Respiratory System Flashcards
What is the function of respiration?
Gas exchange
*CO2 produced through oxidative processes in body and exhaled by lungs
Supply of O2 to the cells
What is the respiratory tract?
Order and functions
mouth and nose –> lungs
1. nasal septum + nasal turbinates: clean air of big dust particles, moistens and warms up air
2. Pharynx: comon for air and food
3. Larynx (vocal cords)
Periphery of lungs (share chest cavity with heart, great vessels and esophagus):
4. Trachea
5. 2 main bronchi
6. Each divides into lobar and segmental bronchi (2x2):
Right main bronchus»_space; 3 lobar bronchi (right lung has 3 lobes)
Left main bronchus»_space; 2 lobar bronchi (left lung only has 2 lobes)
7. Divides into smaller branches until terminal bronchioles (smallest airway without alveoli)
What are the 2 sections of the respiration airways?
Conducting zone (Mouth/nose –> Trachea, Bronchi, Bronchioles, terminal bronchioles)
Functions:
- Defense against bactriral infections/foreigh particles
- Warm and moisten inhaled air
- Sound/speech w/ vocal cords
- Regulation of air flow (smooth muscles contract to increase resistance, not desired, seen in asthma)
- Don’t contribute to gas exchange so contribute to ANATOMICAL DEAD SPACE
Respiratory zone (respiratory bonchioles (have alveoli opening in their lumen), Alveolar ducts, Alveolar sacs)
Functions:
- Gas exchange (approx. 300 millions alveoli, each associated with 1000 capillaries)
What is the pleura and the pleural space?
Pleural = thin sheet, parietal pleural attached to thoracic cage and visceral pleura attached to lungs surface, for 2 pleural sacs (1/lung)
Pressure in pleural space always negative bc 2 sides pulling to extend it
(positive pressure is when push to compress)
What is the difference between bronchi and bronchioles?
Bronchi have cartilage around them
What is an acinus?
What is lobule?
The smallest physiological unit of the lungs:
one bunch of repspiratory bronchioles and their alveolar ducts and sacs
Lobule = group of acinus attached to one terminal bronchiole
Blood Supply to the lungs?
(2 circulations)
Pulmonary circulation:
comes from right ventricle by pulmonary artery (deoxygenated blood) and gas is exchanged via capillaries, then leaves via pulmonary veins
Bronchial circulation:
Part of systemic circulation, oxygenated blood comes via bonchial arteries from aorata supply air walls with O2. (very small amount), leaves via pulmonary veins with oxygenated blood, makes no big difference bc so little
What are the Alveolar cell types?
Epithalial type 1 and 2 cells:
form epithelial layer sealed together by tight junction, type 1 = regular, type 2 produce pulmonary surfactant (decreases surface tension of alveoli)
Endothelial cells:
constitute walls of pulmonary capillaries (very thin for better diffusion)
Alveolar macrophages:
remove foreign particles in alveoli that may have escaped mucociliary defense system
*Between alveoli and capillaries, a bit of intersitial fluid (Interstitium)
What is surface tension? (formula)
What are the roles of pulmonary surfactant?
Pressure inside alveoli like in soap bubble makes alveoli want to collapse
(more impotant in smaller alveoli)
P = 4T/r
Surfactant produced by endothelial cells of type 2 reduces it bc if not, smaller alveoli would empty to bigger and bigger and we couldn’t breathe
Functions of pulmonary surfactant:
- Equilibrates pressure (prevents pressure in small alveoli to exceed pressure in larger alveoli by reducing surface pressure more in smaller alveoli)
- Reduce overall surface tension
What are the inspiratory respiratory muscles?
Principals:
- External intercostals (when contract, elevate the ribs)
- Parasternal intercartilageous muscles (elevate ribs)
- Diaphragm (domes descend to increase volume, increase longitudinal dimension of chest + elevates lower ribs)
**Diaphragm splits thorax from abdominal section
Diaphragm innervated by nerves from cervical segments 3, 4, 5
Neck muscles may assist (accessory)
- Sternocleidomastoid (elevate sternum)
- Scalenus (anterior, middle, posterior) (elevate and fix upper ribs)
*Innervation of these muscles also appears is asthma and other disorders
What the expiratory respiratory muscles?
Quiet breathing:
- Expiration results from passive recoil of lungs (brain tells respiratory muscles to relax)
Active breathing (exercise, higher level of ventilation)
- Intercostal extercostal, except parasternal intercartilageous (depress ribs)
Abdominal muscles (depress lower ribs, compress abdominal content, pull diaphragm up):
- Rectus abdominis
- External oblique
- Transversus abdominis
*Forcing would lead to decrease of cardiac output bc bc increase in pressure in thoracic cage
*Important in coughing, singing, talking, vomiting
What is a Spirometry?
What is a Spirometer used to measure?
Measuring lung volume
*Cannot measure functional residual capacity (air left in lungs forced expiration), total lung capacity (max air the lungs can contain) and residual volume (air left after forced expiration)
What are the following definitions?
Tidal volume (TV)
Inspiratory reserve volume (IRV)
Epiratory reserve volume (ERV)
Residual volume (RV)
Vital capacity (VC)
Inspiratory capacity (IC)
Function residual capacity (FRC)
Total lung capacity (TLC)
Tidal volume (TV) = volume of quiet breathing - 500 mL
Inspiratory reserve volume (IRV) = volume of air inpired more than TV with forced inspiration - 3000mL
Epiratory reserve volume (ERV) = volume of air exhaled more than TV with forced expiration - 1200mL
Residual volume (RV) = volume remaining in lungs after max expiration (mixes with fresh air w/ next inspiration) - 1200mL
Vital capacity (VC) = Amount of air exhaled with max effort after max inspiration (strength of thoracic cage) - 4700mL
Inspiratory capacity (IC) = max amount of air inhaled starting from normal (TV + IRV) - 3500mL
Function residual capacity (FRC) = Amount air in lungs after tidal respiation (RV + ERV) - 2400mL
Total lung capacity (TLC) = Max amount of air lungs can contain (RV + VC) - 5900mL
How can FRC be measured ?
FRC = functional residual capacity = Amount air in lungs after tidal respiation
Not by spirometer bc this air is in the lungs
put He in air inhaled and measure concentration
C1V1 = C2(V1 + FRC)
What is minute ventilation vc Alveolar ventilation ?
Ve (minute ventilation) = Vt(tidal volume) x f = mL/min
But not all air inhaled into lungs participates in gas exchange, some aire remains in anatomical dead space –> 150 mL(/respiration) in adult
Va (alveolar ventilation = amount of air participating in gas exchange/minute) = (Ve - 150mL) x f
What is the alveolar dead space?
Some alveoli get reduced or blocked blood flow so no gas exchange
Pathological dead space = Physiological dead space + Alveolar dead space
What are the normal pressure in Normal Alveolar Ventilation?
Partial pressures in air
Partial pressures in alveoli
In different section of circulation
VA keeps PaCO2 at cste level
Air: PO2 = 160 mmHg, PCO2 = 0.3 mmHg
Alveoli: PO2 = 105 mmHg, PCO2 = 40 mmHg (coming from circulation)
Pulmonary Arteries: PO2 = 40 mmHg, PCO2 = 46 mmHg
Pulmonary veins: PO2 = 100 mmHg, PCO2 = 40 mmHg
Systemic arteries PO2 = 100 mmHg, PCO2 = 40 mmHg
Systemic veins = PO2 = 40 mmHg, PCO2 = 46 mmHg
O2 oxy = 100 mmHg, O2 deoxy = 40 mmHg
CO2 oxy = 40 mmHg, CO2 deoxy = 46mmHg
*bigger change is O2 than CO2!!!
What is Alveolar hyperventilation?
What is Alveolar hypoventilation?
Hyperventilation
When + O2 supplied and + CO2 removed than metabolic consumption
Result: PAO2 ↑ PACO2↓
*Does not consider exercise bc in exercise, metabolic rate increases also
Hypoventilation
Result: PAO2 ↓ PACO2↑
*Can occur w/ disorders ex: chronic obstructive lung disease, damage to respiratory muscles, CNS depressed, pneumothorax
*If breathe air with low PO2 (high altitude) → decrease in PO2, but no change in PCO2 bc not more production
*If change in metabolic rate, both affected
What is the diffusion rate proportional to?
How does EDEMA affect diffusion rate?
- Surface of exchange
- 1/Thickness
- partial pressure gradient
*For gas to diffuse, has to be soluble with liquid, CO2 20x more soluble than O2 so diffuses 20x faster
As blood goes through capillaries, diffusion rate decreases bc gradient decreases bc some diffusion has already been made
- Since O2 has way bigger gradient, diffuses faster but CO2 = more soluble so takes approx same time to diffuse O2 and CO2
EDEMA increase thickness in intersitial space, thicker membrane = less efficient diffusion
How long is the transit time through the pulmonary capillaries?
transit time = 0.75 sec
In normal lungs, diffusion is completed within 1/3 fo the red blood cell transit time
Someone with EDEMA would still have time to diffuse but is it deos exercise and blood flow increases, may not have time
How is vascular resistance different in systemic circulation than in pulmonary circulation?
Flow = pressure/resistance
pressure drop in pulmonary ciruclation = 10 mm Hg
pressure drop in systemic ciruclation = 100 mm Hg
So pulmonary resistance = 1/10 of systemic (to have same flow)
+ high complicance (too offer less resistance) of pulmonary system to accept cardiac output
What is accommodation of pulmonary blood?
Drugs, Nitric Oxide, reflex vasoconstriction
Pulmonary circulation has capacity to accomodate 2, 3 fold increase in cardiac output with little of pulmonary arterial pressure: Increase cross sectional area!!
Recruitment (cardiac vessels may open)
Distension (blood vessels already perfused increase their caliber)
Drugs causing contraction of smooth muscles → increase resistance of pulmonary arteries (Serotonin, histamine, norepinephrine)
Drugs causing smooth muscles to relax → decrease pulmonary vascular resistance (acetylcholine, isoproteranol)
Reflex vasoconstriction in regions of poor oxygenation
Nitric oxide produced by endothelial cells relax smooth muscles → vasodilatation
What are the effects of gravity on pulmonary blood?
Pulmonary blood flow differs with body posture and is affected by gravity
Uneven distribution of blood flow from top to bottom of the lungs
Top:
Alveolar pressure > Pulmonary arterial pressure so capillaries are compressed when low arterial pressure or positive ventilation
*for young healthy subjects, doesn’t happen bc arterial pressure in high enough
Middle:
Pulmonary arterial pressure > alveolar pressure > venous pressure so flow depends on difference between arterial and alveolar pressure, bc if not enough pressure lung will collapse shortly later
Bottom:
pulmonary arterial pressure > venous pressure > alveolar pressure, flow depends on artery-venous difference
*Measure with radioactive xenon
How does gravity affect the distribution of ventilation?
For upright, at rest subject
SLINKY
alveoli at the top of the lungs are more open than bottom ones at rest so during breathing, bottom ones can have more new air so preferrential ventilation for bottom part of lungs
*measured with inhaled radioactive Xenon (instead of infused in blood)
What is ventilation-prefusion ratio?
It’s the ratio between ventilation and perfusion of blood in capillaries depending on hydrostatic pressure/gravity effects
Ventilation increases slowly from top to bottom
blood flow increases rapidly so ventilation-perfusion ratio abnormally high at the top and much lower at bottom
*Normal lung not perfect!
If there was no gravity, we would have a much better ventilation-perfusion ratio
*For subject lying vs standing it is top to bottom in the other sens
How do we calculate O2 consumption/minute?
VO2
It’s O2 taken up by blood in the lungs in 1 minute.
CaO2 = O2 entering the lungs (from artery)
CvO2 = O2 leaving the lungs via the veins (measured w/ catheter)
VO2 = Q(CaO2 - CvO2)
Q = pulmonary blood flow = VO2/(CaO2-CvO2)
What does Henry’s Law state?
gas molecules dissolved in liquid proportional to partial pressure of the gas above the liquid.
Amount of Gas carried by blood directly proportional to the partial pressure of the gas
O2 relatively insoluble in H2O → 0.3 volume % when equilibrated with PO2 of 100 mmHg
BUT consumption much greater → at rest = 300mL O2/min
How are the O2 needs fufilled as O2 is not soluble in H2O?
O2 bound to Hemoglobin
Hb = 1/3 weight of RBC (147g O2/L blood)
Hb = 4 subunits, each has Heme (w/ F++ ion) bound to a globin, every Heme can bind 1 O2 (4/molecule)
cooperative binding → binding of O2 to first subunit increases affinity for second, etc.
O2 bound to Hb = 19.5 volume %
+ 0.3 vol.% dissloved → O2 in arterial blood 20 vol.%
O2 bound to Hb does NOT contribute to PO2 of blood, but PO2 of plasma determiens amount of O2 that combines with Hb
Hb + O2 → HbO2 is REVERSIBLE
O2 dissociation curve
Determines amount of O2 bound to Hb for given partial pressure:
- flat at high alveolar levels of PO2
- steep at low peripheral tissue levels of PO2, bc at low levels, Hb desaturates to let O2 get used
So PO2 has to drop to 60 mmHg for HbO2 drops significantly
Important bc in peripheral tissues, if minor drop in PO2, a lot of Hb desaturates: HbO2 → Hb + O2
*If O2 needed, Hb desaturates, if not, transports it other place where needed
*Peripheral tissues can only use dissolved O2 so needs to desaturate
At rest, Hb still 75% saturated at end of tissue capillaries, protective measure bc when need more, its there (ex: exercise)
So total amount of O2 in blood determined by Hb concentration (ex: anemia)
What is the role of myoglobin in the muscles?
intracellular carrier to facilitate diffusion of oxygen throughout muscle cell (similar to Hb)
Ressembles Hb but only binds 1 O2 at the time Follows hyperbolic shape, only release O2 at very low PO2 in the msucles
What is the Bohr Effect?
Shift of HbO2 dissociation curve to the RIGHT when blood CO2, Temperature of blood pH decreases
ex: when exercice (produce acid, generate heat, increase CO2) → additional amount of O2 released for higher PO2 to prevent from going down to much
Little effect on amount over 80 mm Hg still
Same effect seen when 2, 3-DPG (end product of RBC metabolism) increases → chronic hypoxia
*↓ T˚, ↓ CO2, ↑ acid have opposit effect 9shift to left)
Why is Carbon monoxide poisoning so dangerous?
- CO has higher affinity with O2 binding sites in Hb than O2
- Shifts O2-Hb curve to left reducing unload of O2
- Little stimulation to incrase ventilation bc PaO2 remains normal
How is CO2 carried in the blood?
- Physically dissolved in blood (10%) (Henry’s Law)
- Combined with Hb → HbCO2 (11%): no competition with O2 bc binds to the globin part of Hb
*Reversible - As bicarbonate (79%): in RBC,
CO2 + H2O → H2CO3
H2CO3 → HCO3- + H+ (ionized with Cl-)
*Reverible reaction!! (happens in tissues and reversed in lungs)
What is the Haldane effect?
In capillaries, Hb free of O2 combines with H+
HbO2 → HHb + O2 because HHb less acidic than HbO2 (Hb act as buffer)
Helps blood loading of CO2
That’s why venous blood can carry more CO2 than arterial blood
What is the CO2 dissociation curve like?
no steep of flat portion, relationship between CO2 content and PCO2 in linear
If hypoventilate → alveolar PCO2 ↑, CO2 everywhere ↑ so doubling alveolar ventilation halves alveolar PCO2
What can be the causes of respiratory failures?
- Gas exchange capabilities of the lungs (ex: EDEMA)
- Neural control of ventilation (drive to breathe)
- Neuromuscular breathing apparatus (respiratory muscles and their innervation)
What is arterial Hypoxia?
Whats can be its causes?
Low PaO2 below 60 mm Hg, low % Hb saturation, O2 content in arterial and venous blood becomes lower than sea level values
Causes:
1. Inhalation of low PO2 (high altitude)
2. Hypoventilation ← disease affecting CNS, neuromuscular diseases, barbiturates, other drugs and narcotics
3. Ventilation/perfusion imbalance in lungs: when fresh gas reaching alveolar region/breath is too low for flow through capillaries of that region (ex: asthma)
4. Shunts of blood across the lungs: venous blood bypasses the gas exchange region of lungs and returns to systemic circulation (ex: foramen ovale)
ex: for babies, oxygenated via lungs of mom so redirected directly to brain for greater dev. and then when born, doesn’t adapt
5. O2 diffusion impairment (pulmonary EDEMA)
What is the breaking point of voluntary breathing?
when reach PCO2 reaches 50 mmHg, arterial PO2 = 70 mmHg, voluntary control is over-ridden and involuntary respiration takes back.
*Depends on receptors to CO2 and O2 levels (in arterial blood and/or cerebrospinal-spinal fluid)
*Voluntary breathing comes from cerebral hemispheres
What are the 3 components of the control of breathing?
All in brain stem!! (Pons and medulla)
- Sensors: info about lung volume (pulmonary receptors) and O2/CO2 content (chemoreceptors)
- Controllers: Pons and medulla, get info from sensors via afferent neural fibres and from higher structures on CNS → info is integrated
- Effectors: respiratory muscles!!
Receive info from controllers via spinal motoneurons, ventilation is adjusted to metabolic needs
What is the role of the Medulla in the control of breathing?
Pattern of breathing
pacemaker cells in medulla (2 groups)
- Ventral respiratory group (contains pre-Botzinger complex) → basic rythm
- Dorsal respiratory group → receive sensory inputs and connect to motor neurons
*Connect with each other, basic respiration rythmicity
*If problem with medulla, irregular breathing
What is the role of the rostral (upper) pons in the control of breathing?
*In pneumotaxic center
Pattern of breathing
Turn-off inspiration → smaller tidal volume → increase in breathing frequency to maintain adequate ventilation
*Cutting pneumotaxic center → deep and slow breathing (same as cutting vagus nerve which brings afferent information)
What is the role of the lower pons in the control of breathing?
*Apneustic center
Pattern of breathing
Cells of Apneustic center promote inspiration by sending excitatory impulses to respiratory groups of medulla
*If just lower pons (removed upper and vagus nerve) → apneustic breathing: tonic inspiratory activity interrupted by short expirations
Seen in severe brain injury
What are the roles of CENTRAL chemoreceptors?
PCO2, pH in arterial blood detected by central chemoreceptors → change in ventilation to return to normal values.
On ventral surface of the medulla → detect pH of CSF (influenced by those of arterial blood)
Bathed in brain extracellular fluid, CO2 diffuses easily from blood to CSF → CO2 reduces CSF pH → stimulates chemoreceptors (H+, HCO3- can’t easily cross blodd brain barrier)
Main drive to breathe under normal conditions!!!
*Paper bag test
Info carried out to respiratory neurons → activity of respiratory neuron will adapt.
PaO2 under 60 mmHg or PaCO2 higher than 40 mmG → activity will increase, inversibly
What are the roles of PERIPHERAL chemoreceptors?
Mainly sensitive to changes in PO2 (a bit by changes in PCO2 and pH)
Located in carotid bodies and aortic bodies (structures made up of blood vessels, supporting tissues, end of sensory neurons of glossopharyngeal → carotid bodies and vagus nerves → aortic bodies
Afferent fibers of receptors → dorsal group of respiratory neurons in medulla
What means normocapnia?
Normal levels of CO2 in blood
What are the 3 types of MECHANICAL receptors in lungs?
What happens if vagus nerve sectioned?
Pulmonray Vagal Receptors:
1. Plumonary stretch receptors
2. Irritant Receptors
3. Juxta-capillary of J receptors (C-fibers)
*All afferent fibers of these receptors travel in vagus nerves
If vagus nerve sectioned → slow, deep breathing
What is the role of the Pulmonary Stretch Receptor?
*Mechanical receptor in the lungs
In smooth muscles of trachea down to terminal bronchioles
Innervated by large myelinated fibers, discharge when distension (swelling?) of lungs
Activity phasically increases as lung volume increases during each inspiration
Hering-Breuer Inflation Reflex: when pulmonary stretch receptors innervated → prologation of expiratory time → decrease in respiratory. frequency
Because in ↑ Lung volume → inhibit beginning of next inspiration (negative feedback)
*Noticeable in infants and animals (not rlly in adults unless TV exceeds 1L as in exercise)
What is the role of the Irritant Receptors?
*Mechanical receptor in the lungs
Between aiway epithelial cells in the trachea down the respiratory bronchioles (myelinated fibers)
Stimulated by noxious gases, cigarette, histamine, cold air, dust
Stimulation leads to bronco constriction + hyperpnea (deaper breathing)
ex: histamine released w/ allergies → asthma(
What is the role of the Juxta-Capillary Receptors?
*Mechanical l receptors in lungs
Located in alveolar walls close to capillaries
Innervated by non-myelinated fibers
Short and lasting burst of activity
Stimulated by ↑ in interstitial fluid (pulmonary congestion, EDEMA)
Reflex effect = rapid, shallow respiration, intense stimulation → apnea
*May play role in dyspnea (sensation of difficulty breathing) associated with left heart failure, lung EDEMA or congestion
What happens to the pleural pressure after pneumothorax?
goes to 0 just like outside, lungs collapse, rib cage expands
*Pleural space filled with liquid that allows the lungs to slide against the internal wall of the chest during breathing
How do we evaluate elastic properties of the lungs and the chest wall?
Measure the recoil pressure of each separated structure for given change in lung volume
Lung volumes measured by spirometry
For respiratory system → use of manometers or pressure transducers as ref to atmospheric pressure (=0)
Recoil pressure = pressure difference between outside and inside → transmural pressure
How is measured the recoil pressure of the chest wall?
Trans-chest-wall pressure (Pw)
Ppl - pressure at body surface (Pbs = 0)
How can the Ppl be measured?
Using a flexible balloon introduced into esophagus
Bc esophagus located between 2 pleural spaces, esophagus pressure = close approx. of pleural pressure
How is the recoil pressure of the lungs transpulmonary pressure (Pl) when no air flow, closed mouth and nose?
*Palv and pressure at mouth = same
Pl (transpulmonary) = Palv - Ppl
How is the recoil pressure of the total respiratory system calculated? (
*Trans-respiratory pressure (Prs)
Prs = Palv - Pbs
where Pbs = Ppl-Pw and Palv = Pl + Ppl
So Prs is sum of P lungs and P chest wall = Pl + Pw
How is compliance of the respiratory system normally measured in human?
What is the equation for lungs compliance?
Static pressure relationship while long volume is decreased step by step from TLC
Compliance = volume change in lungs/ unitary change in pressure = ∆V/∆P
Compliance of the lungs = ∆V lungs/ (∆Palv - ∆Pppl)
What is the elastance of the lungs?
The inverse of the compliance
El = (∆Palv - ∆Pppl)/∆V
Elastic recoil of the lungs produced:
Elasticity of the lung tissue (a bit)
Properties of the liquid film lining the inside of the lungs (mostly) → surface tension of this film is important bc surface area very large
How does respiratory disorders affect the compliance of the lungs?
Emphysema: high compliance (too floppy), high TLC, but no recoil
Firbosis: less compliance, lower TLC for higher pressure
How is the compliance of the chest wall calculated?
Cw = ∆V/ ∆Ppl
*∆P = pleural - outside (0) = pressure accross the chest wall
∆P sometimes positive, sometimes negative
What is the relationship between the %Vial Capacity and rip cage pressure?
At 60% Vital Capacity → Pressure = 0
Under 60% → negative pressure (rib cage wants to expand)
Pressure at Residual Volume = -40 cm H2O
Over 60% Vital Capacity → positive pressure (rib cage wants to collapse a bit)
At TLC (100% VC) → approx. 15 cm H20
What is the equation for the compliance of the respiratory system?
Crs = ∆V/∆Prs = ∆V/∆(Pl + Pw)
1/Crs = 1/Cl + 1/Cw
How is FRC pressure determined?
When equilibrium between positive pressure of lungs (wants to collapse) and negative pressure of the rib cage (wants to expand)
Prs = 0
What happens when their is a pneumothorax?
Air enters pleural space bc Ppl < atmospheric
Lungs collapse to resting position (below RV)
Chest wall expands to resting position (60% TLC)
What determines the flow of air coming through the airways?
F = (Palv - Patm)/R
if Palv > Patm → air flows out
How does the dynamics of breathing work?
- Respiratory muscles contract
- Thoracic cage expands
- Ppl becomes more sub atmospheric
- Transpulmonary pressure increases
4.5 Volume lungs ↑, Palv ↓ below Patm - Air flows in
- Air flow gradually decreases as air flows in and pressure gradient decreases
- Palv = Patm
- Onset of expiration → diaphragm relaxes, elastic recoil of resp sys. compresses gas in lungs
- Palv > Patm
- Air flows out
- Lung volume decreases →Ppl slowly returns to resting level
What is the air flow, Palv and Ppl at FRC?
air flow = 0ml/s
Palv = 0 cmH2O
Ppl = -5 cm H2O
*Voir slide avec schéma (p.113)
On what does the pleural pressure during inspiration depend?
contraction of diaphragm and airway resistance
*Need more pressure than juste balancing out Ppl bc of airway resistance
How is the airway resistance calculated?
What is the link with asthma?
Raw = (Palv - Pao)/Flow
*Pao = P airway opening
*Flow = change in volume/time
In asthma, airway constrict so less flow → bigger resistance (smaller airways = more resistance)
What is the link between the flow-volume curve and the effort put into expiration and inspiration?
*Talk about forced expiration
Inspiration → more effort = steeper flow-volume curve
Expiration → constant slope, doesn’t depend on effort
Forced expiration:
During forced expiration, intra-pleural and alveolar pressure increase. Flow drops along the airways (bc goes to 0 at the mouth?) so point at which pleural-pressure > airway pressure which collapses the airways
What is the the link between expiratory flow and breathing disorders?
FINIR
Restrictive → higher expiration flow
Obstructive → lower expiration flow
How are the Tidal Volume and Breathing Frequency influenced by exercice?
*Both determining factors of pulmonary minute ventilation
At start, both increase proportionally
TV plateaus (bc max compliance after which too much work/air) → high ventilatory rates during hard exercise due to higher FREQUENCY
Inspiratory and expiratory times decrease but expiratory time increases more than inspiratory time
What is the relationship between minute ventilation and metabolic rate during exercise?
Untrained and trained subjects, minute ventilation (Ve) increases linearly with metabolic rate (VO2) to about 50%-65% of VO2 max
After, Ve increases disproportionally greater tha change in VO2 → Hyperventilation
Traning delays ventilatory inflection point (Hyperventilation)
Is ventilation a limiting factor in aerobic performance as sea level? (Ve/Q)
What receptors are responsible for ventilation control during exercise?
NOT Central Chemoreceptors mostly at rest
NOT peripheral Chemoreceptors PaO2 remains cst during exercise, PaCO2 is decreased during exercise, pH decreases
But possible that fluctuation in PaO2 increase sensitivity of peripheral chemoeceptors to CO2 and H+
still very poorly understood
*Believe it is Humoral bc can see an onset even before start of exercise and big dip just after (than continues to go down gradually)
How does Minute ventilation, Arterial PO2, Arterial PCO2, Arterial H+ change with exercise (with O2 consumption)?
Minute ventilation increases
Arterial PO2 constante
Arterial PCO2 decreases
Arterial H+ (mol/L) increases
What is the definition of Asthma?
Chronic inflammation of airways
Airway Obstruction + enhanced airway responsiveness to contractile agonist/allergens
What is the definition of Emphysema?
Enlargement of air spaces bc destruction of walls of alveoli
Lungs self-destruct attacked by proteolytic enzymes secreted by leukocytes.
Loss of radial traction so aiways tend to collapse
What is the definition of Fibrosis?
Progressive distortion of alveolar architecture with inflammation and accumulation of fibrotic tissue
