Respiratory system - Lectures 17-18 Flashcards
4 functions of respiratory system
- gas exchange
- pH regulation (by means of CO2)
- removal of pathogens
- sound
respiratory system bulk flow
- flow takes place from regions of _______ to _______ pressure
- a ________ pump creates pressure gradients
- resistance to air flow is influenced primarily by the ________ of tubes through which air is flowing
- higher to lower pressure
- muscular pump
- diameter
Resistance of air flow
- 90% due to what bc what
- 10% due to what bc what
- 90% due to trachea and bronche –> has cartilage: cannot change size of diameter/change resistance
- 10% bronchioles –> can have dilation and constriction to modify resistance
what is the conducting zone vs respiratory zone?
CONDUCTING ZONE: air just passing through
- nose –> pharynx –> larynx –> trachea –> bronche –> bronchiole
RESPIRATORY ZONE: gas exchanges (mostly in alveoli)
- respiratory bronchioles –> alveoli duct –> alveoli
** bronchiole leads to respiratory bronchiole
what is external respiration vs internal respiration?
EXTERNAL: exchange of air between atmosphere and lungs (+ btw lungs and blood?)
INTERNAL: exchange of gases between blood and cells
4 steps of external respiration ish
- exchange 1: atmosphere to lung (= ventilation)
- exchange 2: lung to blood
- transport of gases in blood
- exchange 3: blood to cells (internal respiration)
CONDUCTING SYSTEM
- upper respiratory tract (4)
- lower respiratory tract (4)
WHAT IS THE SITE OF GAS EXCHANGE?
- UPPER: mouth, nasal cavity, pharynx, larynx
- LOWER: trachea, 2 primary bronchi, their branches, lungs
ALVEOLI! (singular alveolus)
THORACIC CAGE:
- includes what (4 + 1 has 4 subtypes)
- bones and muscles of thorax that surround the lungs
- spine
- rib cage
- muscles: diaphragm, intercostal muscles, sternocleidomastoids, scalenes
- pleural sacs each surround a lung
4 types of muscles in thoracic cage + functions
DIAPHRAGM:
- btw lung cavity and digestive cavity
- contraction = decrease rib cage size
INTERCOSTAL MUSCLES:
- btw ribs
- internal –> contraction = decrease thoracic cage size
- external –> contraction = increase thoracic cage size
- 2 dif layer muscle in different directions
STERNOCLEIDOMASTOIDS:
- neck muscle, linked to sternum
- moves head + lifts rib cage = increase size
SCALENES:
- neck muscle
- linked to 1st and 2nd rib & collar bone
- lifts rib cage up = increase size rib cage
lungs are wrapped by 2 layers of ____A_____ (what type of tissue?) = the ______ _____
- what is contained in the layer of _____A______ –> 2 functions
- what happens if ____A_____ is pierced?
- pleura = connective tissue –> pleural sac forms a double membrane surrounding the lung, similar to a fluid-filled balloon surrounding an air-filled balloon (lung)
- pleural fluid
1. lowers friction between membranes
2. holds lungs tight against thoracic wall –> the pleural fluid prevents pleura from coming apart = hold lung tissue and thoracic wall together as unit - if pleura is pierced –> rib towards outside and lungs collapses bc not held together as a unit anymore = pneumothorax bc air in thorax
Right vs Left lung size and shape
R: shorter and wider
L: longer + has cardiac notch to accommodate apex of heart
which muscles are involved in inhale vs exhale vs forced respiration?
NORMAL INHALE:
- diaphragm contract (flattens) + external intercostal muscle contract = thoracic volume increases
FORCED INHALE:
- diaphragm + external intercostal muscle + 2 neck muscles (sternoclidomastoid + scalenes) = increase thoracic volume
NORMAL EXHALE:
- diaphragm + external intercostal muscle RELAX = thoracic volume decreases (diaphragm is bombé vers le haut)
FORCED EXHALE:
- internal intercostal muscle + abdominal contract to decrease rib cage size
R ventricle –> lung –> pulmonary vein
- long or short distance?
- high or low blood pressure?
short + low blood pressure
each alveoli has 3 types of cells
- describe
+ 2 types of connective tissue
- Type 1 alveolar cell –> gas exchange
- type 2 alveolar cell (surfactant cell) –> synthesizes and secretes surfactant to decrease surface tension
- alveolar macrophage –> ingests foreign material
+ collagen and elastin
primary bronchi ________ out a lot = increase what?
- total cross-sectional area of alveoli/exchange surface
- branches out a lot! = increase surface area
- 75 m^2
- what contains your vocal cords?
- what is your windpipe?
- larynx
- trachea
what do your airways do to the inspired air? (3)
- warming air to body temp
- adding water vapor and muscu to air
- filtering out foreign material
why do we have runny noses during the winter?
because cold air stimulates gland secretion = mucus
- cilia (move extra fluid from nose to mouth to swallow in oesophagus) don’t work well in cold air so mucus/extra fluid comes out from nose
which cells produce mucus?
- what moves mucus toward pharynx? what does the mucus also remove?
- goblet cells
- cilia! mucus removes trapped pathogens and particulate matter
how is saline secreted by airway epithelial cells? (4 steps)
- Na+/K+/2Cl= symporter (NKCC) brings Cl- into epithelial cell from ECF
- apical anion channel including CFTR (Cystic fibrosis transmembrane regulator channel) allow Cl- to enter lumen of airway
- Na+ goes from ECF to lumen by paracellular pathway, drawn by electrochemical gradient (drawn to negative charge of Cl- in lumen)
- NaCL movement from ECF to lumen creates a concentration gradient so water follow to lumen
*Cystic fibrosis: NO CFTR –> no Cl-, Na+ or water in lumen —> mucus blocked in trachea/airways
describe Boyle’s law and Dalton’s law
BOYLE’S LAW:
- P1V1 = P2V2
- pressure volume inverse relationship
DALTON’S LAW:
- total pressure equals sum of all partial pressures
- Pt = pp1 + pp2 + pp3
in humid air, water vapor ______ the contribution of other gases to the total pressure
- what is the normal atmospheric pressure?
- how to calculate partial pressure of a gas in humid air?
- DILUTES!
- 760 mm Hg
- at 25°C, 100% humidity: 155 mmHg O2 (21% of air) + 0.24 mm Hg CO2 (0.03% of air) + 24 mmHg water (100% humidity)
- Pgas in humid air = (Patm - PH2O) * % of gas
ie: PO2 = (760-24) * 0.21 = 155 mmHg
what is
- TIDAL VOLUME (VT)
- INSPIRATION RESERVE VOLUME (IRV)
- EXPIRATION RESERVE VOLUME (ERV)
- RESIDUAL VOLUME (RV)
- VT: volume that moves during a respiratory cycle (air that gets in/out during normal breathing) (kinda like stroke volume)
- IRV: additional volume above tidal volume (when you use neck muscles)
- ERV: forcefully exhaled after end of normal expiration (when you use abs and internal intercostal muscles)
- RV: volume of air in respiratory system after maximal exhalation
what machine can do pulmonary function tests?
spirometer!
can measure difference in volume during inspiration and expiration
IRV, VT, ERV and RV for males vs females
- total lung capacity?
MALES:
- IRV = 3000 mL
- VT = 500 mL
- ERV = 1100 mL
- RV = 1200 mL
- total = sum = 5800 mL
FEMALES:
- IRV = 1900 mL
- VT = 500 mL
- ERV = 700 mL
- RV = 1100 mL
- TOTAL = 4200 mL
air flow is proportional to what?
- inspiration occurs when what decreases/increases?
- vs when does expiration occur?
- flow proportional to deltaP / resistance (just like blood flow)
- inspiration –> alveolar pressure decreases
- expiration –> alveolar pressure increases
__________ pressure inside the pleural cavity keeps the lungs inflated –> how much?
- in normal lung at rest, ______ _____ keeps lung adhered to chest wall –> what happens to pressure when we inhale?
- subatmospheric pressure –> -3 mm Hg
- pleural fluid keeps lung to chest
- inhale = lungs get bigger = pressure decreases (-3 to -6 mmg Hg) –> air gets in through pressure difference
Compliance vs elastance?
- what does compliance depend on? high vs low compliance?
COMPLIANCE:
- ability to stretch (how easy to pull lung tissue)
- depends on 1) elastic fibers 2) surface tension
- HIGH = stretches easily
- LOW = requires more force
- restrictive lung diseases (fibrosis and NRDS) = low compliance
ELASTANCE:
- ability fo return to resting volume when stretching force is released/recoil to original shape
what is LaPlace’s law?
Pressure = 2 T / r
- where T is surface tension and r is radius
what are surfactants?
- contain what?
- functions
- more concentrated where
- premature babies have surfactants?
- surfactants = surface active agents –> disrupts cohesive force of water
- mixture of proteins and phospholipids
- 1) prevent collapsing of small alveoli (bc there’s more surfactant) and 2) increase recoil and decrease surface tension
- more concentrated in smaller alveoli
- premature babies don’t have surfactants (newborn respiratory distress syndrome) = used to die –> now, there are artificial surfactants
- if same surface tension but one bubble has bigger radius, which bubble has bigger pressure? –> consequence?
- how to make sure they have the same pressure?
- smaller radius = bigger pressure
– > if the 2 are linked, air will move from smaller bubble to larger bubble - more surfactants in the smaller bubble to decrease surface tension!
what factors affect airway resistance? (same formula as for blood flow)
- what factor can be regulated?
- R = 8Ln / pi * r^4
- length of system, viscosity of air –> all pretty constant
- most important factor = diameter of airways!
- UPPER AIRWAYS: doesn’t change much bc cartilage prevents dilation BUT physical obstruction could affect
- LOWER AIRWAYS/bronchioles –> bronchoconstriction and bronchodilation –> 10% of resistance but can be regulated because of smooth muscles!
how is bronchoconstriction (3) and bronchodilation (2) mediated?
CONSTRICTION:
- parasympathetic neurons (muscarinic receptors, M3)
- histamine: constrict tubules = increase resistance
- leukotrienes
BRONCHODILATION:
- carbon dioxide
- sympathetic neurons: epinephrine (b2 receptors on smooth muscles relax) from adrenal medulla
- what is total pulmonary ventilation? formula?
- what is alveolar ventilation? formula + example
PULMONARY:
- volume of air moved in and out of lungs per minute
- ventilation rate x tidal volume
- ie: 12 breaths/min * 500 mL/breath = 6000 mL/min
ALVEOLAR:
- more accurate: how much fresh air reaches alveoli bc fresh air in dead space doesn’t get to alveoli
- ventilation rate * (tidal volume - dead space)
- ie: 12 * (500 - 150 mL) = 4200 mL/min
- end of expiration, lung volume = 2200 mL + dead space (150 mL) is filled with what air?
- inhale 500 mL fresh air: first 150mL to reach alveoli is what air? only ____ mL of fresh air reaches alveoli + dead space filled with what air?
- end of inspiration: lung volume = ______ mL + dead space filled with what?
- exhale 500 mL (tidal volume): first 150 mL exhaled air is what air? only _____ mL leaves the _____
- dead space = 150 mL stale air
- first 150mL to reach alveoli is stale air –> only 350 mL of fresh air reaches alveoli –> dead space is now filled with fresh air
- 2700 mL + dead space = fresh air
- first 150 mL exhaled is fresh air. only 350 mL leaves the alveoli. lung volume back to 2200 mL
if you increase respiration rate, tidal volume might decrease/increase, so total alveolar ventilation will decrease/increase?
- Vt might decrease –> more shallow breathing
- alveolar ventilation will decrease bc 150mL dead space remains the same
does alveolar gas composition vary a lot during normal breathing? how come?
- fresh air into lungs is about __% total lung volume at the end of inspiration
- what 2 things are matched to ensure efficiency of gas exchange between alveoli and capillaries?
nope! varies little because O2 entering alveoli (environ =) O2 entering blood
- fresh air into lungs is about 10% total lung volume at the end of inspiration
- ventilation and alveolar blood flow are matched
- if alveolar ventilation increases, what happens to PO2 and PCO2
- vs if alveolar ventilation decreases?
VENTILATION INCREASE:
- PO2 increases and PCO2 decreases
VENTILATION DECREASE:
- PO2 decreases and PCO2 increases
what is perfusion? vs ventilation?
- both are ________
- perfusion = blood flow to alveoli
- ventilation = air into alveoli
- both are matched! to maximize gas exchanges
what happens if ventilation decreases in a group of alveoli? consequence?
- PCO2 increases and PO2 decreases –> blood flowing past those alveoli does not get oxygenated
- consequence: arterioles around that under ventilated alveoli constrict (reduce blood flow to that area) –> diverting blood to better ventilated alveoli
bronchiole diameter is mediated primarily by _____ levels in exhaled air passing through them
- local control of arterioles and bronchioles by ______ and _______
(Check tableau of what happens to bronchioles and pulmonary arteries when PCO2/PO2 increases/decreases!!!!)
- CO2 levels!
- O2 and CO2
how is O2 transported from lungs to cells? (2)
- how is CO2 transported from cells to lungs? (3)
- O2: in blood: dissolved in plasma or bound to Hb inside RBCs
- CO2: in blood: dissolved in plasma OR bound to Hb OR as HCO3-
PO2 and PCO2 in arterial vs venous?
PO2:
- arterial = 95 mm Hg
- venous = 40 mm Hg
- HUGE difference!
PCO2:
- arterial: 40 mmHg
- venous = 46 mm Hg
- smalle difference
how is there a similar gas exchange efficiency even if difference between arterial and venous PO2 is so different than difference for PCO2?
because CO2 is much more soluble in blood than O2!!
- breathing is _____ ______ of air into and out of lungs
- individual gasses diffuse along ______ _______ gradients until equilibrium
- exchange btw alveoli and blood
1. PO2 alevolar air (> or <) PO2 blood
2. PCO2 blood (> or <) PCO2 alveolar air - exchange btw blood and tissues
3. PO2 blood (> or <) PO2 tissue
4. PCO2 tissue (> or <) PCO2 blood
- bulk flow
- partial pressure gradients
1. PO2 alevolar air > PO2 blood
2. PCO2 blood > PCO2 alveolar air
3. PO2 blood > PO2 tissue
4. PCO2 tissue > PCO2 blood
what does O2 and CO2 have to diffuse through to get from alveolar air space to blood capillary lumen? (4)
- surfactant
- alveolar epithelium
- fused basement membrane
- blood vessel epithelium
Pathologies can cause hypoxia
- diffusion proportional to (2)
1. emphysema
2. fibrotic lung disease
3. pulmonary edema
4. asthma
- surface area x barrier permeability/distance^2
1. destruction of alveoli = less surface area for gas exchange
2. thickened alveolar membrane slows gas exchange
3. fluid in interstitial space increases diffusion distance –> arterial PCO2 may be normal due to higher CO2 solubility in water
4. increased airway resistance (bronchioles are constricted) decreases alveolar ventilation
movement of gasses is directly proportional to (3)
- pressure gradient of gas
- solubility of gas in liquid
- temperature (increase temp ie while running = increase diffusion)
- at equilibrium, PO2 in air and water are ______. high/low solubility of O2 in water means concentrations are equal/not equal
- what would we have to do to dissolve O2 in champagne (instead of CO2)
- partial pressures are equal, but concentrations are now bc O2 has low solubility
- would have to increase pressure a lot to have same amount of O2 as CO2 in champagne to make it pop! (increase pressure = increase solubility)
how much O2 is dissolved in blood vs bound to Hb?
- how many O2 can bind to 1 Hb
- formula for O2 binding to Hb
- O2 binding obeys law of mass action –> increase PO2 shifts rxn to R/L? vs decrease PO2?
- <2% dissolved vs 98% bound to Hb
- 4 O2 to 1 Hb
- Hb + O2 <–> HbO2 (oxyhemoglobin)
- increase PO2 –> shifts to R
- decrease PO2 –> shifts to L
- what determines oxygen-Hb binding? (2)
- oxygen binding is expressed as what?
- PO2 in plasma! + available O2-binding sites on Hb
- as a percentage! percent saturation of Hb = amount of O2 bound / maximum that could be bound
How is O2 delivered from alveoli to cells? (4 steps)
- O2 diffuses into blood and dissolves into plasma (<2%)
- O2 binds to Hb so that more O2 can enter the blood
- RBC containing Hb-O2 transports in bloodstream to reach cell
- O2 detaches from Hb, dissolves in plasma and diffuses to cell
what can alter O2-binding affinity (3 + extra)
- how can these 3 be modified (increase/decrease) to increase vs decrease O2 released?
- pH, temperature, PCO2 –> + hemoglobin shape
INCREASE O2 released (shift to right) = decreased affinity - decrease pH, increase temp, increase PCO2 –> all represent an increase in metabolic activity so O2 will be more released from Hb
DECREASE O2 released (shift to left) = increased affinity
- increase pH, decrease temp, decrease PCO2
- decrease in metabolic activity
what is the Bohr effect?
- shift in hemoglobin saturation curve resulting from a pH decrease –> saturation curve will shift towards the right
what does 2,3 biphosphoglycerate do to the Hb saturation curve?
shifts curve to the right! = decrease affinity
- chronic hypoxia (ie high altitude) increases RBC production of 2,3 BPG
- RBC don’t have organelles (mit) –> rely on glycolysis for energy –> increase activity = increase glycolysis = increase 2-3BPG –> curve moves to R to increase release of O2 from Hb
what is cooperative binding?
when 1 O2 binds to Hb, Hb will change conformation and increase its affinity to O2
does maternal or fetal Hb have better hemoglobin saturation/O2 binding properties?
- fetal curve more to the left = better affinity to O2 = less O2 released
- maternal curve more to right = lower affinity to O2 = more O2 released
- how is carbon dioxide transported in blood (3 + give %)
- write out equations
- dissolved in plasma (7%)
- bound to Hb (23%)
- Hb + CO2 <–> HbCO2 (carbaminohemoglobin) - converted to HCO3- (70%)
- CO2 + H2O <–> H2CO3 <–> H+ + HCO3-
- use carbonic anhydride for 1st rxn
- H+ binds to Hb: Hb + H <–> HbH (respiratory acidosis)
what is the chloride shift?
- exchanges HCO3- for Cl- to maintain electrical neutrality
- when HCO3- diffuses out of RBC, Cl- enters RBC to keep a negative charge in RBC
CO2 transport from cell to alveoli (8 steps)
- CO2 diffuses out of cells into systemic capillaries
- Only 7% of CO2 remains dissolved in plasma
- in RBC: 23% CO2 binds to Hb, froming carbaminohemoglobin
- in RBC: 70% of CO2 is converted to bicarbonate and H+. Hb buffers H+ (forming HbH)
- HCO3- exits RBC and enters plasma in exchange for Cl- (chloride shift)
- near lungs/alveoli, HCO3- from plasma is pulled back into RBC and converted into CO2
- by law of mass action, CO2 unbinds from Hb and diffused out of RBC
- at lungs, dissolved CO2 diffuses out of plasma
what is the haldane effect?
- binding of O2 on HBCO2 will increase dissociation of HbCO2 into Hb and CO2
- allows for expiration of CO2 when O2 comes in!
REGULATION OF VENTILATION:
- neural networks in _____ ___ behaves like a central pattern generator
1. respiratory _____ in the _______ control inspiratory and expiratory muscles –> control the _______ of breathing ish
2. neurons in the ______ integrate _____ info and interact with ______ neurons to influence ventilation
3. rhythmic pattern of breathing arise from a neural network of spontaneously ________ neurons (need more research)
4. ventilation is subject to continuous modulation by _______ and _________-linked reflexes and higher brain centers
- brain stem
1. neurons in the medulla –> control the starting of breathing
2. pons –> integrate sensory info and interact with medullary
3. spontaneously discharging neurons
4. chemoreceptor and mechanoreceptor-linked reflexes
what are the 3 respiratory groups in medulla that control breathing?
- DORSAL RESPIRATORY GROUP (DRG)
- located in nucleus tractus solitaries (NTS)
- induces respiration (contraction of diaphragm and intercostal muscles)
- sensory input from chemo- and mechano receptors to pons - PONTINE RESPIRATORY GROUP (PRG)
- receive info from limbic system/cortex and medulla –> integrate and send to medulla again - VENTRAL RESPIRATORY GROUP (VRG)
- pre-Botzinger complex –> basic pacemaker activity
- areas for active expiration and force inspiration
PERIPHERAL CHEMORECEPTORS:
- located where
- sense changes in (3): (increase/decrease) will increase ventilation? how?
- specialized ______ cells
- O2 must fall below ____ mmHg to trigger reflex
- carotid bodies
- PO2, pH and PCO2
- decrease PO2, increase pH and increase PCO2 –> initiate ventilation –> closes K+ channels –> depolarization –> opens Ca2+ channels –> release neurotransmitters in glomus cells
- glomus cells! exist in aortic and carotic body –> have receptors that respond to PCO2, PO2, H+
- 60 mmHg
CENTRAL CHEMORECEPTORS:
- located where
- respond to changes in what? –> what is actually detected tho?
- located in CNS
- in PCO2 –> if increase PCO2 –> CO2 crosses into brain ECF –> CO2 is converted to bicarbonate and H+ –> H+ is actually detected!
will acidosis in blood vessels increase ventilation?
no! bc H+ can’t go in brain!
- if increase PCO2 –> CO2 can go into brain –> makes H+ ions which activate central chemoreceptors
what protective reflexes guard lungs? (4)
- bronchoconstriction: irritant receptors in airway mucosa send signals through sensory neurons
- sneezing
- coughing
- Hering-Breuer inflation reflex: bronchiles expand too much –> induce contraction reflex to go to normal size
______ _______ _____ affects patterns of ventilation but is not required for ventilation!
- ______ and _______ can change control of _____ _____ on breath rate and depth
- _____ system can affect breath rate and depth –> can bypass _____ ______
- can these override chemoreceptor reflexes?
- higher brain centers! can affect but are not required!
- hypothalamus and cerebrum can change control of brain stem –> ie you can voluntarily breathe
- limbic system (emotions) –> can bypass brain stem
- higher brain centers cannot override chemoreceptor reflexes –> if we voluntarily stop breathing –> increase in CO2 will activate chemoreceptor reflexes and force you to breathe!!
