Physiology of Resp Flashcards
Name the 4 main gas laws and their definitions.
- Boyle’s Law: P~1/V and gases flow from high pressure to low pressure
- Dalton’s Law: Total pressure = sum of all partial pressure of the individual gases.
- Charles’ Law: Volume is directly related to temperature
- Henry’s Law: the amount of dissolved gas depends on volume of the gas and the solubility of the gas
How much is the fluid in the pleural cavity
5 mL
3 purposes of the pleural cavity
- allow the pleural membranes to slide past one another
- reduce the friction, no pain, less work
- adhesion between the lung and the muscles lining the thoracic cavity (thoracic wall has the tendency to expand while the lungs have the tendency to recoil, the pleural fluid keeps these opposing forces in balance)
Name the muscles used inspiration vs expiration
Inspiration: diaphragm + external intercostal muscles
expiration: abdominal muscles + internal intercostal
name the direction of action of each of these respiratory muscles
diaphragm (superior/inferior)
external/internal intercostals (lateral and posterior/anterior)
Why is asthma expiratory wheeze
during expiration, intra thoracic pressure increases and everything gets smaller and therefore, expiration is more affected on top of the already constricted bronchi
The different types of thoracic pressures and their definition
PA: alveolar/intrathoracic pressure - pressure inside the thoracic cavity
Pa: arterial pressure
Pip: intrapleural pressure - pressure inside the pleural cavity, ALWAYS negative in healthy lungs, but will become less negative during expiration (during inspiration, the pleural walls try to pull away from one another while in expiration, they compress against one another and therefore Pip becomes more positive during expiration)
PT: transpulmonary pressure - (PA-Pip) ALWAYS positive in healthy lungs because Pip is always negative and even when PA is negative, Pip is more negative.
Volume of the anatomical dead space
150 mL (although the air in the alveolar dead space is not for exchange, it will affect alveolar ventilation)
difference between pulmonary and alveolar ventilation
pulmonary/minute ventilation: total air movement in and out of lungs.
Alveolar ventilation: amount of air reaching the alveoli and actually being available for gas exchange.
list and define all the volumes during breathing cycles (there are 10)
Tidal volume: 500mL - volume of air going in and out of lung per breath at rest
Expiratory reserve volume: 1100mL - max volume of air that can be voluntarily expelled at the end of normal expiration (after tidal volume)
Inspiratory reserve volume: 3000mL - max volume of air that can be drawn into the lungs after normal inspiration (after tidal volume)
Vital capacity: 4.6L - TV + ERV + IRV (this is the volume tested in lungs function tests)
Residual volume: 1200mL - remaining air in the lung after expiration, cannot be expelled voluntarily
Total lung capacity: 5.8L - VC + RV
Inspiratory capacity: 3500mL - IRV + TV
Functional residual capacity: 2300mL - ERV + RV
FEV1 (forced expiration volume in 1 sec): 4L
FVC (forced vital capacity): 5L
explain why breathing is only 70% effective
because out of the 500mL tidal volume, 150mL becomes stuck in alveolar dead space.
what are the two things that affect alveolar ventilation, and which is the main determinant?
- depth of breathing (MAIN determinant)
2. rate of breathing (you can be breathing fast and still hypoventilate if you don’t breathe deeply enough)
percentages of O2, N2, and CO2 in the air we breathe
O2 - 79% (160mmHg/21kPa)
N2 - 21%
CO2 - 0.03% (therefore if there is build up of CO2 in the body, it is not from breathing, but rather from metabolism waste product that we cannot get rid of fast enough)
explain why PO2 in the body is 100mmHg (13.3kPa) instead of 160mmHg (21 kPaa)
there are 3 reasons
- air gets saturated with water vapor as it goes down
- some of the O2 gets stuck in dead space
- fresh air gets diluted with the residual volume composed of stale air
state the normal PO2 and PCO2 in respiration
PO2: 100mmHg/13.3kPa
PCO2: 40mmHg/5.3kPa
forces to overcome during inhalation (there are 3). After overcoming these three forces, it would be very easy to increase or decrease lung volume
- surface tension from the surfactants
- tissue inertia
- elasticity
Why does the alveoli have inward force surface tension?
Because the air we breathe in is saturated with water vapor, and when these coat a spherical surface of the alveoli, it will generate inward pulling force.
Why is surfactant more effective in reducing surface tension in smaller alveoli?
because the surfactant molecules can sit in between more water molecules due to it being more concentrated on a smaller surface area
Law of Laplace
P=2T/r
(P=pressure needed to keep the alveoli patent, T= surface tension, r=radius)
(this means that you will need more pressure to keep smaller alveoli open, but that is OK because surfactants are more effective in smaller alveoli. Without surfactants, the small alveoli would close and the gas inside would be pushed into larger alveoli with less pressure, decreasing the available surface area for gas exchange)
difference of breathing in saline before and in air after birth
3 times as hard without surfactants
breathing in saline is like breathing with surfactants
4 things that determines lung compliance
- surface tension
- elastic forces
- airway resistance
- elevation (whether you are lying down or standing up, which direction gravity is acting on)
compliance vs elasticity
compliance = how easy it is to get air into the lungs (how much is change in intrapleural pressure is needed for a certain change in volume) elasticity = how easy it is for the lungs to recoil after expansion
compliance and elasticity in emphysema
high compliance but low elasticity
the elastic structures lining the alveoli and destroyed, therefore although they can get air in, the lungs cannot contract and they have trouble exhaling because there is no passive elastic recoil, exhalation done with extra work
compliance of lungs in different areas and different times
lungs are more compliant at the base due to gravity
gets more compliant at the end of inspiration and expiration as the initial resistance is overcome.
Obstructive vs restrictive lung diseases
Obstructive = obstruction of airflow, increased airway resistance, issue when exhaling, can sometimes be associated with elasticity problem
restrictive = restricted lung expansion, loss of compliance, requires you to put in more effort in breathing in than normal
examples of obstructive lung diseases
Asthma - inappropriate constriction of the bronchial smooth muscle
COPD - emphysema (loss of elasticity), chronic bronchitis (inflammation of bronchi and obstructive airflow)
examples of restrictive lung diseases
fibrosis - caused by idiopathic, asbestos
infant respiratory distress syndrome (lack of surfactants)
edema (fluid build up around alveoli, limiting expansion)
pneumothorax (air leakage between the lungs and the chest wall, limiting expansion)
injury to the ribs (leads to pneumothorax)
volumes that can be measured directly by spirometry
(only the ones that you can voluntarily move, not anything with RV in it)
- tidal volume
- ERV
- IRV
- vital capacity
- inspiratory capacity
FEV1/FVC ratio in obstructive lung disease
reduced
- FEV1 would decrease because there is obstruction especially in exhalation and the amount of air exhaled in 1 sec is greatly reduced
- FVC would also decrease because tidal volume decreased, but otherwise you should be able to get FVC up to normal if you try to exhale hard enough.
- in either case, FEV1 decreased more than FVC
FEV1/FVC in restrictive lung disease
unchanged or increased
in this case, there is nothing obstructing the airways, the issue lies with getting air in and out
- FEV1 is reduced because less air got in in the first place.
- this will also affect the FVC
- since both are affected, the ratio would remain unchanged, or it will even increase if a large proportion of volume can be exhaled in the first second.
Why is the pulmonary circulation under much less pressure but higher flow compared to the systemic circulation although the amount of blood going through it is the same?
it has dense capillary networks.
Average systolic pressure in pulmonary artery vs systemic artery
25mmHg (8mmHg diastolic)
120mmHg
PO2 and PCO2 in peripheral tissue and alveoli
PAO2 (alveolar)= 100 mmHg PACO2 = 40 mmHg PaO2 (arterial)= 100 mmHg PaCO2 = 40 mmHg PvO2 (venous) = 40 mmHg PvCO2 = 46 mmHg
Since the difference in PO2 in arterial and venous blood (btw the lungs and tissue) os 60 and PCO2 is 6, you would expect the rate of diffusion of O2 to be 10 times greater like the size of the pressure gradient, but why is this not the case?
because O2 has much less solubility than CO2 in water, so even with 10 times difference in gradient, the rate of diffusion of O2 and CO2 are not that different: 250mL/min in O2 and 200mL/min in CO2
describe PO2 in emphysema
destruction of alveoli reduces surface area for gas exchange
PAO2 normal
PaO2 low
describe PO2 in fibrotic lung disease
thickened alveolar membrane slows gas exchange, but there may also be less tidal volume due to restrictive nature of the lungs
PAO2 normal or low
PaO2 low
describe PO2 in pulmonary edema
fluid in the interstitial space increases diffusion distance, but the exchange surface is normal otherwise
PAO2 normal
PaO2 low
*this will affect O2 more than CO2 because CO2 is more soluble in water, so often PCO2 is normal
describe PO2 in asthma
increased airway resistance, decreased ventilation but normal gas exchange (this is unlike the other ones because the issue lies with ventilation rather than diffusion) PAO2 low PaO2 low (although gas exchange is normal, there is little gas in the first place)
describe blood flow and ventilation distribution throughout the lungs
blood flow is greater than ventilation at the base and less than ventilation at the apex of the lungs. Both decreases with height, but blood flow is decreases faster than ventilation.
which rib is perfusion and ventilation the same
rib 3
below rib 3, the ratio is pretty close to 1, but above that the ratio becomes drastically different. Above rib 3 is where we get the least effective gas exchange
2 types of V/Q mismatch
type 1: V>Q, ratio>1.0
type 2: V
define alveolar dead space and response mechanism of the lungs to offset this effect (type I V/Q mismatch)
area of the lung that is more ventilated than perfused and therefore not effective gas exchange. There will be an increase in PAO2 and decrease in PACO2 .
the ultimate response is 1. vasodilation to increase perfusion and 2. mild bronchial constriction to decrease ventilation to that area
response mechanism to type II V/Q mismatch
there is more blood flow than ventilation, PAO2 decreases while PACO2 increases. The blood that goes through this region will remain deoxygenated (called shunt).
Response 1. enzyme in the lungs detect hypoxia in that region of the lung and constricts the blood vessel in that region so that there is no blood being uselessly sent there (note that while pulmonary vessels constrict here, the systemic supplying that part of the lung would actually dilate). 2. the deoxygenated blood would mix with oxygenated blood from other parts of the lungs when it returns to the heart 3. increase in CO2 results in mild dilation of the bronchi that will help ventilate that area
Amount of O2 dissolved in plasma (which is 95% water)
3mL O2/1L plasma
with Hb, this increases to 200mL/L
Arterial blood pressure define
only refers to O2 that is dissolved in plasma rather than O2 content of the whole blood.
how is CO2 transported?
dissolved in plasma, wither as CO2 or as bicarbonate
Name 2 determinants of arterial pressure
- the solubility of O2 (fixed)
- the partial pressure of O2 in gaseous phase that is driving the O2 from the lungs into the solution (PO2 in solution in plasma would be equal to the gaseous PO2 in the alveoli that drove O2 into solution, therefore, PAO2 = PaO2) (variable) - this is the major determinant
Is PO2 in the alveoli and plasma the same?
yes, PAO2 = PaO2, however, their concentrations are different. There is 30 times more molecules of O2 in 1L of gas than water (plasma)
how many percent of total arterial O2 content is used?
250 mL (25%) of arterial O2 is used in peripheral tissue per min at rest total O2 content is 200 mL/L of plasma (197mL in Hb, 3mL in solution), multiply that with CO of 5L/min --> 1000mL/min O2 circulating the body each minute
how long does it take for Hb saturation?
How long is the blood in contact with alveoli for?
- 25 seconds
0. 75 seconds
explain the body’s mech of maintaining optimal uptake of O2 even when PO2 falls
Even when PO2 has dropped to 60%, Hb saturation is still above 90%, meaning that the peripheral gas delivery is normal. If it falls below 60%, then the fall in Hb concentration would be very steep, gets dangerous. Normally, the reservoir in Hb is not used even in critical conditions, we would instead compensate by breathing faster and deeper
describe the partial pressure of O2 and O2 content in anaemia
PO2 would be normal although the O2 content would decrease, because the Hb are working fine, there is just less of them. PO2 has nothing to do with O2 content, but rather the PAO2 that is the driving pressure of O2 to dissolve in plasma, as long as PAO2 is the same, PaO2 would not change. Saturation of Hb would also be normal
Is it possible to have low PaO2 and normal O2 content?
No, because PAO2 determines the saturation of O2 in plasma and therefore its content
Things that decreases O2 binding to Hb (there are 5 things) (graph shifting to the right) - this means that it is more likely to give off O2 to peripheral tissues rather than retain it
- decrease in pH (acidosis)
- increase in CO2 levels
- increase in temperature
- increase in DPG (when RBCs are working hard, they will release DPG - diphosphoglycerate, like when there is not enough O2 intake, in order to maintain adequate O2 delivery to body)
- CO (high affinity for Hb, 250x greater than O2) - inhaling this will result in cherry red skin color, brain damage, death, etc.
what happens when you inhale CO?
fall in PO2
normal PCO2 - therefore resp rate unaffected
5 types of hypoxia
- hypoxaemic hypoxia - the most common, reduced PO2 at alveolar level, even before gas exchange. Caused by lung disease or not enough O2 outside
- anaemic hypoxia - reduction of O2 carrying capacity of blood, like in anaemia
- stagnant hypoxia - inadequate tissue perfusion, caused by either inadequate pumping of blood to the lungs for gas or inadequate perfusion of tissues
- histotoxic hypoxia - poisoning that prevents cells from utilising or getting O2, like CO
- metabolic hypoxia - O2 delivery cannot meet increased demand
explain CO2 transport
23% of CO2 will bind to Hb (deoxygenated Hb will have more affinity to CO2) - forms carbomino compound
7% will dissolve in plasma as CO2
70% will go into Hb and act with carbonichydrase in Hb to form carbonic acid and dissolve in the plasma.
what happens to the carbonic acid that is dissolved in the plasma
will dissociate into H+ and bicarbonate ion.
H+: bind with deoxygenated Hb
bicarbonate ion: chloride shift, where it will exchange across the surface of Hb with Cl- , the Cl- will go into the Hb while bicarbonate ion comes out and dissolves in the plasma. later at the alveoli, chloride shift happens again but in reverse, bicarbonate goes into the RBC and reacts with the H+ to form H2O and CO2. At the lungs, we need all the CO2 inside the RBC as much as possible so it can participate in gas exchange
can you respond to metabolic acidosis by hyperventilation?
Yes
Is breathing entirely dependent on the brain?
Yes
it relays information through the phrenic nerves to the diaphragms
dorsal vs ventral respiratory groups
dorsal: activating inspiratory muscles (sends info through phrenic and intercostal nerves)
ventral: expiratory muscles, accessory muscles of inspiration, mostly muscles in the pharynx, larynx, and tongue
both of these are regulated by the pontine respiratory group
list two main functions of the respiratory centers
- set automatic rhythm of breathing - through coordinating the firing of smooth and repetitive bursts of APs in in the dorsal resp group to the inspiratory muscles. This is a smooth recruitment of neurons, followed by abrupt switching off for expiration, which still allows gentle relaxation of muscles to ease into expiration, before starting smooth recruitment for smooth inspiration again.
- adjusts breathing pattern in response to stimuli
stimuli that affect the rhythm in respiratory centers
- emotion from the limbic system in the brain
- voluntary override through higher centers in the brain (but this cannot override involuntary stimuli from the chemoreceptors, at least not for long)
- mechano sensory input from stretch receptors in the thorax. I have inflated your thorax too much, this receptor will send signals to inhibit inspiration
- chemoreceptors detect changes in the composition of blood, like changes in PO2, PCO2, and pH
describe central chemoreceptors
Found in the medulla and responds to PCO2 in the plasma, it responds directly to the changes in H+ concentration in the CSF around the brain (although H+ actually cannot cross the BBB, CO2 can, and that will dissociated into H+ in the CSF, so there is build up of H+ for the chemoreceptor to detect anyway. this also means that the source of H+ that this can detect is only from CO2).
main ventilatory drive.
10% increase in PCO2 will bring about 100% increase in ventilation
define hypercapnea
increase in PCO2
why do divers hyperventilate before diving?
this is to trick the chemoreceptors into thinking that there is low PCO2 and reduce the drive to breathe, thus lessening the O2 consumption from the tank
describe peripheral chemoreceptors
responds to changes in PO2 and are found in the aortic and carotid bodies located in the aorta and carotid arteries. responds mainly to SIGNIFICANT fall in PO2. Also responds to changes in H+ conc, the only difference is that this H+ can be from metabolic processes and any other source while central chemoreceptors only respond from H+ that comes from CO2 dissociation in water.
only used in hypoxic drive
describe hypoxic drive
happens in those with lung diseases who have high PCO2 for such a long time that their central chemoreceptors become insensitive. these ppl rely on the lack of O2 to stimulate the peripheral chemoreceptors rather than increase in CO2
what happens to respiration rate in anaemic patients with half the blood O2 content?
it will stay the same
this is because PO2 remains unchanged and the amount of DISSOLVED O2 remains the same
what happens to ventilation when
- acidosis
- alkalosis
- plasma pH falls, increase in H+ –> increased ventilation
- plasma pH rises, decrease in H+ –> decreased ventilation
how does peripheral chemoreceptors send information to the medulla?
afferent sensory neurons
central chemoreceptors already located in the medulla
how does the resp centers in the medulla send information to the resp muscles?
somatic motor neurons
why is inhaling more CO2 bad?
it will increase PCO2 in the alveoli, which will decrease the gradient that will remove CO2 from the blood. Since CO2 remains in the blood, there is also loss of the gradient to pull CO2 from the periphery, so CO2 begins building up in body cells as well.
name 4 drugs that depress resp centers
- barbiturates (sleeping pills)
- opioids
- most gaseous anaesthetic agents - will increase resp rate but decrease tidal volume –> hypoventilation
- NO (sedative/light anaesthetic) - blunts peripheral chemoreceptors, so there will be no effect in normal ppl, but deadly in those who have insensitive central chemoreceptors
can we administer O2 to those with insensitive central chemoreceptors?
No
since their PO2 is fine now, the peripheral chemoreceptors would decrease the drive to breathe, but in actuality they are not breathing enough and PCO2 is going through the roof, but there is no chemoreceptor to detect that.
