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respiratory - Coggle Diagram
respiratory
Ventilation and Lung volumes
Function of lung: gas exchange between alveoli and blood in the pulmonary capillaries (oxygen and carbon dioxide)
Anatomy
Pleurae
Visceral pleurae: surrounds the lungs
Parietal Pleura: lines the chest
Function
Reduces friction
create pressure gradient
compartmentalisation
cellular structure of airway gets progressively thinner from bronchus to alveolus, lose muscle layer and fibrous coat
Epithelium
Basement membrane
Smooth muscle
Fibrous coat
Alveoli (gas exchange): need thin membrane for efficient diffusion (slow process) and wider the membrane, the longer the diffusion takes
Pleural sac
double walled closed sac, separates each lung from thoracic cavity and surrounding structures
inside sac: pleural cavity
surface of pleura creates thin intrapleural fluid, lubricates pleural surfaces as slide past each other during respiration
Conducting zone
Trachea, Bronchi, Bronchiole and terminal bronchiole
warm and humidify air
distribute gas
serve as part of the body's defense system
Respiratory zone
site of gas exchange
Respiratory bronchiole, alveolar duct and alveolar sac
large total cross sectional area/ SA for diffusion
How is blood supplied to alveoli?
need capillaries so gases can transport oxygen to cells when needed
Pulmonary capillaries occupy 70-80% of alveolus S.A. and the alveoli receive all cardiac output
Systemic circulation: certain % goes to different parts of body (Brains, organs etc...)
Alveolar-capillary membrane separates air in alveoli from blood in pulmonary capillaries
Facilitates gas exchange and the air-pulmonary blood interface has larger SA for exchange
Respiratory muscles
Diaphragm
Structure: dome-shaped
innervated by phrenic nerve
Function: separates abdominal thoracic cavity
During inspiration, it moves down and flattens out. Increasing volume in thoracic cavity and pulls lungs open for forced inspiration
External Inter-coastal muscles
accessory muscle
structure
in-between ribs
external lies on top of internal Coastal muscles
only plays a role during inspiration
Inspiration
Contraction of inspiratory muscles (diaphragm and intercostal muscles)
enlarges thoracic cavity
diaphragm descends downwards, increasing vertical dimension and pushes abdomen contents downwards and forwards (75% enlarge)
External intercostal muscles elevate ribs + sternum upward and outward
Note: accessory inspiratory muscles: neck, raise ribs + sternum (enlarge upper portion of thoracic cavity)
air flows in lungs since atmospheric pressure > intra-alveolar pressure and same no. of air molecules occupy large volume
end of preceding expiration, there is no flow as the intra-alveolar pressure equals atmospheric pressure and during the onset of inspiration, the contraction of muscles occur and so forth
Expiration (not as active as inspiration)
diaphragm relaxes (dome shaped) and the elevated rib cage falls due to gravity| external intercostal muscles also relax
no forces expanding chest wall, so chest walls and stretched lungs recoil
elastic recoil to pre-inspiratory size. Therefore, lung size becomes smaller (decreasing volume)
intra-alveolar pressure rises above atmospheric pressure = no pressure gradient exists
Forced expiration
expiratory muscles contract further reducing volume of lungs and thoracic cavity
muscle of abdomen wall pushes further up into thoracic cavity and reduces vertical dimension
ribs contracted and therefore pulled inwards and downwards which flatten chest wall and decrease size of thoracic cavity
lungs small and therefore intra-alveolar and atmospheric pressure difference large, therefore more air leaves
Pulmonary pressures: pressures in interpleural cavity, alveoli and airways (also pressure across the airway and across the aleveolar wall) prevent the alveoli/ respiratory passage from collapsing
Transairway pressures (pta): Pta = Paw-Ppl
prevents airways collapsing during forced expiration
pressure difference between airway opening and intrapleural pressure
The higher the flow, the higher the pressure; the higher the resistance for an equivalent flow, the higher the pressure required to overcome that resistance
Transpulmonary pressure (Pl = Pa - Ppl)
Prevents lung collapsing
pressure difference between alveolar pressure and the intrapleural pressure in the pleural cavity
lower the compliance of the lung, the higher the transpulmonary pressure necessary to achieve an equivalent tidal volume
Determined volume of lung and is dependent on the compliance of lung
intrapleural pressure
pressure within pleural sac and this pressure is exerted by lungs on thoracic cavity
changes during different phases of breathing
remains approximately -5 cm H2O OR 756MM HG AT REST
why is interpleural pressure more negative at base?
effect of gravity and posture (affects the mass of the lungs), the pressure towards the base of the lungs, and tends to counteract the negative intrapleural pressure, the intrapleural pressure is more negative near the top, or apex of the lung and less negative near the base
how does negative intrapleural pressure prevent lung collapse?
When pleural pressure is lower than the pressure of alveoli they tend to expand. This prevents the elastic fibres and outside pressure from crushing the lungs
Ventilation
Alveolar Ventilation: amount of air exchanged between atmospheric and alveoli/ min and amount of wasted air in/ out anatomical dead space must be consistent
pulmonary ventilation: amount of air breathe in and out per min
determined by tidal volume and breathing frequency
good to have an increase in tidal volume than respiratory rate = since depth of breathing increases more than frequency
Anatomical dead space: air in respiratory passageways that never get down to site of gas exchange in alveoli = dead space
remains in conducting airways
150ml anatomical dead space
affects efficiency of pulmonary ventilation as only 350/ 500ml exchanged between atmosphere and alveoli
forces affecting alveolar stability
which forces tend to keep alveoli open?
transmural pressure gradient and pulmonary surfactant
which forces promote alveolar collapse?
pulmonary elasticity and alveolar surface tension
Gas exchange and transport
Composition of air
Nitrogen (0.7862)
Oxygen (0.2084)
CO2 (0.0004)
water (0.005)
Alveolar Po2
when consuming 250ml O2/ min the normal Pao2 is 104mmHg and alveolar ventilation is 5l/min
If increase consumption of oxygen, need to increase ventilation to maintain normal alveolar Po2
Alveolar Pco2
At 200ml Co2/min the normal alveolar pressure for Co2 is 44mmHg and if increase Co2 consumption need to increase ventilation to maintain normal alveolar Pco2
Diffusion capacity
Surface area
Diffusion is a slow process, larger surface area more efficient or space for diffusion
Thickness
thinner the alveolus-capillary membrane, the larger the diffusion capacity
Partial pressure gradient
Steeper the oxygen gradient (less soluble than co2) faster the O2 diffusion
pressure difference drives flow/ movement/ diffusion from high to low
Diffusion coefficient
dependent on solubility and size of gas molecule
co2 more soluble than oxygen hence require a less partial pressure difference for efficient diffusion
Oxygen transport
Hb transport (98.5%)
Dissolved gas (1.5%)
Hb-O2 dissociation curve
sigmoid shape
flat plateau region promotes O2 loading
steep slope Po2 < 60mmHg promotes unloading
small changes in Po2 causes large change in Hb saturation decrease
increase = promotes offloading (as muscles are using up more oxygen so Po2 decreases) exercise
temperature >> increase heat >> offloading
under acidic conditions offloading O2 (high Pco2 and low blood pH - Bohr effect)
Increase levels of 2,3 Diphosphoglycerate more oxygen offloaded
CO2 transport
Dissolved gas (5%)
Carboamino Hb (5%)
Bicarbonate ion (90%)
control of ventilation
respiratory centres in CNS
medullary respiratory centre: bi-laterally paired groups and cross- communication
Dorsal respiratory group
inspiratory neurons
associated with nucleus tractus Solitarius
ventral respiratory group
inspiratory neurons
inactive during tidal breathing
kicks in when require extra respiratory drive (exercise)
Signals from DRG spills over to VRG (expiratory area)
activated (mainly forced expiration) also inspiration
internal intercostal and abdominal muscles contract
1 more item...
force inspiration (inspiratory area) activates expiratory area
diaphragm, external intercostal muscles contract and other accessory muscles for forceful inspiration
associated with nucleus ambiguous, nucleus paraambiguus and nucleus retroambiguus
expiratory neurons
Pre Boetzinger complex
contains pacemaker neurons
spontaneous generation of action potential for basic rhythm generation
AP stimulate cells in DRG
pons respiratory centres
pnuemotaxic centre
switch off inspiratory neutrons in DRG (inhibitory signals)
limits duration of inspiration
Increases breathing frequency at expense of tidal volume
Apneustic centre
stimulatory signals to inspiratory area (extra boost)
control of overall respiratory centre activity
chemical control (negative feedback system)
central chemoreceptors
changes in Pco2 in arterial blood (not pH), since H+ cannot pass the blood-brain barrier
H+ concentration stimulates central chemoreceptors
stimulated chemoreceptors affects respiratory control centres and increases ventilation
increase H+ = Increase ventilation
peripheral chemoreceptors
carotid body and aortic bodies (aortic arch)
respond changes in Po2
respond to Pco2 and pH (lesser extent)
stimulated by decrease in Pao2 (60-30mm Hg) and corresponds to when Hb saturation is low
so increase in ventilation to get more oxygen into system and increase Hb saturation
exercise
increase in ventilation increases volume of oxygen demands
steady state: increase ventilation but Pao2, Paco2 and pH do not change
what stimulates increase in ventilation?
higher cortical centres
proprioception
increase body temperature: skeletal muscles metabolically active and increase heat have an effect on ventilation
increase sensitivity of chemoreceptors: assist when signal for increase in ventilation overshoots (start of exercise) causing a drop in Paco2 and ventilation drops off quickly (end of exercise) causing an increase in Paco2 so chemoreceptors will fine tune and rectify situation
voluntary control
cerebral cortex and bypasses brain stem
override normal breathing rhythm (esp. during singing, speaking and whistling)
voluntary breath-holding and Hyperventilation
hyperventilation: voluntary over breathing >> increases ventilation but does not change Pco2 and Po2
ventilating more air than provided, metabolism hasn't changed so oxygen consumption and carbon dioxide production stays same as resting values. Hyperventilate so our Pao2 increase and we blowing off more CO2 (hypercapnia)
hypoventilation: voluntary breath holding)
don't ventilate enough, so Pao2 will decrease and you're not removing enough CO2 which will increase Pco2
limit to breath holding and Pco2 reaches 55mm Hg, the need to breathe overrides voluntary control and take breath or else no oxygen to brain and pass out
defensive reflexes
Hering-Breuer Inflation reflex
lung inflation signals limit inspiration
pulmonary stretch receptors in smooth muscle layer in conducting airways
protective mechanism
Irritant receptor reflex
receptors lie between airway epithelial cells
respond to irritation of airways by touch or noxious substances
stimulation causes excitatory responses (cough, gasping, prolonged inspiration time)
Generation of basic rhythm
pre-boetzinger complex contains pacemaker neurons, therefore generates action potentials
stimulate cells in DRG
Inspiratory area active (2 secs)
diaphragm relaxes
normal quiet inspiration
inspiratory area inactive (3 secs)
Diaphragm relaxes and elastic recoil of chest wall and lungs
normal quiet expiration
Mechanism of breathing
Factors that determine flow
Lung compliance
Distensibility/ stretch of lung
Change in volume of lung produced by change in pressure
DeltaV/ DeltaP = V2-V1/ P2-P1 => this is the slope of the static pressure volume curve. In other words the slope of P/V curve when there is no airflow and the pressure thus represents transpulmonary pressure
Compliance decreases with lung volume, so an empty lung has a higher compliance than a filled lung
Factors that affect lung compliance
Elastic fibres in alveoli which consequently affects elastic recoil of lungs (overstitching --> loss of elasticity)
Pulmonary surfactant in alveolar fluid and surfactant reduces surface tension of alveoli and prevents them from coalescing
pressure required to keep alveoli inflated = (2 surface tension)/ r
higher surface tension, more pressure required to inflate alveolus
Lower radius size of alveolus, more pressure required to inflate alveolus
surface tension: alveolar air-liquid interface
inwardly directed force --> tends to reduce alveolar diameter , since cells pack tightly to each other creating inward directed force reducing alveoli diameter. Therefore the greater the alveolar surface tension (less compliance)
air water interface where each (air In alveoli and liquid in cells) water molecules attracted to surrounding water molecules then air causing unequal attraction producing force. The liquid layer resists any force that increases surface area and opposes expansion of alveolus since water hate being pulled apart
dyne/cm
surfactant
Complex mix of liquids and proteins secreted by Type 2 alveolar cells: lipoprotein, rich in phospholipids, dipalmitoyl-phosphatidylcholine (DPPC)
Aveolar cells: hydrophilic and hydrophobic part lines interface between air and water within alveoli
no surfactant: lungs have poor compliance and have exhaustive muscular efforts, since tremendous surface tension of pure water counteracted by pulmonary surfactant. Therefore they counteract strong water forces around alveoli
If lined with water alone (forces are stronger) and there's high surface tension and recoil force (elastin fibres) exceeding opposing stretch force of transpulmonary pressure
The hydrophilic particles push water molecules spart and reduce surface tension. The decrease in surface tension in smaller alveoli more than larger alveoli = tightly packed. This equals pressure in both different sized alveoli = even gas flow
surfactant lowers alveolar surface tension by decreasing hydrogen bonding between alveolar air and water interface. This increases pulmonary compliance reducing work of inflating lungs and lungs tendency to recoil and collapse easily
measured in L/cm H2O
emphysema: high compliance = lungs have trouble deflating because they lost their elasticity due to restriction of elastic fibres (no inhaling and difficulty in exhaling)
Restrictive lung disease: low compliance = overproduction of collagen and therefore difficulty in inhaling and expanding lungs. Also occurs with lack of surfactant
Airway resistance
Airway resistance = Patm - Pa/ V(flow of air)
Relationships
Lower the flow, the higher the airway resistance
Higher the pressure difference required to maintain flow, the higher the airway resistance
resistance determined by airway diameter
R(aw) inversely proportional to radius (1/r^4)
Small passageways have greater resistance (lower radius) and larger airways have high flow and low resistance
Anatomy: region of greatest resistance
terminal bronchioles have low resistance due to highest total cross-sectional area. (add in parallel, their combined resistance is low)
medium sized bronchi too, but terminal bronchioles have lower resistance comparatively
Lung volume vs Airflow
Lungs expand, the resistance to airflow decreases because total airway cross-sectional area increases with lung volume, decreasing total resistance
collapsed lungs: maximal resistance to airflow
Muscular effort