Physiology (Respiration) Flashcards
Functions of Lung
Main function - Gas exchange (respiration - take in O2 and remove CO2)
Other functions:
1. Filter inspired air
2. Defends against inhaled particles - done through hair cells in nose and trachea + mucous (Bronchi are lined with Psudostratified ciliated columnar epitheliam + biofilm mucous –> traps small particles)
- Smaller things = can’t be filtered (Ex. viruses/bacteria = can escape protection mechanisms)
3. Immunologic survelece –> lung is exposed to the envirnment = need protective mechanism
- Example - Ling transplant patients ahve unique challenges
4. Peptide processing –> regulates functions (Ex. Regulates BP)
Breathing control
Breathing = autonmic but can be induced conciouslly
Circulatory = autonmic
Respiration = autonmic (affected by envirnment)
What do we need to breath
- Brain function - have breathing center in brainstem
- Brain tells us to breath
- Brain death = damage to brain stem that don’t trigger breathing
- Ventilation
- Circulation - transport oxygen to tissues and CO2 away
- Respiration
- Exchnage of gas at the tissue level across the alveolar capilary (O2 i and CO2 out)
- Blood flow much match ventilation
Breath Steps
- Decide to breath (conscious or unconscious)
- Air comes into lungs - Lings are able to expand (Intercaustal muscle and diaphram contract = creates negative pressure in chest = expand lungs = air comes in)
- Oxygen goes into capillaries - Air diffuses from capilary to Aveoli space
- Oxygen gets picked up by hemoglobin
- Oxygen gets circulated in blood and delivered to tissues + CO2 is released from tissues has to be taken to blood
- CO2 in blood gets carried to the lungs
- Exhaled air with Oxygen and CO2 gets out (exhale O2 not picked up and CO2 released)
- Start over
Regulation of respiration
Respiration = regulated in the brainstem
Overall - regulated by CO2 level and pH
- Only partially reglated by O2 level
- Have receptors for CO2 in the brain
What is located in Pulimnary veins
Pulminary veins = have arterial blod (have oxugenated blood)
Blood will go form Pulimnary vein –> left ventricle –> Aorta –> Systemic circulation
Breaths per minuts
Around 25 breaths per minuts
Affected by stress + excitment + excersize
Anatomy of respitory bronchi + Aveolai
Respitory brichiole - Last airway
- Lined by cilated colomnar epithelial cells –> Cells will transition to flt epithelium
Aveolar sac - ball shape –> strcuture = increases Surface area
Celular level of brochi
Type 1 Aveolar cells - Flat cells (nuceli are flat and small)
Type 2 Averolar cell – Bigger nucleus
- Basal lamina = unver aveoli cell = Air goes from cytoplasm –> basal lamina –> cytoplasm –> Air space
Capilaries - contain RBCs
- Lined by endothelial cells (have permeable cytoplasm) + junctions bteween cells
- Permability chnages backed on conditions (Ex. Opens during inflamation)
Macrophages - seen in aire space
- macrophages = clean up
- IF macrophages can’t clean up space = macrophages will fuse together (Form foriegn body giant cell + Langerhans cels)
Type II Pnuemocyte
Secretes Serfacton –> Serfacton = decreases tension = keeps space open
In genetic disease where body doesn’t make serfcaton = bodies cant breath = die
In prematur babies = have same issues as genetic disease –> clincians will give sterioirds + give <100% O2 to babies –> steroids accelerate maturation of cells (THIS limits how premature a baby can be born and survive)
Anatomy of brochi/aveoli duct (histology)
Respirtoru bronchi –> opens to duct –> Goes to atrium –> goes to aveolar sac
Respitory Bronchia = cilaited columnar epithelial cells –> have transition to flat cells in aveolar duct
How do we decide to breath
Brain stem (central conrtol) gives out put to effectors (repsitory muscles) –> muscles move/contract –> go to sensors (chemoreceptors and stretch receptors) –> receptors tell brain to increase breathing or decrease breathing
Have sensors monitoring blood CO2 and pH content
- Includes chemorecptors + stretch receptors (stretch receptors = measure expansion of lungs)
Central Chemoreceptors
Loated near the ventral surface of the medulla (in brain)
- Have chemoreceptors in fluid capilaries
- CO2 can get into extracellular fluid –> CO2 gets to CSF –> CO2 decreases pH ; Acid can’t leave BBB –> pH of CSF = bathes cheorecptors to tell you to breath
-Chemoreceotor respond to CO2 in extracellular fluid that bathes the CSF
Sensitive to PCo2 9 (NOT Po2) and pH
- CO2 and bicorbinate and H+ ions = affect pH –> diffuse to extracellar surface where the chemorecptor is –> chemorecetor recat to CO2 and pH
Responds to chnages in pH of the ECF/CSF when CO2 diffused out of cerebral capilaries
CO2 and O2 stimulate ventilation
Right - Ventilation respond to elavated CO2 (CO2 increases = ventilation increases ; slope (rate) based on oxygen content in air –> lower content bretah faster)
- CO2 increases = stimulate respiration
- Main imput of chemoreceptors = CO2
- Respiration response depends on O2 content of air
- Ventilation response is enhances in presence of hypoxia + metabolic acidosis (low pH and high CO2)
- Ventilation response to pH and CO2 decreases with age
- Dropping O2 barley increases ventilation but increase CO2 but few points increases ventilation by a lot even if Oxgen is normal –> shows CO2 is one of the main drivers of breathing
Left - Body temp and pressure (measure of ventilation) on Y axis AND O2 content in Aveolar on X-Axis
- Increase CO2 level = need higher ventilation to keep the same level of O2 (breath faster to keep same level of O2)
- CO2 is low = need to get really hypoxic before increase ventilation BUT if have higher CO2 then get an increase of O2 earlier
Peripheral chemoreceptors
Loxaed in coatoid and aortic bodies
repsond to decreases arterial Po2 and increase PCo2 and H+
Rapidly responding
Ventilatory response to Hypoxia
During hypoxia = Only the peripheral chemorecptors ae involoved (NOT in brain)
There is negblible control during normoxic conditions
The control becomes important at high altitude + in long term hypoxia (caused by chronic lung disease)
Lung (overall)
Lung = has air ways AND air spaces
Image - see tree with branching (cast of human airways - prune away aveoli)
- See trachea and branches to left and right and continues branching
- If took all aireways and put ened to end = 1500 miles = huge area in lung of conducting system
- End of all trees = puff of aveoli
Trachea = splits –> goes to bronchioles –> have primary, secondary, tertiary levels of branching
- terminal bronchials split to respitory bronchias –> then split to aveolai ducts
Bronchioles = have less cratilegde
Airways
Divided into a conducting zone and a respitory/transitional zone
- Traachea branches in two –> keeps branching –> at 16 branches start to get the nubs of aveoli (starts in respitory bronchials and then fully formed aveoli sacs)
Volume of the anatomic dead space = 1500 mL
- - No resporation in conducting zone –> dead space = 1500 mL
Volume of aveolar region (Aveolar volume) = 2.5-3 liters
Gas movement in aveolar region is ONLY done through diffusion
Branching of bronchial
Have 23 levels of splitting (have 16 levels of branching once reach terminal bronchials)
In clinic – If have to go to level 6/7 with scope –> each airway branches 2/3 times –> if you go to the wrong place = end up far from target = use computer to guide
Space in airway
Space in airway (conducting zoon) = conducts air to the aveoli -> Space in airways do not preform respiration
- Aveoli = where respiation is occuring
Respitory bronchials = Aveoli dead space = does take part in respiration
Conducting zone = Anotomical dead space
Conducting zone + respirtpry bronchioles = physiological dead space
Respirtory bronchials = alveolar dead space
Trabslation and respirtory zone = respitory brinchiols + aveolar duct + aveolar sacs
= Aveolar space = aveolar venticlation (can varyvs anaotomcal dead space stays fairly conatsnt)
Air way exponential chart
At trachea level = can see gas would flow form velocity of inhiblation but once at transitional/respitory zone = mostly by diffusion
See in chart - cross sectional area with airway generation –> once get to respirtory zone = have huge crossectional area
Cell types in trachea branching
Respitory bronchials = colimnar cilaited epitheliam
Aveleor ducts = Type 1 and Type 2
Airway generation
Surface vs. airway genertaion
At 16 aireays = where you have the terminal broncshi –> THEN have exponetial growth in surface Area
Airway resistence
How do you get air in ling without resistnce - because of cross sectional area
Highest in the medium sized bronchi ; low resistnce in the small airways
Resitnce and airway gnertaion –> as you breath resistnce increases (trachea gets smaller into branches) –> oce devide furtehr with airway geenrtaion = decreae resistnce
Resistnce decreases as lung volume increases because the airways are being pulled open
- Because large airways are not changed but small airways with mucous and elatic tissue can expand –> elastic fibers in aveoli wall excpand more –> have negtaive pressure –> opens the capilary and the airway = blood flow and air flow is easier when breathing in
- Small airways don’t collapse fully when breath out
Bronchial smooth muscle is controlled by the autonimic nervous system
- Stimulation of Beta anderogenic receptors causes broncho dialtion (realxes airway)
Breathing a dense gase increases resistence (Ex. when diving)
Give pateints who have narrow airways a less dense gas (helium) = decrease resistnce = better flow
Disease where smooth muscle doesn’t function
Disease where smooth muscle doesn’t function mostly affects small airways
Example - Asthma –> smooth muscle contracts = don’t open when inhale + astma glands have more cells that make mucous = closes airway
- Treat with a steroid = can decrease inflamation + decrease mucous production + relax muscle
Airway resistnce chart
Air goes through pipes = have resustnce
Resistnce changes depending on size of airways
Chart - have high resistnce at 5 airways –> resistnce decreases to zero at terminal bronchi
Lung ventilatiion equation
Overall - ventlation is affected by respitory rate + Tidal volume
Minute ventilation = respotory rate X Tidal volume –> Ve = RR X Vt
- Minute ventilatoion = how many liters per minute is moving into lung
Equation - gives how much air you move in a minute
- Depends on how many times you breath and how much air you breath
Ex. breath 500 mL ; breath 15 times –> 7,500
Tidal volume equation
Overall - Tidal volume = normal amount of air going in/out
Vt (tidal volume) = Vd (dead space) + Va (Aveolar volume)
- Anatomic dead space = space at the begining of the airway where there is no gas exhnage
Example:
Averolar space = 3 L (3000 mL) –> X 15 breaths = 5.2 L/ minuts
Tidal volume = 500 mL –> off the TOTAL ventilation (7500)sed for aveoli respiration
Ventilation itself is usless unless you have profusion –> blood flow is 70 mL in capilary –> X flow –> 5000 mL/minute
- Putting the blood through the capilaries in 1 minutes
- Have good match between how blood flow goes and how air exchnage is happening
Image - note have volume on left and flow (rate - volume X frequencey) on right
Lung Volume
Total lung volume = 4 liter liters
Tital volume = 1/2 liter in/out (2.7-2.2)
Inspirtory reserve volume = 1st peak on chart = if took in a big breath (abive TV) –> blow air out until ciundlt blow out = expirtory volume (peak below TV)
- Residual volume = amount of air left in lung at the end of full respiration (airways collapse and keep some air in lung)
- Asthma = higher resipdual volume
Terms:
1. Max inspitory level = max airway can breath in
2.Expitpry reserve = air above normal exhale during forcful repsiration
3. Residual volume = vilume air that you can’t exhale = keep lings opens
Emphyzema
Get barrael chest
Chest barley moved = ise doaphram to breath
Lung capacity acornyms
TLC = how much air you can get into whole lung = RV + EV + TV + IRV
FRC = how much air is in lungs at end of a normal breath
- If open animals chest = lungs collaspe becaus elungs want to collapse ; chest wal expands out –> force ebtween the lungs wnating to collapse and chest wall wanting to expand thatd etrmines FRC –> caises tension between lunch and chest wall
Pnumothrorax
Normal - lungs are covered by Plura (layer of mesoythelia cells + flat cells)
- Mesothelial cells = make pritein rich fluid –> fluid helps move the plura around the chet wall to slide
IF puncture the chest wall or lungs = air goes in = space increases
- Increase vertabra space = get pnumothroax
- Lose negative pressure during inhalation = lungs collapse
Image - Normaly pressure in lung is zero ; pressure outside plural surface is 0 –> but becasue lung wants to collapse and chest wall wnats to expand = have negative pressure in plural pressure
- IF lose that negative pressure = damage to chest wall or damage to lung = all pressures go to zero –> nothing tents the wall open = lung collapses in
Slide 21 IMAGE (ON NEW SLDIES)
Right side = no space below viscera and parietal plura
Left = Have black space = have air
Lung collapse
Black space = lung collapse (in lower lobe)
How to deal with lung colapse –> suck air out –> might need to put somthing to mkae the plura surface stick together
- Usually chest tube is enough
Spontenous pnumothroax –> lung collapse BUT there is no trauma (no reason)
- After treatment they stop occuring