chapter 38 guyton Flashcards
Enlist the muscles of inspiration and expiration in quiet breathing Enlist the muscles of inspiration and expiration in labored breathing Explain the components of the work of breathing Discuss the mechanics of pulmonary ventilation Explain periodic breathing Explain the causes and pathophysiology of sleep apnea
what are the two ways in which the lungs expand and contract?
- diaphragm
- ribs
how is diaphragm used in normal quiet breathing?
- inspiration: contraction pulls lower surfaces of lungs downwards, increases V, dec P, air flows in
- expiration: relaxes; elastic recoil of lungs, chest wall and abdominal structures compresses the lungs and expels air
muscles of inspiration
- external intercostals
- sternocleidomastoid
- trapezius
- pec major and minor
- scaleni
- anterior serrati
PASTES
muscles of expiration
- internal intercostals
- abdominal muscles
- push on lungs, compress, force exhalation
pleural pressure and its changes in inspiration
- pressure of the fluid in thin space between lung pleura and chest wall pleura.
- beg of insp -5cmH2O; amount req to hold lungs open to resting level
- inspiration: -7.5cmH2O
- lung V inc by 0.5l
alveolar pressure
- air pressure inside the lung alveoli
- glottis open: 0cmH2O
- inspiration: -1cmH2O
- expiration: +1cmH2O
transpulmonary pressure
- difference between pleural pressure and alveolar pressure.
- measures elastic forces trying to collapse lungs at each point in inspiration , called recoil pressure
lung compliance
- extent to which lungs will expand for every unit increase in transpulmonary pressure
- total in both lungs 200ml/cmH2O
what cells secrete surfactant
type 2 alveolar epithelial cells
surfactant composition
dipalmityl phosphatidylcholine, surfactant apoproteis and calcium ion.
how does surfactant work
- parts of llipoproteins dissolve while the rest spreads over surface of water in alveoli
- has 1/12th to 1/2 of surface tension of pure water
formula for pressure in occluded alveoli
p=(2*surface tension)/ radius of alveolus
why do premature infants have increased risk of alveolar collapse
- smaller radius = increased pressure
- surfactant produced b/w 6th and 7th month of gestation, so premature = extreme tendency to collapse
- causes RDS of newborn - needs to be treated with continuous positive pressure breathing
components of work of breathing
-compliance/elastic work: work req to expand lungs against lung and chest elastic forces
- tissue resistance work: “ overcome viscosity of lung and chest wall
- airway resistance work: req to overcome airway resistance to movement of air into lungs
mnemonic: CAT
what are 4 pulmonary volumes and what happens if you add them together
- tidal
- inspiratory reserve
- expiratory reserve
- residual
- mnemonic TIRE
- gives maximum volume to which lungs can be expanded
tidal volume
v of air inspired or expired with each normal breath
- around 500ml for avg male
inspiratory reserve
- extra v of air that can be inspired over and above normal tidal when inspires with full forces
- 3000ml
expiratory reserve volume
- max extra vol of air that can be expired with forceful expiration after enf of normal tidal expiration
- 1100ml
residual volume
- vol of air remaining in lungs after the most forceful expiration
- 1200ml
inspiratory capacity
tidal + inspiratory reserve
functional residual capacity
- expiratory reserve + residual
- amount of air that remains in the lungs after normal expiration
vital capacity
- inspiratory reserve + tidal + expiratory reserve
- max amount of can expel after max inspiration and max expiration
total lung capacity
- vital capacity + residual volume
- max vol lung expanded to greatest possible effort
minute respiratory volume
- tidal volume x respiratory rate per minute
- gives total amount of air moved into lung passages each minute
what us alveolar ventilation
- rate at which new air reaches gas exchange areas
what is dead space air
air that fills nose, pharynx etc not gas exchange areas
why is dead space disadvantageous for expiration
- because its removed first, before the gaseous exchange air
value of normal dead space volume
- 150ml for young man
- increases slightly with age
anatomical vs physiological dead space
- anatomical measures volume of all space in respiratory system except alveoli and closely related gas exchange areas
- some alveoli non functional bc of absent/poor blood flow through adj capillaries, so also considered dead space
- anatomical dead space + dysfunctional alveoli dead space = physiological dead space
anat + physiological dead space in healthy humans vs diseased
- in healthy almost equal as all alveoli are functional
- in diseases physio can be 10x anat
alveolar ventilation
- respiratory rate per min x (tidal volume - phys. dead space)
- VA=freq*(VT-VD)
describe cough reflex
- afferent nerve impulses from vagus nerve to medulla
- up to 2.5litres of air rapidly inspired
- epiglottis closes, vochal cords shut tightly to trap air
- abdominal muscles contract forcefully
- internal intercostals also contract forcefully
- pressure rises rapidly to 100mmHg or more
- vocal cords and epiglottis suddenly open widely, air explodes outwards
describe sneeze reflex
- afferent impulses in 5th cranial nerve to medulla
- same as cough reflex, but uvula is depressed so large ampunts of air can pass rapidly through the nose
functions of lungs beyond respiration
systolic pulmonary arterial pressure
25mmHg
diastolic pulmonary arterial pressure
8mmHg
mean pulmonary arterial pressure
15mmHg
what is pulmonary wedge pressure
- pressure measured through catheter inserted into pulmonary artery until its wedged tightly
- 5mmHg
what happens in hypoxia conditions in alveoli
- vessels constrict, allow blood to flow to areas with sufficient oxygen where its more effective
- opposite in systemic vessels
zone 1 of lung
- no blood flow during all parts of cardiac cycle; capillary pressure never rises above alveolar
- only present in pathological conditions where pulmonary systolic pressure is too low or alveolar pressure is too high
– e.g. if breathing against positive air pressure, or severe blood loss
zone 2 of lung
intermittent blood flow during systole but not diastole
zone 3 of lung
continuous blood flow bc capillary pressure is greater than alveolar throughout the cardiac cycle
what happens to zones in lung during exercise
- pulmonary vascular pressures increase enough to convert zone 2 into zone 3
how do the lungs accommodate extra blood flow during heavy exercise
- increasing no. of open capillaries
- distensing capillaries, increasing rate of flow
- increasing pulmonary arterial pressure
– usually only 1st 2 required so art. pressure rises very little
— conserves energy of right side of heart
— prevents inc pulm capillary pressure and pulm oedema
how does left sided heart failure affect the heart and lungs
- left ventricle cant pump blood efficiently
- blood dams in left atrium
- pressure rises in left atrium
- transmitted backwards into pulmonary veins
- pulmonary venous congestion
- transmitted into pulmonary capillaries
- after 7/8mmHg, any increase in LA = concomitant increase in pulmonary arterial pressure
- causes increased load on right side of heart
- above 30mmHg = pulmonary oedema
- leads to hypoxia and hypercapnia
- hypoxic vasoconstriction further worsens right side of heart and left
- vicious cycle
normal left atrial pressure
+6mmHg
how long does blood stay in pulmonary capillaries
- 0.8s
- 0.3s in heavy exercise
causes of pulmonary oedema
- L-sided heart failure or mitral valve disease inc pulmonary capillary pressure - flooding of interstitial spaces and alveoli
- damage to pulmonary blood capillary membranes due to infections eg pneumonia or breathing noxious gases like chlorine gas or sulfure dioxide
concept of safety factor
capillary pressure must rise to value at least equal to colloid osmotic pressure of plasma inside capillaries before significant pulmonary oedema occurs
acute safety factor against pulmonary oedema
21mmHg
chronic safety factor against pulm oedema
- lungs become more resistant to oedema after chronically elevated capillary pressures as lymph nodes expand greatly
how long until high capillary pressures become chronic
2 weeks
what is a respiratory unit
- aka resp lobule
- respiratory bronchiole
- alveolar ducts,
- alveolar atria
- alveoli
how are co2 o2 and no limited in resting conditions
they are perfusion limited
how are co2 and o2 limited in strenous exercise
they are diffusion limited
what are the layers of the respiratory membrane?
- fluid surfactant
- alveolar epithelium
- epithelial basement membrane
- interstitial space
- capillary basement membrane
- capillary endothelium
- red blood cell - has to squeeze through capillary as theyre so narrow, meaning less diffusion distance for gases as its close to membrane
factors affecting diffusion rate through respiratory membrane
- thickness of membrane
- surface area of membrane
- diffusion coefficient of gas
- partial pressure difference of the gas between 2 sides of membrane
what causes thickness of respiratory membrane
- edema fluid in interstitital spaces; gas now has to diffuse through that as well
- pulmonay diseases can cause fibrosis - inc thickness
what causes decrease in surface area of respiratory membrane
- removal of entire lung
- emphysema; alveoli coalesce, walls are destroyed, reduces total surface area
what is the diffusing capacity
volume of gas that will diffuse through the membrane each minute for a partial pressure difference of 1mmHg
diffusing capacity of oxygen
21ml/min per mm Hg
- gives a total of 230ml
diffusing capacity of co2
- cant be directly measured as co2 diffuses so fast
- diffusion coefficient 20x that of o2 so 400-450ml/min per mmHg
types of VA/Q
- normal; ventilation and perfusion is normal
- zero; ventilation zero, still perfusion
- infinity; ventilation, zero perfusion
what condition causes physiological shunt
- VA/Q less than normal (approaching zero)
- blood not ventilated
- upper part of lung
- bronchial obstruction due to smoking
what condition causes physiological dead space
- VA/Q more than normal
- more o2 than can be carried in blood, so wasted
- lower part of lung
- emphysema; alveolar walls destroyed, inadequate blood flow to transport the gases
composition of alveolar air and atmospheric air are:
- different as alveolar air only partially replaced with atmospheric with each breath
- o2 constantly absorbed from alveoli, co2 added
- dry atmospheric air humidified before reaching alveoli
