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
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.
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
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
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
draw a dissociation curve for myoglobin
hyperbolic relationship
much higher affinity
myoglobin acts as a temp store for O2 in muscles.
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 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 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.
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)
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.
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
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
