RESPIRATORY Flashcards
draw volume/time graph of a spirometer…
TLC = 90ml/kg - 6L
TV = 6-8ml/kg - 500ml
IRV = 3000ml (30-40ml/kg)
ERV = 1500ml
VC = 5000ml (60ml/kg)
FRC = 2500ml (40ml/kg)
RV = 1500ml (20ml/kg)
define tidal volume, residual volume
TV = the amount of air moving in and out of lungs during normal restful breathing
Residual volume = the amount of air remaining in the lungs after max forced expiration
define FRC…
FRC = the sum of Residual volume and expiratory reserve volume. the volume of air remaining in the lungs at the end of normal tidal expiration
define inspiratory reserve volume and expiratory reserve volume..
inspiratory reserve volume = the amount of air that can be inhaled on top of the tidal inspiration
exp reserve volume = the amount of air that can be exhaled on top of normal tidal expiration
define vital capacity
sum of IRV + TV + ERV
total amount of air that can move into and out of lungs in max inspiration and expiration.
which lung volumes can be measured with spirometry?
TV, IRV, ERV, VC
(cant be measured FRC, TLV, RV)
what is the physiological relevance of FRC ?
FRC is the volume of air remaining in the lungs at the end of normal tidal expiration
in normal health in supine = 2500ml
it exists due to the equilibrium between outward chest spring and inward elastic recoil of the lungs
no. of physiological roles
- Oxygen reservoir - O2 diffuses throughout the lungs in normal tidal breathing and thus the FRC acts as a reservoir such that diffusion of O2 between lungs and capillaries can continue in expiration and inspiration. Also utilised in anaesthesia.
- preventing airway collapse - means that some air remains in lungs to prevent all alveoli collapsing hence improves compliance and reduces work of breathing. V:Q is maintained during expiration too.
- optimal lung compliance - the volume at FRC means the lung sits at the steep part of compliance curve because of the above
- optimal PVR - the FRC volume also is the volume for optimal PVR.
State some factors that increase and decrease FRC…
Decrease:
Physiological
- Pregnancy
- lying down
- obesity
Anaesthetic:
- anaesthesia and muscle relaxation
- pneumoperitoneum in surgery
- lithotomy position / head down
Pathological:
- fibrosis
- bowel obstruction
- kyphoscoliosis
increase:
physiological:
- male
- height
- PEEP
pathological:
- emphysema
- asthma (gas trapping)
age has no effect
what are the effects of pre-oxygenation?
FRC = 2500ml
by preoxygenating with 100% can fill this with 100% O2 (or near 100%)
without pre-oxygenation = 21% O2 - infact by time it gets to FRC around 15%. so 2500ml x 0.15 = 375 ml of 02
O2 consumption = 250ml/min
hence without preoxygenation 375ml/ 250ml = 90 seconds
with oxygenation 2500ml/250ml = 10mins
hence increases apnoea time
This is theoretically never can reach this high
during pre-oxygenation, the theoretical apnoea time with 100% O2 is 10mins. why is this likely an over-estimation?
never reaches 100% O2 in FRC due to constant diffusion of CO2 out.
FRC may be lower than 2500ml esp when lying down on induction.
O2 consumption may be higher e.g. children, sepsis
draw a pressure volume curve of the lung, what does this demonstrate?
in normal health FRC lies at the steep part of the curve meaning less work is needed for normal tidal breathing as the lung is very compliant at this point.
what is compliance?
Compliance is the measure of distensibility of the lung. specifically the change in volume in response to a change in transpulmonary pressure. i.e. the more compliant the larger the change in volume for a given pressure change. C = ΔV/ΔP
Normal lung compliance at FRC is 200ml/cmH20 (this excludes chest wall)
draw a compliance curve for saline filled lungs?
draw a normal compliance curve and demonstrate a left shift i.e. more compliant for saline filled lungs
less surface tension
describe factors increasing and decreasing lung compliance…
factors affecting compliance can be divided into…
lung volume - any factor affecting FRC can move lung volume to extremes of compliance curve where gradient is flatter. e.g. pneumoperitoneum, lithotomy positioning etc.
lung elasticity - changes to lung elasticity can affect its ability to distend with pressure changes.
increases in compliance = age, emphysema
Decrease in compliance = Fibrosis, pulmonary oedema
surface tension factors - changes to surface tension affect the forces opposing the opening of alveoli.
reduced compliance in ARDS in neonates
atelectasis - reduced compliance
draw a curve for the relationship between pulmonary vascular resistance and pulmonary and lung volume…
FRC lies at the base of the curve in physiological range part
define elastance?
This is the reciprocal of compliance
Elastance in lung physiology is the measure of the lung’s tendency to return to its original size after being stretched or expanded.
ΔP/ΔV - i.e. reciprocal
what is specific compliance?
compliance / FRC
compensates for different body sizes
what is meant by static and dynamic compliance?
Static compliance is the compliance measured at static points within the ventilatory cycle (during inspiratory pause). therefore it is only affected by chest wall compliance and not by resistance to air movement.
dynamic compliance is the compliance measured in real time throughout the ventilatory cycle. It is affected by both lung compliance and airway resistance. This is always lower than static compliance because of airway resistance too. It is inversely related to rate of breathing.
how is lung compliance measured?
using oesophageal pressure probe to measure transpulmonary pressure and
what factors affect airway resistance?
Answer this by using hagen poiseulle equation.
r4/ nl = resistance
radius
viscosity
length
in turbulent flow this would be density instead.
what are the components that make up total compliance of the lung?
chest wall compliance + lung compliance
1/ lung compliance + 1/ thoracic compliane = 1/ total
usually
1/200 + 1/200 = 1/100
hence respiratory compliance = 100L/cmH20
describe the role of surfactant…
surfactant is a molecule secreted by type 2 alveolar pneumocytes. (epithelial cell)
it is made of a mixture of amphipathic molecules e.g. phospholipids that interact with with water at surface of alveoli to reduce surface tension.
hydrophobic head H bonds with water and hydrophobic tails stick at the surface preventing any bonding / hydrophillic interactions.
pressure generated within an alveoli is described by La Place’s law..
T = PR / 2. rearrange to give P= 2T/R.
Without surfactant, smaller alveoli would have higher pressure due to smaller radius and hence would be harder to open/ overcome the tension. Also empty into larger alveoli.
with surfactant added the pressure difference becomes more balanced. this is because surfactant has a bigger effect on smaller alveoli due to being more compact and hence reduces tension more in these.
overall surfactant reduces surface tension (stabilises alveoli), increases compliance and helps to prevent pulmonary oedema.
define surface tension…
surface tension is the tendency of liquid surfaces to shrink into the minimum surface area possible due to attractive forces between the surface molecules. e.g. alveoli to collapse.
state la place law?
describes relationship between pressure and tension in a sphere…
T = PR/2
what is meant by the term closing capacity?
closing capacity is the volume of lung in which the small airways begin to close of during expiration.
it is made up of the closing volume + residual capacity.
in health this is well below the FRC so in normal tidal breathing, small airways don’t close
if FRC is reduced, CC can encroach on normal breathing and airways can collapse leading to gas trapping and atelectasis.
state some situations where closing volume/ capacity can extend above FRC and effect tidal breathing..
how can this be reduced
reduction in FRC - anaesthesia, lithotomy, pneumoperitoneum, pregnancy etc
age - increase in closing volume due to less ability to hold open airways with connective tissue.
other causes of increased closing volume = asthma, COPD, smoking.
can add PEEP to splint open the airways at end of expiration.
what is hysteresis ?
phenomena whereby the state of a system depends on its history i.e. if the measured value is rising or falling.
in respiratory physiology, hysteresis describes the change in pressure-vol curve of the lung in expiration and inspiration
this is because in expiration, there is no need to overcome elastic forces and surface tension. hence the pressure required to inflate the lungs is more than to exhale.
draw a graph to demonstrate lung hysteresis in spontaneous ventilation…
draw a graph to demonstrate lung hysteresis in controlled ventilation and calculate the work of breathing..
rearrange equations
work = area in curve = P x V
not pressure and volume arent at 0.
due to residual volume and PEEP. could draw the pressure at 0 and then demonstate adding PEEP moves the curve towards more compliant region.
the curve is exactly the same in spontaneous however - the values on x are negative i.e. more negative towards right.
what are the main components of work of breathing?
elastic work - work needed to overcome elastic forces of chest wall, lungs and surface tension
resistive work - work against friction to air flow e.g. asthma/ bronchoconstriction
what is dead space?
volume of inspired air that does not take part in gas exchange i.e. ventilated areas of lung that are not perfused.
in a typical healthy individual
TV = 500
Alveolar ventilated volume = 350
deadspace 150ml (around 2ml/kg)
how can dead space be classified ..
physiological DS = anatomical DS + alveolar DS
anatomical = volume of conducting airways e.g. nose, pharynx,larynx, up to terminal bronchi
alveolar DS = poorly perfused alveoli that do not take part in gas exchange.
in anaesthesia DS is increased by apparatus e.g. HMEF, tubing, facemask, bronchodilators , neck extension/jaw thrust.
how is dead space measured?
anatomical dead space = fowler method (nitrogen washout)
physiological = bohr equation
Derive the Bohr Equation…
all expired CO2 comes from alveolar gas
FACO2 x VA = FECO2 x TV
alveolar vent volume = TV - VD
FACO2 x (TV-VD) = FECO2 x TV
the FACO2 can be approximated to PaCO2 and FECO2 to PECO2 (pp of expired CO2)
PaCO2 (TV-VD) = PECO2 x TV
Rearrange
VD/VT = PaCO2- PeCO2 / PaCO2
usually the ratio is around 0.2-0.4
how does spirometry work?
Spirometry is a test that measures lung function by assessing the volume and flow of air that a person can inhale and exhale. It is commonly used to diagnose and monitor respiratory conditions like asthma, COPD, and other lung disorders.
2 types - water sealed spirometry and dry spirometry
in water sealed spirometry - patient breaths into a closed chamber that is partially submerged in water. breathing in and out causes it to be displaced up and down causing a pen to move on a piece of paper (diagram)
dry - air moves bellows which move a pen to draw.
what is body plethoysmography?
method used to measure FRC , RV , TLC
relies on boyles law.
it can also measure airway resistance - can be used for asthma etc
person sits in air tight box and breathes in and out through a mouth piece connected to outside world.
there is a pressure sensor within the cabin that measures cabin pressure
pressure sensor in mouth piece that measures pressure inside lungs
as patient breaths in, the thorax increases in volume, the cabin reduces in volume and hence increases in pressure.
after some normal breathing, a valve in mouth piece closes before inspiration. now patient inspires and pressure reduces in lung but no airflow. this negative pressure generated is measured at a pressure transducer in the mouth. can use the pressure
through various calculations and application of boyles law, FRC and TLC can be measured.
describe the helium dilution method…
measurement of total lung capacity..
patient breaths in O2 and helium
helium is not very soluble - goes in and comes out. (not absorbed)
CO2 is absorbed by soda time.
conc of helium inspired is known
conc of helium at end of expiration is measured.
volume in is known
hence
CxV = CxV. can work out unknown volume.
describe the nitrogen washout method for measuring FRC….
air has 79% N2
FRC should have 79% N2 as N2 is not absorbed.
patient breaths in and out into closed system of 100% O2.
The N2 in lungs will equibrillate into the bag of O2.
after equilibration, the conc of N2 is measured in the bag.
N2 conc in bag x vol = FRC x 0.79
as the amount of N2 should be the same as it is not being added / removed.
what are the problems of nitrogen washout and helium dilution methods?
under estimation as poorly ventilated areas of lung are not measured.
body plethysmography has the advantage here.
what is Fowlers method?
measures dead space
via a single nitrogen wash out test
after normal breathing of 79% N2, the subject takes one vital capacity breath of O2
the expired gases after this are measured over time.
N2 concentration is plotted on y axis and volume/time on x axis.
phase 1 = anatomical dead space filled of 100% O2
phase 2 = rise in N2 as deadspace is mixed with alveolar N2
Phase 3 = alveolar gases containing N2 so plateus. no dead space
phase 4 = steep rise as poorly ventilated alveoli empty - these had minimal O2 entering them as poorly ventilated. also determines the closing volume. just before this is the closing capacity.
deadspace is calculated by measuring midpoint of phase 2 and it is the volume before that point (including phase 1)
draw a flow volume curve for normal vital capacity breath
note volume decreasing on x axis
max flow in expiration = 8-10L/sec
max in inspiration = 4-6L/sec
during expiration - more forceful and the flow rates peak more due to elastic recoil of the lungs
less explosive in inspiration so less of a peak.
what are the methods of measuring FRC, RV and TLC
body plethosmyography
nitrogen wash out
helium dilution
normal value for physiological deadspace
2ml/kg
how does pregnancy and age effect dead space
pregnancy = progesterone causes airway dilation
age - loss of elastic tissue, number of alveoli diminish so relatively deadspace is increased
how does changes to RR and TV affect deadspace?
changing minute vent by increasing RR and reducing TV will increase proportion of deadspace
describe factors increasing deadspace…
physiological
- pregnancy
- age
- standing
- shallow faster breathing > slow deep breathing for same MV
- cardiac output - reducing cardiac output
pharmacological
- bronchodilators
equiptment and anaesthesia
- more tubing/ face mask/ HMEF
- jaw thrust
factors that decrease deadspace?
decrease transporting airways e.g. tracheostomy, bronchoconstriction
increase perfusion of alvolei - increase CO
how do different lung volumes change with age?
increase in dead space and RV
decrease in TLC and VC
how does FRC change with age?
almost 0 before birth
then increases gradually from birth to 5yrs
then static for rest of life. no change with elderly
how do lung volumes vary with height and gender?
the taller you are the larger the lung volume
all slightly lower in female than males for a given height
draw a curve to demonstate lung and chest wall compliance and combined compliance
chest wall - always trying to expand so in the negative values.
lung is always trying to collapse - in the more positive region.
note both start at RV
combined curve in dark blue - this is combined values for each e.g. at bottom -20 vs 0 means it starts at -20. at the top +5 and +20 = +25. at the point where both are equal e.g -10 and +10 = 0 this is equivalent to FRC as this is the resting state where outward recoil balances inward recoil of lungs.
the compliance of chest wall and lung separately is similar - can be demonstrated by similar shape.
however compliance of them together is slightly flatter so reduced compliance
la place equation in a cylinder?
T = PR
(no division by 2)
how does surfactant reduce pulmonary oedema?
reduced inward pressure of alveoli - hence less drawing effect on fluid into lungs
draw a flow volume loop for obstructive and restrictive lung disease
obstructive disease - top image blue line.
- can see during expiration peak expiratory flow not as high due to resistance, scalloped appearance due to airway collapse so early decline in flow
- also increased RV and increased TLC due to gas trapping or loss of elastic tissue in emphysema
restrictive disease - bottom
smaller volumes - shifted to right (remember values are decreasing on x axis). max flow rates are reduced.
thinner curve - reduced VC - smaller stiff lungs
draw a curve for fixed upper airway obstruction.. give examples of when this may occur
e.g. tracheal stenosis , external compression - goitre
volumes are unchanged but peak flow rates are less due to resistance to flow in both inspiration and expiration.
how does flow rate in inspiration/ expiration alter with intrathoracic and extrathoracic obstruction? give examples
intra thoracic - effects expiratory flow
extra thoracic - effect inspiratory flow
for upper airway both effected
intrathoracic e.g. bronchial tumour, tracheomalacia, bronchoconstriction.
extrathoracic e.g. goitre, oesophageal tumour.
draw a volume time curve - compare this for obstructive and restrictive disease
subject takes deep breath in and then exhales as quickly as possible until forced expiratory reserve exhaled.
FVC = forced vital capacity = volume at end of expiration
FEV1 = volume exhaled in 1 second of max expiration.
FEV1/FVC normally 0.75 to 0.8
in obstructive - eventually get to FVC but slower, hence lower FEV1. thus ratio <0.7.
in restrictive - lower lung volumes due to small fibrotic lungs so reduced FVC. FEV1 same or slightly reduced. may get an increased ratio.
what is transfer factor?
measure of diffusion capacity
defined by the volume of carbon monoxide transferred across alveolar membrane into the blood per minute per unit partial pressure of CO.
= TLCO
patient inhales single VC breath of 0.3% CO and hold breath for 10seconds.
inspired and expired CO is then measured. the difference between them is how much eas taken up by lungs.
normal value = 17-25ml/min/mmHg
what reduces and increses transfer factor?
increase = pulmonary haemorrhage, polycytheaemia, exercise, obesity
decrease = fibrosis, emphysema, pulmonayry oedema, P.E , lobectomy , anaemia
what is the difference between a capacity and lung volume?
capacity is the sum of 2 or more lung volumes.
e.g. FRC = RV + ERV
how is COPD severity classified?
FEV1 = GOLD criteria
FEV1 >/= 80% = class 1
50-79% - class 2
30-49 - class 3
<30 - class 4
describe process of physiological ventilation…
ventilation is the process of moving air into and out of the lungs for gas exchange
inspiration:
- diaphragm & external intercostals contracts
- causes chest wall expansion
- increases intrathroacic volume and hence reduces pressure
- transmits to negative pressure in alveoli
- flow of gas down pressure gradient
expiration
- relaxation of muscles
- recoil of lungs and chest wall to resting state
- reduced volume, increased pressure
- gas flows out.
under normal ventilation inspiration is active = work needed to overcome elasticity of lung and surface tension and chest wall. expiration is passive as recoil to resting state.
forced expiration involved internal intercostals and abdominal muscles to help force further air out.
how is the PEFR measured?
gradient of volume time curve during forced expiration
more commonly using mini wrights peak flow meter.
define intrapulmonary, transpulmonary, intrapleural pressure…
intrapleural pressure = pressure between parietal and visceral pleura (negative pressure)
intrapulmonary pressure = pressure inside alveoli and resp tract
transpulmonary = difference of the above (intrapulmonary - intrapleural) = always positive because intrapleural is negative.
describe the different patterns of flow within the airways…
flow in the airways can be laminar or turbulent
describe laminar and turbulent flow at this stage.
laminar = flow in parrallel lines, obeys hagen poiselle equation.
turbulent = flow disorganised, eddie currents, swirls. does not obey hagen poiseulle.
reynolds number can determine which type of flow
Re = V p d / n
p = density, V = velocity, d = diameter, n = viscoity.
>2000 turbulent, <2000 laminar
hence laminar flow more likely at low velocity, small diameter airways. also smooth surfaces.
hence large airways = turbulent - beneficial as helps filter particles as currents colide with walls and particles are trapped by mucus.
smaller airways = laminar - less work of breathing, more efficient
what is the hagen poiseulle equation
FLOW = ΔP πr4 / 8nl
what is reynolds number
reynolds number dimensionless number that can determine which type of flow is more likely.
Re = V p d / n
p = density, V = velocity, d = diameter, n = viscoity.
>2000 turbulent, <2000 laminar
what factors promote turbulent flow in the airways…
increased resp rate = increases velocity
increased diameter = more likely in large areas
obstructions in airway / at bifurcations
increasing density of gas - e.g. diving
how can laminar flow in airways be promoted?
Heliox = 21% O2, 79% helium
helium is less dense than N2
so reduces reynolds number
more likely to promote laminar flow
less work of breathing - laminar breathing is proportional to ΔP. whereas turbulent is proportional to root ΔP so more negative pressure needs to be created in turbulent to have same effect on flow. i.e. more work.
define resistance in lung physiology?
the opposition to flow in the airways.
change in pressure for a given charge in flow
cmH20 / L/ second
what do you understand by term time constants?
different lung units take different times to fill and empty
the time constant defines the time taken for a lung to fill by 63% of its total volume.
it is a product of the compliance and resistance of that lung unit.
time constant = resistance x compliance
this means different parts of lungs empty/ fill at different rates.
(the more compliant, the more volume for a pressure change hence takes longer to fill)
when is the time constant of a lung high or low ?
high = asthma = slow filling and emptying
low = ARDS = lower volume
how does the compliance of base and apex compare?
apex = lung is pulled down by gravity - high resting volume - at top of compliance curve where it flattens out. hence poor compliance
base = less distended, on steeper part of the curve - more compliant
Explain the different west zones of the lung…
west zones describe the relationship between alveolar pressure, venous pressure and arterial pressure to determine whether alveoli are perfused or not.
west zone 1 = PA> Pa >Pv - top of lung
West zone 2 = Pa>PA>Pv - middle of lung
west zone 3 = Pa>Pv >PA - base of lung
in Z1 lung is stretched out by gravity and PA is high. blood pressure reduced due to gravity. pulmonary arteries are compressed by alveoli = dead space. In health not seen.
In Z2 - artery pressure is more than alveolar due to less gravity effects/ better systolic. perfusion occurs and is determined by Pa-PA difference. blood flow only in systole
In Z3 - pulmonary and venous pressure both higher. perfusion dependant on PA-Pv difference. some alveoli may be compressed in this zone - shunt.
how does the intrapleural pressure at top and bottom of the lungs compare?
top = -8cm H20
bottom = -1.5cm H20
hence apex the alveoli are more distended
what increases and reduces likelihood of zone 1 occuring?
in health unlikely to occur because Pa is adequate.
however in IPPV the PA can increase > Pa
or if high intrinsic PEEP e.g. asthma
OR hypovolaemia - reduces Pa
on the other hand - exercise increases blood flow and reduces likelihood of Z1
what is the V:Q ratio
represents ratio of ventilation to perfusion in the lungs.
normally around 0.8
in an ideal lung they would be perfectly matched at 1.
decribe the V:Q with increased shunting and deadspace…
high V:Q >1 = deadspace
more common at top of lungs
low V:Q <1 = shunting
more common at base of lungs
what are the regional differences in V:Q ratio… draw a graph
both ventilation and perfusion reduced at apex but perfusion more so. so high V:Q
both ventilation and perfusion increased at base (ventilation due to better compliance, perfusion due to gravity) but perfusion more so increased. so low V:Q
what is the cause of high and low V:Q?
high V:Q - causes of deadspace
- respiratory - bronchodilation , emphysema
- circulatory - hypovolaemia/ P.E
low V:Q - causes of shunt
- physiological - atelectasis from obesity, age, pregnancy
- pathological - pneumonia, atelectasis behind obstruction e.g. tumour, pneumothorax/ collapsed lung.
what happens to end tidal CO2 if there is a lot of deadspace
falls as less perfusion
more ventilation to dilute CO2
derive the shunt equation…
from the picture
QTCaO2 = Qs(CvO2) + (QT-Qs)(CcO2)
expand and rearrange..
QTCaO2 = Qs(CvO2) + QTCcO2 - Qs(CcO2)
Qs(CcO2)- Qs(CvO2) = QTCcO2 - QTCaO2)
Qs (CcO2-CvO2) = QT (CcO2-CaO2)
Qs/QT = (CcO2 -CaO2)/ (CcO2-CvO2)
Qs/QT normally around 0.2
QT = cardiac output
CcO2 can be calculated from PAO2 - alveolar gas equation and then using O2 dissociation curve. (cant be measured directly)
CvO2 - from mixed venous gas e.g. central venous catheter (pulmonary artery)
CaO2 - arterial O2 gas
what does a shunt do to PaO2 and PaCO2?
reduced PaO2
no change in PaCO2
define a shunt?
An area of lung that is perfused but not ventilated. blood that passes through the lung without participating in gas exchange.
this blood will then mix with oxygenated blood and enters systemic circulation.
can be categorised into
phsyiological
- bronchial circulation = bronchial veins drain into pulmonary vein and LA
- Thebesian veins = coronary venous blood draining into LV
- normal pulmonary shunting - some areas of lung will be collapsed e.g. bases when lying down.
pathological
- extrapulmonary = congenital heart disease (R to L shunts), pulmonary AV fistula.
- pulmonary = atelectasis, pneumonia
why does a shunt not affect CO2?
CO2 diffusion is fast, other areas that are ventilated can compensate. if PaCO2 rises, increase resp rate to compensate.
what is meant by venous admixture?
the blood mixed from shunted blood and oxygenated blood from capillaries involved in gas exchange
describes the amount of shunting.
how does a shunt respond to increasing FiO2?
minimal effect because those areas that are not ventilated are still adding deoxygenated blood to the arterial blood. the more shunting , the less of an effect increasing FiO2 has.
define respiratory failure…
respiratory failure describes the failure of the functions of the respiratory system either in oxygenation or removal of CO2
can be divided into type 1 or 2
type 1 = hypoxia, normal CO2
type 2 = hypoxia, hypercapnia
normal values PaO2 >8kpa, PaCO2<6kpa
what is meant by ventilatory failure?
pathological reduction in alveolar ventilation below levels required to maintain normal gas tensions.
respiratory failure may result from ventilatory failure (normally type 2)
what are the causes of type 1 and type 2 respiratory failure?
type 1
- V:Q mismatch / shunting
- pneumonia , P.E, pulmonary oedema
- hyperventilation will keep CO2 normal or lower it. it will also reduce PaO2 via alveolar gas equation but not enough to account for V:Q/shunts.
type 2
- hypoventilation
- now CO2 effected
- failure of respiratory centre - opioids, anaesthesia, COPD
- chest wall issues - flail chest, neuropathic (guillian bare), muscular dystrophies/ relaxation, fatigue (asthma attack)
what are the causes of ventilatory failure
describe as the pathway of ventilatory control
higher centres - damage by tumours etc, changed sensitivity by opioids, anaesthesia
upper motor neurons - distruption of UMN to spinal cord connection. lesions above C3/4/5 e.g. brainstem stroke/ trauma
anterior horn cells - affects connection between UMN and LMN polio
lower motor neuron - e.g. GBS, phrenic nerve palsy (interscalene block), MND
NMJ - myasthenia gravis, lambert eaton, organophosphate poisoning,
muscles - affects ability to contract e.g, muscular dystrophies, splinted diaphragm from increased abdominal pressure
lung and chest wall - disrupted mechanics e.g. kyphoscoliosis, flail chest.
increased resistance of airways - COPD/ asthma
upper airway obstruction - foreign body, tumour
how does PaCO2 change with changes to minute ventilation?
inversely proportional
as MV increases, PaCO2 decreases
rectangular hyperbolic relationship
what factors affect rate of diffusion across biological membranes / alveolar membrane… how are lungs adapted to maximise this?
This can be described by Ficks law of diffusion and grahams law of diffusion
diffusion rate = (Conc difference x area x solubility) / (thickness x root molecular weight)
conc gradient - maintained through ventilation and blood flow
area = high surface area from many alveoli
thickness = minimal epithelial, BM, endothelial. high cap density
solubilty = higher for CO2 than O2
how does the diffusion of O2 and CO2 differ in lungs?
CO2 much quicker due to higher solubility factor in blood.
hence diffusion defects effect PaO2 first.
state the alveolar gas equation…
PaO2 = FiO2 (Atm - SVP) - PaCO2/R
SVP = 6.3 kpa
R = 0.8
this is used to estimate the PaO2 in alveolus.
describes the relationship between O2 delivery to alveoli and removal.
The O2 removal is deduced from the PaCO2 and respiratory quotient.
PaCO2 is a better predictor of ventilation and not affected by shunting like PaO2 is and hence used instead of PaO2
what is the respiratory quotient ?
the ratio of CO2 produced to O2 consumed
depends on respiratory substrate
carbs = 1
protein = 0.8
fats = 0.7
european diet around 0.8
PECO2 / PiO2 - PeO2 = RQ
what assumptions does the alveolar gas equation make?
assumes full saturation with H20 at alveoli
assumes no CO2 in inspired air
assumes CO2 and O2 are ideal gases
assumes RQ
PAO2 and PaO2 assumed to be in equilibrium
what factors does PAO2 depend on?
use alveolar gas equation to explain
e.g. FiO2, Patm, alveolar ventilation (PACO2 is inversely proportional to alveolar ventilation so used as a surrogate)
what is the Aa gradient?
PAO2 - PaO2
describes the difference between alveolar O2 and arterial O2
always >0 due to shunting
in normal health around 1.5Kpa
increases with increased FiO2 because PAO2 increases much more than PaO2 (FiO2 doesnt really improve shunt)
can also be increased if there is impairment in diffusion and equilibrium not reached.
Descirbe the way O2 is carried in the blood… what is the equation for O2 content of the blood?
mostly bound to Hb
small amount dissolved in blood
Total O2 content = (Hb x sats x 1.34) + (0.0225 x PaO2)
(if in mmHg use 0.003 instead of 0.0225)
hb in g/100ml
answer is in ml O2 /100ml plasma
what is the huffner constant?
describes the mls of O2 carried per g of Hb
theortical value in vitro = 1.39
in vivo = 1.34ml/g
due to presence of other forms of Hb e.g. methamoglobin and carboxyHb
describe the structure of a RBC and Haemaglobin
RBC
- 6-8 um
- biconcave
- no nucleus / mitochondria - glycolysis only
- extensive cytoskeleton - flexible
Hb
- 4 chains polypeptide = 2a and 2b
- globular protein with quarternary structure
- each has heme group with Fe2+
what forms of Hb do you know
physiological:
- HbA = 2a,2b = adult, most abundant
- HbA2 = 2%, 2a,2d, not as efficient
- HbF = 2a2g , increased affinity for 02, <1% by 6month
pathological
- HbS = sickle cell, abnormal B
-MetHb = methamoglobin (Fe3+ cant bind 02)
COHb = usuallty <2%, higher in smokers
draw the Hb O2 dissociation curve..
labelled x = O2 in kpa
labelled y = % saturation
important points
p50 = 3.5 - 50%
venous = 5.3 - 75%
arterial around 100% = 13
explain the sigmoid shape of O2 dissociation curve…
due to cooperative binding
whereby before any O2 are bound Hb is said to be in tense state whereby binding sites are less accessible hence binding is harder
after first binds, conformational change, increases affinity for next O2
moves to relaxed state.
hence shallow gradient to start with then increase then at the end shallow gradient as less binding sites available. so rate of saturation reduced.
what % of blood is extracted of O2 at rest, what does this tell you about venous blood?
25% extracted
hence venous saturations around 75%
what conditions alter the binding of O2 dissociation curve?
To the right
- hyperthermia, hypercapnia, acidosis, 23DPG , sickle cell, pregnancy, exercise
to the left
- opposite of above, fetal Hb, COHb
what is the bohr effect?
rightward shift due to increase H+
hence acidosis promotes unloading. this occurs due to changes in Hb affinity for O2 in presence of H+. this couples metabolism to oxygen delivery.
draw a dissociation curve for myoglobin
hyperbolic relationship
much higher affinity
myoglobin acts as a temp store for O2 in muscles.
what is 2,3 DPG and what are its roles?
organophosphate molecule
produced during glycolysis in RBC
binds Hb residues and reduces affinity for O2 hence promotes unloading of O2 at tissues - right shift.
links metabolism to O2 delivery.
increase in metabolism, chronic hypoxia (altitude, anaemia), pregnancy, exercise
describe the difference between lungs and tissues in Hb affinity for O2 and hence adaptations?
at lungs
- low CO2, higher pH - left shift, increases affinity
at tissues
- metabolism - right shift - increases unloading.
describe the production of RBCs…
Erythropoeisis is the production of RBC
which occurs in the bone marrow of axial skeleton in adults.
in the fetus this occurs in liver and spleen
in neonates this occurs in all bones.
RBC are produced from pleuripotent haemopoietic stem cells which are driven by the hormone Erythropoietin (EPO)
reticulocytes are released into the plasma where they mature into RBC
this is controlled by EPO which is produced by renal parenchyma and liver in response to hypoxia.
stimulates haemopoeitic stem cells to differentiate to proerythroblasts which undergo series of transformations to reticulocytes
what is sickle cell disease?
autosomal recessive
genetic condition
resulting from a point mutation (A to T) that causes an abnormality of B chain of Hb (glutamate to valine)
leading to sickling of Hb and RBCs
results in sickle crisis and anaemia
more prevelent in africa, asia and southern europe.
what are the different sickle genotypes?
HbSS = homozygous = sickle cell disease
HbAS = heterozygous = sickle trait.
the presence of other Hb varients can promote/ inhibit sickling of HbS
describe the pathogenesis of sickle cell anaemia
A–> T
glutamate –> valine
hydrophobic pocket - promotes polymerisation of Hb
RBC less flexible and resistant to changes in shape.
result in haemolysis and anaemia and various crisis …
- haemolytic crisis
- vaso-occlusive crisis - inflammation of vascular endothelium +/- sickling of Hb blocking vessels - thrombosis and vascular stasis. ischaemia (acute chest syndrome, stroke, bony pain)
- visceral sequestration crisis = massive pooling in spleen, splenomegaly, anaemia, hypotension, abdo pain
- aplastic crisis - parvovirus triggers this. drop in Hb and reticulocytes.
precipitants of vaso-occlusive crisis?
acidosis
dehydration
hypoxia
infection
key considerations when anaesthetising a sickle cell patient?
avoid sickling
- avoid hypoxia = preoxygenate etc
- avoid dehydration - pre op IV fluids
- avoid infection - micro discussion r.e. additional prophylaxis
- avoid acidosis - good MV to maintain normal CO2
- avoid hypothermia - bear hugger
Tell me about thalassemia…
autosomal recessive genetic disease
involving imbalance in alpha and beta chains of Hb.
2 forms
alpha thalessemia - deletion of alpha gene
beta thallesemia - deletion of beta gene
various degrees of severity depending on how many chains absent/ mutated.
e.g. B thal minor = 1 chain mutated, may have microcytic anaemia, but relatively assymptomatic.
e.g. B thal major = severe anaemia and tranfusion dependant. becomes apparent from 6 months when gamma is replaced by beta.
similarly alpha thalaessmia can be trait where 1 mutated gene to 4 mutated genes is incompatible with life and results in hydrops fetalis and death in utero.
found more in mediterranean and south asian populations.
how does carbon monoxide effect Hb O2 carrying capacity?
CO binds Hb x300 more affintiy
hence fewer binding sites for O2
conformational change increases the affintiy for O2 of the remaining binding sites
hence reduced ability to off load O2
describe the pathway for Hb breakdown…
RBC are removed by reticuloendothelial system macrophages in liver spleen and blood.
globin chains are broken down to aa and reused.
iron also reused.
porphyrin ring is converted to bilirubin and then undergoes conjugation by liver
converted to bile which is excreted in small bowel.
tell me about the oxygen cascade…
describes a stepwise reduction in pp of O2 between atmosphere and mitochondria
21% O2 inspired = hence 101x 0.21=21kpa
humidification in trachea and airways
(101 - 6.3) x 0.21 = 19 kpa
alveoli - this air mixes with PaCO2 and O2 is taken up. hence less O2. can be calculared by alveolar gas equation = 13.3
capillary blood - small drop to maintain diffusion gradient however equilibrium basically reached so 13kpa
arterial blood = mixing of shunted blood A-a gradient. in health usually 1- 1.5kpa. now drops to 12kpa
at mitochondria - steady drop as it diffuses throughout tissue. by time it reaches mitochondria 1.5-4kpa depends on capillary density, how deep mitochondria is etc
what is pasteurs point?
the minimum partial pressure of O2 at which oxidative phosphorylation occurs in mitochondria.
0.13Kpa
usually O2 reaches mito at 1.5 kpa so large safety margin
what is meant by the O2 flux?
term used to describe flow and consumption of O2 throughout the body. i.e how much is delivered.
O2 flux (DO2) = CO x O2 content of blood
what is meant by the critical DO2?
critical DO2 is the minimum O2 delivery needed to meet the oxygen consumption of the tissue.
this can be explained using VO2 max
VO2 = consumption of O2 by tissues
DO2 = delivery of O2 to tissues.
initially VO2 is limited by delivery of O2 to tissues and by increasing delivery, VO2 can increase. At VO2 max, DO2 is no longer the limiting factor
how is VO2 calculated?
VO2 = oxygen consumption
= CO x (CaO2 - CvO2)
what is the oxygen extraction ratio?
VO2 / DO2
consumed / delivered
normally around 0.25 i.e. 4 x more delivered than needed.
cardiac muscle is highest at around 0.6
OER increases if VO2 increases (sepsis) or DO2 decreases (low CO/ hypoxia)
what factors suggest that the oxygen delivery to a tissue is not adequate
high lactate = anaerobic respiration
venous sats <75%
bigger difference in arterial venous sats - i.e. higher extraction of O2
define hypoxia
defined by the inadequate delivery of O2 to tissues or by the inability of tissues to use O2 that is required to meet metabolic demands of the tissue.
may be systemic or regional.
what is the difference between hypoxia, hypoxaemia and cyanosis?
hypoxaemia = low PaO2. may be the cause of hypoxia
hypoxia may occur without hypoxaemia e.g. cyanide poisoning (unable to use) or anaemia
cyanosi s = clinical signs associated with hypoxaemia e.g. deoxy Hb visible in capillaries of skin/ mucus membranes.
how can the causes of hypoxia be classified?
hypoxic hypoxia - PaO2 <12. also reduced saturations of Hb due to dissociation curve. e.g. high altitude, pneumonia, oedema/ fibrosis.
anaemic hypoxia - low Hb or CO poisoning
ischaemic / stagnant hypoxia - regional embolism/thrombus, systemic - low CO , microcirculatory failure (sepsis)
histotoxic hypoxia - unable to use O2 e.g. cyanide poisoning uncouples oxidative phosphorylation (high PaO2 and high PvO2)
how do the O2 dissociation curves vary for different types of hypoxia?
draw a normal curve - O2 sats at 13.3 100%. venous sats at 5.3 75%. p50 at 3.5
hypoxic hypoxia = both O2 sats and venous lower
histocytic - both high
stagnant bigg A-v difference.
anaemia = normal sats but scale for content is lower.
what are the consequences of hypoxia?
can be categorised into the effects of
- lack of aerobic respiration
- by products of anaerobic respiration
lack of aerobic respiration
- cells have creatine phosphate stores that last about 90 seconds. glycolysis can produce 2ATP from then on. normally aerobic respiration produces 38ATP. without aerobic respiration a lot les ATP for cellular processes to occur e.g. cardiac muscle cant contract and will fatigue, neurons can’t maintain membrane potential and hence fire AP. Cells become stressed and can apoptose.
anaerobic resp - lactic acid - lowers pH - effects on enzymes and membrane potential
cell death - release of K+ - hyperkalaemia
inflammation
how does the body detect and respond to hypoxia?
This can be divided into short term and long term measures
immediate term/ local:
- local tissue hypoxia - anerobic respiration - metabolites cause reactive hyperaemia.
- bohr effect - release of more O2
short term
- peripheral chemoreceptors found in carotid bodies and aorta - detect low PaO2 and low O2 content. When PaO2 <13 they discharge and send impulses (via glossopharyngeal and vagus) to the medulla (nucleus tractus solitarius)
- increase in minute ventilation (however mostly sensitive below 8Kpa)
- sympathetic activation - increase HR and CO. overall vasoconstriction to divert O2 to important places.
later
- kidneys detect hypoxia and release EPO
- EPO acts on bone marrow to stimulate erythropoiesis
describe how the brain, heart and lungs respond to hypoxia..
local effects of hypoxia in cardiac tissue and heart is to cause vasodilation to improve blood flow in response to hypoxia.
this would increase cerebral blood flow, although this is only significant below 6.7kpa
similarly in the heart.
lungs however have opposite effect - hypoxic vasoconstriction. this is to improve V:Q
how is content of O2 in blood calculated..
O2 content = (Hb x 1.34 x sats ) + (Kpax0.0225)
O2 is carried via Hb - majority
and dissolved in blood - v small amount
huffner constant = amount of O2 in ml per g of Hb
how is O2 consumption calculated?
VO2 = CO x (CaO2 - CvO2)
how is CO2 transported in the blood?
CO2 has a number of modes of transport in the blood.
Mostly as Bicarbonate (HCO3)
- in RBC, carbonic anhydrase catalyses H20+CO2 –> H2CO3 –> HCO3 + H+
- H+ buffered by haemaglobin
- HCO3 exchanged for chloride and travels in plasma.
Also some as Carbamino compounds
- carbaminohaemaglobin formed when CO2 binds Hb amino acid residues.
- deoxy Hb is x3.5 more affinity for CO2 than oxy (haldane)
and a small amount dissolved in the blood
- CO2 more soluble in blood than O2
- henrys law states amount dissolved is proportional to partial pressure
- PaCO2 x 0.223 at 37 degrees (or 0.03 mmHg)
tell me about carbonic anhydrase…
enzyme that catalyses CO2 +H20 to H2CO3 (carbonic acid) which can further dissociate to HCO3.
This is found in RBC, kidneys, lungs, aqueous humour of the eye and GIT.
major role in CO2 transport
what is the haldane effect?
This decribes the ability for deoxyHb to bind to CO2 with higher affinity and thus have better carrying capacity than oxygenated Hb.
This couples O2 release and CO2 removal. It means Hb binds to CO2 at the tissues where Hb is deoxygenated and then releases it at the lungs where Hb is more likely to be oxygenated.
Draw the CO2 dissociation curve demonstating different ways CO2 is carried…
pink line = dissolved in plasma
purple = dissolved + bicarb
blue = dissolved + bicarb + carbamino
biggest jump between pink and puple, hence mostly as bicarbonate.
could point out some typical values
- venous blood 50ml/100ml blood at 6.1kpa
- arterial blood 40ml/100ml blood at 5.3kpa
drawing O2 curve on top of this - sigmoid shape. plus total content is half so the top of sigmoid curve should end half way of emax of CO2.
Describe the control of ventilation…
ventilation is controlled by tight neuronal homeostatic mechanisms in order to maintain PaCO2, PaO2 and pH of the blood.
As with all homeostatic mechanisms, it involves sensors, control centre and effectors.
Sensors - peripheral and central chemoreceptors, pulmonary stretch receptors, irritant receptors, joint receptors
control centre = all feed in and are integrated at the medulla and pons.
effectors = muscles of inspiration (diaphragm, intercostals ) and muscles of expiration.
The control centres have 4 main nuclei
- dorsal respiratory group (DRG) - medulla
- ventral respiratory group (VRG) - medulla
- pneumotaxic centre - in pons
- apneustic centre - pons
how does doxapram work?
stimulates peripheral chemoreceptors to stimulate ventilation
what are the peripheral chemoreceptors and what is their role?
carotid and aortic bodies contain chemoreceptors. (arch of aorta, carotid bifucation)
mostly responsible to detecting and responding to low PaO2 (rather than PaCO2).
carotid bodies: very high blood flow of 2L/100g of tissue / min. hence have a small AV difference, hence small changes to arterial PaO2 can be detected through reduced ATP production which results in dopamine NT release. The response is augmented with pH changes. hence carotid bodies increase in firing when PaO2 low or pH low.
Aortic arch - less sensitive than carotid bodies because blood flow not as high. but also can to some extent respond to content of O2 (i.e anaemias) as well as PaO2
what is the role of central chemoreceptors?
located on ventral surface of the medulla
respond to changes in PaCO2 which results from changes to pH of CSF
CO2 crosses BBB. in CSF reacts with H20 to form carbonic acid. lowers pH of CSF. the increased H+ conc is detected by the chemoreceptors. leads to increased firing to respiratory centre to increase MV
less protein and HCO3 in CSF, hence less buffering capacity so sensitive to small changes
However slightly slower response time as it relies on this reaction.
how do central chemoreceptors adapt?
after 48 hrs of persistently high CO2
HCO3 is transported into CSF to correct for pH changes. now pH of CSF is normalised for that level of CO2
hence now the set point for CO2 is higher.
the central chemorecpetors will respond to further CHANGES in PaCO2
peripheral chemoreceptors are now more significant hence CO2 retainers may rely more of hypoxic drive to stimulate ventilation.
what factors reduce or alter the central chemoreceptor response?
chronically high CO2
Opioids / anaesthetic agents/ barbiturates
other factors - age, genetics, exercise
describe the respiratory centre in more detail..
located in the brainstem nuclei that lie in medulla and pons
4 main anatomical areas
medulla:
- dorsal respiratory group -
- ventral respiratory group
these are collectively called central pattern generator and responsible for main control
pons:
- pneumotaxic group
- apneustic area
collectively called the pontine respiratory group and fine tune the resp patterns.
dorsal resp group
- found on floor of 4th ventricle and most neurons within nucleus tractus solitarus where the sensory afferents of CN IX and X end.
- responsible for sending outputs to inspiratory afferents involved in normal breathing - intercostals nerves and phrenic nerve
ventral resp group
- located in ventral medulla and more responsible for active expiration and forced inspiration
pneumotaxic centre = modulates outputs of DRG to reduce depth of inspiration hence involved in fine tubing. stimulation causes a terminaiton in inspiration
apneustic centre = modifies activity of DRG to prolong inhalation time. again fine tunes
is there any voluntary control of ventilation?
inputs from the cortex can overide the respiratory centre basal output and modulate ventilation e.g. hyperventilate, breath hold etc
however eventually brainstem control overides i.e. cant hold breath until death.
other than the respiraotory centre, are there any other inputs that influence ventilation?
cortex - voluntary control
limbic system - emotions / anxiety
pain pathways
pulmonary stretch receptors - protect lungs from over inflation - when there is an increase in transpulmonary pressure they will inhibit inspiration = Hering Breuer reflex
irritant receptors = respond to chemical and cold. involved in coughing and bronchoconstiction but also modulate vent
J receptors = stimulated by oedema in alveoli and chemicals in pulmoanry circulation.
joint and muscle proprioceptors - exercise increases MV before PaCO2 builds up
muscle spinal in diaphragm and intercostal - negative feedback
Draw a graph to show the relationship between CO2 and minute ventilation..
how does this vary with opioids.
MV on y axis - L/min
Kpa on x axis - KpA
Increase in PaCO2 increase in MV - linear reponse from about 5 to 10Kpa
at 10Kpa - falls - CO2 narcosis.
in opioid use. this is shifted to the right
how does low and high O2 change the response of MV to CO2? what about pH?
in response to hypoxia - increased response to PaCO2 - towards the left and more exponential
similarly low pH also shifts to the left.
draw a graph for effector of PaO2 on MV? what happens in presence of hypercapnia?
not much affect until <8kpa
then exponential rise
before 8kpa, MV much more sensitive to PaCO2 than PaO2
if PaCO2 is low, then hypoxic curve shifted to the left - doesnt rise until below 5kpa
describe the changes seen in MV with exercise?
muscle and joint proprioceptors - at start of exercise before CO2 builds up
increase inputs to DRG to prepare for rise in PaCO2
metabolism - increase PaCO2 - increases ventilation via central chemoreceptors.
due to tight control, PaCO2 wont change in exercise. may even decrease (over compensation)
describe the effects of raised CO2…
These can be considered as local effects and systemic effects
locally
- pCO2 causes vasodilation in most organs due to reactive hyperaemia. allows blood flow to the tissue to match metabolism
- including the brain - increases CBF and ICP if v high.
- lungs have opposite effect - vasoconstriction and increase in PVR
- cardiac - myocardial depressive effects and arrhythmias.
systemically
- chemoreceptors detect - increase in MV, increase in sympathetic response - HR and CO. helps in removal.
- O2 dissociation curve - shifted to right
clinical signs - tachycardia, bounding pulse, raised BP, tachypnoea, confusion, tremor, narcosis and coma.
what are the causes of hyper/hypo capnia?
hypocapnia
- reduced production e.g. hypothermia, hypothyroid reduces BMR
- increased elimination - hyperventilation from anxiety, hypoxia, pain.
hypercapnia
- increased uptake - more inspirated (exhausted soda lime), pneumoperitoneum
- increased production - sepsis, MH, hyperhyroid
how are the lungs affected by general anaesthesia?
general anaesthesia can affect the respiratory system in many ways. can be divided into the effects of airway devices, drugs, PPV , positioning, and anaesthetic drugs…
airway devices:
- manipulation of airway can cause laryngospams and bronchospasm.
- bypass humidification process - irritation of mucosa, increased risk of infections and crusting. (HME can help prevent)
- loss of physiological PEEP e.g. endotracheal tube. 3-5cmH20 normally created by larynx to help splint open alveoli. without can lead to atelectasis
- increased work of breathing - narrow ET tube , increased resistance (r^4)
- deadspace increased by tubing/eqiptment
positioning:
- usually supine and pneumoperitoneum or trendelenburg
- reduces FRC
- can result in closing capacity > FRC –> atelectasis and V:Q mismatch –> hypoxaemia
- lower on compliance curve - reduced compliance - increased work of breathing/ airway pressures.
- less O2 reservoir, increased risk of hypoxia
PPV:
- increased airway pressures
- risk of pneumothorax
- also reduces blood flow by reducing preload/venous return hence increases deadspace
- increase in west zone 1 (due to drop in CO / pulmonary BP and increase in alveolar pressures) hence V:Q mismatch
drug effects:
- muscle relaxants including volatiles - reduced FRC
- volatiles inhibit hypoxic vasocontriction - worsening of V:Q mismatch
- opioids and benzos - depression of MV response to CO2
- volatiles - dose dependant reduction in TV (also increase RR)
- propofol - apnoea and drop in VT, supresion of airway reflexes
- ketamine - preserves airway reflexes and spontaneous ventilation.
- certain ones cause histamine release and bronchospasm - atracurium, morphine , NSAIDs
what are the post op complications of anaesthesia on lung function?
atelectasis –> pneumonia
bronchospasm –> hypoxia
pulmonary oedema (negative pressure e.g. from laryngospasm
risk of aspiration
how can post op complications of anaesthesia be minimised?
pre - op - assess and make good aanesthetic plan e.g. asthma avoid using atracurium, could you use regional anaesthesia if bad COPD
intra op - PEEP, spinal, pressure control ventilation?
post op - promote deep breathing after (pain releif, adequate reversal of NMBA)
which patients are most at risk of respiratory complications from anaesthesia?
prolonged operation / positioning that reduces FRC - leads to atelectasis and risk of pneumonia. can reduce by using PEEP
pre-existing lung disease e.g. asthma and copd - more reactive airways - bronchospasm
inadequate analgesia /addo surgery - reduces depth of breathing after - atelectasis etc.
describe the role of pulmonary circulation in metabolism..
endothelium of pulmonary vasculature is metabolically active
ACE = conversion of angiotensin 1 to 2.
breakdown of certain hormones - NA, 5HT3, progesterone. COMT enzyme present
Production of arachidonic acid metabolites - leukotrienes, thromboxane (bronchoconstriction), prostaglandins (bronchodilation)
what are the functions of respiratory system
ventilation and gas exchange- uptake of O2, removal CO2
pH homeostasis - compensation via excretion of CO2
metabolism - breakdown of NA and 5HT3
endocrine functions -ACE
filtration and protection - cilia and goblet cells, macrophages,
vocalisation
temp regulation - evapouration, latent heat of vapourisation
describe the relationship between particle size and inertial impaction/ sedimentation..
where a particle settles depends on its size and speed of inhalation.
30um - sediment in larger airways and are filtered / prevented from reaching alveoli
3-15um - smaller airways
1-3um - alveoli
<1um - inhaled and exhaled out, too small to settle so just diffuse in and out.
breath holding can promote sedimentation.
what is meant by the double bohr effect?
refers to the situation across the placenta
CO2 travels down conc gradient into maternal blood…
increased CO2 in maternal circulation - promotes unloading of O2
decreased CO2 in fetal - promotes O2 uptake
(plus fetal Hb has higher affinity than mum)
how does ventilation / perfusion change in dependant and non dependant lungs in SV and IPPV
In spontaneous ventilation
- dependant lung (lower down lung) - both ventilation and perfusion are higher here due to gravity (perfusion) and sitting further down on compliance curve (ventilation). However Q>V hence, low V:Q
- independant lung (higher lung) - both V:Q are lower here but perfusion more affected than ventilation due to gravity. hence V>Q so high V:Q in these areas.
overall the V and Q follow same pattern so V:Q is more matched than in IPPV…
Whereby
dependant lung - better perfused but less well ventilated V:Q still low but even more so than in SV
independant lung - worse perfusion, better ventilation. again bigger mismatch in V:Q - higher.
overall more V:Q mismatch in IPPV - mostly due to ventilation favouring independant lung in IPPV vs dependant lung in SV. this is because compliance is low in independant lung and hence takes more force of SV to open it, whereas postive pressure can fill this more easily.
how do you measure a patients lung function before critical care admission / general aanesthesia?
age, BMI
functional history
smoking
respiratory disease - how severe, inhalers, hospital admissions etc
may need CXR, spirometry , transfer factor testing.
what does cardiopulmonary exercise testing involve?
non invasive, objective measure of evaluating both cardiac and pulmonary function. slowly increase intensity of exercise whilst monitoring
breath to breath analysis of CO2, O2 hence can work out CO2 production, O2 consumption
VO2 max can be deduced and anaerobic threshold.
why are bronchioles narrowed in emphysema?
emphysema= breakdown of elastin in alveolar walls. results in larger less numerous alveoli. less capacity for gas exchange (reduced S.A)
elastin is also present to hold terminal bronchi open via radial traction. this is lost so they collapse - gas trapping.
in following image - point out where the respiratory centre lies..
picture of brain stem
very top, not labelled = midbrain
next = pons
last = medulla
top arrow points to pneumotaxic centre
next = apneustic centre
in medulla = at the back = dorsal respiratory group
in front = ventral respiratory group
(ventral group made up of 4 other nuclei)
nucleus tractus solitarus lies at top of dorsal respiratory group within medulla
explain the following diagram …
shows the CO2 dissociation curve
bottom line shows dissolved content can see how increasing PaCO2 increases CO2 dissolved in blood - minimal amount compared to total
next line = dissolved + Bicarbonate = can see this is the biggest increase hence bicarb is the biggest contributor to CO2 carriage
next 2 are as carbamino compounds in arterial vs venous blood. top one is venous which we can see carries more than arterial. this is because of the haldane effect
