Kin 132 CV Flashcards
What is ventilation
Air exchange between the atmosphere and the alveoli
What are the two gas exchanges? Explain the process
1st gas exchange: Gas exchange at the lungs
- External respiration: gas exchange between the alveoli and the pulmonary capillaries
Gas transport:
- Gas movement by pulmonary and systemic circulation between gas exchange locations
2nd gas exchange location: Gas exchange at tissue
- Internal respiration: gas exchange between tissue capillaries and Interstitial fluid/ tissue
How is ventilation driven?
Air pressure differentials
What is the air pressure at sea level. how can a change be shown as
~ 760 mmHg is considered 0 and and rise or decrease in it will be shown and a plus or minus
Explain the pressure gradients when breathing
Inspiration: High pressure in the atmosphere, low pressure in the alveoli
Expiration: Higher pressure in the alveoli lower pressure in the atmosphere
What factor can we manipulate to control inspiration and expiration?
Alveolar pressure is altered
How are pressure and volume related according to boils law
they are inversely proportional.
How does build law affect inspiration and expiration
- Increasing volume decreases pressure
- Decreasing volume increases pressure
creates pressure gradients which produces ventilation
What are the 3 pressures of ventilation
Atmospheric pressure:
- Pressure from surrounding enviroment
Alveolar pressure
- Pressure in the alveoli
Intrapleural pressure
- Pressure in the intrapleaural space
- Always less than the atmospheric pressure
Explain how the inter pleural pressure holds the chest together
- lower intrpleaural pressure than alveolar pressure causes outward pressure preventing lung elastic recoil
- Lower intreapleural pressure than the atmospheric pressure causes inward force preventing chest elastic recoil
What do the combined effects the outward and inward force due to the low intrapleural chest do?
Links lungs and chest wall together so they move as a unit
What is eupnea
At rest breathing
Explain ventilation (inspiration) at eupnea
due to 2 muscles:
- Diaphragm contracts downward which causes the thoracic cavity to increase in volume = larger lung capacity = lower pressure = alveolar pressure becomes sub atmospheric = inspiration following pressure gradient
- Contraction of the external intercostals cause out and upward movement of the chest wall = larger thoracic cavity volume = inspiration
Explain ventilation (inspiration) at more forceful scenarios
- Same process as in eupnea, but the diaphragm and the external intercostals contract harder causing a even larger increase in thoracic cavity and lung volume
- If this isn’t enough then accessory muscles are recruited which contract and cause the chest wall to expand even more = Palv decreases even more below Patm causing a even greater inspiration
What are some accessory muscles of inspiration?
Sternocleidomastoid, Scalenes, pectoralis minor
Explain ventilation (expiration) at eupnea
- Recoil of diaphragm and external intercostals cause the lung volume to decrease to its original volume
- Contraction squeezes alveoli causing a increase in Palv
- Larger Palv than Pam causes a expiration of air out of lungs
Ventilation (expiration) at more forceful scenarios
- Diaphragm and external intercostals stop contracting and a larger recoil occurs
- Can recruit accessory muscles of expiration to contract which cause the inward and downward movement of the chest wall
- Palv becomes even lower than Pat causing a larger expiration
What is the main center for the respiratory center and what are its sub centres
Medullary respritory center:
- In medula obliongata
- Pre-Bozinger complex:
- Pacemaker sending signals to the dorsal respritory group to initiate treating cycle - Dorsal respritory group:
- Composed of inspiratory neurons - Ventral respritory group
- Composed of inspiratory and expratory neurons
Explain how these centres control ventilation at eupnea
Dorsal respritory neurons:
- Cycle between active and inactive. 2 seconds active = 2 seconds inspiratory and 3 seconds inactive = 3 seconds expository
- total of 5 seconds for inspiration and expiration for a breathing frequency of 12bpm at eupnea
How do drugs affect breathing
They can suppress the dorsal respiratory group inspiratory neurones making it so you can’t breath in
How can more forceful breathing happen
- dorsal respritory neurons are still cycling between active and inactive, causing stronger muscle contractions
- If even stronger contractions are needed and accessory inspiratory and expository muscles are needed, then there DRG recruits Ventricle respritory group inspratory and excretory neurons to activate the accessory muscles
Explain how the dorsal respritory group controls ventilation intensity
- It has control over how strong of a signal it sends to make the inspiration and expiration larger
- It controls when to recruit the ventricle respritory group for even larger contractions
What is the pontine respritory group and how does it affect ventilation
- In pons
- Sends signal to the dorsal respritory group to switch between active and inactive to modify breathing rate, which changes inspiration and expiration rates
- Strong signal to DRG in activities such as breathing and swimming
How do proprioceptors affect respiration
- When movement is detected by proprioceptors, it sends a signal to the dorsal respritory group to match ventilation to the needs of the body due to movement
- Proprioceptors are most likely what tells the DRG when to recruit the VRG at a certain intensity of movement
How do chemoreceptors influence ventilation
Peripheral chemoreceptors:
- In corotis sinus and aortic arch
- Detects chemical changes in the blood
Central chemoreceptors:
- In medulla oblongata
- Detects chemical changes in the interstitial fluid in brain
- Changes in chemicals in blood/ brain interstitial fluid detected by the peripheral (blood) and central (interstitial) chemoreceptors send a signal to the dorsal respritory group to change ventilation
What chemical changes do the chemoreceptors detect
- Lower arterial oxygen
- Increases firing of peripheral chemoreceptors
- Increases Dorsal respritory group active/inactive firing = increase in ventilation - Increase in arterial co2
- Either raises H+ concentration in blood or in brain interstitial fluid
- If interstitial fluid = increase central chemoreceptor firing
- If in blood = increase in peripheral chemoreceptor firing
- Both of these result in increased DRG active/inactive cycling
Explain how the higher brain centres influence ventilation
If oxygen levels get too low or co2 levels get too high then you pass out and involuntary breathing occurs
Explain the 4 breathing volumes
Tidal volume:
- Air volume inspired or expired in one breath
Inspiritory reserve volume:
- Amount of additional air volume that could be inspired after a tidal volume inspiration
Expiritory reserve volume:
- Amount of air volume left over after a tital volume expiration that would still be expired
Residual volume:
- Air volume remaining in the lungs after maximal expiration
Explain the different combinations of the breathing volumes
- Vital capacity:
- Air expired from max inspiration to max expiration
- Tv + ERV + IRV - Total lung capacity
- Total volume of air able to be held in lungs
- Tv + IRV + ERV + RV
Explain how changing one breathing volume effects the others
- Increasing tidal volume = decrease IRV and ERV
- No change in RV Total lung capacity or Vital capacity
What is forced vital capacity?
- Air volume expired from maximum inspiration to maximum expiration as fast as possible
- Forced vital capacity 1: Air volume expired in 1 second of forced vital capacity. Measured as a percent
What is Forced vital capacity 1 a good test of
Can be a sign of:
- Obstructive lung disease
- Difficulty with full expiration of lungs
- Both FVC and FVC1 decrease, but FVC1 decreases more leading to the the percent to decrease - Restrictive lung disease
- Difficulty fully inspiring
- Both FVC and FVC1 decrease by the same amount leading to no change in the percent
What is minute ventilation?
- Air flowing in or out of lungs per unit time (L/min)
- Minute ventilation = tital volume x breathing frequency
How does minute ventilation, Tital volume, and breathing frequency increase with exercise?
Minute volume:
- Increases linier to threshold points where it increases exponentially
Tidal volume:
- Increases linearly until moderate intensity where it begins to plateau
Breathing frequency
- Increases Linearly
What is dead space? What are the different types
- Portion of the minute ventilation not reaching the alveoli
Types:
1. Anatomical dead space:
- Conducting zone part of airway (no alveoli)
- Alveolar dead space:
- Damaged or blocked alveoli - Physiological dead space:
- Anatomical dead space + alveolar dead space
What is alveolar ventilation
- Air volume reaching alveoli per unit time
- Alveolar ventilation = (Tital volume - physiological dead space) x breathing frequency
What is effective ventilation?
Percent of the minute volume that reached alveoli for gas exchange
What results in the best effective ventilation?
Larger tital volume and smaller breathing frequency. Leads to having a lower physiological dead space resulting in a higher effective ventilation
Explain daltons law of partial pressure
The total pressure exerted by a mixture of gases is equal to the sum of the partial pressures from each individual gas
How to determine partial pressure
partial pressure = Atmospheric pressure of the gas x abundance of the gas in air
Explain external respiration
- Its the gas exchange between the lungs (alveoli) and the blood stream (pulmonary capileries)
- Alveoli has higher P02 than the pulmonary capillaries resulting in the movement of oxygen from the alveoli to the capileries
- Results: Blood enters capileries de oxygenated and leaves oxygenated
- The blood going to lungs also has a higher CO2 partial pressure than in the alveoli leading to the movement of CO2 from capileries to alveoli which gets expired out
What is ventilation perfusion matching?
- Matching the amount of blood flow to the amount of air flow
- Decreased ventilation = vasoconstriction = lower blood flow = additional blood is diverted to areas with higher air flow
- Decreased perfusion = bronchioconstriction = lower air flow = extra air is diverted to areas with high perfusion
Explain internal gas exchange
- Gas exchange between tissue capillaries and the interstitial fluid (goes to tissue)
- Oxygenated blood comes in with high O2 partial pressure. Oxygen flows into interstitial fluid where theirs lower O2 partial pressure
- Blood leaves tissue capilleries deoxygenated and goes back to heart via systemic circulation
- Aswell the partial pressure for CO2 is higher in the interstitial fluid than in the tissue capillaries leading to the movement of CO2 from interstitial fluid to capillaries
What is the atriovenous oxygen difference
- Difference between oxygen going into the tissue capillary bed and the oxygen coming out of them
- Lower difference at eupnea, higher at exercise
- Controlled by vaso contraction/dilation of the arterioles and the contraction/relaxation of the pre capillary sphincters
What is oxygen consumption?
- its the volume of oxygen consumption per unit time
- Achieved by multiplying the cardiac output by the atriovenous difference
- think about it as the amount of blood being deceived multiplied by how much oxygen is in that blood
What is the key factor for gas exchange
- Pressure gradients
What are the 3 smaller factors that affect gas exchange?
- Surface area
- Higher surface area = higher gas exchange - Thickness of membrane
- Thinner membrane = higher gas exchange - Diffusion coefficient of gas (amount of gas that can cross a area in 1 second)
- Higher diffusion coefficient = higher gas exchange
What is henrys law state?
- The concentration of a gas in a liquid = (Partial pressure of the gas moving into the liquid) x (solubility coefficient)
- If only looking at one gas ignore the solubility coefficient. Only depends on partial pressure of gas
Explain what affinity is during gas transport
- Since not enough oxygen can be dissolved in blood for the needs of the body, 4 oxygen molecules are bonded to each hemoglobin for transport which don’t count as dissolved
- Since only dissolved gasses can be used for gas exchange affinity (how tightly the gas is bonded to the hemoglobin) is altered
- (loading) Higher affinity causes a higher hold on the oxygen, which is good for transport
- (Unloading) Lower affinity causing a weaker bond between the oxygen and the hemoglobin, making it more likely for the gas to de attach
what percent of oxygen is transported dissolved in blood or carried on hemoglobin?
1.5% is dissolved in blood
98.5% is carried on heme disks of hemoglobin
What does saturated vs unsaturated hemoglobin mean?
Saturated: All 4 heme disks in hemoglobin carry a O2
Unsaturated: Not all 4 heme disks are being used. eg 25% saturated means 1 oxygen is bonded
What is a saturation curve?
What the saturation of hemoglobin is at a given partial pressure of oxygen
- (Loading) Increasing the partial pressure of O2 increases the Hb-O2 saturation. wanted in transport
- (unloading) Decreasing the partial pressure of O2 decreases the Hb-O2 saturation. wanted in unloading
Explain Hb-O2 saturation during external respiration
During external respiration the partial pressure of O2 in the pulmonary capillaries increases resulting in a increase in Hb-O2 saturation
Explain O2 saturation and O2 partial pressure levels before and after resting external respiration
- Before external resting respiration PO2 is ~40mmHg with a saturation of 78%.
- After external resting respiration the PO2 ~ 100mmHg with a saturation of 100%
- Results: 22% saturation difference added from alveoli to blood
Explain Hb-O2 saturation during internal respiration
- During internal respiration the partial pressure of O2 decreases as it moves from the tissue capillaries into the interstitial fluid resulting in a decrease in Hb-O2 saturation
Explain O2 saturation and O2 partial pressure levels before and after resting internal respiration
Before internal respiration:
- PO2 = 100mmHg
- Saturation = 100%
After respiration:
- PO2 = 40 mmHg
- Saturation = 78%
Results: 22% saturation difference from oxygen going to interstitial fluid
Explain the portions of the saturation curve
- Saturation curve is linear then plateaus at the top
- Broken into two pieces: Plateau portion and steep portion
Plateau portion: Changes in the partial pressure of O2 Barkly change the O2 saturation level
Steep portion: Changes in the partial pressure of O2 result in large changes in the saturation level
Explain O2 saturation and O2 partial pressure levels before and after external respiration at exercise
Before external respiration:
- PO2 = 20mmHg
- Saturation = 38%
After external respiration
- PO2 = 100mmHg
- saturation = 100%
Results: 62% increase in saturation due to oxygen coming from alveoli to pulmonary capillaries
Does the increase in exercise intensity result in a lower oxygen saturation?
No, pretty much always the blood will leave the pulmonary capillaries with 100% saturation and a PO2 of 100mmHg
Explain O2 saturation and O2 partial pressure levels before and after internal respiration at exercise
Before internal respiration:
- PO2 = 100mmHg
- Saturation: 100%
After internal respiration:
- PO2 = 20mmHg
- Saturation = 38%
Results: 62% decrease in saturation as the oxygen moves from tissue capileries to the interstitial fluid
What is a curve shift and what does it do?
- Curve shifty is a minor way to alter the saturation level
Shift right: Decreases saturation level, decreases affinity = increases unloading
Shift left: Increases saturation level, increased affinity = increases loading
What factors cause a curve shift?
Shift right:
- High acidity (H+ concentration)
- High temp
- High CO2
Shift left:
- Low acidity
- Low temp
- Low CO2
Explain the Bohr effect
- During exercise H+ and CO2 levels are high
- Oxygenated blood enters the tissue capillaries and meet high acidity and CO2
- These factors cause a curve shift right causing a lower saturation and lower affinity
- Oxygen is released from hemoglobin into dissolved state which goes into interstitial fluid
- Hemoglobin now binds with the H+ and CO2 to transport them to lungs for expiration
How is CO2 transported?
- 7% is dissolved in blood (more than O2 because higher solubility constant)
- 23% carried in hemoglobin
- 70% converted to bicarbonate formed in red blood cells and stored in the plasma
How does the movement of the negative bicarbonate in and out of the red blood cell get its charge balanced?
Cl- moves in and out of the red blood cell to counteract the movement of the bicarbonate
