The Respiratory System Flashcards
lecture 13 and 14 week 7
What is the basic structure of the lungs
- lungs are inside the ribcage
- 23 generations of airways between alveoli and outside air
- around 300 million alveoli in adult lungs creating a surface area for gas exchange around 60-80m2
- trachea and primary bronchi held open by c-shaped rings of cartilage, smaller bronchi by overlapping plates of cartilage and no cartilage in bronchioles
- smooth muscle is present in the walls of airways
What is Boyle’s law
- the pressure exerted by a gas is inversely proportional to its volume
inspiration: increased lung volume —> pressure in lungs falls below atmospheric pressure —> air flows in
expiration: reduction of lung volume —> pressure in lungs rises —> air flows out
How are the lungs held open
- interpleural pressure holds the lungs open
the elastic recoil of the chest wall tries to pull chest wall outwards
the elastic recoil of the lungs creates an inwards pull
the pull in opposite directions creates a negative/sub atmospheric pressure
What are the muscles used in respiration
main muscles in pulmonary ventilation are intercostal muscles and diaphragm
inspiration: active process, muscles contract
expiration: passive process, muscles relax
inspiration: thoracic cavity expands, external intercostal muscles contract, diaphragm contracts
expiration: thoracic cavity reduces, external intercostal muscles relax, diaphragm relaxes
What are the factors affecting pulmonary ventilation
- elastic recoil/pulmonary ventilation
- airway resistance
What is elastic recoil/lung compliance
elastic recoil
- the ease in which the lung rebounds after stretching
compliance
- ease in which the lungs stretch/expands
- these are inversely related
compliance is mainly determined by elastic fibres in lung tissue and alveolar surface tension, the fibres are present in connective tissue
alveolar surface tension is reduced by surfactant secreted by alveolar type ii cells
What is air way resistance
- airflow is inversely proportional to resistance
- resistance depends on tube diameter and type of flow
- resistance highest at medium-sized bronchi, as even though small airways have greater resistance the combined surface-area means a lower resistance
What are the pressure changes during breathing
at rest: interpulmonary pressure =atmospheric pressure, negative interpleural pressure
inspiration: as thoracic cavity expands, interpleural pressure decreases, causing lungs to expand, decreasing intrapulmonary pressure. air then flows into the lungs and intrapulmonary pressure slowly reaches atmospheric pressure
expiration: decrease of thoracic cavity volume, increases intrapleural pressure, lung volume decreases due to elastic recoil, intrapulmonary pressure then increases and air flows out of the lungs until intrapulmonary pressure = atmospheric pressure
What does a spirometry do
- measures lung volume
when using a bell spirometry
inspiration: air from bell, upwards movement on chart
expiration: lifts inverted bell, downwards on chart
How are gases exchanged for respiration
- gas exchange between alveoli and capillaries occurs by diffusion
- gases diffuse from a region of high partial pressure to a region of low partial pressure
What is Fick’s law of diffusion
- describes the rate of transfer of a gas through a sheet of tissue
dV/dT = A/T x D x (P1-P2)
How is oxygen transported in the blood
- oxygen solubility in blood is low 3ml O2/l blood so not enough to support the body
- haemoglobin increases capacity of blood to transport oxygen to 5 litre/ minute so sufficient supply to the body
What is the structure of haemoglobin
2 alpha-chain and 2 beta-chains with a heme group
- each Fe2+ can reversibly bind one molecule of oxygen (oxyhaemoglobin)
What is a haemoglobin oxygen-dissociation curve
sigmodial shaped curve from cooperative O2 binding
- binding of one O2 molecule leads to conformational change of haemoglobin that increases binding affinity of remaining heme group for additional O2
high partial pressure: flat curve —> drop in PO2 leads to little change in saturation
low partial pressure: steep curve —> facilitates release of O2 for diffusion into tissues
How is carbon dioxide transported into the blood
- CO2 diffuses from tissues into blood vessels —> some CO2 binds to haemoglobin —> this releases carbonic anhydrase in red blood cells which catalyses C02 + H2O <—> H2CO3 reaction
- H2CO3 dissociates into HCO3- and H+, HCO3- is exchanged for Cl- and H+ is buffered by haemoglobin
in the body
CO2 gas, HCO3- and carbamino (CO2 + amino acid from haemoglobin)
How is breathing controlled
- respiratory muscles have NO intrinsic rhythmic control
- a group of neurones located in the pons and medulla (brainstem) discharge action potential with an intrinsic rhythm corresponding to respiratory cycle. neurons activate neurons of the phrenic and intercostal nerves and activate intercostal muscles and the diaphragm
What is the effect of blood gases on breathing
- peripheral and central chemoreceptors sense changes in PO2 + PCO2 and pH
- signals are sent to respiratory centers to adjust rate and depth of ventilation
How do peripheral chemoreceptors work
- carotid and aortic bodies are main peripheral chemoreceptors
i. glomus cells in carotid bodies detect low PO2 in blood vessles
ii. K+ channels close in response to the low PO2
iii. cell depolarisation occurs
iv. voltage-gates calcium channels open
v. Ca2+ enters the cell
vi. the influx of Ca2+ triggers exocytosis of vesicles containing neurotransmitters
vii. neurotransmitters bind to receptors on sensory neurons, leading to cation potential generation
viii. sensory neurons stimulate neurones of respiratory centres to increase ventilation rate and depth
How do central chemoreceptors work
- located on ventral surface of medulla, respond to changes in pH of cerebrospinal fluid (CFS)
- CO2 can diffuse from blood to CFS, in CFS reactions lead to the formation of H+
- higher partial pressure of CO2 in CFS, more H+ produced which causes a lower pH
-H+ stimulates central chemoreceptors which sends signals to respiratory centres increasing ventilation
How is breathing controlled
higher brain centres modulate respiratory activity for non-respiratory activities eg. swallowing
streton receptors in smooth muscles of upper airways protect lungs from overinflation
irritant receptors respond to chemical/mechanical irritation, activation induced coughing and bronchoconstriction
receptors in muscles and joints that are activated when muscles contract have stimulatory effect on ventilation
ventilation can also be modulated as a response to emotional stimuli and pain
What are the pulmonary defense mechanisms
- mucus produced by mucous cells inside ciliated columnar epithelial and movement of cilia slowly moves mucus to pharynx where it is swallowed. any particles reaching alveoli are phagocytosed by alveolar macrophages
- some material is also trapped in the nasal cavity
What are the two different types of lung disease
obstructive
- airway obstruction increases resistance to air flow eg. COPD (chronic obstructive pulmonary disease)
restrictive
- reduced compliance limits expansion eg. pulmonary fibrosis
What is COPD and the effects of COPD
- causes tobacco smoke, air pollution, some genetic factors
continual bronchial irritation and inflammation —> CHRONIC BRONCHITIS (excessive mucus, chronic productive cough) —> airway obstruction, dyspena, frequent infection —> respiratory failure
breakdown of elastin in connective tissue of lungs —> EMPHYSEMA (destruction of alveolar walls, loss of elasticity) —> airway obstruction, dyspena, frequent infection —> respiratory failure
What is the cause of pulmonary fibrosis and the effects
- cause is unknown in most cases, but thought to be from infection or autoimmune disorders
scars form in lung tissues causing a thickening of the alveolar walls which impairs O2 diffusion
- the stiffness leads to decreased compliance (stretch and expansion of lungs)
