Physiology (Respiration) Flashcards

1
Q

Functions of Lung

A

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)

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2
Q

Breathing control

A

Breathing = autonmic but can be induced conciouslly

Circulatory = autonmic

Respiration = autonmic (affected by envirnment)

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3
Q

What do we need to breath

A
  1. Brain function - have breathing center in brainstem
    • Brain tells us to breath
    • Brain death = damage to brain stem that don’t trigger breathing
  2. Ventilation
  3. Circulation - transport oxygen to tissues and CO2 away
  4. Respiration
    • Exchnage of gas at the tissue level across the alveolar capilary (O2 i and CO2 out)
    • Blood flow much match ventilation
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4
Q

Breath Steps

A
  1. Decide to breath (conscious or unconscious)
  2. Air comes into lungs - Lings are able to expand (Intercaustal muscle and diaphram contract = creates negative pressure in chest = expand lungs = air comes in)
  3. Oxygen goes into capillaries - Air diffuses from capilary to Aveoli space
  4. Oxygen gets picked up by hemoglobin
  5. Oxygen gets circulated in blood and delivered to tissues + CO2 is released from tissues has to be taken to blood
  6. CO2 in blood gets carried to the lungs
  7. Exhaled air with Oxygen and CO2 gets out (exhale O2 not picked up and CO2 released)
  8. Start over
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5
Q

Regulation of respiration

A

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

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6
Q

What is located in Pulimnary veins

A

Pulminary veins = have arterial blod (have oxugenated blood)

Blood will go form Pulimnary vein –> left ventricle –> Aorta –> Systemic circulation

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7
Q

Breaths per minuts

A

Around 25 breaths per minuts

Affected by stress + excitment + excersize

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8
Q

Anatomy of respitory bronchi + Aveolai

A

Respitory brichiole - Last airway
- Lined by cilated colomnar epithelial cells –> Cells will transition to flt epithelium

Aveolar sac - ball shape –> strcuture = increases Surface area

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9
Q

Celular level of brochi

A

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)

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10
Q

Type II Pnuemocyte

A

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)

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11
Q

Anatomy of brochi/aveoli duct (histology)

A

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

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12
Q

How do we decide to breath

A

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)

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13
Q

Central Chemoreceptors

A

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

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14
Q

CO2 and O2 stimulate ventilation

A

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

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15
Q

Peripheral chemoreceptors

A

Loxaed in coatoid and aortic bodies

repsond to decreases arterial Po2 and increase PCo2 and H+

Rapidly responding

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16
Q

Ventilatory response to Hypoxia

A

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)

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17
Q

Lung (overall)

A

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

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18
Q

Airways

A

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

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19
Q

Branching of bronchial

A

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

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20
Q

Space in airway

A

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)

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21
Q

Air way exponential chart

A

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

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22
Q

Cell types in trachea branching

A

Respitory bronchials = colimnar cilaited epitheliam

Aveleor ducts = Type 1 and Type 2

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23
Q

Airway generation

A

Surface vs. airway genertaion

At 16 aireays = where you have the terminal broncshi –> THEN have exponetial growth in surface Area

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24
Q

Airway resistence

A

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

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25
Q

Disease where smooth muscle doesn’t function

A

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

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26
Q

Airway resistnce chart

A

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

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27
Q

Lung ventilatiion equation

A

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

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28
Q

Tidal volume equation

A

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

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29
Q

Lung Volume

A

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

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30
Q

Emphyzema

A

Get barrael chest

Chest barley moved = ise doaphram to breath

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31
Q

Lung capacity acornyms

A

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

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32
Q

Pnumothrorax

A

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

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33
Q

Slide 21 IMAGE (ON NEW SLDIES)

A

Right side = no space below viscera and parietal plura

Left = Have black space = have air

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34
Q

Lung collapse

A

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

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35
Q

Pulminary sufactant

A

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

36
Q

Steps of breathing

A

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

37
Q

Circulation

A

O2 goes to blood

38
Q

Vessles in lungs

A

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

39
Q

Blood gas interface

A

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)

40
Q

Blood vessles

A

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

41
Q

vessles + artery+ branch image

A

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

42
Q

Flow of blood in pulminay circulation

A

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

43
Q

Pulminary vs. Systemic circulastion

A

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

44
Q

What is in pulminary vein

A

Pulminary vein has arterial blood - any chnage in pulmianry vein pressure = affects resustnce

45
Q

Mechanisms of increased blood flow

A
  1. Get more blood vessels
  2. 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)

46
Q

Pulminary vessels and lung volume

A

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

47
Q

Pulminary vessels and lung volume (IMAGE 2 - in his new Ppt)

A

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

48
Q

Air flow and blood interactions

A

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

49
Q

V/Q mismatch

A

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

50
Q

High VQ

A

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)

51
Q

Low VQ

A

Aka Sunt

IF decrease air flow –> VQ decreases (Adqueet profusion and inadqeuet ventilation)
- Occurs if have obstructed airway

52
Q

Oxygen Diffusion

A

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

53
Q

O2 concetration and transport

A

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)

54
Q

Blood O2 content

A

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

55
Q

Hemglobin content and Oxygen content

A

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

56
Q

Bigger driver for oxygen content

A

Hemoglibin concteration = bigger driver for oxygen content

57
Q

What affects association between O2 content and hemoglobin

A

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

58
Q

Gas concetration in different compartments + hemoglobin

A

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

59
Q

Gas concetration in different compartments

A

Gas concetration chnages in circulation

Arterial blood = decreased O2

Venous blood = has constant PCO2 then PO2 increases durig respiration

60
Q

Gas concetration in different compartments (IMAGE NOT IN SLIDES)

A

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

61
Q

Lung Diseases

A
  1. Airway disease
    • Ex. Asthma
  2. 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
  3. Parachymal disease
    • Example - interstitial lung disease
62
Q

Emphyzema

A

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

63
Q

Normal Lung histology

A

See pigment around airway

Red circle in lower left corner = artery

64
Q

Inflamation lung histology

A

Image = has some inflamation (Has macrophages _ cytokines)

ALSO see terminal bronchiole

65
Q

Respitpry brochiole histology

A

See pigment in lung –> pigment is macrophages + inflamation
- Could be from smoking

66
Q

Asthma Lung histology

A

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

67
Q

Asthma Lung histology #2

A

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)

68
Q

Pulmonary hypertension histology

A

Dense purple area (se in center bottom area) – Artery = big
- Pink - fibrosis

69
Q

Pulmonary hypertension histology #2

A

Red area - Atery wall= big (lumen is narrow = have thick walls)

70
Q

Pulmonary hypertension with thrombosis histology

A

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

71
Q

Emphyzema histology

A

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

72
Q

Emphyzema histology #2

A

Normal lung = no big spaces (dense pattern + don’t see holes)

Emphyzema – have spaces
- Black pigment = entraotic pigment = macrophages = breathing dirty air

73
Q

Emphyzema histology #3

A

Emphysema = spaces are not uniform

74
Q

Emphyzema histology #4

A

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

75
Q

Interstitial fibrosis Histology

A

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

76
Q

Interstitial fibrosis Histology #2

A

Left - fibrotc lung = shrinks + harder

Right - Air sacs are replaced by fibrosis

77
Q

Interstitial fibrosis Histology #3

A

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

78
Q

Interstitial fibrosis Histology #4

A

Image - can’t find aveoli lungs

No respiration occirs - just diffusion and destruction

Spaces = cystic space –> filled with mucus

79
Q

End Stage lung Fibrosis Histology

A

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

80
Q

Name for end stage fibrosis

A

Called restrictive lung disease - get rid of tissue in lungs = lungs can’t expand = airflow decreases –> overtime Total lung capacity decreases

81
Q

Decrease in Total lung capacity

A

Total lung capcity decreases:
1. No ventilation because aveoli are destroyed
2. Airways dilate + get fibrosis –> Lung can’t expand = airflow is combroised

82
Q

Affect of inflmiation

A

Inflimation results in restcive pattern in lungs

83
Q

High vs. low VQ

A

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

84
Q

Carbon monoxide

A

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

85
Q

Lung Cancer

A

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

86
Q

Lower lobe of lung

A

2/3 of repsiration occurs in the lower lobe –> easuer to lose top lobe if need