibres: Obliquely, inferiority, ant to post
Action: forced expiration they will contract bringing ribs down and in
Nerve supply: Major bundle below costal groove -intercostal nerve between each rib bundled with intercostal artery and vein. Minor bundle (collateral branches) run slightly above the rib.
Describe the diaphragm, their nerve supply and actions in respiration?
Nerve supply: Phrenic nerve
Action is contraction to increase thoracic volume during inspiration.
Expiration relaxation
Musculophrenic artery, inferior phrenic artery, pericardiacophrenic arteries - supplies the diaphragm muscle.
Central tendon of diaphragm - is the middle portion of the diaphragm.
Describe the course of the intercostal nerves, arteries and veins
Intercostal nerve is a branch off the spinal column from the ventral ramus- sympathetic nerve.
Major branch - run beneath costal groove
Minor branch - runs above costal groove
Major and minor branches both have intercostal arteries and veins in them.
Dual blood supply to intercostal muscles therefore increasing risk of blood loss if there is damage.
Anterior perforating branches of intercostal vessels and ant. cutaneous branch of intercostal nerve cover the anterior portion of the muscle and come over to the skin.
Lateral branches of the intercostal nerve and vessels come out the sides to cover the lateral portion of the area.
Blood goes up and down the thoracic cavity in the anterior part next to the body of the sternum called internal thoracic artery and vein.
Blood goes up and down the thoracic cavity in the posterior part ant to the vertebrae called posterior intercostal artery and vein.
They vessels run between the internal and innermost intercostal muscles.
How would you insert a chest drain/ pleural tap and avoid damaging any neurovascular supply to the surrounding tissues?
Insert slightly above the rib as this is where there is a less risk of damaging important neurovascular supplies.
At what vertebral level do the following pass through the diaphragm:
Vena cava
Oesophagus
Aortic hiatus
Vena cava - T8
Oesophagus - T10
Aortic hiatus - T12
What is the venous drainage of the ribs?
Left T1 - T3 = goes into superior vena cava at T2
Left T4 - T8 = Accessory hemiazygous vein L side which then crosses over to R side into the azygous vein
Left T9-T12 = hemiazygous vein on L side then crosses at T9-T10 into the azygous vein
Right T1 - superior vena cava at T1-T2
Right T2-T4 = Into opening of the azygous vein into the SVC at T4
Right T5-T12 = Azygous vein
What nerves roots innervate the diaphragm?
C3/4/5
Keeps the diaphragm alive
What is the part of the lung called where the trachea bifurcates?
Carina
What separates the lobes of the lung?
Fissures
Right lung - Transverse fissure and oblique fissure
Left lung - oblique fissure only as there are only 2 lobes.
Describe the pleural cavity and pleura incl nerve supply and role of pleural fluid and seal in lung expansion?
2 layers of pleura: visceral pleura and Parietal pleura. It is a potential space.
Between there is 10ml of serous fluid that acts as lubricant to allow easy chest expansion. Surface tension creates a seal which ensures that when the thorax expands on inspiration the lungs expand too.
Visceral pleura is on the surface of the lung and the parietal is on the surface of the thorax. Visceral pleura has somatic innervation and so is painful to pierce or irritation occurs.
Describe the blood supply to and from the lungs
Pulmonary trunk - right and left pulmonary arteries.
Left (2) pulmonary veins
Right (3) pulmonary veins
Blood supply to the lungs for its own blood supply = Superior left bronchial artery + inferior left bronchial artery
Right bronchial artery - branch from right third posterior intercostal artery
On surface markings what is the height of the diaphragm at rest?
Right side up to 5th rib (higher) and left side up to 5th intercostal space (lower) in the mid-clavicular line
Describe in simple terms in relation to the trachea what happens in a tension pneumothorax as seen in an x-ray?
Tracheal deviation
Black areas where the lung should be - due to air entrapment
Lung would be scrunched up in the middle where the air has been removed
What is the gap between the diaphragm and the ribs at the base of the thorax called?
costo-diaphragmatic recess
Peripheral gutter around the outer edges of the diaphragm into which only the parietal pleura extends.
How does the epithelium change in the respiratory system?
Nasal cavity - Bronchioles= pseudostratified ciliated epithelium with goblet cells
Terminal bronchioles = simple columnar epithelium with cilia and club (clara) cells but no goblet cells
Respiratory bronchioles - alveolar ducts = simple cuboidal epithelium with a few sparsley scattered cilia and club (clara) cells.
Alveoli - simple squamous/ type 1 (+septal/type 2) cells.
How does the cartilage change in the respiratory system?
Trachea - cartilage rings encircle the lumen anteriorly - semi-circle rings.
Sec and tertiary bronchi - cartilages arranged as irregular crescent plates or islands rather than rings
Bronchus-bronchioles - small diameter bronchis with cartilage reduced to small islands
Bronchiole - no subepithelial cartilage
What is contained in the secretions of the epithelium and submucosal glands of the trachea and bronchi?
Mucins, water
Serum proteins
Lysozyme (destroys bacteria)
Antiproteases (inactivated bacterial enzymes)
Lymphocytes contribute immunoglobulins (esp IgA)
Why is the absence of cartilage in walls of bronchioles problematic and in which condition specifically?
Air passages constrict and almost close down when smooth muscle contraction becomes excessive. Such bronchoconstriction can become excessive in asthma and cause more difficulty with expiration than inspiration (during expiration the bronchial walls are no longer held open by the surrounding alveoli - by traction.
When do clara cells become apparent in the respiratory tract?
Bronchioles get smaller and goblet cells give way to club cells interspersed between ciliated cuboidal cells.
Club cells secrete a surfactant lipoprotein, which prevents the walls sticking together during expiration.
What are the connections of an alveolus?
Respiratory bronchiole
Alveolar duct
Alveolar sac
Another alveolus (via an alveolar pore)
Why are alveoli good at their function?
Abundant capillaries
Supported by a basketwork of elastic and reticular fibres
Have a covering composed chiefly of type 1 pneumocytes
Have a scattering of intervening type 2 pneumocytes
What cells of the respiratory tract produce the surfactant?
Type 2 pneumocytes
What is the shape of the type 1 and 2 pneumocytes?
Type 1 - squamous - 90%
Type 2 - cuboidal - 10%
Describe what happens in emphysema?
Destruction of alveolar walls and permanent enlargement of air spaces which can result from smoking or alpha-1antitrypsin deficiency.
Alveolar walls normally hold bronchioles open, allowing air to leave the lungs on exhalation.
When these walls are damaged, bronchioles collapse making it difficult for the lungs to empty. Air becomes trapped in the alveoli.
What is chronic bronchitis?
Productive cough that lasts for 3 months of the year and for at least 2 years in a row. Infection of the bronchi.
(Acute bronchitis is inflammation that is temporary and lasts up to 3 weeks)
What is pneumonia and what are the common bacteria causing is?
Inflammation of the lung caused by bacteria. The lung consolidates as the alveoli fill with inflammatory cells.
Most common organism is strep pneumoniae
Others: Haemophilus influenzae, Staph. aureus, Legionella pneumophila and Mycoplasma pneumoniae.
How could you tell the difference between bronchi and bronchioles histologically?
Bronchus - small islands of cartilage and glands in submucosa with cilia.
Bronchiole - no cartilage or glands and very few if any cilia.
Bronchus is much larger in diameter compared to the bronchiole
What structures are included in the upper respiratory tract?
Nostrils to the lower border of the cricoid cartilage of the larynx and comprises of the nose and paranasal sinuses, pharynx and larynx.
What cells line the paranasal sinuses?
Respiratory epithelium - pseudostratified ciliated columnar epithelium.
What is the name of the junction between the manubrium and the body of the sternum?
Sternal angle
What costal cartilage articulates with the sternum at the level of the sternal angle?
2nd costal cartilage
What is the area above the manubrium called?
Jugular notch/ suprasternal notch
How much of chest expansion in quiet respiration is due to diaphragm contraction?
> 70%
What defines the beginning and end of the trachea?
Beginning - lower border of the cricoid cartilage (of the larynx) in the neck and terminates by dividing into the right and left main bronchi at the level of the sternal angle
What is a bronchopulmonary segment?
Area of lung supplied by a segmental bronchus and the accompanying segemental branch of the pulmonary artery. It is drained by a segmental pulmonary vein. These segments are pyramid shaped with the apex facing towards the segmental bronchus and the base toward the lung surface
How many lobes are there in each lung?
Right lung 3 lobes and left lung 2 lobes
Where does the blood in the bronchial artery end up?
Pulmonary vein via a shunt. A small amount of blood returns via the bronchial veins which drain via the azygous vein into the SVC atrium.
What does a bronchial artery supply?
Bronchial tree (but not the alveoli) and visceral pleura with oxygenated blood.
Why in PE’s is not all the distal portion of the lung affected?
In PE’s if a clot occurs then due to the dual blood supply of the bronchial arteries some parts of the lung can be saved. The blood comes from bronchial arteries and the pulmonary arteries which anastamose at the precapillary level and capillary level (these maintain some blood supply to lung parenchyma in patients with PE’s)
What is the lymphatic drainage from the lungs?
Drain into the hilar nodes, also known as the bronchopulmonary nodes. Effects from these nodes run to tracheobronchial nodes. Enlared tracheobronchial nodes can cause widening of the carina.
What is the nerve supply to the lung?
Fibres from right and left vagus nerves and the sympathetic trunk. Parasympathetic efferent fibres from the vagus are motor to the bronchial smooth muscle (bronchoconstrictor), and secretomotor to mucous glands. The vagal afferent fibres are those for the cough reflex and some subserving pain.
The sympathetic efferent fibres are bronchodilator and vasoconstrictor.
How far does the oblique fissure on either side extend using surface markings?
Spinous process of T2 vertebra posteriorly to the 6th costal cartilage anteriorly. The surface marking of the oblique fissure approximately follows the medial border of the scapula when the arm is abducted.
What are the surface markings for the horizontal fissure?
Horizontal fissure only on Right side. Extends from the mid axillary line anteriorly along the 4th rib, to the anterior edge of the lung, separating the right upper and middle lobes.
What can cause blunting of the costophrenic angle?
Pleural effusion - fluid in pleural cavity that collects in the costo-diaphragmatic space in the upright position.
COPD when the diaphragm maybe pushed down and the lungs fail to expand - air trapping
Define and give an approximate Tidal volume
The volume of air which enters and leaves the lungs with each breath
Volume: 500ml
Define and give an approximate Inspiratory reserve volume
During normal respiration the increase in lung volume is not maximal. It is increased to the extend of the inspiratory reserve volume.
Volume: 3000ml
Define and give an approximate expiratory reserve volume
During normal respiration the decrease in lung volume is maximal and extends to the expiratory reserve volume
Volume: 1000ml
Define and give an approximate residual volume
We cannot however empty our lungs completely, so even after normal expiration a residual volume will remain.
Volume: 1200ml
Define and give an approximate inspiratory capacity
End of quiet expiration to maximum inspiration.
Tidal volume + Inspiratory reserve volume
500ml+3000ml=3500ml
Define and give an approximate functional residual capacity
Expiratory reserve volume + Residual volume
1000ml+1200ml=2200ml
The resting volume at which the elastic recoil pressure of the lung inward equals the elastic recoil pressure of the chest outwards
Define and give an approximate vital capacity
Tidal volume + Expiratory reserve volume + Inspiratory reserve volume =
Inspiratory capacity + expiratory reserve volume
500+3000+1000=3500+1000 = 4500ml
Define and give an approximate total lung volume/ capacity
Tidal volume + Expiratory reserve volume + Inspiratory reserve volume + Residual volume
500+1000+3000+1200=5700ml
What are the fixed points in the breathing cycle?
Maximum inspiration
Maximum expiration
End of quiet expiration
Define anatomical dead space
The volume in the conducting airways
Define alveolar dead space
Air in alveoli which are not perfused or are damaged also do not take part in gas exchange and ventilation of these alveoli, are wasted
Define physiological dead space
Anatomical dead space + alveolar dead space
Define and calculate pulmonary ventilation rate
Total pulmonary ventilation (aka minute volume) = tidal volume x respiratory rate
Define and calculate alveolar ventilation rate
(Tidal volume - dead space) x resp rate
Explain what is resting expiratory level
At rest, (i.e. end of quiet respiration, when the respiratory muscles are relaxed) the lung is subject to two equal and opposing forces. One is directed inwards and the other outwards.
Inward: lungs elasticity and surface tension generate inwardly directed force that favours small lung volumes
Outward: muscles and various connective tissues associated with the rib cage also have elasticity. At rest these elastic elements favour outward movement of the chest wall.
Net effect: at rest two forces balance each other and also creates a negative pressure within the intra-pleural space relative to atmospheric pressure.
Describe the mechanism of normal quiet inspiration
Contraction of muscles and the pleural seal ensure that the lungs expand along with the thorax. As the lung volume increases, the air pressure within the lungs fall below atmospheric pressure and air flows into the lungs.
Describe the role of inspiratory muscles of normal quiet inspiration
Contraction of diaphragm
External intercostal muscles expand the thoracic cavity outwards
Describe the mechanism of quiet expiration and the role of elastic recoil
Muscle contraction eases. Elastic recoil of the lung results in thoracic cavity and lung returning to the original equilibrium position. Thus quiet expiration is a passive process. The pleural fluid between the two layers has surface tension- which holds the outer surface of the lungs to the inner surface of the chest wall. It is this seal which ensure that the chest wall and lungs move together.
Explain the changes in alveolar pressure during respiratory cycle
Alveolar pressure changes but only relatively small amounts compared to the pleural pressure.
The pressure during inspiration becomes more negative compared to atmospheric pressure which then forces air into the alveoli for the first part but as the time goes along the pressure equilibriates with the pleural pressure till it reaches the end of inspiration. Then at expiration the pressure of the alveoli become positive compared to the atmosphere which forces air out of the lungs. But this goes on for half of the duration of expiration after which the pressure starts to fall as the pressure equilibrates with the atmosphere.
Explain the changes in pleural pressure during respiratory cycle
The intrapleural pressure which is negative at rest becomes more negative during the inspiratory phase due to expansion of the thorax and returns to the resting (negative) pressure at the end of quiet expiration. The resting intrapleural pressure is -4 mmHg compared to the atmosphere and reaches -8 at the end of quiet inspiration.
During quiet inspiration what is the percentage of the muscles of respiration used and what is the split?
Diaphragm - 70%
External intercostal muscles - 30%
During quiet expiration what is the percentage of the muscles of respiration used?
None passive due to the elastic recoil
Describe the mechanism of forced inspiration and the accessory muscles of inspiration
Forced inspiration - when ventilation is increased during exercise or resistance to respiration is present - accessory muscles of inspiration are used. These are Sternocleidomastoid muscle and scalene muscles of the neck, serratus anterior and pectoralis major muscles of the chest wall
Describe the mechanism of forced expiration and the accessory muscles of and expiration
Muscles - internal intercostal muscles and abdominal wall muscles (external and internal oblique and rectus abdominus muscles).
Define the term ‘compliance of the lungs’
Stretchiness of the lungs is known as compliance.
Compliance is defined as the volume change per unit pressure change.
To stretch the lungs the elastic recoil of the lung must be overcome by: elastic tissue in the lungs and surface tension forces of the fluid lining the alveoli (surfactant).
Describe the factor which affect the compliance of the lungs?
Surfactant production by type 2 pneumocytes and the surface tension they create.
What is the lung surfactant made of in simple terms?
phospholipids and proteins with detergent properties
How does the surfactant work in the lungs?
Hydrophilic heads - inside the alveolar fluid and hydrophobic tails project into the alveolar gas. The surfactant molecules disrupt the interaction between fluid molecules on the surface thereby reducing the surface tension.
How does the surface tension of the alveolar fluid vary with the surface area of the alveolus?
Alveolus expands - surfactant molecules spread further apart making them less efficient - surface tension then increases - causing alveoli to shrink down to previous size.
Alveolus shrinks - surfactant molecules come closer together increasing their conc on the surface - more efficient to reduce surface tension - easier to expand the alveolus.
Therefore the force required to expand smaller alveoli is less than that required to expand large ones - because of the amount of surfactant.
How does the law of Laplace on bubbles affect alveoli?
Pressure = 2 x surface tension / radius
The larger the radius the lower the pressure.
Smaller radius the higher the pressure.
Surface tension increases then the pressure increases.
Pressure increases then either radius decreases or sufactant increases - in the body the surfactant amount would be constant but the effect on pressures would be different and the radius would be changing.
What would happen if there were two unequal sized alveoli connected by an airway using the law of Laplace?
Pressure = 2 x surface tension / radius.
One smaller sized alveolus would have much higher pressure and the larger sized alveolus would have much lower pressure. The smaller alveolus air would then enter the larger alveolus due to the change in pressure and then as a result collapse into the larger alveolus creating a huge air-filled space called a bullae.
What happens when we breathe in, in terms of pressure within 2 different sized alveoli?
Higher the surface tension and higher the radius the pressure would be greater.
Pressure = 2x10/5 = 4
Pressure 2x30/10=6 - higher radius higher pressure = pushes air into the smaller alveolus keeping it patent.
The amount of pressure is the same even though there was less
Describe the factors which influence airway resistance in the normal lung. Resistance = pressure/rate of flow = [8 x viscosity of air x length of tube] / Pi x (radius)^4
Resistance of a single tube increases sharply with a reducing radius.
However, the combined resistance of the small airways is normally low because they are connected in parallel over a branching structure where the total resistance to flow in the downstream branches is less than the resistance of the upstream branch. Most of the resistance to breathing is in the anatomical dead space, except when the small airways are compressed during forced expiration.
What is airway resistance?
Resistance of an airway to flow air through it
Describe how airway resistance changes over the breathing cycle
Inspiration - alveoli increase in size and so radius increases. This then causes resistance to decrease by a factor of 4 in a small margin.
Describe the `interstitial space’
Potential space between alveolar cells and the capillary basement membrane, which is only apparent in disease states when it may contain fibrous tissue, cells or fluid
Explain why fibrous tissue deposition in the interstitial space causes a restrictive type of lung disease (ILD)
Fibrous tissue has the following effects in the interstitium:
- Lungs stiffer - harder to expand since collagen is less stretchy than elastin fibres - lung compliance is reduced
- Elastic recoil of the lungs is increased (of elastin and collagen fibres)
- Lungs become smaller than normal
- Causes a restrictive type of ventilatory defect
- On examination chest expansion is reduced
- Thickening of alveolar walls increases distance oxygen has to diffuse. The effect on diffusion of oxygen is much greater than CO2 which is more soluble than oxygen.
What happens to inspiratory capacity, functional residual capacity and vital capacity in ILD?
Inspiratory capacity = TV + IRV = 500+3000mls. TV decreases as reduced lung compliance and IRV also decreases as smaller lungs due to the inc elastic recoil.
FRC = ERV + RV. ERV and RV dec as less compliance and expansion of the lung.
VC = ERV + TV + IRV.
The lung elastic recoil > chest wall elastic recoil. Therefore FRC will be reduced
What is respiratory distress in the newborn?
Disorder resulting in stiffer lungs - reduced compliance
RDS in the new born is caused by a deficiency of surfactant in premature babies particularly in <30 weeks old
From what age is surfactant produced?
From 32 weeks of gestation
What effect does the surfactant levels in RDS in new the born cause?
Reduced surfactant production
Higher surface tension of the fluid in the lungs
Harder to open up the alveoli when breathing in and so there are fewer alveoli open therefore no gas exchange occurring in these.
Increased effort to then breath and overcome the surface tension
Impaired ventilation
Typically babies have signs of respiratory distress (cyanosis, grunting, intercostal and subcostal recession)
What are the signs of respiratory distress?
Cyanosis, grunting, intercostal and subcostal recession
How do you treat RDS in the new born?
Surfactant replacement via an endotracheal tube
Supportive treatment with oxygen and assisted ventilation
How do you treat ILD?
Steroids to reduce inflammation and removal of cause e.g. drugs
How do you treat Emphysema?
Stop causative agent e.g smoking + steroids to reduce inflammation
LAMA+LABA would just increase airways even further which is the problem
What long acting inhalers can you use in asthma treatment?
LABA as want smooth muscle relaxation and NAC to increase secretion viscosity +/- steroids to reduce the causative agent
How do you treat RDS in the new born?
Give surfactant via endotracheal tube + Oxygen + assisted ventilation
What is the pathophysiology of emphysema?
Opposite to those of lung fibrosis
Loss of elastin and breakdown of alveolar walls causing increased lung compliance (stretchiness) and narrowing of small airways due to the loss of elastic fibres exerting an outward pull (radial traction) on the small bronchioles
Lungs are easier to expand - inc lung compliance
Elastic recoil is reduced
Lungs - hyperinflated
Airway narrowing causing an obstructive type of ventilatory defect on spirometry.
What are the symptoms of emphysema?
SOB
Reduced exercise tolerance
What is a pneumothorax?
Disorder where air enters the pleural space, with loss of pleural seal and lung collapse.
Air in the pleural space
What causes a pneumothorax?
An opening is created which allows the pleural cavity to communicate with the outside (e.g. trauma to the chest) or with the lung (spontaneous rupture of a weak area of the lung), air flows into the pleural cavity down the pressure gradient until the pressure in the pleural cavity reaches atmospheric pressure.
What is atelectasis?
Either incomplete expansion of the lungs (neonatal atelectasis) or the collapse of previously inflated lung, producing areas of relatively airless pulmonary parenchyma.
What are the main types of acquired atelectasis?
Compression atelectasis results whenever significant volumes of air (pneumothorax) or fluid (pleural effusion) accumulate within the pleural cavity
Resorption atelectasis - stems from complete obstruction of an airway. Over time air is resorbed from the alveoli which collapse.
What is the main cause of resorption atelectasis?
Bronchial carcinoma
Mucous plug
How does asthma cause airway obstruction?
Broncho constriction prevents air coming in and out of the alveoli. The bronci/oles are narrowed partly due to the excessive secretions, local oedema/ smooth muscle hypertrophy. Narrowed lumen due to the above causing an obstruction to the airways hence an obstructive picture on spirometry
How does COPD (emphysema) cause airway obstruction?
Lung compliance is increased - less elasticity to bring lungs back to normal shape. Hyperinflated lungs. Small airways elastin are destroyed - therefore less radial traction on the terminal bronchioles. Airway narrowing is the result causing obstruction.
Explain the relevance of Boyles law in ventilation of the lung
The pressure of a fixed quantity of gas at a constant temperature is inversely proportional to its volume. Pressure is measured in kPa. The higher the pressure the lower the volume.
Ventilation - inspiration and expiration.
As we inspire the volume of the lungs increases. The higher the volume the lower the pressure. Therefore gas moves from an area of high pressure to low pressure i.e. the lungs hence we inspire
Explain the concept of the ‘partial pressure’ of an individual gas in a gas mixture
Dalton’s law
In a mixture of a gases, each component gas exerts a partial pressure in proportion to its volume percentage in the mixture. Since atmospheric pressure is 101.1kPa and air contains 20.9% oxygen, the partial pressure of O2 in atmospheric air is 101.1x0.209=21.1kPa.
Calculate the partial pressures of constituent gases in atmospheric air and explain the effects of altitude upon them
pOxygen - 21.1kPa pNitrogen - 79.6 kPa pCO2 as 0.04 kPa pH2O as 0.5kPa As altitude increases there is less pressure and although the partial pressures are the same.
Explain the effect of saturated vapour pressure on partial pressure of inhaled gases such as oxygen
Evaporated water <=> dissolved H2O in liquid phase.
At equilibrium the gas mixture is saturated with water vapour, and the pressure it exerts is called the saturated vapour pressure (SVP). SVP depends only on temperature. At body temp 37 degrees the SVP of water is 6.28kPa.
In humidified air, water vapour contributes 6.28kPa which means that the rest of the gases account for 94.28kPa (101-6.28kPa). Since the other gases remain in the same proportions as in dry air the pO2 of humidified air = (100-6.28)*20.9% = 19.8kPa.
Inhaled air becomes more saturated with water vapour as it passes along the resp tract so that in a given volume of air, the percentage of O2 drops to about 20% with a drop in pO2 to about 19.8kPa.
What is meant by “partial pressure of oxygen” in blood and what are the values of it in the arteries, veins and mixed blood from the lung?
Mixed venous blood reaching the pulmonary capillaries has a pO2 of 6kPa and a pCO2 of 6kPa. After gas exchange the blood leaving the alveoli has pO2 of 13.3kPa and pCO2 of 5.3kPa which is the same as that of alveolar air. Partial pressure of oxygen in blood is the pressure exerted in the blood by oxygen
Explain why “partial pressure of oxygen” in blood is different from the “content” of oxygen in the blood.
Partial pressure in blood = alveolar partial pressure.
Henry’s law - the amount of gas that dissolves in a specific volume of liquid is proportional to the partial pressure of that gas in a gas phase and its solubility coefficient. O2 is not water soluble; Solubility coefficient is 0.01mmol/L/kPa.
Plasma = alveolar air pO2 is 13.3kPa but the content will be 0.01x13.3 = 0.13mmol/L.
Blood = amount of gas chemically bound + amount of gas in free solution.
Amount bound to Hb= 8.8mmol/L, O2 content therefore= 8.8+0.13=8.93mmol/L.
How is alveolar pO2 and pCO2 related to inspired air and mixed venous blood related to arterial blood.
Alveolar pO2/ pCO2= equilibrium between rate of uptake by blood and rate of replenishment by alveolar ventilation.
Blood at alveolar capillaries equilibrates to alveolar air therefore having the same partial pressure.
State the normal PO2 and PCO2 in alveolar air, arterial blood and mixed Venus blood
Inspired air= pO2= 21.2kPa
Alveolar air = pO2 = 13.3kPa, pCO2 = 5.3kPa
Mixed venous blood = pO2= 6kPa, pCO2 = 6kPa
Arterial blood = pO2 = 13.3kPa, pCO2 = 5.3kPa.
Inspired air is dry, alveolar air is saturated with H20.
Describe the layers making up the diffusion barrier at the air-blood interphase
Gas in alveoli Alveolar epithelial cell Interstitial fluid Capillary endothelial cell Plasma Red cell membrane 5 cell membranes, 3 layers of intracellular fluid and 2 layers of extracellular fluid.
Describe factors affecting the rate of diffusion across the air blood interphase
Diffusion solubility Distance Blood flow Oxygen concentration gradient Time RBC spend in the alveolar capillary
Name 3 diseases that cause diffusion defects in the alveoli/ blood interphase
ILD
Emphysema
Pulmonary oedema
How does ILD cause diffusion defects in the alveoli/ blood interphase?
Characterised by excessive deposition of collagen in the interstitial space. Thickening of alveolar walls. Increased diffusion distance.
How does pulmonary oedema cause diffusion defects in the alveoli/ blood interphase?
Fluid in interstitium - increased diffusion distance
How does emphysema cause diffusion defects in the alveoli/ blood interphase?
Destruction of alveolar walls - reduced elastin. Small alveoli fall into large airspaces and so reducing the total gas exchange surface area.
Explain why gas exchange depends on the partial pressure gradient across the diffusion barrier
Gases go from an area of high concentration to an area of low concentration therefore having a pressure gradient would be similar where gases would go from an area of high pressure to an area of low pressure. Solubility also has an effect on this.
Describe the role of diffusion resistance in gas exchange
Carbon monoxide is used to calculate diffusion resistance. Single maximal breath of CO and Helium. CO is used because its extreme affinity to Hb. Almost all CO in blood binds to Hb. Conc gradient for PaCO (alveoli to blood) remains the same the entire time blood remains in contact with alveolar gas. Amount of CO transferred is an estimate of the diffusion resistance of the barrier.
State and explain the difference in the diffusion rates of O2 and CO2
CO2 is 21 times faster at diffusing than O2. O2 has a much lower solubility and diffusion time compared to CO2 and so by having less being able to dissolve in the water a carrier is required whereas CO2 doesn’t require a carrier because it is so soluble in liquid.
Define Oxygen saturation (SaO2, ‘Sats’)
How much of the haemoglobin is saturated with O2. Measured as a % comparing oxy-Hb and deoxy-Hb.
Pulse oximetry only detects pulsatile arterial blood NOT venous blood.
DOESN’T say how much Hb in blood
Define Arterial PaO2 (partial pressure of oxygen)
The force exerted by O2 in blood in the arterial system after it has been oxygenated by the lungs. PaO2 = 8.93 mmol/Litre.
Define Oxygen content of blood
O2 bound + O2 dissolved. Usually 8.93mmol/Litre if the blood is exposed to 13.3kPa of O2 in the alveoli.
Draw an oxygen-haemoglobin dissociation curve, label the axes correctly and indicate the normal values of (i) alveolar pO2 (ii) capillary pO2 in a typical tissue
x-axis= PO2 (kPa)
y-axis= % saturation
Alveolar pO2 = 99% at the peak and sigmoid curve.
pO2 = 13.3kPa
Capillary pO2 in tissues= 75% sats. pO2=5.3kPa.
p50= 50% oxygen saturation the curve is at 3.6kPa.
What factors affect the oxygen carrying capacity of Hb in the alveoli and at tissues.
Hb which holds the oxygen molecule. Each Hb has 4 iron atoms and can hold 8 atoms of O2.
2,3-DPG accumulates in RBC when O2 tension is low. Binds to Hb and shifts dissociation curve to the right in both tissues and the lungs - causing low O2 sats in higher O2 kPa therefore more O2 is unloaded in the respiring tissues.
pH- higher respiring tissues have a low pH. More acidic environment. This would shift the curve to the right therefore more O2 released in these respiring tissue areas.
Temperature- higher temperature shifts oxygen sats curve to the right- more O2 released in higher pO2 therefore more released in respiring tissues.
CO2- higher levels of CO2 would also shift the curve to the right as there is more respiring tissues and so more O2 is needed at higher pO2 therefore more is released in the respiring tissues.
Does hyperventilation increase the oxygen content of the blood significantly?
No - it does not significantly effect O2 sats
Define cyanosis and explain its significance
Bluish coloration due to unsaturated Hb
Deoxy-Hb less red than oxy-Hb
Can peripheral due to poor circulation
Central (mouth, tongue, mucous membranes) due to poorly saturated blood in systemic circulation.
Problem oxygenating the blood. Centrally is worse than peripherally
What are the 2 ‘moods’ of Hb?
Relaxed and Tensed states
Low affinity - Tensed - difficult for O2 to bind
High affinity - Relaxed - easy for O2 to bind
At low PO2 what state is Hb in?
Tensed - hard for first O2 molecule to bind
As each O2 binds the molecule becomes more relaxed and binding of the next O2 molecule is easier.
Understand why anaemia causes tissue hypoxia despite normal arterial PaO2 and normal Oxygen saturation (SaO2, ‘Sats’)
Anaemia - low Hb levels in the blood.
Less Hb= less O2 carried around the body
Hypoxia - low [O2] at the tissues or body
Even at normal O2 saturation - all the Hb is oxygenated but that doesn’t mean there is enough O2 being carried around to meet the demands hence hypoxia occurs.
What disease cause local hypoxia due to reduced blood flow?
Shock = reduce blood flow - peripheral vasoconstriction can cause peripheral hypoxia
Name the diseases that cause local hypoxia due to O2 use> O2 delivery to the tissue
Peripheral arterial disease/ Raynaud’s = tissues using O2 faster than it is delivered
Up to how much of the Hb can be saturated with CO before it can cause fatality?
> 50% HbCO
Why is there a need for Hb to react to changes in temperature or pH?
Exercise increases metabolism up to 10x but CO can only go 5x. Therefore needs to be a more efficient method of O2 transfer - improved extraction at the tissues. This occurs by physical changes in Hx due to temp and pH to offload more O2.
Up to how much HbO2 can dissociate in extremely low pO2.
70% HbO2 can be given up due to temp and acidity
What is the Bohr shift?
pH effects the affinity of Hb.
Lower pH more O2 given up at higher pO2.
The shift in the sigmoid O2 sat/PO2 curve to the right is the Bohr shift.
pH promotes a tensed state so more O2 is given up as it is harder to bind O2.
How low can tissue pO2 get and explain why so low.
Tissue pO2 must be high enough to drive diffusion of O2 to cells (down conc gradient)
Can’t fall below 3kPa in most tissues.
What does the body do in tissue where the pO2 needs to get very low to supply the highly metabolically active tissues?
Higher capillary density - the lower the pO2 can fall (doesnt have to diffuse as fa)
Very metabolically active tissues have a higher capillary density
What is a typical pO2 in tissues?
5kPa depending on how metabolically active though.
How could you calculate the amount of O2 given up at tissues?
% O2 sat in Arterial blood - % O2 sat in tissues
100%-65% = 35% given up.
Arterial pO2 = 8.8mmol/L
8.8mmol/L x 0.35= 3mmol/L
What happens to oxygen content in the blood, O2 saturation and pO2 in anaemia where the lungs are functioning normally?
pO2 would be the same as it is the amount of O2 dissolved in the blood
O2 saturation would be normal
Oxygen content would be lower as there is less Hb and this accounts for 8.8mmol/L.
List the reactions of CO2 in blood
H20 + CO2 H2CO3 H+ + HCO3-
H+ + Hb HbH
Describe the buffering action of haemoglobin in red cells
Hb takes H+ and so increases the pH of the surrounding blood/ RBC.
Deoxy-Hb is a better buffer than oxy-Hb which would be the case in the tissues.
Because H+ + Hb HbH it draws more H+ from H20 + CO2 H2CO3 H+ + HCO3-. This then brings the [HCO3-] 20x greater than CO2 (25mmol/L : 1.2mmol/L)
Describe the process of transport of CO2 from tissues to lungs
CO2 enter the RBC. Carbonic anhydrase converts that with H20 to H2CO3. This then produces H+ and HCO3-. H+ reacts with Hb to make HbH. This is a reversible reaction.
CO2 is also dissolved in plasma.
CO2 also reacts with protein part of Hb forming carbamino compounds (carbamino Hb).
State the proportion of CO2 traveling in various forms from tissues to lungs
1L of plasma has 600ml plasma and 400ml of RBC. 600ml plasma = 1.33mmol/L dissolved CO2 600ml plasma = 27mmol/L HCO3 400ml RBC = 0.98mmol/L dissolved CO2 400ml RBC = 2.9mmol/L carbamino 400ml RBC = 11.69 mmol/L HCO3. Then as proportions of each in blood 600ml blood = 0.8mmol/L dissolved CO2 600ml blood = 16.19mmol/L HCO3 400ml RBC blood = 0.39mmol/L dissolved CO2 400ml RBC blood = 1.17mmol/L carbamino 400ml RBC blood = 4.66 mmol/L HCO3. Total 23.21mmol/L blood.
Most is HCO3- in plasma.
Describe the function of carbamino compounds
Carry CO2 that is bound to the protein part of the Hb
State the factors influencing the hydrogen carbonate concentration of plasma
Amount of carbonic anhydrase enzyme in the plasma (little amount anyway)
Buffering capacity of Hb (more so than pCO2)
Define hypoxia
Low amount of O2 in the blood reaching the tissues
Define hypercapnia
Rise in alveolar and hence arterial pCO2
Define hypocapnia
Reduction in alveolar and hence arterial pCO2
Define hyperventilation In terms of CO2 and metabolism
Removal of CO2 from alveoli is more rapid than its production. Ventilation increase without change in metabolism
Define hypoventilation In terms of CO2 and metabolism
Removal of CO2 from lungs is less rapid than its production. Ventilation decrease without change in metabolism
Describe the effects on plasma pH of hyper ventilation
More CO2 removed than produced
Dec alveolar pCO2
Less [CO2] in the blood
Less H+ available and therefore respiratory alkalosis/ increase in pH.
Describe the effects on plasma pH of hypo ventilation
Less CO2 removed than produced
Inc alveolar pCO2
More [CO2] in the blood
More H+ in the blood and therefore respiratory acidosis / decrease in pH
Describe the general effects of acute hypo ventilation
Respiratory acidosis occurs
CO2 is retained in the blood and so becomes more acidic
Decreased O2
Increased CO2
Describe the general effects of acute Hyper ventilation
Respiratory alkalosis occurs (Less CO2 and therefore less H+)
Decreased CO2
Increased O2
Define Respiratory Acidosis
Less CO2 removed than produced
Inc alveolar pCO2
More [CO2] in the blood
More H+ in the blood and therefore respiratory acidosis / decrease in pH
Define Respiratory Alkalosis
More CO2 removed than produced
Dec alveolar pCO2
Less [CO2] in the blood
Less H+ available and therefore respiratory alkalosis/ increase in pH.
Define Compensated Respiratory Acidosis
Respiratory acidosis occurs (more pCO2 more H+)
Kidneys reduce the excretion of HCO3 to mop up the H+ - thus restoring the ratio of [HCO3]/[Dissolved CO2] and pH to near to normal - compensated respiratory acidosis
Define Compensated Respiratory Alkalosis
Respiratory alkalosis occurs (Less CO2 and therefore less H+)
Kidneys inc excretion of HCO3 so the ratio of [HCO3]/[Dissolved CO2] returns to near normal, therefore pH is restored but buffer base concentration is reduced
Compensated respiratory alkalosis
What happens if there is a decrease in O2 but no change in CO2 on RR and then what would be the result on CO2?
Decrease O2
RR increases to bring O2 up
Inadvertently CO2 is blown off
Decrease in CO2 and Increase in O2
Define the term Metabolic Acidosis
If tissues produce acid this reacts with HCO3
Fall in [HCO3] leads to a fall in pH
Metabolic acidosis occurs
Define the term Metabolic Alkalosis
If plasma [HCO3] rises (e.g. after vomiting)
Plasma pH rises
Metabolic alkalosis occurs
Define the term Compensated Metabolic Acidosis
If tissues produce acid this reacts with HCO3
Fall in [HCO3] leads to a fall in pH
Metabolic acidosis occurs
Compensation occurs by changing ventilation
Increased ventilation lowers pCO2
Restores pH towards normal
Define the term Compensated Metabolic Alkalosis
If plasma [HCO3] rises (e.g. after vomiting)
Plasma pH rises
Metabolic alkalosis occurs
Compensation occurs by changing ventilation
Decreased ventilation raises pCO2
Restores pH towards normal
However there is a risk of hypoxia therefore a limit of compensation
Describe the acute effects upon ventilation of falling inspired pO2
Increased ventilation to bring up the pO2
Decreased pCO2 occurs as more is blown off
pH will then increase and become more alkalotic. The kidneys will try and compensate by removing HCO3 to allow more H+ to have an effect and bring the pH back to normal
Describe the acute effects upon ventilation of increases in inspired pCO2
Increased inspired CO2 would then increase pCO2 in the alveoli and therefore the blood
The body would compensate by increasing the HCO3 kept in the blood to neutralise the H+ production.
This would then change respiratory acidosis to a compensated resp acidosis.
RR should increase to try and blow off the rise in pCO2.
Describe the acute effects upon ventilation of falls in arterial plasma pH
Fall in pH = more H+
In order to remove the H+ need to remove the CO2 to then push the equation towards removing the H+ and producing more CO2. As a result RR/ Ventilation will increase
Describe the location of peripheral chemoreceptors and their nerve supply
- Carotid bodies at the bifurcation of the carotid arteries to the brain. Sinus nerve branch of the glossopharyngeal nerve (CN IX)
- Aortic bodies - Found in the arch of the aorta. Aortic nerve a branch of the vagus nerve (CN X).
Describe the response of peripheral chemoreceptors to changes in arterial pO2 and its role in the regulation of respiration
Large falls in pO2 stimulate the carotid and aortic bodies
Increased RR and HR
Change in blood flow distribution - inc flow to brain and kidney
Describe the response of peripheral chemoreceptors to changes in arterial pH and its role in the regulation of respiration
Directly activated by change in the pH of the blood. A low pH results in increased respiratory rate and tidal volume.
Describe the response of peripheral chemoreceptors to changes in arterial pCO2 and its role in the regulation of respiration
Peripheral chemoreceptors are not particularly sensitive to pCO2, needing a large change in pCO2 to stimulate them. They are not crucial for the precise regulation of respiration, due do respond quickly to large changes in pCO2.
What receptors are sensitive for changes in pCO2, pO2 and pH the most?
pCO2 and pH - central chemoreceptors
pO2 and pH - Carotid and aortic chemoreceptors
Describe the location of central chemoreceptors
Located on the ventral surface of the medulla and are exposed to CSF. They respond to a drop in pH which occurs when the arterial pCO2 rises.
Describe the central chemoreceptors response to changes in arterial pCO2 in the regulation of respiration
Arterial pCO2 changes -> CSF pCO2 changes -> pH changes. Which are sensed by central chemoreceptors. Impulses from chemoreceptors travel to the brain stem -> breathing rate changes to feedback on the loop.
Describe the roles of the CSF in the response of central chemoreceptors to changes in arterial pCO2
CSF therefore is sensitive to pH changes as it is maintained by its own [HCO3-]/[Dissolved CO2] buffer system. It contains no Hb.
CSF Dissolved CO2 is determined by arterial dissolved CO2.
Describe the roles of the blood-brain barrier in the response of central chemoreceptors to changes in arterial pCO2
BBB has free passage of CO2 but not HCO3- through it.
Describe the roles of the choroid plexus in the response of central chemoreceptors to changes in arterial pCO2
CSF HCO3- is determined by the activity of choroid plexus cells which pump HCO3- into and out of the CSF and is largely independent of plasma HCO3-.
Thus ratio of [HCO3-] and [dissolved CO2] determines the pH.
Explain the effect of prolonged elevation of pCO2 on the central chemoreceptors.
Persisting changes in CSF pH stimulate the choroid plexus to pump more HCO3- into the CSF and change [HCO3-] to bring the [HCO3-]/[dissolved CO2] ratio back towards normal
CSF pH is corrected much more quickly than blood pH because of small volume. As CSF pH is corrected, changes in ventilation driven by alteration of pCO2 disappear, and the control system is reset to operate around a different pCO2.
2 capillaries exit an alveolus but one of those capillaries is from a poorly ventilated alveolus (due to a mucous plug) how would you work out the combined blood oxygen saturation and pO2? Would it just be average of the two pO2?
Using the oxygen saturation curve you would look at the two pO2’s of each capillary leaving the alveolus. Then you would cross reference that on the curve with the oxygen saturations. The average of the two oxygen saturations should be taken. Then cross reference that on the oxygen sat curve and find the pO2 value of the two. This would give you the combined pO2 of the mixed venous blood returning to the heart.
State the normal range plasma pH
7.35-7.45
Describe the CO2/ Bicarbonate buffer system and the factors influencing pCO2 and [HCO3-]
pCO2 = RR controls this, dissolved CO2, Carbamino Hb
Renal function controls [HCO3-] more so than changes in pCO2
What effect does pH have on serum calcium salts?
Alkalaemia reduces the solubility of calcium salts, which means that free Ca2+ leaves the ECF, binding to bone and proteins
What effect does pH have on enzyme function in general (E.g. in the blood)?
Acidaemia denatures enzymes
What effect does pH have on serum potassium?
Acidaemia = inc H+. H+ moves K+ out of cells, producing hyperkalaemia which can be fatal.
Potassium is replaced by H+ in transporters on the cell membranes (K-ATPase) and so cells become acidotic and blood becomes hyperkalaemic.
What about the relationship of HCO3 and pCO2 causes a change in pH?
It is the ratio of the two that controls pH and not absolute values.
What happens if acid is produced metabolically to HCO3?
Recovery of all filtered HCO3 is insufficient to restore plasma [HCO3] so HCO3 will have to be created within the kidney. This will create H+ ions which are then excreted directly or indirectly into the urine and to avoid damaging the urinary acidity, it must be buffered by either other filtered substances or buffers created by the kidney.
What area of the kidney handles HCO3 reabsorption?
Proximal tubule - 80-90%
Thick ascending limb of the loop if Henle - 15%
Distal nephron
What transporter controls H+ excretion on the apical membrane of the kidney?
H+/ Na+ channel. H+ is excreted for N+, Na moves down its concentration gradient.
What is the reaction that produces HCO3- which then leaves the cell into the blood?
H+ reacts with HCO3- in the lumen. This produces CO2 which diffuses across into the cell (through the cell membrane). The CO2 reacts with water and the reverse reaction occurs to produce HCO3 and H again. The HCO3- is pumped out of the cell into the blood. H+ again moves through the Na+/H+ transporter causing Na to be reabsorbed and the cycle goes again.
What is the reaction in the distal nephron that is the final site for HCO3- absorption?
Through intercalated cells
H+ pumped across apical membrane by H+-ATPase pump as the Na+ ion gradient is insufficient.
What is the reaction in the distal nephron that is the final site for HCO3- absorption?
Through intercalated cells.
H+ pumped across apical membrane by H+-ATPase pump as the Na+ ion gradient is insufficient.
By this point there is little HCO3 remaining - so little CO2 enters the cell.
The CO2 used is produced by the cells own metabolism - so generating new HCO3- to enter the plasma
What buffers the excreted H+ from the urine?
Monobasic phosphate (HPO2 -4) buffers the H+ and becomes more effective as the pH of the urine falls.
How is an amino acid used to remove H+ and produce useful HCO3-?
H+ is held by ammonium ions. (NH4+).
Ammonium ions are produced from the amino acid Glutamine.
Each alpha-ketoglutorate produces 2x HCO3- which enters the blood stream and H+ is excreted.
What is the yield in the reaction with ammonium ions and glutamate producing?
Glutamine –> NH4+ + Glutamate –> NH4+ + alpha-ketoglutorate
What pH disturbance can be caused by hypokalaemia?
Metabolic alklosis
What pH disturbance can be caused by hyperkalaemia?
Metabolic acidosis . Capacity of the kidney to reabsorb and create HCO3- is reduced
Why does ECF pH fall as acid secretion increases?
Large changes in renal tubular pH consequent upon changes in the rate of export of HCO3- to plasma. HCO3- is more controlled rather than pH - which leads to changes to HCO3-.
Explain how the kidneys respond to respiratory acidaemia?
pCO2 rises in the blood. Decreased ratio of HCO3-/pCO2 (less HCO3) therefore decreased pH.
Fall in renal tubular pH induced by diffusion of extra CO2 leads to extra H+ being excreted. With consequent production and export into the plasma of HCO3-, restoring the ratio of HCO3- to PCO2 nearer to normal
Explain how the kidneys respond to respiratory alkalaemia?
Rises in tubular pH induces less HCO3- resorption by reducing H+ export and suppressing H+ secretion - so HCO3- is excreted and [HCO3-] falls, again restoring the ratio of HCO3- to pCO2 nearer to normal
Explain how the kidneys respond to metabolic acidaemia?
If excess acid produced - associated anion (e.g. lactate) will replace HCO3- in plasma which will influence the anion gap.
Broadly name causes of metabolic acidaemia
Excess metabolic production of acids, acids are ingested, HCO3- is lost or there is a problem with renal excretion of acid.
What is an anion-gap?
Difference between the sum of [Na] and [K] and the sum of [Cl-] and [HCO3-]. If HCO3- is replaced by another anion which is not included in the calculation the gap will increase.
([Na+] + [K+]) / ([Cl-] + [HCO3-] = anion gap.
What is the usual reference ranges for the anion gap?
8-14mmol/L
What is the anion gap representative of?
Unmeasured anions in the ECF (anions that aren’t routinely measured)
What does an increase in the anion gap indicate?
Inc in the percentage of one or more unmeasured anions. This occurs with acidic conditions characterised by higher organic acids present in the blood i.e. lactic acid.
