ICL 1.7: Mechanics of Breathing Flashcards
myra and hannah loved cross country. during their first season while running, a group of deer plowed through the runners into the adjacent tree line. myra was thrown into the air upon impact with one of the deer and had to be taken to the ER. hannah was told that myra suffered a fracture of the 4th rib and a pneumothorax. on being asked what it is, she was told that myra’s right lung collapsed!
what caused myra’s lung to collapse?
what are the forces that keep your lung inflated?
loss of negative intrapleural pressure is what caused myra’s pneumothorax –> the penetration of the thorax wall allowed air to flow down its pressure gradient into the pleural cavity
the intrapleural pressure is no loner negative compared to the intrapulmonary pressure and the visceral pleura is separated from the parietal pleura –> these two changes combined with the elastic property of the lung tissue cause the lung to deflate or collapse
surfactant and negative intrapleural pressure helped to prevent the lung from collapsing
lung recoil and high surface tension are the forces acting on the lung that would cause it to collapse
what is a negative intrapleural pressure?
negative means that it’s less than the atmospheric pressure
what is lung recoil?
it represents forces in the wall of the lungs that always favors lung collapse
the higher the lung volume the greater the recoil
collagen and elastin in the extracellular matrix of the lungs are what are responsible for this lung recoil
what is surface tension?
the forces in the fluid-lining of the alveoli
inside the alveoli, is a thin lining of fluid causes contraction due to increased surface tension from the hydrogen bonding between the water molecules! this is causing the alveoli to collapse and the lungs to collapse
what is the alveolar pressure?
P(A) is the air pressure in the alveoli – it’s the same as the intrapulmonary pressure; these terms are interchangeable
P(A) is 0 when no airflow is occurring (same as barometric)
+1 mm Hg means that +1 above the barometric and so on
what is intrapleural pressure?
P(IP) is the pressure inside the intrapleural space
each lung is encased in a pleura which is a fluid filled sac – the inside layer is the visceral pleural physically connected to the lung while the outside layer is the parietal layer and is attached to the rib cage
P(IP) is negative when the lungs are inflated due to the opposing recoil forces of the lungs and the chest wall
what is transpulmonary pressure?
P(TP) is the pressure difference between the outside and the inside of the lungs
it’s the pressure across the wall o the lungs needed to keep them inflated!
it’s analogous to the pressure required to keep the arteries open and is also referred to as the transmural pressure
what keeps the pleural together?
the ribs are pulling outwards on the parietal pleural while the lungs are pulling inward on the visceral pleural so what’s keeping the pleural together? it’s the pleural fluid!
the water molecules want to stick together and don’t want to be separated in either direction so their surface tension creates a negative force inside the pleural space which creates a vacuum!
-4 mmHg is the normal intrapleural pressure and this is what keeps the lung from collapsing, it keeps the lung inflated!
what is the equation for transpulmonary pressure?
P(TP) = P(A) - P(IP)
transpulmonary pressure is the pressure needed to stretch the lung tissue and expand the alveolar surface
PTP = +4 mmHg normally because P(A) = 0 and P(IP) = -4
how do the lungs remain inflated?
- the outward recoil of the chest cavity balanced out the inward recoil force of the lungs
- the intrapleural pressure is less than the alveolar pressure so this negative pressure keeps the lung expanded
what is a pneumothorax?
a collapsed lung caused by the loss of negative pressure between the visceral and parietal pleural membranes that occurs when air abnormally enters the pleural space
penetration of the thorax wall allows air to flow down its pressure gradient into the pleural cavity; the intrapleural pressure is no longer negative compared to the intrapulmonary pressure and the visceral pleura is separated from the parietal pleura
if there’s a puncture and air goes into the intrapleural cavity, this disrupts the vacuum and the visceral and parietal pleura get separated and the lung collapses
these two changes combined with the elastic property of the lung tissue cause the lung to deflate or collapse
will a pneumothorax in the right lung cause both the lungs to collapse?
no
the lungs are separated by the mediastinum so the lungs aren’t connected
do you think myra’s breathing was effected with a pneumothorax?
yes
the loss of negative intrapleural pressure also disrupts the process of breathing
loss of negative intrapleural pressure is very important for the air to enter into the alveoli for gas exchange and without it, inspiration won’t happen because it’s NOT a passive process, it’s an active process!
is inspiration active or passive?
expiration is passive (during quiet breathing)
inspiration is an ACTIVE process!
inspiration starts with the brains control center telling you to inspire; this is passed through the phrenic nerves which give signals to the diaphragm and external intercostal muscles so the they contract
the diaphragm moves down and the thoracic cavity expands and the lung volume increases, alveolar pressure P(A) decreases and air enters the lungs!
is quiet expiration passive or active?
QUIET expiration at rest is passive; it’s a different story with forced expiration like during exercise
the brain stops sending signals to inspire and the diaphragm and intercostal muscles will relax
this causes the lung volume to decrease, alveolar pressure to increase and air leaves the lungs
what is respiration?
exchange of air between the atmosphere and alveoli
what is Ohm’s law?
F = ΔP/R
F = (Palv - Patm)/R
F = air flow
what is Boyle’s law?
P1V1 = P2V2 at a constant temperature
if there’s an increase in volume, pressure decreases and vice versa
what is happening to the different pressures in the lungs when there is no air flow in the lungs like in the split second after you finish quiet expiration?
when there’s no airflow in between breath, there’s no pressure gradient and the atmospheric pressure and the alveolar pressure are the same
P(A) = 0 P(IP) = -4 P(TP) = 4
P(TP) = P(A) - P(IP) = -4 mmHg
what is happening to the different pressures in the lungs at the start of inspiration?
the draphragm and intercostal muscles contract and the thoracic cavity expands and the intrapleural space increases since the parietal pleura is being pulled by the ribs
the intrapleural space is a closed chamber! so when its volume increases the pressure drops according to Boyle’s law (P1V1=P2V2)
when this happens, the trans pulmonary pressure increases and when this happens the volume of the lung increases which decreases the alveolar pressure
this decrease in P(A) is enough to drive inspiration and have air rush into the lungs
P(IP) = -6 P(A) = -1 P(TP) = 5
P(TP) = P(A) - P(IP) = -4 mmHg
what is happening to the different pressures in the lungs at the end of inspiration?
inspiration stops when the intrapleural pressure has reached its maximum negative pressure and the transpulmonary pressure has caught up to the same value
the air that came into the lungs makes the pressure in the alveoli 0 so P(A) is back to being 0
this is when the lungs are done inspiring – alveolar elastic recoil is very high at this point
what is the series of events that happens during inspiration?
- brain initiates inspiratory effort
- diaphragm and external intercostal muscles contract
- thoracic volume ↑ as the chest wall expands
- intrapleural pressure (PIP) becomes more negative
- transpulmonary (PTP) pressure ↑
- alveoli expand in response to the transmural pressure difference
- alveolar elastic recoil increases
- alveolar pressure (PA) < atmospheric pressure establishing a pressure difference
- air flows into the alveoli
- irflow will stop when the PA becomes 0 (atmospheric pressure)
what is happening to the different pressures in the lungs at the start of quiet expiration?
the brain has stopped its inspiration command so the diaphragm and intercostal muscles relax so the intrapleural space volume decreases which causes the pressure to increase and become more positive
transpulmonary pressure also consequently decreases – when this happens, the force exerted on the lungs keeping them inflated drops so the volume of the lungs decreases and the pressure in the lungs consequently increases (P1V1=P2V2)
so now, the trnsplumonary pressure decrease in combination with the increased elastic recoil, the alveoli have increased in pressure and P(A) = 1 which makes the air in the lungs to flow out since P(A) > Patm!
what is the series of events that happens during expiration?
- brain ceases inspiratory command
- external intercostal muscles and diaphragm relax
- lungs deflate and thoracic volume ↓
- intrapleural pressure (PIP) becomes less negative
- transpulmonary (PTP) pressure↓
- the ↑elastic recoil returns alveoli to pre-inspiratory volumes
- alveolar pressure (PA) > atmospheric pressure
- pressure difference is formed in the opposite direction
- air flows out of the alveoli
- airflow will stop when the PA becomes 0 (atmospheric pressure)
does all the air inspired by a person under normal conditions reach the alveoli?
no, there is anatomical dead space!
it’s just because of the structural limitations of how the respiratory system is set up; the air fills the respiratory passages where the gas exchange doesn’t occur like the the nose, pharynx and trachea which are areas that aren’t useful for gas exchange
on expiration, this air in the anatomical dead space is expired first before the air that made if all the way down the alveoli and it never gets the chance to go all the way down to the lungs!
what is anatomic dead space?
the volume in the respitory system where gas exchange doesn’t occur
about 1/3 of each normal breath we take is anatomic dead space = 150 mL
this means the tidal volume has to be >150 mL for fresh air to reach the alveoli!
what is the physiologic dead space?
anatomic dead space + alveolar dead space
alveolar dead space is alveoli that are nonfunctional so in a healthy person, all the alveoli are working and the only dead space should be anatomical dead space
in a normal person, the anatomical and physiological dead spaces are nearly equal
as she was sitting there getting tensed about her friend’s condition, Hannah started taking deep breaths since she remembered her coach’s words that it will help you relax. does all the extra air inspired during her deep breath reach the alveoli?
when you take a deep breath does the alveolar ventilation increase?
YES
what is minute ventilation vs. alveolar ventilation? what is the formula for each?
minute ventilation is the amount of air you’ve taken in in 1 minute:
V(E) = V(T) x RR
V(E) = 500 mL x 12/minute = 6 L/min
however, not all the air you breath in is going to make it to the alveoli! so alveolar ventilation is:
V(A) = (VT - VD) x RR
V(A) = (500 - 150) x 12 = 4.2 L/minute
VD is the anatomical dead space, VT is the tidal volume and RR is respiratory rate
myra’s normal tidal volume is 400 mL with a dead space of 100 mL. as she undergoes a ventilation during surgery with a VT of 700 mL, what was the change in alveolar ventilation if her rate of breathing was constant at 12?
V(A) = (VT - VD) x RR
VA = (400-100) x 12 = 3600
VA = (700-100) x 12 = 7200
it doubles!
if hannah breathes rapidly and shallowly at a rate of 40 breaths per minute with a tidal volume of 150 mL in each breath, what will happen?
there will be no alveolar ventilation and she would become unconscious soon
the tidal volume must be more than 150 mL for fresh air to reach the alveoli!!
so rapid shallow breaths is NEVER good and that’s why hyperventilation is not a good thing!
when you take a deep breath and your alveoli is totally stretched out, the type II pneumocytes will secrete more surfactants which keeps your lungs healthy!
which among the following factors has the most prominent effect in increasing the flow of air through the narrow bronchioles?
A. increasing the diameter
B. increasing the length
C. decreasing the viscosity
D. decreasing the surface tension
A. increasing the diameter
R = 8ηl/πrˆ4
airflow due to pressure gradient is inversely related to airway resistance!
during inspiration, an increase in bronchiole diameter decreases the resistance
this is why in asthma when there’s a narrow airway, you have such difficulty breathing because there’s a lot of resistance
what part of the respiratory system has the highest resistance?
first and second order bronchi
they’re very cartilaginous so there isn’t much change in their pliability and they have a lot of resistance
the alveolar ducts, alveolar sacs have the least resistance even though they have smaller radii because of the connective tissue of lung pulls on the walls of smaller airways which increases their diameter and decreases resistance!
this phenomenon is known as lateral traction
how is airway resistance effected in COPD and asthma?
when there isn’t lateral traction, there is increased airway resistance
expiration is effected more because the air gets trapped in the lungs and the diaphragm gets flattened and it’s unable to generate the pressure gradient for inspiratory flow
then since the diaphragm can’t function, the high lung pressure increases the work of breathing
______ is lung volume/transpulmonary pressure
compliance
what is lung compliance? what is the formula?
pulmonary compliance indicates the effort required to expand the lungs
compliance = Δlung volume/Δtranspulmonary pressure = ΔV/ΔP
more compliant structures become larger for a given increase in pressure compared to less compliant ones
what are the two major components that effect lung compliance?
- elasticity
more elasticity increases compliance and also makes recoil easier
- surface tension of the air-water interface
surface tension opposes compliance!
what increases pulmonary compliance?
- surfactant
- loss of fibrous tissue (emphysema)
slide 29
what decreases pulmonary compliance?
- pulmonary fibrosis
- increased surface tension
slide 29
a preterm infant has a surfactant deficiency. without surfactant, many of the alveoli collapse at the end of the expiration. which set of changes is present in this infant?
increased surface tension
decreased pulmonary compliance
what is surfactant composed of?
it’s a mixture of lipids
mainly dipalmitoylphosphatidylcholine and apoproteins
surfactant lowers surface tension which decreases lung recoil
the hydrophilic part lines up to the water molecules while the hydrophobic portion lines up on the inner surface of the alveoli – the hydrophobic part doesn’t have strong interactive forces so they decrease surface tension!
it’s only in the alveoli! not in other parts of the respiratory system
what is the function of surfactant?
- reduces need for excessively negative intrathoracic pressure
- prevents over-inflation of the lungs
- avoids collapse of smaller alveoli
how does surfactant prevent alveoli collapse?
in small alveoli there can be huge pressures due to the small radii
this could lead to the air being sucked out from the small alveoli into the larger alveoli due to the pressure gradient
so surfactant reduces the surface tension by spreading inside the smaller alveoli and avoids the pressure increase – so basically all the alveoli have the same surface tension
