Pulmonary ventilation Flashcards
gas exchange
the process involved in the movement of O2 from the air to cels and CO2 from cells to the air
trachea and bronchi in airways
cartilage to prevent them from collapsing
bronchioles
smooth muscle to regulate air flow
alveoli
large surface area for gas exchange (lots of them)
conduction zone (dead space)
where there is no gas exchange occurring
what does happen:
- warm the air
- humidify the air
- remove particle from the air
respiratory zone
where gas exchange occurs (at alveoli)
Pbar (barometric pressure)
pressure outside of the lungs
always set to 0
alveolar pressure
pressure compared to air Pbar (which is always 0)
negative alveolar pressure
air flows into the lungs (inspiration)
positive alveolar pressure
air flows out of the lungs (expiration)
pleural pressure
fluid filled area between lung and chest wall
pleural pressure is always (+ or -)
negative
pleural pressure is negative because
lungs want to collapse inward
chest wall wants to expand outward
negative pleural space pressure keeps the lungs
inflated
pneumothorax
hole in the chest wall, air into the pleural space
- pleural pressure goes to 0
- lungs and chest wall no longer connected (lung collapses, chest wall expands outward)
main muscle of respiration
diaphragm
during inspiration diaphragm will
contract and pull down
during expiration the diaphragm will
relax and push up
mechanics of breathing
increase in volume causes a decrease pressure
increase in volume of chest cavity causes decrease in lung pressure
normal inspiration
contract diaphragm - pulls down - increase volume of chest cavity - decrease lung pressure - air into lungs
increased inspiration
contract EXTERNAL intercostal muscles , contract accessory muscle in neck - chest wall pulled up and out - increased volume of chest cavity - decrease lung pressure - air into lungs
normal expiration
relax diaphragm - moves up - decreased volume of chest cavity - increased lung pressure - air out of lungs
increased expiration
contract INTERNAL intercostal muscles - chest wall pulled down and in - contract abdominal muscles - intestines pushed up - decreased volume of chest cavity - increased lung pressure - air out of lungs
increased expiration
contract INTERNAL intercostal muscles - chest wall pulled down and in - contract abdominal muscles - intestines pushed up - decreased volume of chest cavity - increased lung pressure - air out of lungs
increased expiration
contract INTERNAL intercostal muscles - chest wall pulled down and in - contract abdominal muscles - intestines pushed up - decreased volume of chest cavity - increased lung pressure - air out of lungs
in tidal volume each breath is about __ L
0.5
air in is (+ or -) flow
negative
air out is (+ or - ) flow
positive
why is pleural pressure most negative at the end of inspiration
the pleural pressure is at equilibrium with the outside air (Pbar)
tidal volume
amount of air moved each breathe (0.5L)
expiratory reserve volume
extra amount that can be expired after a normal expiration
inspiratory reserve volume
amount of air that can be inspired after normal inspiration
residual volume (RV)
amount of air that always remains in the lungs (1 L)
vital capacity (VC)
total amount of air that can be moved
tidal volume + inspiratory res. vol + expiratory res. vol
5 L
total lung capacity (TLC)
vital capacity + residual volume
6 L
forced vital capacity (FVC)
vital capacity as fast as possible (5 L)
forced expiratory volume in 1 second (FEV1)
the amount that can be expired in the 1st second
FEV1 / FVC
how much of total forced expiration occurs in the first second (used clinically)
normal FEV1/FVCis
4L/5L or 0.8 which is expressed at 80%
normal numbers
FVC = 5L
RV = 1 L
TLC = 6L
FEV1/FVC = 80%
obstructive disorder
person cannot get air out of lungs (expiration)
increased RV and decreased FEV1/FVC, FVC
emphysema
loss of alveoli, loss of elastic recoil
lungs lose ability to collapse
restrictive disorder
cannot get air into lungs (inspiration)
decreased TLC, decreased FVC
fibrosis (scar tissue in lungs) / edema (fluid in lungs)
difficulty getting air into lungs
asthma
reversible airway constriction
primarily obstructive
- forced expiration through constricted airways (airway collapse) which means air is harder to get out
treatment of asthma
beta 2 receptor agonist (epinephrine)
- cause airway dilation
if blood flow is blocked to part of the lungs, then there would be an
alveolar dead space
total ventilation
amount of air moved/minute
Vt = tidal volume X frequency of breathing
alveolar ventilation
amount of air moved that is involved in gas exchange/minute
Va = (tidal volume - anatomic death space) X frequency of breathing
is it better to breathe deep and slow or fast and shallow
deep and slow; because of dead space, deep and slow breathings more effective at ventilating alveoli
resistance decreases dramatically as
radius increases
the greatest total resistance is in the
large bronchi
the most important resistance in the ____ because
bronchioles, they have smooth muscle so they can be regulated
parasympathetic nervous system control of airway
ACh acting on mACh receptors cause airway constriction
sympathetic nervous system control of airway
Ep acting on beta2 receptors causes airway dilation
decreased ___ causes airways constriction
CO2
when blood flow decrease to the lungs, CO2 in the lungs
decreases, causes airway constriction
decreased blood flow causes
decreased airflow
increased compliance
large change in volume for a change in pressure
easy to inflate hte lungs
decreased compliance
small changes in volume for a change in pressure
difficult to inflate lungs
to generate greater pressure difference there is
increased work of breathing
why can increased compliance be bad
there is high compliance but a problem getting air out of the lungs
- increased residual volume, barrel chested
surfactant
lipoprotein made by type II alveolar cells
- gets between water molecules decreasing surface tension and intros way preventing alveoli from collapsing
surfactant decreases surface tension more in ___ which allows for different sized alveoli to exist
small alveoli
surfactant is made late during
fetal development