Physiology Flashcards
what is lung compliance
- distensibility of lung
, ability to swell under pressure
increased lung compliance
- less elastic fibres
- less recoil
- hard to expire
e. g. COPD
decreased lung compliance
- fibrosis/ scarring
- more effort to expand
- breathless
- oedema, pneumothorax
inspiration overview
active process
air into lungs
Expiration overview
air out of lungs
passive/ active process
elastic recoil/ accessory muscles
Control of breathing + nerve origination
phrenic nerve
C3 - C5
Inspiration muscles
Diaphragm - contracts - inferiorly
External costal muscles
- out + up
bucket handle
passive expiration muscles
relaxation of diaphragm + elastic recoil
Active expiration muscles
abdominal wall + internal costal muscles
Process of inspiration
- Phrenic nerve innervation
- Diaphragm contracts
- Decrease in pleural pressure
- Lungs expand
- Air in
Keeps lungs inflated
Intra -pleuric cohesiveness - water in pleural space attracts each other Negative pressure - pleural space has -ve pressure pressure grad., keeps inflated
Pneumothorax
Air into pleural cavity
- increases pressure
No pressure gradient
- lung collapses
passive Expiration process
- decreased phrenic nerve innervation diaphragm relaxes increase in pleural pressure elastic recoil air out
Active respiration
diaphragm relaxes + internal costal muscles contract + abdominal wall contracts
- increased pleural pressure (become +ve)
forces air out lungs
- dynamic collapse
alveolar pressure = to
pleural pressure + elastic recoil pressure
Elastic recoil
- elastic fibres in membrane
- decreases as less stretched
Dynamic Collapse
Positive pressure from active respiration
- Transmural pressure = -ve
- inward pressure on airway
exacerbated if decreased airway pressure
Causes a collapse
- Increases pressure behind collapse
- Airway re opened - pressure grad.
Emphysema + dynamic collapse
decreased elastic recoil (swollen alveoli)
- decreased transmural pressure
- airway more likely to collapse
Alveolar collapse
inward pressure = 2x surface tension/ radius - more likely in smaller alveoli - surfactant = amphipathic reduces tension via repulsion Alveolar independence - one alveoli collapses rest = stretched, elastic recoil, open
Tidal Volume
- normal expiration
0,5L
Vital Capacity
- volume expired after max inspiration
4. 5 L
Inspiratory reserve volume
- volume inspired after tidal volume
- 3L
expiratory reserve volume
- volume exhaled after tidal volume
1L
residual volume
- remaining air in lungs volume
1. 2L
Total lung capacity
Vital capacity + residual volume
= 5.7L
Functional reserve capacity
total air left in lung after tidal volume
- 2.2L
Forced Vital Capacity
- volume of air forcibly exhaled after maximum inhalation
Forced expiratory volume 1
- max air expired 1 second after max inhalation
FEV1/FVC ratio + features of abnormalities
70% = normal <70% = obstructive airway disease - can't expire (narrow lumen) 70% but low FVC + FEV1 = restrictive (cant inflate)
Physiological dead space
anatomical + functional dead space
Anatomical dead space
- recycled air/ not used air
e. g. airways
Functional dead space
- air not diffused
e. g. no blood supply
alveolar resp.
(tidal volume - dead space) x resp. rate
Diffusion - air -> blood
ideal 1:1 ratio - not likely, gravity apex < base lung - vasodilation perfusion/ diffusion limited
perfusion limited O2 uptake
- sub optimal conditions due to inadequate blood supply
determined by unbound gas (no partial pressure if bound)
diffusion limited O2 uptake
- dependent on a diffusion factor e.g. size of membrane
Dead Space
- air not available for perfusion
- anatomical/ functional
anatomical dead space
- air in airways
can’t be perfused into blood
functional dead space
- insufficient blood supply
perfusion limited
4 factors effecting gas perfusion
- partial pressure of gas
- Surface Area
- Thickness of Membrane
- Solubility in membrane
Features of O2 dissociation curve
- sigmoidal
high O2 uptake at slightly low O2 conc. - keeps O2 sats high
Bohr effect
graph moves to right
- increased dissociation of O2 in tissue + uptake in lung
CO2, H+ conc., temp, 2,3 bisphosphoglycerate
Oxygen delivery index =
cardiac output x O2 arterial content
foetal haemoglobin
2 alpha, 2 gamma sub units
higher affinity for O2
- picks up O2 from mother
- less reactive to 2,3 bisphosphoglycerate
Myoglobin
in muscles
carries 1 O2
short term relief of anaerobic conditions
Haldane effect
No O2 bound
- globin has high affinity for CO2
O2 has greater affinity - displaces CO2
- CO2 removal, lungs
Reduce effects of dead space
Heavy deep breathing
Alveolar gas equation
Partial pressure O2 in air - (partial pressure CO2/0.8)
PO2 arterial + alveolar
small grad. = normal
large grad. = circulatory problem
Henrys law
Gas dissolved in liquid = proportional to partial pressure of gas
O2 arterial blood content
1.34 x haemoglobin conc. x 5 saturation
Oxygen delivery Index
Arterial O2 content x Cardiac Output
3 methods of CO2 transport
- plasma
- bicarbonates
- Carbamino Compounds
CO2 transport in plasma
Henrys law
- proportional to partial pressure + solubility
only unbound gas
Bicarbonates
In RBC carbonic anhydrase catalyses:
CO2 + H2O H2CO3 H+ + HCO3-
- bicarbonate exchanged for Cl-
in RBC
Carbamino compounds
CO2 binds to globin
- doesn’t affect partial pressure, bound CO2
Control Of respiration - 2 forms
neural
chemical
Neural control - rhythm
medulla
Pre botzinger complex
- innervates dorsal respiratory group neurones
Stimulation of inspiration
pre botzinger complex causes innervation of diaphragm via dorsal respiratory group neurones via phrenic nerve
Pneumotaxic centre function
- Inhibits dorsal respiratory group neurones, allows respiration
activated by dorsal neurones - ve feedback
Apneustic centre function
Prolongs inspiration
- excites dorsal respiratory group neurones
Expiration
Pre botzinger complex inhibits dorsal respiratory centre innervation of phrenic nerve
- relaxation
Active expiration
- ventral respiratory group neurones stimulated
innervation of internal intercostals + abdomen
Apneusis
Respiration - no pneumotaxic centre
long inspiration, short expiration
hering Breur reflex
Prevents hyper inflation
- inhibits inspiration
Chemical control of respiration mechanisms
Negative feedback of central + peripheral chemoreceptors
Location of central chemoreceptors
- surface of medulla
Main mechanism of resp. control
- H+ ion conc. in CSF via central chemoreceptors
Process of resp. control via central chemoreceptors
- CSF = impermeable to H+ + HCO3- ions very permeable to CO2 CO2 dissolves in H2O produces increased H+ ions low protein levels - low buffering
Peripheral control of respiration
senses PaO2, PaCO2 + Pa H+
Peripheral control - changes in Pa CO2
Hypercapnia - High CO2 increase ventilation expel more CO2 Hypocapnia - acidaemia - decreases ventilation decreases CO2 expelled prevents alkalaemia - process ineffective in severe chronic COPD
Peripheral chemoreceptor control of PaO2
Detects very low O2 levels
Hypoxaemia
very low PaO2
- increase ventilation
Mechanism of cough initiation signalling
Afferent signals
-cough receptors on posterior trachea + pharynx + carina
internal laryngeal nerve -> superior laryngeal nerve -> vagus nerve
Mechanism of cough signalling - efferent
Contraction of diaphragm + external intercostals - short breath in Closure of larynx - rima glottis shut by vocal chords - active expiration contraction of abdomen + internal intercostal muscles - larynx opens - air expulsed
