Respiratory Physiology Flashcards
4 functions of respiratory system
- gas exchange - O2 to blood from air, CO2 from blood to air
- Acid-base balance - regulation of body pH
- protections from infection - cilia/epithelial tissue?
- communication via speech
what 2 systems are required to deliver fuel to active cells within tissues and remove waste products
CVS and respiratory system
compare cellular (internal) to external respiration
- Cellular - biochemical process releasing energy from glucose either via glycolysis or oxadative phosphorylation. Latter requires oxygen and depends on external respiration
- External respiration: movement of gases beteen the air and the body’s cells via both the respiratory and CVS
compare function of pulmonary and systemic circulation
Pulmonary: Delivers CO2 to lungs and collects O2 from the lungs
Systemic: delivers O2 to peripheral tissues and collects CO2
what does pulmonary artery carry
deoxygenated blood
what does pulmonary vein carry
oxygenated blood
Give an example of the integration between the CV and respiratory systems
Inc energy demand but working muscle leads to:
Resp: inc rate and depth of breathing; speeding up a)substrate (O2) aquisition and b) waste disposal (CO2)
CV: Ince HR and force of contraction; speeding up a) substrate delivery to muscle via blood and b) waste removal via blood
what is the net volume of gas exchanged in the lungs per unit time
250ml/min O2 and 200ml/min CO2
what does the net volume of gas exchanged in the lungs per unit time equal?
the net volume exchanged in the tissues
what does; net gas exchange [lungs] = net gas exchange [tissues] prevent?
gas build up in circulation which would hamper gas exchange and helps ensure supply = demand
normal and excercising respiration rate
12-18 breaths/min - rest
40-45 at max exercising capacity in adults
what 2 levels are O2 and CO2 exchanged at
lungs, peripheral tissues
equation of life
Nutrients + O2 = Energy (ATP) + waste (incl. CO2)
(intracellular respiration)
7 parts of respiratory system
Nose: airs enters, cilia and mucus trap particles and warm/moisten air
Pharynx: air moves down into pharynx (throat) which is shared with digestive system
Epiglottis: small flap of tissue folds over trachea and prevents food from entering it when swallowing
Larynx: “voice box” containing vocal chords
Trachea: stiff rings of cartilage (support and protection)
Lung: soft, spongy texture due to thousands of tiny sacs (alveoli) that compose them
Bronchus: air moves from trchea to right and left bronchi which lead inside the lungs
parts of upper respiratory tract
mouth, nasal cavity, pharynx, larynx
parts of lower respiratory tract
trachea, bronchi, lungs
number of lobes in left/right bronchi
Left: 2 lobes
Right: 3 Lobes
how many secondary bronchi in left/right lungs
Left: 2
Right: 3
name parts of right lung
- Superior lobe
- —horizontal fissure
- middle lobe
- — oblique fissure
- inferior lobe
name parts of left lung
- superior lung
- — oblique fissure
- inferior lobe
pericardium
(heart related…)
a protective, fluid-filled sac that surrounds your heart and helps it function properly
conc gradient aka…
partial pressure gradient
explain branching of airways
trachea branches into 2 bronchi. Each bronchus branches 22 more, terminating in cluster of alveoli
how many times do the airways branch
24
parts of repiratory system showing patancy
larynx, trachea, bronchi (primary + secondary)
patancy
the condition of being open or unobstructed
what maintains patancy
semi-rigid tubes, patancy of airway is maintained by C-shaped rings of cartilage
order of branching within the lungs
bronchi, bronchioles, alvioli
bronchiole
no cartilage, patency maintained by physical forces in thorax
alveoli
point of gas exchange
conducting zone
all of the structures that provide passageways for air to travel into and out of the lungs: the nasal cavity, pharynx, trachea, bronchi, and most bronchioles
NOT alveoli
compare shape/size of bronchi
Right: larger/wider and more verticle
aspirated foreign bodies found more commonly here
respiratory zone
alveoli
where is there most resistance to air flow
in least branched areas (e.g. bronchi, trachea)
conducting vs respiratory zone
conducting zone is everything apart from place of gas exchange (alveoli) which is respiratory zone
what does air in the conducting zone sit in
dead space
what can be altered by activity of bronchial smooth muscle
airway diameter, and therefore resistance to airflow
explain relationship between bronchial contraction and resistance
contraction dec diameter = ince resistance
relaxation inc diameter = dec resistance
what is each cluster of alveolis surrounded by
elastic fibres and a network of capillaries
what doe elastic fibres allow for
expansion/contraction of alveoli during respiration
give a common pathology of elastic fibres
emphyseama
types of cells found in alveoli
Type 1: gas exchange
Type 2: synthesise surfactant
what other cell (not type 1 or 2) is found in alveolar structure
alveolar macrophages ingest foreign materil that reaches the alveoli
type 2 (surfactant cells)
produce surfactant so not involved in gas exchange
what are always directly abuted together
capilallary (endothelial) cells and type 1 cells - minimises diffusion distance for gas exchange
what is good about alveoli in terms of gas exchange
large surface area - 80m2
where is gas exchange between lungs and blood only possible
at alveoli: due to their thin surface
what do areas of the upper airways contain and why
anatomical dead space - unable to participate in gas exchange as the walls of the airways are too thick
airway resistance
how much air flows into the lungs at any given pressure defference between atmosphere and alveoli. Major determinant of airway resistance is the radii of the airways
approx vol. of lungs
6L
ventilation
air in/out of lungs (nothing to do with gas exchange)
lung volume/capacity diagram
see pic 1
dead space volume
150m volume of gas occupied by the conducting airways and not available for gas exchange
tidal volume
volume of air breathed in and out of the lungs at each breath
see pic 1
expiratory reserve volume
max vol of air which can be expelled from the lungs at the end of a normal expiration
see pic 1
inspiratory reserve volume
max vol of air which can be drawn into the lungs at the end of a normal inspiration
see pic 1
residual volume
volume of gas in the lungs at the end of a maximal expiration
see pic 1
vital capacity
TV + IRV + ERV
see pic 1
total lung capacity
VC + RV
see pic 1
Inspiratory capacity
TV + IRV
see pic 1
functional residual capacity
ERV + RV
see pic 1
FEV1:FVC
fraction of forced vital capacity expired in 1 second
see pic 1
what is each lung enclosed in
2 pleural membranes (containing pleural fluid)
where do the esophagus and aorta pass through the thorax
between the pleural sacs
viscelral pleura
lung-side membrane
parietal plaura
more superficial membrane (attached to rib cage and diaphragm)
what are the lungs and interior of the thorax covered by
pleural membranses with extremely thin layer of pleural fluid between the membranes
what do the pleural membranes allow for
movement of lungs and rib-cage (during expansion/contraction) in a friction-free mannar
what effectively happen to the lungs through the relationship of the pleural membranes
they are stuck to the rib cage
function of pleural membranes
to stick the lungs to the rib cage
what is visceral pleura stuck to
surface of the lungs
how is the visceral pleura stuck to the parietal pleura
via the cohesive forces of the pleural fluid
what is the parietal pleura stuck to
the rib cage and diaphragm
explain lung expansion/contraction in relation to the pleural cavities
The lungs are effectively stuck to the rib cage and diaphragm and will follow the movements of these bones and muscles as the chest wall expands during inspiration.
The chest wall therefore leads the expansion of the lung during inspiration. In contrast, the elastic connective tissue in the lung leads to recoil of the chest wall in (unforced) expiration.
what is intrapleural pressure always
negative (subatmospheric)
what does negative intrapleural pressure prevent
collapsed lung (pneumothorax)
what happens to much of the lung capacity and when may it be used
not utilised during relaxed breathing at rest (tidal volume) but this “spare” capacity is vital and is utilised during periods of greater energy demand eg. exercise
what is the air imposible to remove from the lungs called
residual volume
what could be used to descibe the action of the pleural fluid
cohesive
how are the lungs stuck to, and expanded by the chest wall
by pleural membranes
what does recoil of the elastic connective tissue in the lungs bring about
recoil of the chest wall in normal expiration (although chest wall may be employed during forced expiration)
boyle’s law
pressure exerted by a gas is inversely proportional to its volume
what allows breathing to occur
the thoracic cavity changing volume
based off Boyle’s law how does inc/dec vol. affect pressure in the lungs/during breathing
Inc vol = dec pressure
dec vol = inc pressure
along what gradient do gases move
from high pressure to low pressure
what muscles are used during inspiration
external intercostal muscles and diaphragm
what muscles are used by expiration
is passive at rest but uses internal intercostal and abdominal muscles during severe respiratory load
give moredetailed list of muscles used for inspiration
diaphragm, external intercostals, sternocleidomastoids and scalenes
what muscles could be used in expiration
internal intercostals and the abdominals
describe movements of diaphragm during inspiration and expiration
Inspiration: contracts, thoracic volume inc
Expiration: relaxes, thoracic volume dec
what nerve innervates the diaphragm
phrenic nerve
bucket tap thinngy?
idea ribs move up and out when breathing and sternum moves up and down but also a little out
(plueral cavity then pulls lungs out too)
summarise the mechanics of breathing for inspiration and expiration
diaphragm motion, effect on vol, effect on airways, resistance to breath
Inspiration: Diaphragm contracts, thoracic vol inc, airways pulled open by physical forces of inspiration, least resistance to breathing
Expiration: diaphragm relaxes, thoracic vol dec, airways compressed by physical forces of expiration (aggravates asthma), most resistance to breathing
Intra-thoracic (alveolar) pressure (Pa)
pressure inside the thoracic cavity (essentially pressure inside lungs). Can be negative or positive compared to atmospheric pressure
Intra-pleaural pressure (Pip)
pressure inside the pleural cavity, typically negative
Transpulmonary pressure (Pt)
difference between alveolar pressure and intra-pleural pressure. Almost always positive because Pip is negative (in health)
good equation to knwo for common pressures…
Pt = Palv - Pip
why is intrapleural pressure negative
help maintain proper inflation of the lungs and to help prevent a pneumothorax (i.e. collapsed lung)
(mechanical?) factors to affect breathing
bit of a long one… confusion?
- Bulk flow of air between the atmosphere and alveoli is proportional to the difference between the atmospheric and alveolar pressures and inversely proportional to the airway resistance: F = (Patm- PA)/R
- Between breaths at the end of an unforced expiration Patm= PA, no air is flowing, and the dimensions of the lungs and thoracic cage are stable as the result of opposing elastic forces. The lungs are stretched and are attempting to recoil, whereas the chest wall is compressed and attempting to move outward. This creates a subatmospheric intrapleural pressure and hence a transpulmonary pressure that opposes the forces of elastic recoil
- Airway resistance determines how much air flows into the lungs at any given pressure difference between atmosphere and alveoli. The major determinant of airway resistance is the radii of the airways
what kind of word could be used to describe lung structure
elastic
What does the lung’s volume depend on
the pressure difference actross the lungs (transpulmonary pressure) and how stretchable the lungs are
summarise the changes in pressure during inspiration and expiration
During inspiration, the contractions of the diaphragm and inspiratory (external) intercostal muscles increase the volume of the thoracic cage.
This makes intrapleural pressure more subatmospheric (negative) and causes the lungs to expand.
This expansion makes alveolar pressure subatmospheric, which creates the pressure difference between atmosphere and alveoli to drive air flow into the lungs.
During expiration, the inspiratory muscles cease contracting, allowing the elastic recoil of the chest wall and lungs to return them to their original between-breath size.
This compresses the alveolar air, raising alveolar pressure above atmospheric pressure and driving air out of the lungs.
what happens in terms of pressure in forced expiration
In forced expirations, the contraction of expiratory (internal) intercostal muscles and abdominal muscles actively decreases thoracic dimensions, reducing duration of breathing cycle and allowing more breaths/min
why is intrapleural pressure always less than alveolar pressure
intrapleural pressure pulls harder and harder on lungs to expand them. Alveolar pressure get negative the back to 0 on inspiration, then get positive and back to 0 on inspiration. Basically air catches up… equilibrium! :)
See pic 2
what is the natural tendancy of the lungs
to recoil (contract inwards)
surfactant
what is it, function
detergent like fluid produced by alveolar cells
Reduces surface tension on alveolar surface membrane thus reducing tendency for alveoli to collapse
what is surface tension and when does occur
the attraction between water molecules and occurs where ever there is an air-water interface
function of surfactant
Reduces surface tension on alveolar surface membrane thus reducing tendency for alveoli to collapse
what effects does surfactant have
- inc lung compliance/distensibility
- reduces lung’s tendancy to recoil
- makes work of breathing easier
compliance
how easy it is to stretch lungs open
where is surfactant more effective and why
iin small alveoli than large alveoli because surfactant molecules come closer together and are therefore more concentrated
what cells produce surfactant
type 2 alveolar cells
give time-line of surfactant production… and what can happen to premature babies…
Surfactant production starts ~25 weeks gestation. Complete by ~36 weeks. (40 weeks = full term). Stimulated by thyroid hormones and cortisol which increase towards end of pregnancy.
Premature babies suffer Infant Respiratory Distress Syndrome (IRDS).
inflation curve with air vs saline (like in IRDS?)
See pic 3
compliance
change in volume relative to change in pressure - stretchability of lungs, not elasticity
High compliance vs low compliance
+ when good/bad
High compliance = large inc in lung volume for small dec in ip pressure - only good if accompanied with high elasticity
Low compliance = small inc in lung volume for large dec in ip pressure - always bad
what can compliance change with
disease states (e.g. fibrosis) and age (dec elastic function
what, in part, determines compliance
action of surfactant (inc ease of expansion —> inc compliance)
what determines compliance
elastic forces, surface tension at the alveolar air-liquid interface and by airway resistance
does surfactant inc or dec compliance
inc compliance (but dec alveolar surface tension)
where is surfactant more effective
in small alveoli
law of laplace
Pressure is inversely proportional to the radius. The smaller the radius, the more pressure.
what is anatomical dead space
volume of gas occupied by the conducting airways and not available for exchange
Roughly 150mL
2 ways to describe ventilation
Pulmonary (minute) ventilation
Alveolar ventilation
Pulmonary (minute) ventilation
total air movement into/out of lungs (relatively insignificant in functional terms)
Alveolar ventilation
fresh air getting to alveoli and therefore available for gas exchange (functionally musch more significant)
units for pulmonary and alveolar ventilation
L/min
describe air that is gained and lost during inspiration and expiration (give volumes/quantities)
see pic 4
average tidal volume
500mL
normal respiratory rate
12-16 breaths/min
what x what = pulmonary ventilation
respiratory rate + tidal volume
terms for not enough/too much ventilation
hypoventilation, hyperventilation
dalton’s law
the total pressure of a gas mixture is the sum of the pressures of the individual gases
where does the CO2 in our cells/blood come from
us making it (and NOT breathing it in)
define partial pressure
Pressure of a gas in a mixture of gases is equivalent to the percentalge of that particular gas in the entire mixture multiplied by the pressure of the whole gaseous mixture
What can vary with hyper/hypo-ventilation
kinda key concept
Alveolar PO2 and PCO2
What happens to PO2 and PCO2 during hyperventilation (inc alveolar ventilation)
PO2 rises to about 120 mmHg (from 100) and PCO2 falls to about 20mmHg (from 40)
normal partial pressures of O2 and CO2
O2 = 100 mmHg (13.3 kPa)
CO2 = 40mmHg (5.3 kPa)
what happens to PO2 and PCO2 during hypoventilation (dec alveolar ventilation)
PO2 falls to 30 mmHg and PCO2 rises to 100 mmHg
why is normal PO2 at 100 mmHg and not atmospheric 160 mmHg
- diluted by anatomical dead space and residual volume
- saturated by water vapour so further diluted
- is in equilibrium with pressure of gas in the blood
what is Pgas in alveoli the same as
Pgas in systemic arterial blood
what is the primary driving force for breathing and what does this make hard
in terms of gases
CO2: hard to hyperventilate
why is CO2 the primary driving force for breathing
Is toxic so cells are sensitive to it/changes in [CO2]
describe the pressure-volume curve and the discrepenceis between the base and the apex of the lung
learn - is confusing so maybe remake?
Varies:
* at base volume change is greater for a given change in pressure
* Alveolar ventilation declines with height from base to apex.
* Compliance is lower at the apex due to being more inflated at FRC. At the base the lungs are slightly compressed by the diaphragm hence more compliant on inspiration.
* A small change in intrapleural pressure therefore brings about a larger change in volume at the base compared with the apex
describe relative alveolar ventilation and compliance at base vs apex of lung
Base: alveolar ventilation high, compliance low
Apex: alveolar ventilation low, compliance higher
what would happen to pressure-volume curve if went from standing up to lying down
It would change - gravity has an effect
Which type of ventialtion is functionally more important and what is it significantly influenced by
Alveolar ventilation (than pulmonary ventilation): anatomical dead space
What is more influential at determening alveolar ventilation and why
Depth of breathing (than rate of breathing) - because of the effect of anatomical dead space
what happens to alveolar ventilation as we move up the lung
declines with height from base to apex due to changes in compliance
does hypo/hyper-ventilation alter partial pressures
yes
what does the pulmonary artery carry
deoxygenated blood AWAY from the heart to the lungs
what does the pulmonary vein carry
oxygenated blood TOWARDS the heart from the lungs
what are the two kinds of blood supply to the lungs
- bronchial circulation (nutritive)
- Pulmonary circulation (gas exchange)
bronchial circulation
nutritive: supplied via bronchial arteries arising from systemic circulation to supply oxygenated blood to lung tissues - 2% left heart output, blood drains to left atrium via pulmonary veins
pulmonary circulation
gas exchange: consists of L and R pulmonary arteries originating from the right ventricle. supplies dense capillary network surrounding the alveoli and returns oxygenated blood to the left atrium via pulmonary vein. High flow, low pressure
is pulmonary circulation in series or parrallel with systemic circulation
series
A
alveolar
a
arterial blood
v
mixed venous blood (e.g. in pulmonary artery)
partial pressures of O2/CO2 in alveolar/arterial/venous blood…
see pic 5
what laws does gas exchange between alveoli and blood follow
simple diffusion - continues until equilibrium is reached
what is the rate of diffusion across the membrane directly proportional to
- partial pressure gradient
- gas solubility (must be in solution to cross)
- available surface area
what is the rate of diffusion across the membrane inversely proportional to
the thickness of the membrane
where is the rate of gas diffusion across the membrane most rapid
over short distances
what does partial pressure in alveoli correspond with
PP in systemic arterial blood
What does partial pressure in pulmonary arterial blood correspond with
(deoxygenated blood)
PP at tissues
PP gradeint for O2 and CO2
PO2 = 100 —> 40 (250ml/min) alveoli to pulmonary artery
PCO2 = 46 –> 40 (200ml/min) pulmonary artery to alveoli
what feature of the alveoli membrane allows for rapid diffusion
thin membrane so short diffusion distance
what part of the heart is bronchial and pulmonary supple to the lungs each from
bronchial - left side (oxygenated blood)
pulmonary - right side
what is pulmonary arterial pressure
low: 25/8
More suseptable to effects of gravity and gives rise to a great degree of vairability in blood flow within the lung
which gs diffuses more rapidly and why
CO2: mose soluble - however overall rates of equilibrium between O2 and CO2 are similar because of the greater pressure gradient for O2
how is the anatomy of the lung adapted to maximise gas exchange
- large surface area
- minimunm diffusion distance
- thin cell membranes
(type 1 alveolar cell, capillary cell)
factors to influence gas diffusion across alveoli
- partial pressure gradient
- gas solubility
- available surface area
- thickness of the membrane
- distances
Emphysema
destruction of alveoli reduces surface area for gas exchange
Fibrotic lung disease
thickened alveolar membrane slows gas exchange. Loss of lung compliance may decrease alveolar ventilation
Pulmonary oedema
fluid in interstitial space increases diffusion distance by seperating the alveoli from the capillary. Arterial PCO2 may be normal due to higher CO2 solubility in water - normally due to pulmonary hypertension
Asthma
Increased airway resistance decreases airway ventilation - PO2 low in alveoli and blood
Effect of fibrotic lung disease on ventilation and diffusion
- Dec ventilation as resists stretch during inspiration
- Dec diffusion as fibrous tissue resists diffusion
What is the physical characteristics of emphysema
breakdown of alveolar membrane and loss of elastic tissue
what can cause emphysema
smoking
effect of emphysema on compliance, elasticity and overall effect on breathing
- increased compliance so big change in lung volume for relatively small change in intrapleural pressure
- Lost lots of elasticity due to breakdown of elastic fibres meaning elastic recoil during expiration less common - may need to invest muscular effort rather than it being passive
Inspiration easier, expiration incredibly difficult
2 big things lost/negatives of emphysema
loss of elastic tissue and loss of surface area
explain the effect of asthma on diffusion
affects airways rather than alveoli so little direct effect. However, can have big impact on ventilation, and therefore PAO2 (dec) and PACO2 (inc), which will subsequently limit diffusion
Obstructive and restrictive lung disease definitions
Obstructive: obstruction of air flow, especailly on expiration
Restrictive: restriction of lung expansion, loss of compliance
Describe some obstructive lung disorders
- Asthma
- Chronic Obstructive Pulmonary Disease (COPD) - chronic bronchitis, emphysema
Impact expiration greater?
Give some restrictive lung disorders
- Fibrosis (idiopathic, asbestosis)
- Infant Respiratory DIstress Syndrome (insufficient surfactant production)
- Oedema
- Pneumothorax (get loss of lung expansion)
restrictive lung disorders
restiction of lung expansion, loss of compliance
Therefore, greater change in intra-pleural pressure required to inc volume by same amount
spirometry
technique commonly used to measure lung function - amount of air inspired or expired
How can spirometry measuremnet s be classed
- Static: only consideration made is the volume exhaled
- Dynamic: time taken to exhale a certain volume is measured
what can spirometry not measure
anything where residual volume is a component
(residual volume, total lung capacity, functional residual capacity)
Explain FEV1/FVC
FEV1: forced expiratoy volume in 1 second - 4L (fit healthy yound adult male)
FVC: forced vital capacity - 5L
FEV1/FVC = 80% - should be able to expel 80% of air in first second
abdolute values decline with age, but ratio remains around 80%
FEV1/FVC for obstructive lung diseases
~42%
FEV1/FVC in restrictive lung diseases
~90%
Airflow is fine but total amount of aire that can be expired is restricted due to restriction in expansion (less air goes into lungs in the first place)
Explain the effect of an obstrictive lung disorder (e.g. COPD) on FEV1 and FVC (and then ratio)
- rate at which air is exhaled is much slower
- Total expired volume (FVC) is also reduced (FRC may be inc)
- Mayor effect is on airways and so FEV1 is reduced to a greater extent than FVC
- Ratio also reduced
FEV1 = big dec
FVC = dec
Ration = dec
Explain the effect of a restrictive lung disorder (e.g. pulmonary fibrosis) on FEV1 and FVC (and then ratio)
- absolute rate of airflow is reduced (but only because total lung volume is reduced)
- total volume is reduced due to limitations to lung expansion
- ration remains constant or can inc as a large proportion of volume can be exhaled in first second
FEV1 = big dec
FVC = big dec
Ratio = unchanged or inc
What is spirometery more effective in diagnosing
Obstructive diseases since people with restrictive lung diseases may still ahve a normal ration of FEV1 to FVC
explain key point with pressure-volume relationship and inspiratory and expiraotry curves - and why this is the case (3 reasons)
Ir requires a greater change in pressure (from FRC) to reach a particular lung volume during inspiration, than to maintain that volume during expiration
This is:
1. overcome lung inertia during inspiration
2. overcome surface tension during inspiration
3. during expiration compression of the airways means more pressure is required for air to flow along them
give effect of emphysema and fibrosis on pressure-volume curves
see pic 6
Describe the pathophysioology of asthma
Over-reactive constriction of bronchial smooth muscle. Inc resistance, expiration phase most affected
what do obstructive and restrictive lung diseases increase the work of
Obstructive: expiration
Restrictive: inspiration
what is tthe ventilation-perfusion relationship
ventilation (air getting to alveol L/min) <—> Perfusion (local blood flow L/min)
ideally V=P
what happens to both blood flow and ventilation across the height of the lung
decrease
what is higher at the base of the lung (blood flow or ventilation)
Blood flow is higher than ventilation because arterial pressure exceeds alveolar pressure. This compresses the alveoli
What is higher at the apex of the lung (blood flow or ventialtion)
ventialtion is higher and blood flow is low because arterial pressure ois less than alveolar pressure. This compresses the arterioles
Where are ventilation and perfusion both greater for both cases (in terms of V+P mismatch)
at the base of the lung
see pic 7
how does the ratio of ventilation to perfusion withing the lung change from base to apex and why
increases - due to effect of gravity
where does the majority of V+P mistatch occur
in the apex - this is then auto-regulated to keep V:P ratio close to 1.0
Describe autoregulation when blood flow>ventilation (at base of lung)
If ventilation decreases in a group of alveoli, PCO2 inc and Po2 dec. Blood flowing past those alveoli does not get oxygenated. Dilution of oxygenated blood from better ventilated areas = SHUNT
Response: Dec tissue PO2 around underventilated alveoli constricts their arterioles (pulmonary vasoconstriction) diverting blood to better-ventilated alveoli. Bronchial dialation also happens due to inc PCO2.
Constriction in response to hypoxia is particular to pulmonary vessels (systemic vessels dilate)
response of pulmonary vessels to hypoxia
constriction
(systemic vessels dilate)
autoregulation when ventilation > blood flow
alveolar dead space - occurs to small extent in apex of lung, and pathologically in pulmonary embolus
Wat happens: Alveolar PO2 inc, PCO2 dec
Response: Pulmonary vasodilation and to a lesser extent bronchial constriction
Effect: act to bring V:P ration close to 1 as possible
Shunt effects
- pulmonary vasoconstriction
- Bronchial dilation
alveolar dead space effects
- Pulmonary vasodilation
- Bronchial constriction
shunt
passage of blood through areas of the lung that are poorly ventilated (V < P)
opposite of alveolar dead space
alveolar dead space
alveoli that are ventilated but not perfused
anatomical dead space
air in the conducting zone of the respiratory tract unable to participate in gas exchange as walls of airways in this region (nasal cavities, trachea, bronchi and upper bronchioles) are too thick
Physiological Dead Space
Alveolar dead space + Anatomical dead space
Respiratory sinus arrhythmia
a normal alteration in cardiac rhythm (HR) generated from the stimulation of the vagus nerve and changes in cardiac filling pressures during respiration
why does Respiratory sinus arrhythmia (RSA) occur
If HR stayed constant then:
* during inspiration… inc Alveolar dead space
* During expiration… inc shunt
Ensures V:P ratio is close to 1 (matched)
How does RSA occur
due to inc bagal activity (parasympathetic nerve innervating heart) during expiratory phase
where in the lung is perfusion higher
base
what makes the lungs more susceptible to the effects of gravity which gives rise to a great degree of variability in blood flow within the lung
low pulmonary arterial pressure (25/8)
why does ventilation change acorss the lung
Changes in compliance
function of respiratory sinus arrhythmia (RSU)
minimise ventilation:perfusion mismatch during breath cycle
2 ways O2 travels in blood and proportion of each
- in solution in plasma - 3ml O2 dissolve per litre plasma
- bound to haemoglobin protein in red blood cells -200ml O2 per litre whole blood, 197ml of which is bound to haemoglobin in red blood cells
volume O2 per litre whole blood
200ml
How is CO2 transported in the blood
2 ways
- 77% in solution in plasma
- 23% stored within haemoglobin
how much arterial O2 is extracted by peroipheral tissues at rest
25%
percentage of oxygen in blood bound to RBC (haemoglobin)
More than 98%
how many O2 molecules does each haemoglobin bind
4
what is the major determinant to which haemoglobin binds (is saturated with) oxygen
partial pressure of oxygen - PO2
what does alveolar ventilation determine… and what does that determine…
Alveolar ventilation –> Po2 of alveoli –> PO2 of plasma (O2 in solution) –> O2 carried in haemoglobin in RBC
how does Hb bind to O2 at the alveoli
Takes O2 from plasma maintaining a partial pressure gradient that continues to suck O2 out of the alveoli, until Hb becomes saturated with O2
Hb + O2 <—> HbO2
How long does it take for Hb to become saturated with O2 and how long is total contact time
O.25s after contact with alveoli
- total contact time of 0.75s
O2-Hb dissociation curve
see pic 8
what does Hb show in binding to O2
co-operative binding
explain the saturation of Hb at different PO2’s
- Hb almost fully saturated at the normal systemic arterial PO2 of 100 mmHg
- Even at PO2 of 60mmHg though haemoglobin is still 90% saturated with O2. This permits a relatively normal uptake of oxygen by the blood even when alveolar PO2 is moderately reduced.
At normal venous PO2, there is still 75% reserve capacity
Big PO2 fall causes relatively small impact on O2 binding to Hb
Anaemia
Any condition with res ults in a decrease in the oxygen carrying capacity of the blood (e.g. iron deficiency, haemorrhage, vit B12 deficiency)
What happens to PO2 in anaemia
Nothing: PO2 normal despite total blood O2 content being low
What will a low PO2 indicate
a low total blood O2 content
Can RBC be fully saturated with O2 in anaemia
Yes: RBC still fully saturated as PO2 is normal
(only caveat is iron deficiency where number of O2 binding sites will be reduced, but those present will be saturated)
what factors can change the affinity of Hb for O2
- pH
- PCO2
- Temp
- DPG
if the Hb-O2 dissociation curve moves up/down x axis what change would be seen
little impact on O2 uploading at lungs
Hb-O2 dissociation curve response to alkalosis
move left
better for retaining O2
Hb-O2 dissociation curve response to acidosis
(e.g. excercisinng muscle)
Move to right
better for offloading O2
Hb-O2 dissociation curve response to dec PCO2
move to left
better for retaining O2
Hb-O2 dissociation curve response to inc PCO2
move to right
better for offloading O2
Hb-O2 dissociation curve response to inc temp
move to right
better for offloading O2
Hb-O2 dissociation curve response to dec in temp
move to left
better for retaining O2
Hb-O2 dissociation curve response to no DPG
move to left
better for retaining O2
Hb-O2 dissociation curve response to added DPG
move to right
better for offloading O2
what causes the Hb-O2 dissociation curve tp move to the right
name it
- Dec pH
- inc PCO2
- Inc body temp
Bohr effect —> aids O2 unloading at peripheral tissues due to dec affinity of Hb for O2 (e.g. when exercising)
when would the Hb-O2 dissociation curve move to the left
to inc affinity of Hb for O2 (but harder for tissues to access O2) - why hypothermia is dangerous
explain binding of 2,3-DPG and how if affects O2 affinity
The affinity of haemoglobin for oxygen is decreased by binding 2,3-diphosphoglycerate (2,3-DPG) synthesised by the erythrocytes. 2,3- DPG increases in situations associated with inadequate oxygen supply (heart or lung disease, living at high altitude) and helps maintain oxygen release in the tissues.
Table of factors affecting arterial PO2
see pic 9
explain effect of CO binding on haemoglobin
CO binds to haemoglobin to form carboxyhaemoglobin with an affinity 250 times greater than O2 - binds readily and dissociates very slowly so very problematic once dissolved in circulation
effect of CO poisining
hypoxia, anaemia, nausea, headache, cherry red skin and mucous membranes. Respiration rate unaffected due to normal arterial PCO2. Potential brain damage and death.
Treatment for CO poisining
provide 100% O2 to inc PaO2
how is CO2 transported (include percentages)
long one ik but important
When CO2 molecules diffuse from the tissues into the blood, 7% remains dissolved in plasma and erythrocytes, 23% combines in the erythrocytes with deoxyhemoglobin to form carbamino compounds, and 70% combines in the erythrocytes with water to form carbonic acid, which then dissociates to yield bicarbonate and H+ ions. Most of the bicarbonate then moves out of the erythrocytes into the plasma in exchange for Cl- ions & the excess H+ ions bind to deoxyhemoglobin. The reverse occurs in the pulmonary capillaries and CO2 moves down its concentration gradient from blood to alveoli.
see pic 10
what does alveolar PP equal
arteroid PP
What does peripheral tissue PP equal
venous PP
what is the sole determinant of arterial partial pressure of oxygen (PaO2) and in health is in equilibrium with alveolar partial pressure of oxygen (PAO2)
Oxygen in solution
what is the main determinant of how much oxygen binds to haemoglobin (saturation)
PaO2
what directly determines how much oxygen can bind to Hb and what else can influence it
- PaO2
- number of RBC
- amount of Hb in each RBC
Influence:
* PaCO2
* Bondy temp
* Plasma pH
* levels of 2,3 DPG
explain the action of carbonic anhydrase in CO2 transport
Once inside the RBC, the enzyme carbonic anhydrase catalyses the conversion of CO2 into carbonic acid (H2CO3). Carbonic acid is then hydrolysed into H+ ions and HCO3– (bicarbonate). The H+ ion is bound by haemoglobin which buffers the process.
factors to favour CO2 unloading into the lungs
Same that inc O2 loading:
* High pH
* Low CO2
* Low temp
* No DPG
Haldane effect
maybe check???
what is PaO2 not the same as
arterial O2 content
what determines PaO2 (O2 in solution in the plasma)
- O2 solubility
- PO2 in the gaseous phase that is driving O2 in solution
What is the PaO2 (oxygen tension)
100mmHg
What is PP not the same as and why
concentration: conc varies on the form the molecule is in
Do gases travel in the gaseous phase in plamsa
No (although bound to Hb), if they did they would cause air embolism
how many ml of O2 bind to each gram of haemoglobin
1.34ml
Types of Hb
- 92% HbA
- 8% mad up of HbA2, HbF, and glycosylated Hb
Myoglobin
another O2 carrier molecule found exclusively in cardiac and skeletal muscle (only made of 1 poplypeptide chain)
HbF
foetal haemoglobin
Affinity of HbF and myoglobin for O2 compared to HbA
have higher affinity: necessary for extracting O2 from maternal/arterial blood
why does myoglobin have a higher affinity for O2 that Hb
allows skeletal/cardio muscle to extract more O2 from blood
difference between partial pressure and gas content
PP: amound dissolved in solution/plasma
Gas content: amount dissplved in plasma plus bound to Hb
hypoxia definition
inadequate supply of O2 to tissues
5 types of hypoxia
- Hypoxaemic Hypoxia: most common. Reduction in O2 diffusion at lungs either due to decreased PO2atmos or tissue pathology. (e.g. altitude)
- Anaemic Hypoxia: Reduction in O2 carrying capacity of blood due to anaemia (red blood cell loss/iron deficiency).
- Stagnant Hypoxia: Heart disease results in inefficient pumping of blood to lungs/around the body
- Histotoxic Hypoxia: poisoning prevents cells utilising oxygen delivered to them e.g. carbon monoxide/cyanide
- Metabolic Hypoxia: oxygen delivery to the tissues does not meet increased oxygen demand by cells.
partial pressure
amount of oxygen in solution in plamsa
what does higher affinity of HbF for O2 allow
them to extract O2 from (maternal) systemic circulation that would not otherwise have access too
