1
Q
What are the fxns of Respiration?
A
- Gas Exchange (primary)
- Both O2 and CO2 are transported by blood.
- Both Respiratory and Cardiovascular system are involved in respiration
2
Q
Pathway of air in respiratory tract
A
- Conducting zone
Nose
Nasal Turbintes
Pharynx
Trachea (cartilage rings)
Main L/R Bronchus (i)
Secondary/Lobar bronchi
Bronchioles
Terminal bronchioles - Respiratory zone
Repiratory bronchioles
Alveoli ducts & sacs
3
Q
How do we inflate lungs?
A
- Muscles of ribcage (intercostals, diaphragm)
- Pleura space (visceral, parietal, pleural fluid)
4
Q
Describe pleural space
A
Closed fluid-filled sac.
Parietal, visceral
NEGATIVE pressure
High surface tension = pull on lungs
5
Q
Pneumothorax
A
- It shows how ribcage and lungs are coupled (work together)
- Pressure increases in pleural space (hole)
- Air go into pleural space (down pressure gradient)
- No more coupling between lung and ribcage
- Lung collapse
6
Q
What is the “Mechanical pump” (model of how we breathe)
A
Seringe
Piston go down (diaphragm)
Balloon inflate
7
Q
What surrounds/makes the respiratory airways?
A
Smooth muscles = Involuntary
- if contract = bad, cant breathe = asthma
8
Q
Functions of the Conducting zone? (4)
A
- Defense against bacterial infection and foreign particles : cillia, glands for mucus = Mucociliary Defense System
- Warm and moisten inhaled air : form blood
- Sound and speech : air goes through vocal chords for speech
- Regulation of air flow : smooth muscle can contract/relax air resistance to air flow (redirection, asthma, etc.)
9
Q
What does nicotine do to the respiratory system?
A
Paralyze cilia
10
Q
Functions of Respiratory zone?
A
Gas exchange : huge surface area
11
Q
How many circulations does the LUNGS ONLY have?
A
Two.
Pulmonary circulation & BRONCHIAL circulation (part of systemic circulation to supply lungs)
12
Q
What are the alveolar cell types?
A
- Epithelial I and II
= 1 regular
= 2 secrete pulmonary surfactant to DECREASE SURFACE TENSION - Endothelial
= walls of pulmonary capillaries THIN - Alveolar macrophage
= immunology
= remove cells that escaped the mucociliary system
13
Q
Surfactant: baby
A
Develop in LATE gestation
if baby doesnt have
1. steroids to produce = premature baby
2. artificial surfactant or animal = without notice
14
Q
Repiratory Muscles (10)
A
Inspiratory (elevate ribs)
- Principal
1. Diaphragm (C3-5) bucket-handle
2. Parasternal Intercartilaginous
3. External Intercostals
- Accessory
4. Sternocleidomastoid
5. Scalenus
Expiratory (depress ribs)
- Quiet Breathing
= Passive recoil of lungs
= no muscles
- Active breathing
6. Rectus Abdominis
7. External Oblique
8. Internal Oblique
9. Tranversus Abdominis
15
Q
Define: Spirometry
A
Measure lung VOLUMES with spirometer
Breathe out = spirometer go up so pen go up
Breathe in = spirometer go down so pen go down
16
Q
What is a Tidal Breathe
A
Its the tidal volume (when ur breathing at rest)
volume : breathe in OR out
17
Q
What is Functional Residual Capacity - FRC
A
You do not breathe out ALL the air from lungs u still got air in lungs at rest
Reasons
1. Require too much energy to expire all the air out
- Remaining air allows for gas exchange to be continuous
18
Q
What is Total Lung Capacity
A
All air that can be contained in lungs
19
Q
What is Residual Volume
A
Forceful expiration
still some air inside lungs
20
Q
What is Inspiratory Reserve Volume
A
Difference between Tidal Breath and Total Lung Capacity
(the potential air volume that you could still breathe in more after inspiring)
20
Q
What is Vital Capacity
A
Difference between Total Lung Capacity and Residual Volume
(max air in and max air out)
21
Q
What is Expiratory Reserve Volume
A
Difference between Functional Residual Capacity and Residual Volume
(what more can you breathe out after resting breathing)
22
Q
What is Inspiratory Capacity
A
Forceful insipration
DEEP BREATH
Difference between Total Lung Capacity and Functional Residual Capacity
23
Q
Breathing Frequency - What is Minute Ventilation
A
Amount of air inspired or expired over 1 minute
Ve . = Minute ventilation
vT = tidal volume
f = number of breaths per minute
24
What are Anatomical Dead Spaces
Not all air inhaled reach the exchanging zone
APPROX. 150 ML
(same as weight in pounds)
and stay in conducting airways = anatomical dead space
25
What is / How to measure Alveolar Ventilation (vA)
vA . = (Tidal volume - 150ml) * 12 breaths /min
Adult male = 150 ml dead space & 12 breaths/min
26
Pathological Conditions creating Dead Space
Alveolar Dead-Space
1. Blood Clot: Capillaries are obstructed
2.
27
Physiological Dead-Space (vD) is....
Total Dead-space (vD) from Alveolar (pathological) and anatomical (conducting airways)
28
Pressure
Barometric P ?
Fractional [O2] ?
Fractional [CO2] ?
*Fx = dry gas
*Consider H2O vapor ?
760 mmHg
21% O2
0.03% CO2
H2O Vapor = 47 mmHg
29
What is partial pressure of O2 in air - normal conditions?
*values can vary
PO2 =
(760 mmHg - 47 mmHg)*0.21
= 150 mmHg
30
Why is there a big difference in partial pressures of O2 in air vs. in alveoli?
Because as soon as you breathe in, the pressure gradient between capillaries and alveoli or O2 is so big that O2 will immediately diffuse into capillary
31
What controls Pa CO2?
Alveolar Ventilation (air inhaled/exhaled per minute)
keeps CO2 at constant pressure of 40 mmHg in ARTERIAL BLOOD (oxygenated)
32
What is Alveolar Hyperventilation? + symptom
1. Ventilation exceeds body's needs
2. More O2 supplied, More CO2 removed than METABOLISM required
3. Alveolar & arterial PO2 increase
4. Alveolar & arterial PCO2 decrease
Symptom: Fainting
= lack of CO2 in brain = blood vessel constrict
33
What is Alveolar Hyporventilation? + cause + symptom
1. Ventilation not enough for body's needs
2. Less O2 supplied, Less CO2 removed than METABOLISM required
3. Alveolar & arterial PO2 decrease
4. Alveolar & arterial PCO2 increase
Cause:
- Chronic Obstrucitve Lung disease
- Damage in resp. muscles (ribcage injury)
- CNS depression/problem
34
35
Gas Diffusion (rate)
- Where
- How (type)
- Pros/Advantages
- Laws
- etc.
- Alveolar-Capillary membrane
- Passive Diffusion
- Huge Surface Area + Thin membrane
- Fick's Law: Diffusion RATE
1. Proportional to: surface area
2. Proportional to: partial pressure gradient
3. Proportional to: 1/thickness
- Gas must be soluble in liquid
- Gas dissolved Proportional to partial pressure
- CO2 >>> O2 (solubility in water)
- O2 >>>> CO2 (pressure)
THEREFORE time for diffusion equilibrium between alveolar and capillary = same for both gases
36
Transit time
idk
37
Edema in lungs + Exercising
1. Interstitial space is thicker (layers between alveoli and capillaries)
2. Transit time and (De)Saturation time increase
Exercising
1. O2 CO2 Less time in pulmonary capillaries
idk
38
Pressure Equation
Force / Area
38
What happens if you have TOO HIGH pressure from the heart pump?
1. Leakage
2. Edema
3. Thicker Alveolar-Capillary membrane
4. Slower Diffusion
39
What are the differences between Pulmonary and Systemic circulations regarding PRESSURE
1. Right ventricle ~25 mmHg systole VS. Left ventricle ~120 mmHg systole
2. pulmonary pressure <<< systemic pressure
3. Walls of Blood vessels THINNER & LESS SMOOTH muscle than systemic
40
Why: 3. Walls of
Blood vessels THINNER & LESS SMOOTH muscle than systemic
Because you have same flow in both circulation (volume per time) BUT higher pressure in one. To maintain SAME FLOW IN BOTH CIRCULATIONS.
You must decrease resistance in pulmonary systemic to accomodate more blood.
41
Flow Equation
Pressure / Resistance
or
Volume / time
42
Pulmonary vs. systemic : VASCULAR RESISTANCE
1. Pressure drop in pulmonary = 10mmHg
2. Pressure drop in systemic = 100 mmHg
3. Pulmonary resistance is ~1/10 of systemic resistance
43
Accommodation of Pulmonary Blood Vessels by Pulmonary circulation : 2 ways + drugs (for 2-3x cardiac output)
1. Recruit blood vessels
2. Distend blood vessels (vasodilation)
Drugs:
- Serotonin, histamine, Norepinephrine = CONSTRICT
- Acetylcholine, Isoproteranol = RELAX
- Reflex Vasoconstriction (poor oxygenated to redirect)
- Nitric Oxide (endothelial cells) = RELAX VASODILATION
44
T or F:
Pulmonary BLood Flow is affected by Gravity
True.
Use Radioactive Xenon
45
Effects of Gravity on Ventilation
at rest, normal gravity
- Alveoli at top = more open
- Alveoli of bottom = close due to gravity
at beginning of breathe
- same elastic property, so all alveoli open at same volume
- air will go bottom due to pressure gradient (bottom alveoli collpase vs. top alveoli half full alr)
46
What is Fick's Principle
- To measure Blood Flow (Q)
- Oxygen consumption per min = O2 taken up by lungs/cells per min
CaO2 = [ ] = ml O2/ml blood
CvO2 = [ ] = ml O2 /ml blood
VO2 = ml/min
Q = ml / min
47
What is Henry's Law
Amount of gas dissolved is proportional to its partial pressure
48
O2 bound to Hb _________ contribute to the PO2 of the blood. Only _________________ are responsible for PO2. However, the __________does determine the amount of O2 that ________ with Hb.
1. does not
2. molecules dissolved in the blood plasma
3. PO2 of the
plasma
4. combines
49
Hemoglobin: what leads to sygmoidal shape of curve
Quaternary structure = Cooperative Binding (increase affinity)
50
Myoglobin
In Skeletal muscle
- Hyperbolic
- ONE O2 molecule only
- ONLY releases O2 at low PO2
51
Total Amount of O2 in blood depends on ...
Hemoglobin Concentration
Less Hb (anaemia) = less O2 carried in blood
52
What is the Bohr Effect
Shift in HbO2 curve to the RIGHT when
- CO2 and/or TEMPERATURE INCREASE
or
- Blood pH DECREASE (acid)
Effect: Decrease affinity to O2 to let it go at higher O2 pressures when (stated above)
THE OPPOSITE IS TRUE (move to left)
53
Carbon Monoxide poisoning
1. High affinity to O2 binding sites on Hb (210x >>> O2)
2. Reduce O2 bound to Hb
3. Shifts O2 Hb to LEFT (bc so much CO that O2 has extra affinity to Hb)
4. Very little stimulation to increase ventilation bc PO2 remains normal (though you have more CO, you still have O2 dissolved in plasma, just not on Hb)
54
Transport of CO2 (3)
1. Physical: dissolved (10%)
2. Combined w/Hb (bind to globin portion) (11%)
3. Bicarbonate
CO2 + H2O → H2CO3 (carbonic acid-Carbonic anhydrase)
H2CO3 → HCO3- + H+
(spontaneous ionization)
55
Now if CO2 decrease what happens to Hb and the rxns/equations?
The equations go opposite
1. Take CO2 from plasma into alveoli
2. HCO3- turn into CO2 and diffuse into alveoli
56
Name and Explain this curve
CO2 Dissociation Curve
Linear for CO2 and PCO2
- Increase in ventilation = increase in removal of CO2
(directly proportional)
double ventialtion = half CO2
57
Repiratory Failure is...
Occurs when respiratory system does NOT
1. Gas exchange
2. Neutral control of Ventilation (drive to breathe)
3. Neuromuscular breathing apparatus (respiratory mscules and innervation)
58
Arterial/Blood Hypoxia (Hypoxemia) is....(5)
Deficiency of O2 in blood
Causes
1. Inhalation of low PO2 (high altitude)
2. Hypoventilation (less O2 for same CO2 produced) - PCO2 increase
3. Ventilation/Perfusion imbalance in lungs: asthma, chornic obstructive disease. smooth muscle constrict. Less airflow.
4. Shunts of Blood across lungs: physiological. venous blood bypass lungs (mixing of blood)
5. O2 Diffusion Impairment: thickening of alveolar/capillary membrane - EDEMA
59
Control of Breathing: Type + Structures
Voluntary: Cerebral Hemisphere
Involuntary: Brainstem (Pons and medulla)
CNS control gas exchange
Structures
1) Sensors: Chemoreceptors-pH, lungs, etc.
2) Central Controllers: pons, medulla, brain
3) Effectors: respiratory muscles
60
Breathing: Breaking Point
Hold your breathe Voluntarily...
Involuntary takes over when
- PCO2 reach about 50 mmHg
- PO2 reach about 70 mmHg
61
Breakdown of Brainstem
+ Midbrain
--------------------- CUT : normal breathing pattern
--------------------- CUT VAGUS: Deep/slow breathing
+ Upper Pons
--------------------- CUT : Deep/slow breathing
--------------------- CUT VAGUS: Apnosis
+ Lower Pons
--------------------- CUT (& w/Vagus) : Irregular volume, proper rhythm
+ Medulla Oblongata
--------------------- CUT : No breathing
+ Spinal Cord
62
Medulla Oblongata: Breathing Roles
RHYTHM
A) Ventral Respiratory group = Rhythm + Pacemaker cells
||
(they connect)
||
B) Dorsal Respiratory group = Sensory inputs
63
Rostral/Upper Pons: Breathing Roles
TURN OFF INSPIRATION
= smaller tidal volume
= increase breathing frequency
so WITHOUT IT
= big deep and slow breaths same as cutting vagus above upper pons
64
Lower Pons: Breathing Roles
PROMOTE INSPIRATION
sends excitatory impulses to medulla
65
Chemoreceptors: PO2, PCO2, pH in arterial blood
Change in Pressures or pH will change Ventilation
Chemoreceptors --> Repiratory neurons (medulla etc.)
Changes:
INCREASE RESPIRATION
1) PaO2 < 60 mmHg
2) PaCO2 > 40 mmHg
DECREASE RESPIRATION
3) PaO2 > 100 mmHg
4) PaCO2 < 40 mmHg
66
Types of Chemorepectors: Central
- Ventral medulla (in brain tissue)
- Detect pH of CSF (pH affected by PCO2 and pH of arterial blood)
- Main drive to breathe under normal conditions
Steps
1) CO2 in arterial blood will cross Blood-Brain-Barrier bc it can (easily diffusable)
2) This CO2 will decrease pH (more acidic)
3) Central Chemoreceptors will detect this decrease in pH
4) Changes/sensitivity (Test: CO2 REBREATHING-HYPERCAPNIA)
a) VE. = VT x f = amount of air expired in1 min
b )Graphs are independant such that if frequency increase, the tidal volume is constant
67
Types of Chemorepectors: Peripheral
- in Carotid (Glossopharyngeal IX) & Aortic bodies (Vagus X) - w vessels
- Mostly sensitive to changes of PO2
- also increase in PCO2 and decrease in pH
- Go towards dorsal resp. neurons in medulla
Steps for sensitivity
1) Breathe with decreasing PO2 - HYPOXIA
2) with normal CO2 (normocapnia), PO2 can be reduced to 60 mmHg
3) Below 60mmHg, ventilation INCREASE A LOT
4) Hypercapnia = for same O2, ventilation increase
68
Types of Mechanoreceptors of Vagal X : Pulmonary Stretch (1) + Hering-Breuer Inflation Reflex
- Smooth muscle of Trachea to Terminal Bronchioles
- Stimulated by DISTENSION of lung (i.e. lung volume)
- Activity as long as lung is distended/expanded
- Firing rate increase as lung volume increase during each inspiration
MAIN REFLEX/PRODUCT:
1) Hering-Breuer Inflation Reflex
+ Decrease in Respiratory Frequency due to Prolongation of Expiratory Time
+ Negative Feedback
+ Weak in adults unless : tidal volume exceeds 1L (exercise) - noticeable in infants/animals
69
Types of Mechanoreceptors of Vagal X : Irritant (2)
- Airway epithelial cells of Trachea to Terminal Bronchioles
- Stimulated by Noxious gas, cigarette smoke, histamine, cold air, dust
- PRODUCT:
1) Bronchoconstriction
2) Hyperpnea (increase breathing depth)
- Bronchoconstriction is triggerd by histamine release during allergic asthmatic attack
70
Types of Mechanoreceptors of Vagal X : Juxta-Capillary / J (3)
- In Alvolar walls close to capillaries
- UNMYELINATED (slow) short outburts
- Stimulated by Pulmonary Interstitial Fluid
- PRODUCT:
1) Rapid/shallow respiration (apnea: pause of airflow)
2) Dyspnea : shortness of breath (associated w/left heart failure and lung edema/congestion)
71
What controls ventilation during exercise?
We dont know.
Heres the evidence
(trained and untrained people)
1) VE. increases linearly with O2 consumption up to 65% max
2) After 65%, VE. increases at rate DISPROPORTIONAL greater (more slope) = hyperventilation
*endurance training = to delay ventilatory inflection point
A) Not PO2 bc when hyperventilating consume more O2 but more O2 come in lungs so PO2 remains constant --> Peripheral chemoreceptors NOT stimulated --> so theyre not the cause of increasing ventilation
B) Not PCO2 bc when hyperventilating CO2 decrease --> CO2 decrease so les acidic (H+) --> so chemoreceptors of medulla NOT stimulated --> so VE. /ventilation decrease --> BUTTTTT STILL HYPERVENTILATING DURING EXERCISE SOOOO NOT PCO2
C) MAYBE Acid (lactid)
72
Onset and Recovery from Exercise
Onset/Recovery = Neural
During exericse = Humoral
73
Static Properties of Respiratory System: Elastic Define
How easy and difficult to inflate/deflate lungs.
Recoil Pressure (same as pressure pushed in) for a given change in volume
Manometer (used to measure pressure)
74
Pressure of lungs...
With reference to its surrounding
so its 0 bc same as atmospheric MINUS the pressure in pleural space.
Esophagus = subject to same pressure changes as pleural space
75
Elastic properties of Lungs: Compliance
Pl = pulmonary pressure
Palv = alveolar "
Ppl = pleural "
Pbs = body surface " = Patm
Pao = air opening "
Prs = respiratory system "
Pw = chest wall "
Compliance: ease w/which each of these can be distended/expanded
C= V/P = change in volume/ change in pressure
actually....
C = V/Palv-Ppl
(all variable have a delta, except for C)
76
Compliance: Static Pressure-Volume Curve + Diseases
Take lungs w/manometer
Inflate at Total Lung Capacity
(want to recoil at 30mmHg)
Deflate to Residual Volume
Observation
Slope = compliance
Its harder and harder to inflate lungs at Larger volumes
(compliance decrease with increasing lung volume)
DISEASES
- Fibrosis : Stiff lung = compliance decrease ALOT
- Emphysema: floppy = compliance increase ALOT
77
Elastance
1/Compliance
78
Compliance of Ribcage
= Difference Pleural pressure and Body surface (0 mmHg)
So its just pleural pressure!
1. Take ribcage out of subject
2. Manometer
3. Ribgcage is solid: If expand itll want to collpase. If compress itll want to spring out.
4. Resting volume of ribcage = 60% Vital capacity = rest = no pressure
5. Low volume = negative pressure
6. Cw = V/ Ppl (delta everywhere)
79
Compliance of Respiratory System
Prs= Palv-Pbs
Palv = Pl + Ppl
Pbs = Ppl-Pw
Pressure of Respiratory system is the same as the Pressure drop across LUNG and CHEST WALL
therefore
Crs = V/Prs
Crs = V/(Pl+Pw)
1/Crs = 1/Cl + 1/Cw
80
Dynamic Properties of Rspiratory System: Flow
FLOW-RESISTIVE properties
Flow = Palv-Patm / R
(negative flow = inspiration)
(positive flow = expiration)
80
Airways resistance (Raw) - Asthma
Raw = (Palv-Pao) / Flow
(ao = airway opening)
Asthma
= Inflammatory disease
= lots of cells, mucus accumulation in airway
= bronchoconstriction
= HIGH RESISTANCE
81
Flow-Volume curve: Dynamic compression of airways
From TLC to RV
Descending portion
= same slope
= independent of effort
= due to Compression of airways by INTRATHORACIC pressure
(i.e. FORCED EXPIRATION = pressure so high it collapes the airways
RESTRICTIVE (stiff) : lower volumes all around (can have better outflow than normal at certain volumes)
OBSTRUCTIVE (flop) : bc floppy, collpse easy = difficult to exhale = air trapped. so much more volume and sudden drop of flow (scooped out) and longer expiration
Asthma = same as normal but smaller peak bc of constriction but same volumes?
82
Ventilation: VE. Tidal volume and Frequency : What happens when you reach high tidal volume?
Bc you reach tidal volume
= Compliance plateau
so instead increase frequency
83
When you increase frequency dueing exercise = less time inspiring and expiring (Which?)
Less time expiring!
Peak Expiratory Flow rate >>>> peak inspiratiry flow rate
bc its forced (muscles)
jenn phgy 210
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