mechanisms of ventilation Flashcards
what is the function of respiration
provide O2 and remove CO2
5 ways the respiratory system achieves its goal (O2/CO2 exchange)
- pulmonary ventilation (air-> alveoli)
- regulation of ventilation
- matching of pulmonary blood flow to alveolar ventilation
- movement of O2 between alveoli and blood
- transport of O2 and CO2 in blood and body fluids
non respiratory function for the RT
foreign body expulsion (coughing); infection defense mechanism
how many mmHG are in 1 atm
760
pressure-force equation
P = F/A
what is BTPS
the condition of gases within the body - body temp (37), pressure, saturation (with water - 100% in alveoli)
what is ATPS
ambient temperature, pressure, saturation
what is STPS
standard temperature (0C/273K), pressure (1atm/760mmHg), saturation (0%)
what is Boyle’s law
P1V1=P2V2
what is Charles’ law
V1/T1 = V2/T2
what is the ideal gas equation
PV=nRT
how does air move in the bronchi
convection currents
how does O2 move from blood to cells
diffusion
what is Dalton’s law
total pressure = pG1 +pG2
(G is the gas)
=>
pG1 = n x total pressure
what is Henry’s law
total amount of gas dissolved in a liquid = partial pressure x solubility
how many generations of bronchi are anatomical dead space
16 - 17th is the first GE system
what is the bronchiole/alveolar duct structure and why is it significant
no cartilage, lots of smooth muscle; susceptible to collapse during expiration
why does the velocity of air rapidly decrease after generation 5
switch from convection to diffusion begins
what are the 2 blood supplies to the lungs
pulmonary arteries (deoxygenated), bronchial arteries (oxygenated)
where do bronchial arteries branch from?
aorta
where do the majority of bronchial arteries drain and what does this cause
into the pulmonary veins (carrying newly oxygenated blood) creating an admixture
what are pores of kohn
apertures in the alveolar septum, which allow the communication of two adjacent alveoli
transmitter, receptor and effect of cholinergic system on respiratory bronchial smooth muscle
transmitter: Ach
receptor: Muscarinic
effect: constriction
transmitter, receptor and effect of adrenergic system on respiratory bronchial smooth muscle
transmitter: adrenaline
receptor: B2 adrenergic
effect: dilate
transmitter, receptor and effect of peptidergic system on respiratory bronchial smooth muscle
transmitter: vasoactive intestinal peptide (VIP)/ substance P
receptor: VIP, Neurokinin
effect: VIP -dilate, neurokinin - constrict
what is tidal volume
the volume of air inspired/expired within one normal breath (500ml)
what is inspiratory reserve volume (IRV)
extra volume of air that can be inspired above tidal volume (2500ml)
what is expiatory reserve volume (ERV)
max extra volume of air that can be expired by force at the end of normal tidal breathing (1100ml)
what is residual volume (RV)
volume of air remaining in lungs after most forceful expansion (1200ml)
what can impact the IRV
current lung volume; lung compliance; muscle strength; comfort; flexibilty of the skeleton; posture
what is alveolar ventilation
the rate at which new air reaches the gas exchange areas
what is minute ventilation
the total amount of air breathed in in 1 min (TV x RR)
what is dead space air
air that is breathed in but never reaches the gas exchange areas, just fills the airways (nose, trachea, pharynx etc.)
alveolar ventilation rate equation
VA (alveolar ventilation) = RR x (TV - dead space volume)
what do the lung have a tendancy to do when not filled with air and why
collapse inwards due to their elastic structure
is the lung attached to the chest wall?
no - it floats in the thoracic cavity surrounded by a thin layer of pleural fluid that acts as a lubricant
how are the lungs held in the pleural cavity
lymphatic drainage of excess fluid between lung pleural membrane and pleural surface of the thoracic wall leads to a suction effect
what is the FRC determined by
the equilibrium of pressure between the lung and chest wall
what pressure is the pleural space under?
negative - chest wall naturally wants to recoil outwards, lungs want to collapse in
what does physiologically coupled mean
changes in one affects the other - lung, pleura and chest wall are physiologically coupled
what is the transpulmonary gradient
the difference between mean pulmonary arterial pressure and pulmonary capillary wedge pressure; determines alveolar size
transpulmonary gradient equation
TPG = alveolar pressure - intrapleural pressure (this is usually -ve)
where are alveoli largest and why
alveoli at the top (apex) are larger due to increased negative intrapleural pressure (meaning that TPG is larger for them); this is due to gravity as there is greater lung tissue below the apex for gravity to act on, so there is a large force pulling the lung away from the pleural space here - intrapleural pressure is more negative
when are alveolar apex largest (what position)
when stood up
describe the pressure changes during inspiration
at start of respiration pleural pressure is -5cmH2O -> rib cage pulls pleural cavity outwards and downwards -> pressure drops to -7.5cmH2O -> this is lower than outside pressure so air rushes in;
reversed in exhalation
what are the most important muscles for raising the ribcage (4)
external intercostals
sternocleidomasteoid (lift upward on sternum)
anterior serratus (lift many ribs)
scaleni (lift first 2 ribs)
what are the most important muscles for lowering the rib cage
abdominal recti
internal intercostals
what is the V/Q perfusion ratio
evaluates the matching of ventilation (V) to perfusion (Q) - normal is around 0.8
why is the V/Q ratio different for different areas of the lungs
V: alveoli are larger at the apex and smaller at the bases - while this means that ventilation acc increases at the base rather than the apex, the ratio of perfusion increase is so great in the base that the V/Q ratio is actually decreased in the bases and increased in the apex
Q: apex of the lungs is well above the level of the heart while the base is below it => blood flow to the apex is decreased due to gravity => decreased perfusion in apex (and vice versa for base)
what is “pump handle” breathing
movement of the diaphragm to allow for inspiration/expiration (change in anterioposterior diameter of the chest) - rib moves in a pump handle like motion
what is “bucket handle breathing”
movement of the ribs that allows for lateral throacic expansion
where is V/Q highest and lowest in the lungs
highest - apex
lowest - base
examples of conditions that decrease the V/Q ratio (3)
pneumonia; COPD (although in late stage the capilaries are damaged so perfusion also decreases and ratio balances out); pulmonary odema
examples of conditions that increase the V/Q ratio (3)
late stage COPD (capillary damage); pulmonary embolism;
what is absolute physiological/pulmoary shunt
when there is perfusion but no ventilation - re-diversion of blood from its usual path through pulmonary circulation.
what is an absolute dead space (in alveoli)
gas enters the alveoli but there is no gas exchange (bc no perfusion)
what are the accessory muscles used for deep breathing
scalene; sternocleidomastoid; pectoralis major; trapezius; external intercostals; abdominals (rectus abdominis, external oblique, internal oblique, and transversus abdominis)
what is the average amount of air pulled into the lungs during inspiration
0.5L
what is static lung compliance
pulmonary compliance when there is no airflow, like an inspiratory pause - the extent to which lungs will expand for every unit increase of transpulmonary pressure
lung elastance equation (measure of elastic recoil)
E=1/C
E is elastance, C is compliance - AKA high compliance = low elastic recoil
lung compliance equation (lung volume, trans pulmonary pressure)
C = ΔV/ΔTPP
what 2 elastic forces determine compliance
- elastic forces of the lung tissue itesslf (elastin and collagen fibres among lung parenchyma, deflated lung fibres are contracted and kinked)
- elastic forces caused by surface tension of fluid that lines alveoli
what spirometry values are decreased in pulmonary fibrosis
RV, FRC, TLC
what happens to lung compliance in pulmonary fibrosis
decreases - smaller than normal change in Lung volume for the same pressure change
what happens to lung compliance in COPD
increaes - larger than normal changes in lung volume for the same pressure change (airways may collapse inwards on expiration)
what is hysteresis and why does it happen in the lung
the phenomenon in which the value of a physical property lags behind changes in the effect causing it;
The lung is an imperfect elastic body and for this reason dissipates energy; The energy applied to the lung in inspiration is not recovered in expiration. The property of dissipating energy receives the name of hysteresis
what happens to hysteresis if the lungs are filled with water
the gradient of the graph is steeper due to reduced surface tension (water/air interphase removed) and s hysteresis disappears
what is surface tension
a measure of the force acting to pill a liquid’s surface molecules together at an air-liquid interphase;
the wate-air interphase means that the H2O molecules at the surface aren’t H-bonding with with air molecules leaving one side unbalanced -> creates a cohesive force between these surface water molecules which causes them to reduce to the smallest SA possible (hence inward collapsing force on the alveoli)
what is the consequence of surface tension in the lungs
water lines the alveoli, creating surface tension and so this will result in the alveoli trying to collapse as the force of surface tension draws them in
what stops the alveoli collapsing (normal lung) and how
surfactant - this is a phospholipoprotein layer that acts to decrease surface tension, it consists of DPPC, and some proteins e.g. surfactant proteins A and D
what is La Place’s law
the pressure within the alveolus is dependent on the surface tension of fluid (T) and radius of alveolus
P = 2T/r
what cells release surfactant
type II alveolar pneumocytes - cuboidal cells that contain lamellar bodies
how is surfactant produced
lipid components enter type II cells from bloodstream -> secreted by type II cells
how does DPPC reduce surface tension
due to its amphipathic nature - hydrophilic phosphate + amine group, attached to two hydrophobic 16-carbon saturated chains ->
The hydrophilic end adheres to the surface of the water film that lines the alveolar wall, while the hydrophobic tails float in the air towards the center of alveoli - the lack of attractive forces between hydrophobic tails reduces the surface tension
how is surfactant degraded
with the aid of alveolar macrophages; the rest is taken up and recycled/destroyed by type II cells
how does surfactant affect the speed of alveolar expansion
rapid expansion - alveolus expands rapidly reducing the surface density of surfactant meaning that surface tension and elastic recoil rise => expansion stopped
slow expansion - surfactant is less diluted and so there is less resistance against expansion here and the alveolus continues to expand
what are the dynamic components that must be over come to allow for respiration
inertia and resistance of tissues and air molecules
pressure/flow/reisitance equation
R=P/F (a version of Ohm’s law where V is P, I is F)
airway resistance equation (Hagen-Poiseuille’s law)
R = (8μl)/πr^4 ;
where μ is dynamic viscosity and l is the length of tube
airways resistance in healthy people
<1.5 cmH20/L/s
which airways have the most resistance
major airways - trachea
how does alveolar tethering reduce resistance
alveolar attachments that transmit an outward force on these airways, which increases as the lungs expand - increasing outward force increases airway radius, thus decreasing airway resistance
total effort equation
total effort = -ve TPG (static component, overcoming elastic forces, maintaining current lung volume) + alveolar pressure(dynamic component, overcoming resistance and inertia, producing airflow)
what systems are involved in voice production (4)
respiratory; CNS (specific speech centres in brain); respiratory centres in brain; mouth/nasal cavities (articulation and resonance structures)
what is the primary function of the layrnx
protect the tracheobronchial tree
what structures are involved in preventing food/saliva entering the respiratory tract
vocal chords + epiglottis sphincter action
what nerves supply the laryngeal muscles
cricothyroid - superior laryngeal nerve
all other muscles - recurrent laryngeal
what are the afferent (sensory) nerves for the glottis, subglottis and supraglottis
glottis + subglottis - recurrent laryngeal;
supraglottis - superior laryngeal
function of the larynx during phonation
acts as a vibrator - vocal chords are the vibrating elements, they protrude from the lateral walls of the larynx towards the centre of glottis; during phonation the chords move together so the passage of air between them causes vibration, the pitch is determined by stretch of chords
what are the 3 major articulation organs and the 5 resonators
articulation - lips, tongue, soft palate;
resonators - mouth, nose, associated nasal sinuses, pharynx, chest cavity
