respiration

types of respiration

external and internal (cellular respiration)

external respiration

• ventilation or breathing: exchange of air between atmosphere and lungs

• exchange of O2 & CO2 beteen lungs and blood

• - transport of O2 and CO2 by blood

• exchange of O2 and CO2 beteen blood and cells

internal or cellular respiration

intracellular reaction of O2 ith nutrients to produce CO2, ater and energy

functions of the respiratory system

• regulation of blood pH

• additional route for water loss and heat elimination (not as effective in humans)

• enhances venous return via respiratory pump

• enables vocalisation and smell

• defends against inhaled foreign matter

CO2 content

• more concerned about CO2 homeostasis rather than O2

• as it determines blood pH, CO2 generates H+ in the blood

• changes in pH are disastrous for cells

the parts of the respiratory system

• upper (everything in the head) and lower tract

branching of airays

• branch in a fractal pattern

• every alveolus is equidistant from the trachea

why is every alveolus equidistant from the trachea?

• ensures they all have the same resistance and thus inflate equally

• if they weren’t equidistant, some wouldn’t inflate during quiet breathing

hat affects resistance?

• length of vessel

• diameter of vessel

• viscosity

viscosity of air

• increased by humidity

cartilage of the airays

blue, asthma usually involves constriction down at the levels of the bronchioles here there is smooth muscle. cartilage keeps the airways open everyhere else

total cross sectional area

• greatest at the alveoli

• resistance decreases as e move through the system

• here all the exchange takes place

hat keeps the lung inflated?

• pleural sac attaches the lung to the thoracic all (prevents lung from collapsing hen e exhale)

  • pressure differences

pleural sac

• to membrane structure surrounding the lungs,

• inner membrane attached to lungs, outer membrane attached to thoracic all

• filled ith fluid

pressure difference beteen lung and pleural sac

• for the lung to remain inflated, the pressure in the pleural sac must be less than the pressure ithin the lung

• atmospheric pressure at sea level is 760 mm Hg, hich is the same as the pressure of the lungs. pressure in the pleural sac is 756 Hg mm

transmural pressure gradient

• pressure gradient across the chest all

• if the pressure becomes loer in the lungs, air ill rush into the lungs

pneumothorax

• disruption of pleural space can lead to collapsed lung

• if air enters the fluid layer, it loses its pressure and the lung collapses inwards

• can occur in lung diseases here inflammation causes blisters in the pleural sac, if one blister ruptures it disrupts the membrane

tension pneumothorax

• hen air entering the pleural space cannot exit so every time you breathe in the pressure gets higher and higher

• pressure on organs and heart, compress the heart

• need to pull the air out of the pleural space

Boyle’s la

• if pressure is halved, volume must be doubled

pressure changes during inhalation

• the volume of the lungs increases, decreasing the pressure

• intra-alveolar pressure decreases

• intrapleural pressure decreases (as the chest all is expanding, this pulls the intrapleural space ith it, increasing volume)

• air flows into the lungs

graph of pressure changes during inspiration

• V shape in alveolar pressure is due to initial drop in pressure when you first breathe in, but as air moves in, it re-equilibrates ith atmospheric pressure

pressure changes during expiraton

• lung volume must decrease

• intra-alveolar pressure must increase

• intrapleural pressure must increase

graph of pressure changes during quiet breathing

muscles used for breathing

• diaphragm

• 
  

quiet breathing (stage 1 breathing)

• should be able to breathe just using your diaphragm ithout the ribs expanding

stage 2 breathing

• recruit external intercostals (pull ribs out)

stage 3 breathing

• recruit sternocleidomastoids and scalenes hich lift ribs up and out

expiration

• normally passive, occurs due to passive elastic recoil of lungs and thoracic cage, saves energy

• muscles of expirationused only in forced breathing or voluntary exhalation, internal intercostals pull ribs in

reflex control of ventilation

• chemoreceptors in the brain detects CO2 levels (primary mechanism)

• other sensors detect O2 and pH

• high CO2 triggers respiratory centres in the brainstem to trigger outputs to respiratory muscles

neural networks that control ventilation

• higher brain centres

• medullary chemoreceptors

• other chemoreceptors and mechanoreceptors

• very complex as you have to regulate depth vs rate, vocalising, eating and swallowing

neural activity cycles during quiet breathing

factors that affect airay resistance

• upper airays more affected by physical obstruction because the cartilage keeps them open

• resistance in bronchioles dependent on bronchoconstriction and bronchodilation

formula for resistance

bronchoconstriction

• parasympathetic neurons (muscarinic receptors)

hat affects the ork of breathing?

• airay resistance (decreased airay diameter leads to increased airay resistance hich increases ork of breathing)

• lung compliance

lung compliance

• ability of lung to stretch

  • decreased lung compliance makes it harder to stretch the lungs, increasing ork of breathing

lung compliance vs elastance

lung compliance = ability of lung to stretch (inspiration)

lung elastance = ability of lung to spring back after being stretched (ho ell they can do passive expiration)

relationship between lung compliance and lung elastance

independent of each other

here is lung compliance affected?

• decreased in diseases such as pulmonary fibrosis hen inelastic scar tissue is formed hich reduces the ability of alveoli to stretch

here is lung elastance affected?

• decreased in diseases such as emphysema hen elastin fibres around alveoli are destroyed

ho does alveolar surface tension affect lung compliance?

• surface tension due to hydrogen bonds beteen ater molecules hich are more attracted to each other than gases at air-fluid interface

• attraction beteen ater molecules resists any force that increases its surface area, thus opposes expansion of alveolus creating surface tension

• liquid surface area tends to shrink due to attraction beteen ater molecules, thus reducing alveolus size

law of LaPlace

• the smaller the alveolus, the more inward pressure from the surface tension

• to prevent smaller alveoli from collapsing:

  • surfactant

  • alveolar interdependence

surfactant

• disrupt cohesive forces between water molecules and replace water at the surface, decreases surface tension and resistance of lung to stretch

• surfactant is more concentrated in smaller alveoli, decreasing surface tension and pressure

• produced by type 2 alveolar cells, higher proportion in smaller alveoli to make all the alveoli of the same compliance

alveolar interdependence

• the alveoli are all connected

• if one collapses, the others start pulling it outards

types of respiratory diseases

• obstructive

  • restrictive

obstructive lung diseases

• narrowing of lower airways

• increased airway resistance

• more difficult to expire

• issue ith the airays themselves which is reducing rate that you can move air, issue ith airflow

• e.g. asthma, emphysema, chronic bronchitis, COPD

restrictive lung diseases

• decrease in lung compliance, reduces volume you can breathe in as the lungs can’t stretch as well

• more difficult to inflate lung

• pulmonary fibrosis

spirometry

• measurement of lung volumes

tidal volume

• amount of air breathed in a normal quiet breath, around 500 mL.

• less than 10% of the air in your lungs is exchanged in one breath (the capacity is 5800 mL)

• left of graph

expiratory reserve

• the breath that you can continue to breathe out after a quiet expiration

• yellow

inspiratory reserve volume

• extra amount that you can inhaleafter a normal inhalation

vital capacity

biggest breath you can take

residual volume

• you can breathe out all you ant, but your lungs are still held open by your rib cage

• even when breathing our vital capacity, we do not exchange 100% of our breath, so the oxygen and carbon dioxide content ill never be equal to that of the atmosphere

can e measure residual volume?

• yes, using the helium dilution method

• fill the bell ith helium and oxygen, if you kno the intial concentration of helium and volume of the bell and the person breathes out of it for an extended period of time and the helium concentration equilibrates between their lung and the bell you can remeasure the concentration of helium and calculate the overall volume of the lung

forced expiratory volume in one second (FEV1)

• breathe all the ay in, and breathe all the air out as quickly as you can

• measure what percentage of the air you exhaled in the first second

• set up a FEV1/FVC ratio

• FEV1 = how much you breathe out in the first second

• FVC = total amount breathed out

• 80% is normal

• if there’s something wrong, there is an issue with the airways rather than the lungs as it is an issue with airflow

hallmarks of obstructive lung disease?

• FEV1 and FEV1/FVC are affected as there is a flow issue

• exhalation is usually more affected than inhalation, as exhalation causes increased pressure in the thoracic cage, so if your airays are already constricted to begin ith, this causes microcollapses of the airays hich traps air in the lungs

• vital capacity drops, trapping air in the lungs as it is harder to exhale because of the microcollapses of the airays, this means that residual volume therefore increases

types of COPD

• chronic bronchitis, asthma, emphysema

• all cause inflammation of the airways, causing them to narrow

• bronchitis has mucus

• emphysema = elastance is decreased

hallmarks of restrictive lung disease?

• total lung capacity decreases, as residual volume can’t decrease, this decrease comes out of the vital capacity

• therefore FVC also decreases, as does FEV1 as you have less air in total to be breathing out, so also less in the first second

• as FVC drops so much, there might sometimes be an increase in FEV1/FVC ratio

reduction in surfactant

• decreases compliance

• artificial surfactant can be given to babies ho don’t produce surfactant

• stimulate endocrine system to promote surfactant

anatomic dead space

• alveoli are the only sites in your lungs for air exchange

• conducting airays knon as anatomical dead space as the air there doesn’t reach the interface for exchange

• hen e breathe out, the atmospheric air gets kicked out, stale air fills the airays, hen e breathe in, e re-breathe in the stale air folloed by atmospheric air

• this volume is around 150mL

• as the total inhalation during quiet breathing is usually 500mL, the effective air moved is 350 mL

minute ventilation (Ve)

• total amount of air breathed in a minute

• tidal volume x respiratory rate

alveolar ventilation (Va)

• better measure of effective rbeathing

• (tidal breath - deadspace) x respiratory rate

• air reaching alveoli every minute

is there a functional difference beteen these situations?

• yes, an increase in alveolar ventilation is achieved more efficiently by increasing TV than frequency

normal breathing rate

500mL x 12 per minute, just uses diaphragm instead of other muscles such as intercostals, most efficient rate of breathing

• usually results in pulmonary ventilation 6 L/min, alveolar ventilation 4.2 L/min

maximum voluntary ventilation

125-170 L/min

eupnea

normal quiet breathing

hyperpnea

increased respiratory rate and/or volume in response to increased metabolism e.g. during exercise

hyperventilation

increased respiratory rate or volume ithout increased metabolism, if you breathe off too much CO2 you become alkalotic

dyspnea

difficulty breathing

apnea

cessation of breathing

breathing through a tube underater

• transmural pressure gradient: if pressure from ater is greater than air pressure breathed in, the lungs on’t be able to expand properly

• in scuba diving, the air is pressurised to match the ater pressure

• thinner tubes increase resistance

• ider tubes increase dead space