RS Learning Objectives Flashcards
Boyle’s Law and its importance.
- volume and pressure inversely related to get pressure gradient as well as prevent rupture of the lungs
- volume changes → pressure changes → pressure gradient → producing ventilation
- volume decreases = pressure increasing and air going out (expiration)
- volume increases = pressure decreasing and air going in (inspiration)
Role of pressure gradients (including alveolar, atmospheric, intrapleural pressures) to get inspiration and expiration.
- atmospheric pressure: environment pressure
- alveolar pressure: pressure in alveoli
- intrapleural pressure: pressure in between parietal and visceral pleura
- always subatmospheric
- in between breathes: atmospheric = alveolar
- role of pressure gradients
- between alveolar and intrapleural: oppose lung elastic recoil (0 push on -4 →)
- between atmospheric and intrapleural: oppose chest wall elastic recoil (0 push on -4 ←)
- both these effects = lung and chest wall moving together as one unit as they’re both pushing against the intrapleural space
Respiratory muscles role creating pressure/volume changes to produce inspiration and expiration from eupnea to forceful breathing.
Eupnea
- inspiration
- diaphragm flatten downwards
- external intercostals: outward upward chest wall movement
- muscles contract → thoracic cavity volume increase → lung volume increase → alveolar pressure subatmospheric → air flow into lungs (connecting Boyle’s law)
- expiration
- diaphragm recoil to dome shape
- external intercostals: inward and downward chest wall movement, recoil of chest wall
- muscles relax → thoracic cavity volume decrease → lung volume decrease → alveolar pressure greater than atmospheric → air expiration
More forceful
- inspiration
- same diaphragm and external intercostals
- recruit accessory muscles of inspiration (SCM, scalenes, pectoralis minor) to help chest wall movement
- greater increase in lung volume → greater subatmospheric pressure in alveoli → more air flow into lungs
- expiration
- same diaphragm and external intercostals
- recruit accessory muscles of expiration (internal intercostals, abdominals) to help chest wall movement
- greater decrease in lung volume → alveoli compression → greater increase above atmospheric pressure for alveolar pressure → greater air flow out of lungs
Role of medullary respiratory centre and changes from eupnea to forceful breathing. (think of chart cycle thing)
Medullary respiratory centre
- pre-botzinger complex possible pacemaker and sends signals to…
- dorsal respiratory group made of inspiratory neurons that starts breathing cycle
- ventral respiratory group made of both inspiratory and expiratory neurons that helps when more forceful breathing needed
roles in breathing
- eupnea: during relaxed breathing, the dorsal respiratory group is the only group working by cycling between active and inactive since nothing more is needed for expiration (eg. all muscles and stuff are just relaxing with no outside influence)
- more forceful breathing: DRG still cycling but more active contraction and less inactive recoil. This leads to the VRG being recruited and the neurons activating the muscles of inspiration and expiration
Contributions of pontine respiratory group, proprioceptors, chemoreceptors, and higher brain centres to ventilation.
Pontine respiratory group
- sends signals to DRG to influence switching between active and inactive and modifying breathing cycle
- strong signal when speaking or exercising (ex. switching to active breathing just for a second to accommodate a long, run-on sentence)
Proprioceptors
- in joints and muscles to respond to changes in body movement (rest to exercise, very relevant to changing breathing)
- send signals to DRG to match ventilation to movement needs (strong or weak depending on movement)
Chemoreceptors
- peripheral chemoreceptors: carotid sinus and aortic arch, respond to changes in arterial blood
- central chemoreceptors: medulla oblongata, respond to changes in interstitial fluid surrounding brain
- send signals to DRG to increase ventilation, needs a dramatic shift though for chemoreceptors to be necessary
- refer to flow chart in mind
Higher brain centre
- anything above brainstem, mainly cerebrum or cerebellum
- apnea: stopped breathing when voluntary signal over rides involuntary
- two ways, arterial oxygen low enough and you pass out and involuntarily breath again or arterial CO2 high enough and you start breathing voluntarily to compensate
Respiratory volumes and capacities plus relation to each other.
Volumes
- tidal volume: air volume inspired or expired (tidal __) in a single breath
- inspiratory reserve volume: how much more air volume could be inspired
- expiratory reserve volume: how much more air volume could be expired
- residual volume: air volume remaining after maximum expiration
Capacities
- vital capacity: IRV + ERV + TV, air volume from maximum inspiration to maximum expiration
- total lung capacity: all 4 volumes added together, maximum air volume lungs can contain
Relation to each other
- volumes make up capacities
- residual volume determines whether vital or total lung for capacities
Ventilation changes from rest to exercise.
- tidal volume increases because more air needs to be inspired and expired in a single breath
- reserve volumes decrease since they are being used
- residual volume stays the same
- since tidal volume and reserve volumes have a sort of inverse relationship, the capacities don’t change much
Forced vital capacity and relation to lung diseases.
forced vital capacity: air volume expired from max inspiration to max expiration as fast and hard as possible
forced expiratory volume in one second: volume of air expired in 1st second of FVC effort
- %FEV1 = FEV1/FVC
Relation to lung diseases
- obstructive lung diseases: blocking air expiration making difficult to fully expire air, FEV1 decreases much more than FVC so % goes down a lot
- restrictive lung diseases: block inspiring making difficult to fully inspire air, both FVC and FEV1 decrease so percentage remain similar
Minute ventilation and its components.
equation: VE = VT x f
- air flowing into or out of lungs per unit time (L/min or mL/min)
-VE = minute ventilation
-VT = air volume in one breath either inspired or expired
-f = breathing frequency in bpm
Graphs changing with exercise intensity
- minute ventilation: linear until moderate intensity, then two exponential increases (VT1 and VT2, ventilary threshold points)
- tidal volume: linear from eupnea until moderate where it plateaus
- breathing frequency: linear from eupnea to maximum intensity
Concept of dead space and the different types.
Dead space: portion of minute ventilation not reaching gas exchange
types
- anatomical: conducting zone like main and lobar bronchi above
- alveolar: damaged or blocked alveoli
- physiological dead space: anatomical + alveolar
Alveolar ventilation and its importance. (remember chart with different values for VT, VE, VD, VA, and EV)
equation: VA = (VT - VD) x f, basically taking the air that’s making it to the exchange areas and multiplying by the breathing frequency
- air flowing into or out of alveoli per unit time
Effective ventilation: how much minute ventilation reaches gas exchange areas in alveoli as a percentage (VA/VE = %)
Breathing patterns
- different ones don’t affect VE
- however, VD at lowest with slow, deep breaths which means VA is highest, this means EV is higher too since more air is reaching the target alveoli
Dalton’s Law and its importance
equation: PG = Patm x FG
- PG = individual gas partial pressure in air
- Patm: atmospheric pressure
- FG: fraction of gas in air
- total pressure exerted by mixture of gases is sum of pressures exerted by each gas in mixture
- ex. at sea level, Patm = 760mmHg, FO2 (FG) = 21 % → PO2 (PG) = 760 x 0.21 = 159mmHg
- ventilation driven by air pressure gradients, respiration driven by individual gas pressure gradients (partial pressure gradients)
Gas exchange for oxygen and carbon dioxide at external respiration sites.
remember: external respiration is between alveoli and pulmonary capillaries
oxygen
- alveoli has 105mmHg while arterial blood arriving in pulmonary capillaries only has 40mmHg, thus the gradient favours alveoli to pulmonary capillaries
- results: arterial blood n pulmonary capillaries is oxygenated with 100mmHg and can pump blood to systemic circulation to do it’s thang!
carbon dioxide
- alveoli has 40mmHg and arterial blood arriving in pulmonary capillaries has 46mmHg, but the partial pressure gradient favours pulmonary capillaries to alveoli since we want to limit CO2 in our bodies
- results: arterial blood leaves with slightly less CO2 and obtained. CO2 in alveoli is expired into atmosphere
Process of ventilation-perfusion matching and response to mismatch.
Process: ventilation (air flow to alveoli) and perfusion (blood flow into pulmonary capillaries) try their best to match each other for the most efficient gas exchange
decreased ventilation
- decrease airflow to region of lung
- PO2 of pulmonary bloodgoes down
- pulmonary vessels vasoconstrict
- blood flow decreases
decreased perfusion
- decrease blood flow to region of lung
- PCO2 of alveoli goes down
- bronchioconstriction
- air flow decreases
*both lead to diversion of air and blood flow from unhealthy to healthy areas of lung
Gas exchange for oxygen and carbon dioxide at internal respiration sites.
basically opposite of external respiration (remember, tissue capillaries and interstitial fluid)
oxygen
- tissue cells (<40mmHg) and arterial blood arriving in tissue capillaries have 100mmHg
- partial pressure gradient favours tissue capillaries to tissue cells (makes sense, we want oxygen to get to tissue cells to be used)
- results: arterial blood leaves deoxygenated (40mmHg) and oxygen enters interstitial fluid to send to tissue cells to be used, systemic circulation sends blood to pulmonary circulation to be oxygenated again
carbon dioxide
- tissue cells (>46mmHg) and arterial blood arriving in tissue capillaries with 40mmHg
- partial pressure gradient favours tissue cells to tissue capillaries (makes sense, tissue cells want to get rid of CO2)
- results: blood leaves with more CO2 and heads to heart to be pumped into pulmonary circulation where lungs can take and expire (relating to external respiration)
Role of a-v oxygen difference at rest and exercise plus how it combines with cardiac output to give oxygen consumption.
Definition: difference between oxygen going into tissue capillary bed and oxygen coming out of tissue capillary bed
- a-v O2: a is artery, v is vein
- oxygen leaves blood to interstitial fluid to tissue cells
at rest
- 20mL enters, 15-16mL exits, a-v O2 difference 4-5mL, small difference = less O2 needed to supply tissue cells at rest
exercise
- 20mL enters, 5mL exit, a-v O2 difference 15mL, larger difference = more O2 needed to supply tissue cells during exercise
Cardiac output combination
- VO2: volume of oxygen consumption per unit time (L/min or mL/kg/min)
- fick equation: VO2 = Q x (a-v O2 difference)
- Q: delivery of oxygen in blood
- a-v O2 difference: extraction of oxygen from blood
- max oxygen consumption = VO2 max
Regulation of movement across membranes for external and internal respiration plus how changes would affect respiration.
locations
1. external respiration: alveolar wall → pulmonary capillary (huge for external, not as much for internal)
2. internal respiration: tissue capillary to interstitial fluid
factors/changes
- partial pressure gradient of gas (most important)
- surface area (like capillary beds opening due to relaxation of sphincters)
- thickness of membrane gas is going through (like fluid in alveoli)
- diffusion coefficient of gas (amount to cross area in 1 second)
Henry’s Law and its importance.
Definition: at constant temperature, amount of gas dissolved in liquid (concentration) directly relates to partial pressure gradient that moves gas into liquid (PG) and solubility of gas in liquid (solubility coefficient)
equation: C = PG x S
- C = concentration
- PG = partial pressure gradient
- S = solubility coefficient
single gas in liquid? S constant and concentration only depends on PG
multiple gases? S can differ so concentration depends on both S and PG (ex. CO2 much more soluble in blood than oxygen)
Affinity and loading/unloading and contribution to gas exchange and transport.
Affinity: how tight oxygen binds to transporters
- lower: more likely to unload
- higher: more likely to load
Problem 1
- cant dissolve enough oxygen and CO2 into blood for metabolic needs
- solution is gas transporters binding gases and moving enough to meed metabolic needs, gas does not count in dissolved concentration when bound to a transporter
Problem 2
- only dissolved gas can participate in gas exchange
- solution is transporters being able to let go as well after binding and let molecules return to dissolved state to participate
Processes for transporting oxygen.
- Hemoglobin binds between 0-4 oxygen molecules at a time
- 100%/saturated means all sites occupied by oxygen
- lower means not all sites
- 1.5% oxygen dissolved in plasma, rest bind to hemoglobin for gas transport as oxyhemoglobin inside an erythrocyte (red blood cell)
- process: alveolus gives dissolved O2 → erythrocyte picking up and making oxyhemoglobin → oxyhemoglobin splitting near tissue cells in interstitial fluid → dissolved O2 being consumed by cell mitochondria
Oxygen-hemoglobin saturation curve at rest and exercise plus causes and effects of curve shifts.
Resting external respiration
- arrival: deoxygenated blood (40mmHg) at 78% saturation
- exit: oxygenated blood (100mmHg) at 100% saturation
- difference in saturation (22%) from oxygen from alveoli being added to blood in pulmonary capillaries
Resting internal respiration
- arrival: oxygenated blood (100mmHg) at 100% saturation
- exit: deoxygenated blood (40mmHg) at 78% saturation
- difference in saturation (22%) from oxygen in blood going to interstitial fluid and tissue cells
Exercise external respiration
- arrival: deoxygenated blood (20mmHg) at 38% saturation
- exit: oxygenated blood (100mmHg) at 100% saturation
- difference in saturation (62%) from oxygen being added to blood in pulmonary capillaries, still reaching 100% saturation since usually enough time under most exercise conditions (unless unhealthy individual)
- oxygen levels are lower but body good at getting oxygen into bloodstream
Exercise internal respiration
- arrival: oxygenated blood (100mmHg) at 100% saturation
- exit: deoxygenated blood (20mmHg) at 38% saturation
- difference in saturation (62%) from more oxygen being released by Hb and heading into interstitial fluid and tissue cells
Saturation curve
- movement to right: increase partial pressure oxygen with more oxygen binding to Hb and Hb-O2 saturation increasing contributing to loading
- movement to left: decrease partial pressure oxygen with less oxygen binding to Hb and Hb-O2 saturation decreasing and contributing to unloading
- sometimes we want high, other times we want load, depends if we want to load for gas transport or unload for gas exchange
- Plateau portion: like a safety margin, only 22mmHg decrease in PO2 and a very small decrease in saturation from 100% to 98%, this is why you don’t feel much effects during the beginnings of a respiratory disease
- Steep portion: 20mmHg decrease in PO2 (from 40mmHg to 20mmHg) and a large decrease in saturation from 78% to 38%, this is where you start to feel effects of respiratory disease quickly and suddenly
- location on curve matters
- Hb-O2 saturation = Hb saturation
Curve shifts
- PO2 most important variable for Hb saturation, but acidity, CO2, and temperature can also cause curve shifts
- right shift: decrease affinity, increase unloading, lower Hb saturation, more oxygen for gas exchange, basically exercising since all things that cause right curve shift result from exercise
- left shift: increase affinity, decrease unloading, greater Hb saturation, less oxygen for gas exchange
- neither shift is bad, just depends on what we want in that moment (more affinity for oxygen transport or less for exchange?)
Importance of Bohr effect.
- active muscles have high CO2 and H+ levels from increased metabolism and lactate production
- as such, oxygenated blood enters tissue capillaries of active muscles
- the high CO2 levels and H+ levels lower affinity of Hb for oxygen (right curve shift)
- oxygen unload from Hb which means it’s released from transporter and in a dissolved state
- dissolved oxygen can cross membrane to interstitial fluid and supply active muscles (internal respiration of oxygen)
- Hb, now with no oxygen, can bind to the high levels of CO2 and H+ from the increased metabolism and lactate during exercise and transport to removal areas (lungs - external respiration, kidneys- urinary output)
Processes for transporting carbon dioxide.
- 7% of CO2 dissolved in plasma and inside erythrocyte (can dissolve more CO2 in blood than oxygen → higher solubility coefficient)
- 23% CO2 binds to Hb as carbaminohemoglobin (HBCO2) inside erythrocyte
- 70% CO2 convert to bicarbonate inside erythrocyte and moves outside erythrocyte once formed (accompanies chloride shift) and dissolves in plasma
- to correct too much negative charge, chloride shift corrects (every bicarbonate take charge out, chloride take charge in)
Dangers of carbon monoxide.
Every hemoglobin only has 4 binding sites, then two gases are competing
- Problem with this is carbon monoxide has high affinity for these sites
- When CO around, it will likely win due to it’s strong affinity
- Sites not carrying oxygen = lesser value of saturation = hypoxia
- Carbon monoxide influences Hb ability to unload oxygen, less gas letting go means staying bound to transporter because has to get to dissolved statese to go to membrane and be delivered, no dissolved oxygen = hypoxia for different reason
First problem
- CO has extremely high affinity for heme sites so it usually beats oxygen to heme sites
- leads to less oxygen binding Hb → less O2 transported to tissues → hypoxia
Second problem
- 4 heme sites can have combination of CO and oxygen
- however, binding CO cause shape change and make it harder for O2 to unload
- leads to less unloading → less gas exchange in internal respiration → hypoxia)
Often need oxygen therapy with pure pressurized oxygen to force CO of heme sites
