Respiratory physiology Flashcards
What is internal respiration?
the intracellular mechanisms which consumes oxygen and produces carbon dioxide
what is external respiration?
sequence of events that leads to the exchange of oxygen and carbon dioxide between the environment and the cells of the body
what are the four steps of external respiration?
Ventilation
The mechanical process of moving gas in and out of the lungs
Gas exchange between alveoli and blood
The exchange of O2 and CO2 between the air in the alveoli and the blood in the pulmonary capillaries
Gas transport in the blood
The binding and transport of of O2 and CO2 in the circulating blood
Gas exchange at the tissue level
The exchange of O2 and CO2 between the blood in the systemic capillaries and the body cells
What is boyles law? and how does this effect ventilation?
At any constant temperature the pressure exerted by a gas varies inversely with the volume of the gas
(as the volume of a gas increases the pressure exerted by the gas decreases)
-air flows down a pressure gradient from a region of high pressure to a region of low pressure
-intra-alveolar pressure must become less than atmospheric pressure for air to flow into lungs
What are the two forces that hold the thoracic wall and lungs in close opposition?
- intrapleural fluid cohesiveness: water molecules in intrapleural fluid are attracted to each other sticking pleural membrane together
- negative intrapleural pressure: the sub-atmospheric intrapleural pressure creates a transmural pressure gradient
What respiratory muscles are at work during inspiration?
Is it an active or passive process?
Does intraalveolar pressure increase or decrease?
ACTIVE
-diaphragm: contracts and descends (increasing vertical dimension of thoracic cavity)
-external intercostal muscles: contracts and elevates ribs (increases side to side dimension of thoracic cavity and causes sternum to move upward and outward which increases front to back dimension of thoracic cavity)
intraalveolar pressure decreases to less than atmospheric
What respiratory muscles are at work during expiration?
is it an active or passive process?
Does intraalveolar pressure increase or decrease?
PASSIVE
-diaphragm and external intercostal muscles relax
-chest wall and stretched lungs recoil
intraalveolar air pressure increases to more than atmospheric pressure
What causes the lungs to recoil during expiration?
- elastic connective tissue
- alveolar surface tension
- alveolar interdependence
What reduces alveolar surface tension? what is this consisted of and how is it secreted?
-surfactant
complex mixture of lipids secreted by type II alveoli
it intersperses between water molecules lining alveoli
What is LaPace’s law and what does this mean for the effect of surfactant on smaller alveoli?
P = 2T/R
P = inward directed collapsing pressure
T = Surface Tension
r = radius of the buble
According to the law of LaPlace: the smaller alveoli (with smaller radius - r) have a higher tendency to collapse
Surfactant lowers the surface tension of smaller alveoli more than that of large alveoli
This prevent the smaller alveoli from collapsing and emptying their air contents into the larger alveoli
What is alveolar interdependence?
If an alveolus start to collapse the surrounding alveoli are
stretched and then recoil exerting expanding forces in the
collapsing alveolus to open it
What are the major muscles of respiration?
- contract every inspiration
- diaphragm and external intercostal muscles
What are the muscles of active expiration?
- contract only during active expiration
- internal intercostal muscles
- abdominal muscles
What are the accessory muscles of inspiration?
- sternocleidomastoid
- scalenus
What is the: Tidal volume inspiratory reserve volume inspiratory capacity expiratory reserve volume residual volume Functional residual capacity Vital capacity
- Tidal volume: Volume of air entering or leaving lungs during a single breath = 500ml
- Inspiratory reserve volume: Extra volume of air that can be maximally inspired over and above the typical resting tidal volume = 3000ml
- Inspiratory capacity = TV + IRV
- Expiratory reserve volume: Extra volume of air that can be actively expired by maximal contraction beyond the normal volume of air after a resting tidal volume = 1000ml
- Residual volume: min. volume of air remaining in the lungs even after a maximal expiration = 1200ml
- Functional residual capacity: volume of air in lungs at the end of normal passive expiration = RV+ERV = 2200ml
- Vital capacity: maximal volume of air that can be moved out during a single breath following a maximal inspiration = IRV +TV + ERV = 4500ml
What is the total lung capacity?
-the maximum volume of air that the lungs can hold
-vital capacity + residual volume
=5700
Does residual volume increase or decrease when the elastic recoil of the lungs is lost? What condition can this happen in?
it increases
-e.g. in emphysema
What is FVC in spirometry?
Forced Vital Capacity
maximum volume that can be forcibly expelled from the lungs following a maximum inspiration
What is FEV1?
Forced expiratory volume in 1 second
-the volume of air that can be expired during the first second of expiration in an FVC determination
What is the normal FEV1/FVC ratio?
How does this change in an obstructive lung disease picture?
How does this change in a restrictive lung disease picture?
How does this change in a mixed obstructive and restrictive lung disease picture?
Normal = >70% Obstructive = <70% (FVC stays the same but FEV1 is reduced) Restrictive = >70% (both FVC and FEV1 are reduced) Mixed = <70% (both FVC and FEV1 are reduced but FEV1 is still proportionally MORE reduced due to obstruction)
What is the formula for air flow?
Normally does air move in and out with a small or large pressure gradient? Why is this?
What is the primary determinant of airway resistance?
Is expiration or inspiration more difficult when there is significant resistance to airflow?
F = change in P/R
F = flow P = pressure R = resistance
Air usually flows in and out of the lungs with a small pressure gradient due to resistance of flow in the airways being very low.
Primary determinant of airway resistance is the radius of the conducting airway
Expiration is more difficult than inspiration
What affect does sympathetic vs parasympathetic stimulation cause in the airways of the lungs?
Parasympathetic simulation = bronchoconstriction
Sympathetic stimulation = bronchodilation
Does the intrapleural pressure rise or fall during inspiration? Does it rise or fall during expiration?
Intrapleural pressure falls during inspiration
Intrapleural pressure rises during expiration
What is dynamic airway compression? is this a problem in normal people? how come? Is this a problem for patients with airway obstruction? How come?
- during expiration the chest wall recoils, this creates a rise in intrapleural pressure
- during active expiration this causes the alveoli AND the airway to become compressed
-in normal people the increased airway resistance causes an increase in airway pressure upstream, this helps to open the airways by increasing the driving pressure between the alveolus and the airway i.e. increasing the airway pressure downstream
-in those with airway obstruction, during active expiration, the driving pressure between the alveolus and the airway is lost over the obstructed segment = fall in airway pressure along the airway downstream. But the intrapleural pressure remains high and therefore these airways are more likely to collapse.
(this problem becomes worse if the patient also has decreased elastic recoil of the lungs)
What is pulmonary compliance? How does the work required to produce a given degree of inflation change if the lungs are less compliant?
compliance is the measure of effort that has to go into stretching/distending the lungs
- volume change per unit of pressure change across the lung
- the less compliant the lungs are, the more work is required to produce a given degree of inflation as a greater change in pressure is needed to produce a given change in volume (stiffer lungs)
List 5 things that could reduce pulmonary compliance?
- pulmonary fibrosis
- pulmonary oedema
- lung collapse
- pneumonia
- absence of surfactant
What pattern is seen on spirometry of people with reduced pulmonary compliance? What clinical feature would be described?
- restrictive pattern of lung volumes
- shortness of breath esp. on exertion
How could pulmonary compliance increase? what does this cause in the lungs?
- if elastic recoil of the lungs is lost
- e.g. emphysema
- patients have to work harder to get air out of the lungs = hyperinflation of lungs
- compliane increases with increasing age
What are the four situations where work of breathing is increased?
-When pulmonary compliance is increased
-When airway resistance is increased
-When elastic recoil is decreased
-when there is a need for increased ventilation
(Breathing usually requires about 3% of total energy expenditure)
What is anatomical dead space? how much is this usually in mls?
some inspired air remains in the airway where it is not available for gas exchange
150mls
What does pulmonary ventilation mean? How do you work out pulmonary ventilation in litres per minute?
Pulmonary ventilation is the volume of air breathed in and out per minute
Tidal volume X respiratory rate
What does alveolar ventilation mean? How do you work out alveolar ventilation? is it less or more than pulmonary ventilation
The volume of air exchanged between the atmosphere and the alveoli per minute
This is less than pulmonary ventilation because of anatomical dead space
Alveolar ventilation = (tidal volume - dead space volume) X respiratory rate
What can be done to increase pulmonary ventilation? What is it more advantageous to increase? why is this?
Increase the depth of breathing (tidal volume)
Increase the respiratory rate
-it is more advantageous to increase the depth of breathing because of anatomical dead space
(if you are doing shallow rapid breathing and tidal volume is only 150mls, you are only moving dead space in and out so this makes alveolar ventilation 0)
What is the difference between ventilation and perfusion?
Ventilation = the rate at which gas is passing through the lungs Perfusion = the rate at which blood is passing through the lungs
Do blood flow and ventilation vary or stay the same from the top to the bottom of the lungs?
blood flow is much higher in the bottom of the lungs whereas ventilation is slightly higher = the average arterial and alveolar partial pressures of oxygen are not exactly the same.
What is alveolar dead space? is this large or small in normal lungs? What happens to this space in diseased lungs?
This is referring to the regions of alveoli that are ventilated but are not adequately perfused with blood
- in normal lungs this is small and of little importance
- this could increase significantly in disease
What is the physiological dead space?
the anatomical dead space + the alveolar dead space
Describe how the smooth muscles of the airways and arterioles are affected in areas where the perfusion is greater than the ventilation i.e. there is more blood flow than airflow
- there’s an accumulation of carbon dioxide in the alveoli due to increase perfusion: local controls act to decrease airway resistance by relaxation of airway smooth muscle= increased airflow
- there’s a low oxygen concentration in the alveoli which causes a contraction of local pulmonary arteriolar smooth muscle = constriction of local blood vessels = increased vascular resistance = decrease blood flow
= there is an increase in airflow and a decrease in blood flow
Describe how the smooth muscles of the airways and arterioles are affected in areas where the ventilation is greater than the perfusion i.e. there is more airflow than blood flow
- if there’s an accumulation of oxygen in the alveoli due to increased ventilation local controls cause relaxation of local pulmonary arteriolar smooth muscle = dilation of local blood vessels = decreased vascular resistanct = increased blood flow
- There’s a decreased conc. of carbon dioxide in the alveoli = contraction of local airway smooth muscle = constriction of local airways = increased airway resistance = decrease in airflow
= there is an increase in blood flow and a decrease in airflow
What happens to pulmonary arterioles vs systemic arterioles when the concentration of oxygen is decreased/increased?
Pulmonary arterioles:
-if there is an increased oxygen conc. this means that there is an area where there is more ventilation than perfusion = the arterioles vasodilate
-if there is a decreased oxygen conc. this means that there is more perfusion to ventilation
= the arterioles vasoconstrict
In systemic arterioles if there’s an increase in oxygen conc. they vasoconstrict and if there’s a decrease in oxygen concentration they vasodilate (because if they want to maximise the oxygen supply to the tissues)
What are the four factors that influence the rate of gas exchange across the alveolar membrane?
1: partial pressure gradient of oxygen and carbon dioxide
2: diffusion coefficient for oxygen and carbon dioxide
3: surface area of alveolar membrane
4: thickness of alveolar membrane
What is dalton’s law of partial pressures?
the total pressure exerted by a gaseous mixture is the sum of the partial pressure of each individual component in the gas mixture
I.E
Total pressure = Pressure of gas 1 + pressure of gas 2 + pressure of gas 3…
What is the partial pressure of a gas?
The pressure that a gas would exert if it were the only gas present in the total volume of the mixture at a given temperature
e.g. if the total pressure of a gas mixture = 100kPa, and gas 1 took up half the mixture the partial pressure of gas 1 would be 50kPa.
if total atmospheric pressure = 760mmHg, and 21% of this is oxygen and 79% of this in nitrogen, what are the partial pressures of oxygen and nitrogen in the atmosphere?
For oxygen:
21% of 760 = 160mmHg
For nitrogen:
79% of 760 = 600mmHg
How can you work out the partial pressure of oxygen in the alveolar air? (PAO2)
partial pressure of oxygen in inspired air - (partial pressure of carbon dioxide in arterial blood/respiratory exchange ratio)
- Pi02 = Partial pressure of O2 in inspired air
- PaCO2 = Partial pressure of CO2 in arterial blood
- Respiratory Exchange Ratio (RER) (i.e. ratio of CO2 produced/O2 consumed) = 0.8
To work out the partial pressure of oxygen in inspired air, you have to work out the pressure of inspired air and find 21% of this.
The pressure of inspired air is atmospheric pressure - water vapour pressure (as water vapour pressure contributes about 47mmHg to the total lung pressure)
do gases move from high to low partial pressures or low to high?
High to low
Describe the gas exchange across pulmonary capillaries vs systemic capillaries
- Partial pressure of oxygen in alveoli = 100mmHg
- partial pressure of CO2 in alveoli = 40mmHg
- Partial pressure of oxygen in venous blood = 40mmHg
- Partial pressure of CO2 in venous blood = 46mmHg
- Partial pressure of oxygen in arterial blood = 100mmH
- Partial pressure of CO2 in arterial blood is 40mmHg
- Partial pressure of oxygen in tissues <40mmHg
- Partial pressure of CO2 in tissues >46mmHg
Therefore across pulmoary capillaries:
- oxygen partial pressure gradient = 60mmHg
- Carbon dioxide partial pressure gradient = 6mmHg
Therefore across systemic capillaries:
- oxygen partial pressure gradient >60mmHg
- Carbon dioxide partial pressure gradient >6mmHg
why can carbon dioxide move across membranes with only a 6mmHg partial pressure gradient whereas oxygen moves across with a 60mmHg partial pressure gradient?
-the diffusion coefficient for co2 is 20 times that of o2
co2 is more soluble in membranes
What would a big gradient between the partial pressure of oxygen in the alveoli vs the partial pressure of oxygen in the arterioles indicate?
A small gradient between Alveolar PO2 (PAO2) and arterial PO2 (PaO2) is normal (ventilation-perfusion match is usually not perfect)
A big gradient between PAO2 and PaO2 would indicate problems with gas exchange in the lungs or a right to left shunt in the heart
(the arteries have less oxygen than the alveoli - problem with gas exchange in lungs OR venous blood is being mixed with arterial)
What is fick’s law of diffusion? How does the anatomy of lungs maximis effective gas exchange?
=The amount of gas that moves across a sheet of tissue in unit time is proportional to the area of
the sheet but inversely proportional to its thickness
The alveoli = increase surface area for gas exchange (with a very extensive pulmonary network)
The thin walls of the alveoli and the narrow interstitial space between alveoli and pulmonary capillaries = small thickness
(walls of alveoli consist of a single layer of flattened type 1 alveolar cells.)
What is henry’s law? so if the partial pressure of oxygen in the gas phase increased, the concentration of oxygen in the liquid phase would…
The amount of a given gas dissolved in a given type and volume of liquid (e.g. blood) at a constant temperature is:
proportional to the partial pressure of the gas in equilibrium with the liquid
if the partial pressure of oxygen in the gas phase increased, the concentration of oxygen in the liquid phase would increase
How is oxygen transported in the blood?
Bound to haemoglobin - 98.5%
Dissolved in the blood - 1.5%
How is oxygen bound to haemoglobin? how many haem groups per one haemoglobin molecule? when is haemoglobin considered fully saturated? what is the primary factor that determines the percent saturation of haemoglobin with oxygen?
- haemoglobin can form a reversable combination with oxygen
- each Hb molecule has 4 haem groups
- each haem group reversably binds one oxygen molecule
- Hb is considered fully saturated when all the Hb present is carrying it’s max. oxygen load
- Partial pressure of oxygen is the primary factor which determines % saturation of haemoglobin with oxygen
What is the oxygen delivery index?
What determines the oxygen content of arterial blood? how can you work this out?
this is the amount of oxygen delivered to tissues in ml/min/metre2
DO2I = oxygen content of arterial blood (Ca02) x Cardiac index
(cardiac index relates the cardiac output to the body surface area)
Haemaglobin concentration and the saturation of haemoglobin of Hb with oxygen determines Ca02
Ca02 = 1.34 X conc. Hb x Sa02 (% Hb sat. 02)
1 gram of hb carries 1.34ml of oxygen when fully saturated
What are the four factors that can impair oxygen delivery to tissues?
- decreased partial pressure of inspired oxygen
- respiratory disease: this can decrease arterial P02 and hence decrease Hb sat. with 02 and therefore 02 conc. of the blood
- anaemia: this decreases Hb conc.
- heart failure: this decrease cardiac output
What does partial pressure of inspired oxygen depend on?
- total pressure (atmospheric pressure) - this is decreased at altitude
- proportion of oxygen in gas mixture
What is co-operatively with regard to oxygen binding? What shape is the curve - why is this significant?
- binding of one oxygen molecule to Hb increases the affinity of Hb for oxygen
- sigmoid curve: at high oxygen conc. (at pulmonary capillaries) the curve flattens out and a moderate fall in alveolar P02 will not affect oxygen loading much, however at lower oxygen conc. (at peripheral tissues) a small fall in alveolar P02 will cause Hb to give up a lot of oxygen molecules easier.
What is the bohr effect?
this is when the oxygen-haemoglobin dissociation curve is shifted to the right, causing an increased release of oxygen from Hb at higher P02. This happens due to certain conditions at tissues e.g. high PC02, high H+ conc., high temperature, high 2,3-biphophoglycerate
What is different about foetal haemoglobin compared with adult? why is this important for oxygen transfer from mother to foetus?
-structurally it has two alpha and two gamma subunits
-interacts less with 2,3-biphosphoglycerate in red cells
= higher affinity for oxygen compared with adult which allows oxygens to be transferred from mother to foetus even if the P02 is low
(the oxygen haemoglobin dissociation curve for HbF is shifted to the left)
for myoglobin:
- where is it present?
- how many Hb groups per myoglobin molecule
- is there co-operative binding of oxygen?
- what shape is the dissociation curve?
- what role does myoglobin have?
- what does the presence of myoglobin in the blood indicate?
-Myoglobin is present in skeletal and cardiac muscles
One haem group per molecule of myoglobin
No cooperative binding of O2
Dissociation curve hyperbolic
Myoglobin releases O2 at very low PO2
Provides a short-term storage of O2 for anaerobic conditions
presence of myoglobin in the blood indicates muscle damage
How is carbon dioxide transported in the blood?
- In solution (10%)
- As bicarbonate (60%)
- As carbamino compounds (30%)
is carbon dioxide or oxygen more dissolvable in solution?
-carbon dioxide is about 20 times more soluble than oxygen
How is bicarbonate produced by carbon dioxide?
What is the catalyst?
Where does this occur?
C02 + H20 - H2C03 - H+ + HC03-
carbonic anhydrase is the catalyst for the formation of H2C03
It occurs in red blood cells
how is carbon dioxide transported in carbamino compounds? what are these?
-Carbamino compounds formed by combination of CO2 with terminal amine groups in blood proteins.
Especially globin of haemoglobin to give carbamino-haemoglobin
Rapid even without enzyme
Reduced Hb can bind more CO2 than HbO2
What is the haldane effect? What does oxygen do to the carbon dioxide dissociation curve? At the lungs when the haeoglobin picks up the oxygen, what does this to the Hb ability to bind carbon dioxide and H+?
- removing oxygen from Hb increases the ability of Hb to pick-up carbon dioxide and carbon dioxide generated H+
- oxygen shifts the carbon dioxide dissociation curve to the right
At the lungs the Hb pick-up the O2 which weakens its ability to bind CO2 and H
What does the bohr effect and the haldane effect work in synchrony to facilitate?
O2 liberation
and
uptake of CO2 and CO2 generated H+
at the tissue level
In the neural control of respiration:
For passive respiration
-where is the major rhythm generator?
-What generates the rhythm here? How does it do this?
-what modifies this rhythm and why is this necessary?
For active respiration:
-what group of neurones are excited? what does this lead to?
respiratory centre in the medulla
- a network of neurones called the pre-botzinger complex demonstrate pacemaker activity
- the pre-botzinger complex excites dorsal resp. group neurones (inspiratory) which fire in bursts = contraction of inspiratory muscles
- when firing stops = passive expiration
- this is modified by neurones in the pons (pneumotaxic centre) which when stimulated they terminate respiration, they are stimulated when dorsal resp. neurones fire and without this breathing = apneusis
When there’s increased firing of dorsal neurones this excites second group of ventral neurones = excited internal intercostals and abdominals = forceful expiration
Where is the apneustic centre and what happens when this is stimulated?
- in the pons
- impulses from these neurones excited inspiratory area of medulla = prolong inspiration
What are the 6 different factors that can influence the respiratory centres?
- higher brain centres
- stretch receptors in walls of bronchi and bronchioles (prevent hyperinflation)
- juxtapulmonary receptors stimulated by pulmonary capillary congestion, pulmonary oedema and PE = rapid shallow breathing
- joint receptors - stimulated by movement of joints
- baroreceptors: increased ventilatory rate in response to decreased BP
- chemoreceptors (central and peripheral)
What is the hering-breuer reflex?
-pulmonary stretch receptors are activated during inspiration to inhibit respiration
How do joint receptors affect breathing?
Impulses from moving limbs reflexly increase breathing
Probably contribute to the increased ventilation during exercise
During exercise what are the 5 different factors that may increase ventilation?
Reflexes originating from body movement
Adrenaline release
Impulses from the cerebral cortex
Increase in body temperature
Later: accumulation of CO2 and H+ generated by active muscles
When is the cough reflex activated and what does afferent discharge stimulate?
activated by irritation of airways or tight airways:
Afferent discharge stimulates: short intake of breath, followed by closure of the larynx, then contraction of abdominal muscles (increases intra-alveolar pressure), and finally opening of the larynx and expulsion of air at a high speed
Where are peripheral chemoreceptors located? what do they sense?
carotid bodies and aortic bodies
-sense tension of oxygen and carbon dioxide and conc. H+ in the blood
-
Where are central chemoreceptors located? what do they respond to? Why is this a good measure of hypercapnia? what happens when there is hypercapnia?
Situated near the surface of the medulla of the brainstem
Respond to the [H+] of the cerebrospinal fluid (CSF)
CSF is separated from the blood by the blood-brain barrier
it is a good measure of hypercapnia because:
- BBB is relatively impermeable to H+ and HCO3- but CO2 diffuses readily
- CSF contains less protein than blood and hence is less buffered than blood
Ventilation increases when there’s hypercapnia
Which chemoreceptors sense hypoxia? what does this cause?
Peripheral chemoreceptors sense hypoxia
-this causes an increase in ventilation
What is the hypoxic drive of respiration? when is this important?
The effect is all via the peripheral chemoreceptors
Stimulated only when arterial PO2 falls to low levels (<8.0 kPa)
Is not important in normal respiration
May become important in patients with chronic CO2 retention (e.g. patients with COPD)
It is important at high altitudes = hyperventilation and increased cardiac output
What are 5 chronic adaptations that happen due to high altitude hypoxia?
inc. RBC production (polycythaemia)
- O2 carrying capacity of blood increased
increased 2,3 BPG produced within RBC
- O2 offloaded more easily into tissues
increase in number of capillaries
- blood diffuses more easily
Increase in number of mitochondria
- O2 can be used more efficiently
Kidneys conserve acid
- arterial pH decreased
During a metabolic acidosis, when there is an increase in H+ ions, which receptors cause hyperventilation to blow off carbon dioxide?
-peripheral chemoreceptors
becuase hydrogen ions do not readily cross the blood brain barrier.
what is the aim target saturations in patients without COPD
-94-98%, get it up and titrate down
What is the aim target saturations in patient with COPD
-88-92%
