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
Pulminary sufactant
Surfactant = reduces the surface tension of the aveolar lining layer
- Keeos surface open
Surfactant = priduced by type 2 avolar epithelial cells
Contans dialmitoly phosphtidycholine
Absence results in reduce slung comppliance + alveolar atelectasis + tendance to pulminary adema
Steps of breathing
Conciously or unconciuosly decide to breath
Air comes in –> signal to activate respirtpry muscles –> Chnage pleural pressure –> Air moes down a series of tubes –> Air into aveoli availibe for gas exhnage
Muscles - bretahing muscles (interconstale mucles and diaphram) contract –> get negative pressure –> air goes in –> ar goes to aveoli
Circulation
O2 goes to blood
Vessles in lungs
Image:
See plura
Subplura; space = has veins + systemic artery + lymphatoc vessels
See arties and veins and lymophatic interacy and run together
See pulminary artery and pulimnary veins
interlobal septa = where the veins and lymphatic chanels run –> collect venous blood from aveoli
Pulminary arteries = run in airways –> carry venous blod from systemic system
Systemic arteries = comes from aorta + carry arterioized blood –> provide O2 t keep lng tissue viable
Blood gas interface
Walls are extrmeley thin (0.2-0.3 um) - wall thickness is fraction of RBC thickness
- Over extend aveolus = damage airways
Enonormas surface area of aveoli space (50-100 m^3)
Large area obtains by have 500 million alveoli - Aveoli space = lots of Surface area
So thin that large increases in capilary pressure can damage barrier
- Aveoli can be injured –> if have too much pressure to get air into lungs –> get positive pressure = get respitory issue
- Over extend lungs = caise damage
Image - Aveoli is thin strcture ; RBCs are black dots
- Cross section through capilary and aveoli wall –> center = center of aveolus and black is teh wall of the aveolus where the capilary runs through (walls are very thin)
Blood vessles
The whole of the output of teh right heart goes to the lung
- Pressure is lower in right heart cimaber + in pulminary arteries
The diamter of capilaries is 7-10 um
- Needs to be at least 7 um for RBCs
The thickness of much of the wall of the capilar is less than 0.3 um
Blood spends 0.75 seconds in the capilaries
Image - holes = spaces between cells where cell components pass ; shows aveoli wall with dense capilary netorks
- capilary segmensta re so shrt that it seems to be a continous set in lungs
vessles + artery+ branch image
Lymphatic chanels = next to artery + veins
- Lymphatic vessles = hard to see because they collaspse –> see when increase ressure in venous system or f have tumor in lymphatic chanel
Flow of blood in pulminay circulation
Pulminary artery and bronchus –> pulmary artery branches off –> goes to cpailaries aling aveloli –> dreai to pulmnary veins –> go t heart
- Pulmary artery = not very thick because low flow
Pulminary vs. Systemic circulastion
Video - all blood in body gos through the lungs BUt an’t ahve same pressure in the lungs because would blow capilaryies
- Blood goes to Right atrium –> right ventricle - have low pressure system in the right ventrcile –> goes to pulminary artery (takes blood to apilaries –> capilaires pick up O2 –> oxygebated blood goes to body (higher pressure at left ventrcile because have to get blood to many capilaries bed in whole body)
- Low pressure system in pulmoinary circulation
Example
Pressure in aorta –> from left venticle have 120/80
Periphery – Capilary beds = 20 ; venous sytem = 10
Osmotic oressure in plasma = keeps proteins in water –> normally fliud does not ozzie to tissue –> if decrease osmotic pressure or increase permability = fluid goes out = get inflamation
Image:
Right heart - pressure = 2
Left heart - pressure = 25-15
- 15 in pulminary artery –> 8 in pulmnary veins
narrow arterioles = get hypertension - increase pressure in capialries = affects gas exchnage
What is in pulminary vein
Pulminary vein has arterial blood - any chnage in pulmianry vein pressure = affects resustnce
Mechanisms of increased blood flow
- Get more blood vessels
- Vessels become bigger
IF have chronic constriction –> increase venous pressure = get proliferation of vessels (not reversible) + have sretching (rapid reversible response)
- Often a cardiac issue - have chronic conjection
- Example - mitral valve anastomosis –> back up of pressure into lungs
- Example for stretch - for infection
- Can recruit smaller capilaries + distend airways (distention is due to air in lung)
Pulminary vessels and lung volume
Breathing in = blood vessels dialatea
Arteriols = have muscular wall = not affected by begative pressure
Capilaies dialte a little
Measure vessel resistnce
- low lung volume = higher vascular resitnce because capilaries are floppy (airways is not distended) - increas elung volume = tent open capilaired BUT if too high lung vilume then compress capilaries from air in aveolar space and increase resistence
- At base line (bottom of u) - normla lung volume = low vasuclar resistnce but when vcolapase or over distnec eyou change resustence in capilaries and make harder for blood to flow through
Image - optimal condition + change in either direction = increase resistnce
Pulminary vessels and lung volume (IMAGE 2 - in his new Ppt)
Right - see capialry
- Breath in - resistnec to blood floow decreases in venous and increases in aveolar vessles (capilaries)
End - get a U shape when add total resistence together
Air flow and blood interactions
Air flow = gases exchnage in averoli = venous blood gets oxygentaed
- Get arterial blood (oxygenized blood)
IF get disruption between ventilation and profusion (ex. if have an onstruction of airflow or change in blood supply or shunt) = then Arterial blood gets less oxygenated
V/Q mismatch
Normal air volume = 4 ; Blood volume = 5 –> V/Q = 0.4/0.5 = 0.8
Image B - IF decrease air flow –> VQ decreases
Image C - IF decrease Blood volume = VQ increases
High VQ
Aka Dead space
IF decrease Blood volume = VQ increases (Adequet ventilation and inadequet profusion)
Example - if have dead space somewhere = have bad produsions = blood flow decreases
- Occurs if have pulminary embolism (clo clot locks flow in vessels)
Low VQ
Aka Sunt
IF decrease air flow –> VQ decreases (Adqueet profusion and inadqeuet ventilation)
- Occurs if have obstructed airway
Oxygen Diffusion
Occurs through diffusion (takes 0.75 seconds for blood to get through capilary)
Right - Normal O2 diffusion (X-Axis = time in capilary)
- normal = get all O2 into capilary in 0.25 seconds –> gives 0.5 seconds (0.75-0.25) for blood to go through the rest of the capialry
- Excersize = blood goes faster (higher HR = blood moves faster) = blood only spends 0.5 seconds in a capilary in lung BUT enough time in normal lung to completley pick up oxyxgen
- MIddle line in A - In abnormal lung (Ex. COPD) = maye take full 0.75 seconds to pick p O2 before RBC leaves capialry –> when they excersize = blood will be out of capialry before it fully picks O2 (called Excersitional hypoxemia - give supemental O2 –> give 100% then higher O2 in Y axos = more oxygen can diffuse across in normal time)
- Bottom line in A - Reallky bad lungs = resting or excersizing they can’t pcick up enough O2 before RBC leavse capilary = low O2 at rest
NOTE - Aveolar O2 level = affects O2 diffusion to the blood –> get exponebtial curve (line flattens on the right = normal)
Left - Different O2 curve BUT get the same response
- Lower aveolar O2 (Example high altitude)
- Can go to high altidtude and not get hypoxia because if their lung is normal then they can still pick up all the oxygen they need iwthin the 0.75 seconds
O2 concetration and transport
O2 transport = Cardiac output X arterial O2 content (PO2 level)
Arterial O2 content = Dissolved O2 - Hbbound O2 (Hemoglobin bound O2)
- Majority of O2 = hemobloglobin bound
- Hemoglobin bound O2 = avaible for oxygenation of tissues
Dissolved O2 = 0.003 mL O2 X PO2
Hb-O2 = 1.39 mL O2 X Hb (mg/mL) X Hb sat/100)
Blood O2 content
Relationship between dissolved O2 and Hemoglobin bound O2
Chart - Po2 (Arterial concetration) = X-Axis ; Hemoglibin saturation = Y-Axis (Left) ; Oxygen concetration = Y-Axis (right)
- As Hemoglobin saturation increases = Oxygen concetration increases in expinential manner
- IF have high hemoglobin = then doesn’t amke a differnence if dissolve more oxygen in blood (doesn’t chnage oxygen concetration)
- Normally dissolved oxyegn is negligible (seen as bottom pink line)
- Oxygen attached to hemoglobin = where most oxygen is
Hemglobin content and Oxygen content
X-Axis = Po2 ; Y-Axs left = O2 concentration ; Y-Axis right = Hemaglobin saturation
Hemoglobin concentration affects O2 content + amount of O2 to reach saturation
- More hemoglobin = realy on less O2 saturatio to result in the same concetration
- If Hemoglibin drops to 10 – for a given Po2 = have lower Oxygen content (Example - at Hemoglobine 10 – 90 Po2 –> oxygen conctertaiion is 12 BUt if hemoglobin is nornal at 90 PO2 then oxygen concetration is 20)
- Low hemoglobin and low O2 saturation = low oxygen concetration
- Low jemoglobine but 100% saturationo = higher oxygen concetration
Male hemogolbin = 13
Normal hemoglobin = 15
Start transfusing pateints at Hb = 7/6
People who live in high altitudes = higher hemoglobine to increase O2 concetration
Bigger driver for oxygen content
Hemoglibin concteration = bigger driver for oxygen content
What affects association between O2 content and hemoglobin
Need hemoglobin to be able to dissoctae from the oxygen
Images = hemoglbin Oxygen dissociation curve
- typical = nice curve –> high Po2 = flatten curve (doesn’t make a big differece on saturatiion) BUT at low Po2 have a steap drop in hemoglobin saturation
Things shift the dissociation curve:
1. Body temperature - decrease body temperture = shift left = less O2 to get to the same saturation = hemoglobin holds onto to oxygen OR if increase temperatire need more O2 = shift right (off load more ocygen)
2. Increase Acid - shoot curve right
3. Increase Hypokpina - shoot curve right
4. Increase DPG - shoot curve right
5. Increase PCo2 (Acidosis) - shoot curve right
PO2 levels = have further curve to the right = less efficnet =need more O2 to get to saturation
Gas concetration in different compartments + hemoglobin
Gas concetration in different compartments = affects how gas is offloaded from hemoglobin
CO2:
Don’t breath in CO2 = no CO2 in air
Lungs have CO2 (less because being offloade din blodd)
Tissues = most CO2
O2:
Highest in air
Less in the lungs
Arteiors = have loss of O2
Lose O2 in tissues = lowest in tissues
Gas concetration in different compartments
Gas concetration chnages in circulation
Arterial blood = decreased O2
Venous blood = has constant PCO2 then PO2 increases durig respiration
Gas concetration in different compartments (IMAGE NOT IN SLIDES)
Left –> tespiration volume in L/minutes
- Increase PCO2 in aveoli = increase respirtory volume (increase PCO2 in space = Increase respiration)
Right –> O2 levels in air – Percent saturated
- At high stauration = lower level of ventilation needed to maintain oxygentaion
- In pateints - if they are short of O2 = don’t start at 100% O2 – give 80% to start –> see if helps –> then increase concetration if needed
Lung Diseases
- Airway disease
- Ex. Asthma
- Vascular disease
- Ex. Pulminary arterial hypertension (can be primary thing or secondary to a different disease like having a primary pulinary embolism that causes hypertension)
- Ex 2. Pulminary embolism
- Parachymal disease
- Example - interstitial lung disease
Emphyzema
Aveoli tissue get destroyed + space gets bigger
- Surface area decreases ; volume increases
- Diffusion is normal
Can get fibrosis in aveolar sac = prevents gas exchnage + atertial volume of lungs decreases + diffusion decreases
Normal Lung histology
See pigment around airway
Red circle in lower left corner = artery
Inflamation lung histology
Image = has some inflamation (Has macrophages _ cytokines)
ALSO see terminal bronchiole
Respitpry brochiole histology
See pigment in lung –> pigment is macrophages + inflamation
- Could be from smoking
Asthma Lung histology
See large airway
See the glands (purple circle in lower left corner)
- Glands make mucus = they are bigger in astma –> put mucus in the airspace –> bulge out
- Airways in astma –> smooth muscle is thicker -> hypertrophic
Asthma Lung histology #2
Big circle in middle –> small bronchiples = smooth muscle is inflamed + too much mucous
V/Q in astma –> <0.8 because the issue is in the airway (inaqadeuqt ventilation _ Adequet profusions)
Pulmonary hypertension histology
Dense purple area (se in center bottom area) – Artery = big
- Pink - fibrosis
Pulmonary hypertension histology #2
Red area - Atery wall= big (lumen is narrow = have thick walls)
Pulmonary hypertension with thrombosis histology
NOW the hypertension is sedondary to the thrombosis (caused by thromosis)
Big circle = artery (has fibrosis)
- Starting vessel
V/Q = >0.8 (issue is with profusion)
Treatment - hard to treat so clincians try to prevent it using anti-coagulation thearpy for rest of life
- Once have hypertension it is hard to treat
Emphyzema histology
Normal - see vessels
- White circhle under lne on right = aorta
Emphyzema - little black holes –> more prominent deeper in the oaranchyma (subplural)
- Black = air ; space = siar
- have destruction of paranchyma
Emphyzema histology #2
Normal lung = no big spaces (dense pattern + don’t see holes)
Emphyzema – have spaces
- Black pigment = entraotic pigment = macrophages = breathing dirty air
Emphyzema histology #3
Emphysema = spaces are not uniform
Emphyzema histology #4
Pink lines - shows you get fibrosis = know occured in vivo
Emphyzema classifcation = based on size of the spacs (ex. variable vs uniform)
V/Q for emphyzema = >0.8 –> secreate srufactnat is off (aveolar destuction) = decrease blood flow = overinflated
- Aveolar tissue is destroyed = elasticity of the lung decreases = small circulation in blood–> paranchyma needs to stay open –> over inflates in emphyzema because loss of elasticity = expandig is not efficient = air stays in lungs
Interstitial fibrosis Histology
White = fibrosis or Ca2+
Black = air
Left side = see little uniform space under plura (starts under the plura)
Know it is not emphyzema vecause have fibrosis (white) = have destruction of fibers in lungs
Interstitial fibrosis Histology #2
Left - fibrotc lung = shrinks + harder
Right - Air sacs are replaced by fibrosis
Interstitial fibrosis Histology #3
See area with normal wall thickness –> diffuse fibrosis (replaced by lungs)
Space woth mucus = lined with red epithelium
Issue = can’t breath
- Parachyma –> fibrosis + repair –> get aveolar air = hits vasculature = bad
- Oxugen can’t diffuse through collegene to capilary
Interstitial fibrosis Histology #4
Image - can’t find aveoli lungs
No respiration occirs - just diffusion and destruction
Spaces = cystic space –> filled with mucus
End Stage lung Fibrosis Histology
V/Q - <0.8 (decrease total lung capacity)
Have mucous in airspace = air canct go in = decrease in lung capacity
- Airlfow and diffision are compromised because of fibrosis
- Couold be issue with airways (airflow) or teh air itself
Name for end stage fibrosis
Called restrictive lung disease - get rid of tissue in lungs = lungs can’t expand = airflow decreases –> overtime Total lung capacity decreases
Decrease in Total lung capacity
Total lung capcity decreases:
1. No ventilation because aveoli are destroyed
2. Airways dilate + get fibrosis –> Lung can’t expand = airflow is combroised
Affect of inflmiation
Inflimation results in restcive pattern in lungs
High vs. low VQ
High VQ = dead space
- Example - block in blood vessels or increase pressure in venous system (blood flow decreasses + hardder for blood to go thorugh campialry)
Low VQ = shunt –> decrease in air flow = blood is shunted away from area
- Example - pulminary edema = blood goes away from the area with low oxygen
You can have both low ventilation and low profusion at the same time
Carbon monoxide
Bad because it binds to hemoglobin more readily than O2
When making wine = have sludge at bottim of barrel –> if take out too muchsludge you start taking out carbin monoxide = people die
- Check to see if have carbon moxide using fire
Lung Cancer
Small cell lung cancer = won’t affect respiration BUT if tumor narrows airway then get low V/Q
OR if have tmor in vessles then affects profusion = get high V/Q
Lower lobe of lung
2/3 of repsiration occurs in the lower lobe –> easuer to lose top lobe if need
