Respiration 1 - 4 Flashcards
2 types of respiration
internal external relies on diffusion and gradients effect of diffusion - linked to distance inc distance = inc time for diffusion
internal respiration
in cell
CO2 produced - glycolysis, Krebs cycle, O2 consumed - Ox Phos
external respiration
ventilation
exchange and transport of gases around body
lungs contain multiple branches
broken into 2 zones
1 - conducting zone
2 - respiratory zone
bronchioles more subjected to collapsing, rely on elastic tissue around them to keep open
conducting zone
not involved in gas exchange
transports gases to respiratory zone
nose, mouth, pharynx, trachea, bronchial tree
functions: conditions incoming air - filter, warm, humidify
solubility of gas decreases with heat inc
humidity stops lower airway drying out
structure of bronchial wall
reinforced with cartilage rings, prevents collapsing
layer of smooth muscle, contraction reduces airway diameter
mucous glands, respiratory epithelium, traps particles
elastic tissue, helps support airways
respiratory epithelium
lines lumen, ciliated epithelial cells, direct mucus out of lungs into throat
goblet cells - produce mucus
sensory nerve endings - help detect noxious chemical in airways
bronchioles
less than 1mm diameter
lack cartilage support, use elastic tissue to stay open
in COPD, elastic tissue is broken down = more likely to collapse
lined by repiratory epithelia
more smooth muscle
alveoli
large SA = huge area, small diffusion pathway
fed from terminal bronchiole
thin walled epithelial layer
air blood barrier
epithelium type 1 = makes up most of area, very thin cells
sandwich created by flattened cytoplasm of type 1 pnemocyte and capillary wall
for gas exchange to take place multiple barriers have to be crossed
large SA for exchange
ventilation
inspiration and expiration, quiet (rest), forced (active)
movement of air down pressure gradient
inspiration vs atmosphere
Patmos > Palv so air moves into lungs
expiration vs atmosphere
Palv > Patmos so air moves out of lungs
quiet inspiration
involves primary muscles of inspiration
diaphragm - contracts and moves down
external intercostals - lifts ribs
effect = inc thoracic space and lung volume
air movement follows Boyles law - inc vol leads to reduced pressure, air moves into lungs and down gradient
forced inspiration
involves secondary muscle (accessory)
scalenes - attach to ribs and pulls up and forward
sternocleidomastoids - attach to sternum - lift and pull forward
= expand thoracic cavity
neck and back muscles - pull pelvic girdle - expand rib cage
upper respiratory tract muscles - reduce resistance to airflow
quiet expiration
passive process using elastic recoil, no primary muscles
relaxation of external intercostal muscles
recoil of lungs (elastic forces returning lungs to original size)
forced expiration
accessory muscles, active process
contraction of abdominal muscles - push diaphragm up
neck and back muscles - push pelvic girdle - bring ribcage in
internal intercostals - bring ribcage back down
pleura
tough membrane lines chest wall and outside lungs
fluid filled space, allows lung and chest wall to move over each other
prevents lungs from sticking to chest wall
enables free expansion and collapse of lungs
elastic forces at rest
elastic forces in lungs and chest balance
elastic nature of lungs would tend to cause them to collapse inwards
chest wall would tend to expand
so inward = outward forces
pressure in interpleural space < Patmos
pneumothorax
collasped lung trauma creates breach in chest wall breaks pleural memebrane on chest inter pleural space is at atmos pressure - eqm = loss of force that keeps lungs inflated elastic nature takes over == collapse
compliance
measure of elasticity
compliance = distensibility
C = delta volume / delta pressure
shows the ease with which the lungs and thorax expand during pressure changes
low compliance
more work required to inspire
e.g. pulmonary fibrosis - lung parenchyma is more rigid - harder to expand
high compliance
difficulty expiring - loss of elastic recoil
e.g. emphysema and COPD - airways can collapse
effect of disease states on compliance
fibrosis - small delta volume
emphysema - larger delta volume
same change in pressure
components of elastic recoil
2 major components
1 - anatomical, elastic nature of cells and extra cellular matrix
2 - elastic recoil due to surface tension generated at air - fluid interface
effect of surface tension on compliance
inflating with liquid - saline
- linear increase in volume
inflating with air
- have to overcome surface tension, inc pressure to overcome then smaller airways open - linear filling
surface tension
due to difference in forces on water molecules at air/water interface
in a gas bubble there is balance between pressure exerted by gas and surface tension at gas/water interface = Laplace’s equation
P= 2xSt/radius
surface of bubble will become smaller due to water molecules pulling away
bubble shrinks = pressure inside increases, then reach point where 2 balance in lung
many air sacs of different volume
larger sacs = lower pressure than in smaller
air will flow from smaller alveoli to larger leading to their collapse
surfactant
overcomes problem of smaller alveoli collapsing
produced by type II pnemocytes - made of lipids and proteins (type I for gas exchange)
lipid molecules partition into air/water interface due to hydrophilic and phobic parts which relieves surface tension by decreasing density of water molecules, because hydrophobic tail pulls surfactant molecule upwards
resultant vector = minimal
small alveoli = more surfactant, balances surface tension and pressure between alevoli and stops smaller ones collapsing
when we breathe in, alveoli = full, surfactant decreases, surface tension increases to stop them overfilling
lung volumes
simple spirometer
measures all volumes apart from residual
dead space
volume not involved in gas exchange
- anatomical = volume of conducting airways, at rest approx 30% of inspired air volume
- physiological = includes anatomical dead space, conducting zone + non functional areas of respiratory zone
normally 2 values are almost identical
vital capacity
completely full lung then breathe out as much as possible
residual volume
air left after vital capacity
total lung capacity
vital capacity + residual volume
forced expiratory volume
fill lungs then empty in one seconds
FEV : VC = helps understand lung disease
dynamic values
ERV + TV + IRV = VC
tidal volume
amount of air in and out in single breath
inspiratory reserve volume
top of tidal volume up to vital capacity
expiratory reserve volume
end of tidal volume down to residual volume
functional residual capacity
ERV + RV
= total amount of air
inspiratory capacity
bottom of tidal volume up to vital capacity
changes in IRV and ERV during exercise
increased tidal volume - bigger breaths
reserves decrease
calculating residual volume
helium dilution
C1 x V1 = C2 x V2
using spirometer, add known conc of helium in container, subject breathes for a few mins, then take sample of container and measure [helium]
airflow in lungs
flow of air is proportional to pressure gradient and iversely proportional to resistance
change in pressure/resistance
impact of resistance on flow = poiseuille’s law
airway resistance is proportional to gas viscosity and length of tube but inversely proportional to radius4
small changes in airway diameter have big impact on resistance and therefore flow rate
in normal individual,
pharynx - larynx = 40%
airways > 2mm diameter = 40%
airways < 2mm diamter = 20%
larger airways = resistance in series - Rt = R1 + R2 + R3….
smaller airways = resistance in parallel - Rt = 1/R1 + 1/R2……
factors that impact airway resistance
airway diameter
inc mucus secretion, dec diameter, inc resistance
oedema - inc fluid retention = swelling and narrowing, inc resistance
airwayd collapse e.g. forced expiration, narrows airways, inc resistance
control of bronchial smooth muscle
ANS
- para - ACh released from vagus, acts on muscarinic receptors = constriction
- symp - norepinephrine released from nerves = weak agonist = dilation
humoral factors
- epinephrine circulating in blood = better agonist = dilation
- histamine - released during inflammatory processes = constriction
composition of air
dry and wet at standard atmospheric pressure of 760mmHg
Daltons law - total pressure of mix of gases = sum of individual partial pressures
gases in solution
henrys law - conc of gas dissolved in solution
[gas]dis = solubility coefficient X partial pressure of gas
O2 transport by blood
O2 has low solubility in saline, 0.003ml per 100ml of blood
so when partial pressure O2=100mmHg, plasma can carry 0.3ml O2 per 100ml of blood
at rest cardiac output = 500ml/min, plasma can provide 15ml O2 per min at most however body requires 250ml
plasma cant provide enough O2 alone, overcome by RBC containg haemoglobin
haemoglobin
tertrameric unit, 4 subunits
each subunit consists of haem unit and globin chain
different combinations of globin chains (alpha, beta, gamma) depending on Hb type
in adults - 2 x alpha, 2 x beta
foetus - 2 x alpha, 2 x gamma
haem unit
porphyrin ring containing single iron atom
for O2 to bind, it has to be Fe2+, enzyme methaemoglobin reductase converts 3+ to 2+
haemoglobin exists in 2 states
tense - low affinity for O2
relaxed - high affinity for O2
as partial pressure of O2 increases, haem saturation increases
haem carries more O2 at low temp
shifting oxygen dissociation curve
right shift in curve = decreased affinity
inc temp, inc CO2, dec pH, inc 2,3DPG ==== shifts right
2,3 DPG binds to beta globin chains in haemoglobin
implications of shifts in curves
tissues undergoing active respiration = inc temp, CO2 and dec pH = lower affinity, O2 released from haem and taken up by tissue
fetal haemoglobin
beta globin chains replaced by gamma chains
left shift in curve = higher affinity for O2 - allow for fetal uptakeof mothers O2 from circulation
CO2 transport by blood
CO2 + H2O = H2CO3 = HCO3 + H CO2 acts as a weak acid H2CO3 - carbonic acid sped up by carbonic anhydrase critical for setting plasma pH
blood carries CO2 in various formats
dissolved in solution carbonic acid bicarbonate carbonate carbamino compound all grouped together as total CO2
pathway of CO2
tissues to capillary
1 - crosses endothelium of capillary
2 - 11% remains in plasma
3 - 6% stays dissolved, small amount goes to carbonate, or binds to plasma proteins (carb amino)
4 - 89% goes across RBC membrane (very high permeability to CO2), 4% stays dissolved in RBC, 21% binds to haem to form carbamino compounds, asit binds - H released so RBC becomes more acidic - shifts harm curve - causesO2 to be released to tissues
5 - 64% forms bicarbonate (sped up by carbonic anhydrase), this is transportedout by anion exchanger, Cl in, HCO3 out - dissolved in plasma in capillary
pathway of CO2
in lungs
all flipped
exchanger brings HCO3 in, converted back in CO2 to be released by lungs
2 types of lung disease
obstructive - decreased flow through airways
restrictive - decreased lung expansion
can have both, both decreased ventilation
graphs for lung disease
flow vs vol
shape of decline can show lung disease
vol vs time
breathe fully in and then out as hard and long as possible
obstructive lung disease
narrowing airways due to excess secretions, bronchoconstriction (asthma), inflammtion
inc resistance airflow
obstructive spirometry
decreased FEV1
vital stays the same but takes longer to get all air out, FEV1 decreases
concaved shape due to resistance of airflow - initial flow and peak flow = similar
diseases
chroninc bronchitis persistent productive cough and excessive mucus secretion ( for 3 consecutive months in 2 years)
asthma - inflammatory disease
COPD - structural changes
emphysema - loss of elastin
asthma
hyperactive airways
trigger can be:
atopic —> extrinsic —> allergies
non atopic —> intrinsic —-> respiratory infections, cold air, stress, exercise, inhaled irrtants, drugs
response
movement of inflammatory cells into airways, release of inflammatory mediators e.g. histamine causing bronchoconstriction
treatment of asthma
short term or long term
short - inhaler, salbutamol, Beta 2 adrenorecptor agonist, causes dilation of airways
long - inhaled steroids, glucocortidcoids e.g. beclometasone, reduce inflammatory response - long acting beta adrenoreceptor agonists
restrictive lung disease
reduced chest expansion: chest wall abnormalities, muscle contraction deficiencies
loss of compliance (fibrosis): normal ageing, increase collagen, exposure to environmental factors
- large decrease in vital capacity compared to predicted vital capacity
decreased VC but FEV1 can stay the same or even increase
shape = normal, reduction in volume of air moved, can also reduce peak flow
asbestosis
slow build up of fibrous tissue leading to loss of complaince
macrophages try to attack foreign asbestos fibres, but can’t
summary
obstructive - patients FEV1 reduced to less than 80% of VC
restrictive - patients VC is lower than expected for height, age and sex
can have mix of both
breathing
automatic, rhytmical process, generated by centres in medulla inputs from various regions act to modify respiratory pattern
- involuntary mechanism - but can be altered concoiusly e.g. hyperventilation, holding breath
dorsal respiratory group = inspiration only
ventral respiratory group = inspiration/expiration
both in medulla that sends signals for contraction
medullary centres
dorsal respiratory group - sends signals to inspiratory muscles, quiet inspiration
spontaneously active - shows period of activity - shuts off - period of activity
ventral respiratory group - controls inspiration and expiration, inactive during quiet respiration
during activation helps control forceful inspiration/expiration
pons
prebotzinger complex generates basic rhythm then sends signals to DRG and VRG
modifiying breathing pattern - pneumotaxic and apneustic centres, outer firing pattern and altering respiratory period - send stimuli to medulla to regulate depth anfd rate of breathing
pneumotaxic centre
increased rate by shortening inspirations, inhibitory effect on inspiratory centre
apneustic centre
increases depth and reduces rate by prolonging inspiration
stimulates inspiratory centre
other feedback mechanisms - stretch receptors
e.g. hering-breuer reflex
stretch receptors in lungs send signal back to medulla to limit inspiration and prevent oer inlfation of lungs
phrenic nerve —– diaphragm contracts —- stretch receptor in lung —– vagus nerve —–inspiratory centre
vagus nerve can be inhibitory if signal is too high, inhibits inspiration to start expiration
chemoreceptors
central chemoreceptors - monitor conditions i cerebrospinal fluid, sensing CO2 and pH level
indirect response to a rise in O2 - stimulation leads to an increase in ventilation
peripheral chemoreceptors - located in carotid body and aortic arch
- respong to: inc CO2, dec pH, dec O2
- stimulation leads to increased ventilation
