Respiratory System Flashcards
upper airway muscles (33)
active during inspiration, keep airway open
nasal and oral cavities, pharynx, larynx (vocal cords)
Trachea
Lungs
- bronchi –> bronchioles –> alveoli
smooth muscle and connective tissue
pulmonary circulation
Sleep apnea
reduction in upper airway path during sleep. Airflow is blocked.
caused by loss of muscle tone, anatomical defects
Risk factors of sleep apnea
Lack of excitatory drive - reduction in muscle tone
Filtering Action regions
conducting zone - mucus-producing (goblet) cells and ciliated cells
trap and remove inhaled particles
muco-cilliary escalator
Role of goblet cells and ciliated cells
Trap inhaled particles and remove them. Prevent it from reaching respiratory zone
SOL layer
low density. Free cilia movement
CILIATED cells that have free movement
GEL layer
Goblet cels (mucous)
high viscosity and elastic properties
traps inhaled particles
Removal of mucous
cilia movements
downward (nasopharynx)
upward (trachea)
eliminated through esophagus
Smoking affect on cilia and goblet cells
chemicals/tar effect cilia movement, preventing the removal of particles
Where are macrophages located
Alveoli
Last defence to inhaled particles
Pulmonary fibrosis
silica duct and abestos
lungs cannot expand due to collagen buildup over time
Spirometry
Pulmonary function test
rate of insp and exp air
measure volume of air inspired and expired by the lungs
AMOUNT AND RATE OF AIR BREATHED IN AND OUT OVER TIME
Atelectasis
complete or partial collapse of lung (or lobe of lung)
Occurs when alveoli become delated/flat
Can you measure residual lung volume?
NO it cannot be measured via spirometry
Tidal volume
volume of air moved IN or OUT of respiratory tract during each ventilation cycle
inspiratory reserve volume
additional volume of air that can be forcibly inhaled following NORMAL RESP
simply inspire maximally, MAXIMAL POSSIBLE INSPIRATION
expiratory reserve volume
additional volume of air that can be forcibly exhaled following normal expiration
simply expire maximally MAXIMUM VOLUNTARY EXPIRATION
residual volume RV = FRC - ERV
the volume of air remaining in the lungs after a MAXIMAL EXPIRATION. cannot be expired at all (no matter what)
RV = FRC - ERV
Capacities
SUM of two or more lung volumes
VC = TV + IRV + ERV
VITAL CAPACITY - maximal amount of air that can be forcibly exhaled after maximal inspiration
IC = TV + IRV
INSPIRATORY CAPACITY - maximal volume of air that can be forcibly exhaled
FRC = RV* + ERV
FUNCTIONAL RESIDUAL CAPACITY - volume of air remaining in the lungs at the end of a normal expiration
cannot be measured by spirometry
TLC = FRC + TV + IRV = VC + RV*
TOTAL LUNG CAPACITY - the volume of air in the lungs at the end of a maximal inspiration
cannot be measured by spirometry
Lung volume
Tidal volume - 0.5 L
Flow (calculation)
Total/minute ventilation
total amount of air moved into the respiratory system per minute
Total/minute ventilation = TV x resp frequency = 0.5L x 15bpm = 7.5L/min
Alveolar ventilation (Va)
amount of air moved into alveoli per minute
depends on the anatomical dead space - constant, not available for gas exchange
AV = (0.5 - 0.15) L x 15/min = 5.25 L/min
Which sis more effective - DEEP breathing or INCREASED RATE (shallow)?
Deep breathing - higher alveolar ventilation
FEV1
FORCED EXPIRATORY VOLUME in 1 sec
health person can empty most air out of their lungs in one second
FVC
FORCED VITAL CAPACITY
amount of air that is blown out in one breath after max inspiration as fast as possible
Spirometry Test Patterns (3)
- normal (age, gender, weight, height)
- obstructive (difficulty exhaling - asthma)
shortness of breath, air comes out slowly - restrictive (difficulty fully expanding - fibrosis, ALS, MS)
stiffness in lungs
Helium dilution technique
helium is insoluble in blood, EQb after a few breaths, Measure the concentration at the end of expiratory effort
measures communicating gas or ventilated lung volume
Mechanics of Ventilation
Static properties of lung (mechanics of ventilation)
NO AIR IS FLOWING maintains chest wall volume Intrapleural ressuer (Pip), transpulmonary pressure (Ptp)
Dynamic properties of lung (mechanics of ventilation)
LUNGS ARE CHANGING VOLUME
air flows in and out
permits airflow
Alveolar pressure (Palv)
Boyle’s Law
for a fixed amount of an ideal gas; fixed temperature
Pressure and volume are INVERSELY proportional
P1V1 = P2V2 (contant T)
gas molecules are in constant motion, creating pressure:
EXPIRATION: decrease volume, increased pressure (alv)
INSPIRATION: increased volume, decreased pressure (alv)
Ventilation
exchange of air between the atmosphere and alveoli
Bulk flow: gas moves from HIGH pressure to LOW pressure
F = deltaP / R
deltaP —> (Palv-Patm)
What creates pressure
movement of gas molecules in a container
How ia airflow created
change in volume and pressure produces airflow
pressure difference is generated, air moves via bulk flow HIGH to LOW pressure
F = deltaP / R
Elastic recoil
interaction between lung and thoracic caste determines lung volume
Lungs tend to collapse due to elastic recoil
chest wall - pulls thoracic cage outward due to elastic recoil
EQb –> inward recoil balanced with outward recoil
Intrapleural Pressure (Pip)
Intrapleural fluid - reduces friction of lung against thoracic wall during breathing
PRESSURE IN THE PLEURAL CAVITY
always subatmospheric
if Pip = Palv —> lungs would collapse
Transpulmonary pressure
FORCE RESPONSIBLE FOR KEEPING ALVEOLI OPEN
grater than 0 to keep lungs expanded
determines lung volume (static) not airflow
airway resistance
- Inertia of respiratory system (negligible)
- Friction
- lung tissue with itself
- lung and chest wall tissue
- resistance of air flow
Laminar flow
relatively little energy in airflow RESISTANCE, small airway are distal to terminal bronchioles
Transitional flow
extra energy needed to produce vortices, resistance increases
airflow is transitional throughout bronchial tree
Turbulent flow
effective resistance to airflow is highest
LARGE AIRWAYS (trachea, larynx, pharynx)
radius is large and linear air velocities may be extremely high
Poiseuille’s law
laminar flow
R = 8nl / pi r^4
airway resistance is proportional to the viscosity of the gas and the length of the tube, but inversely proportional to fourth power of the radius
R to airflow is highly sensitive to the airway radius
Disease conditions of Airway resistance
typically impacted by small airways more than large ones
- smooth muscle wall contraction
- edema occurring on the walls of alveoli and bronchioles
- mucus collection in lumens of bronchioles
Lung compliance
Dynamic vs static
measure of elasticity of lungs, lung expansion
CHANGE IN LUNG VOLUME produced by change in TRANSPULMONARY PRESSURE
static - measured during no gas flow
dynamic - measured during gas flow
Static compliance
no air flow through
Dynamic compliance
measured during air flow
reflection of lung stiffness and airway resistance
Emphysema - high compliance
loss of alveolar tissue (less gas exchange)
floppy lungs, less elastic recoil
Hysteresis
defines the difference between inflation and deflation compliance paths
Grater pressure difference is required to open a previously closed (narrowed) pathway than to keep an open airway from closing
Elastic components of lungs
elastin - weak spring, LOW tensile strength, extensible
collagen - strong twine, HIGH tensile strength, inextensible
What determines Lung Compliance
Elastic components - elastin, collagen
Surface Tension - air/-water interface within the alveoli
alveolar surface tension
water molecules at the surface of a gas-liquid interface are attracted strongly to the water molecules within the liquid mass
surface tension measures the attractive forces acting to pull a liquid’s surface molecules together
Factors that affect pressure-volume relation
air inflation
liquid inflation
Laplace’s equation
describes EQb:
P=2T/r
the smaller the bubbles radius is, the grater pressure needed to stay inflated
Alveolar surfactant
Produced by Type II alveolar cells
Lowers surface tension ( level of alveoli)
Stable against collapse
Surfactant and surface tension
Phospholipids mixture
Dipalmitol-phosphatidylcholine
breaks the strong attractive forces at the surface of water
T/F - there is a constant amount of surfactant in every alveoli
True
Equalizes pressures between alveoli of different sizes
T/F - More dense/concentrated surfactant equalizes alveloi
TRUE
no pressure gradient
small alveoli will not collapse
Infant Respiratory Distress
Premature infants - lack of surfactant decreases compliance, increases work required to breathe
Regional differences in ventilation -
Gravity and Position
Radioactive Xenon inhaled
Highest amount of ventitialtion
Back of lungs
What explains Regional Differences in Pip
Weight of lungs increases pressure near bottom of
How is Inter-pleural pressure created
Gas Exchange
Partial pressure of Gases
Dalton’s Law
In a mixture of gases - each gas operates independently
Ptotal = P1 + P2 + P3 …
Partial pressure of Gases at atmosphere at SEA LEVEL
760 mmHg = Patm
Diffusion: how gas crosses the Blood-gas barrier
Ficks law explains the rate of transfer of has through a sheet of tissue/unit of time
Respiratory Membrane
minimal thickness
Solubility of gases in Liquids
Diffusion constant (D) CO2 solubility is much highter than O2
Henry’s Law
the amount of gas dissolved in a liquid is direction proportional to the partial pressure of gas in which the liquid is in equilibrium
Diffusion of gases in liquids
amount of gas in the liquid is dependent on the solubility
PP of oxygen decreases in alveoly
PP of CO@ increases in alveoli
Why does CO2 partial pressure decrease?
slide 128
Air is warmed up and humidified
Determinants of alveolar Po2:
1 Po2 in atmosphere
2 alveolar ventiliation
3 metabolic rate
4 perfusion
Gas exchange between alveoli and blood
Blood gasses EQb quickly
Perfusion of the Lung
Systemic circulation
High pressure system
Why do we need a low pressure system? What is it called
Pulmonary system
Delivery blood only to lungs and high pressure is risky
Resp membrane damage
Low pressure system
Low resistance system
high compliance vessels
Positive to alveoli collapse
redirect blood to regions where gas exchange can still occur
Ventilation-perfusion relationship
Ventilation and perfusion matching
Bronchoconstriction
Diameter of the airway has become smaller. reduction in ventilation
Oxygen transport in blood
O2 - gas molecule with LOW solubility
Hemoglobin
2 alpha chain
2 beta chains
4 heme groups
Oxygen Dissociation curve
interaction between Hb and the arterial partial pressure of oxygen
porphoryn ring
iron atom binds to oxygen
O2 + Hb HbO2
reversible process
O2 CAPACITY
max amount of oxygen that can combine with Hb.
Depends on how much Hb is present in blood
1 g Hb combines with 1.39 mL O2
Hb SATURATION
Percentage of the available Hb binding sites that have O2 attached
O2 combined with Hb / O2 capacity X 100
What is the Dissociation curve sensitive to?
Arterial pO2 ***
pH
Temperature
pCO2
What influences the sigmoidal dissociation curve?
Cooperative binding
Cooperative Binding
When O2 binds - confirmation change of the HEME group
TENSE —> RELAXED
significance of sigmoidal dissociation curve
- Flat portion 60-100 mmHg
2. Steep portion
sigmoidal dissociation curve plateau
Reduced alveolar Po2
Tense vs Relaxed state
Tense vs Relaxed state steep portion
10-40 mmHg 40-60 mmHg Unload large amounts of oxygen Advantage - reduction of CO2 and PO2 UNLOAD OXYGEN TO PERIPHERAL TISSUE
anemia
reduction in amount go Hb in blood
Polycythemia
increase in Hb amount in blood or reduction of blood volume (increases Hb concentration)
Carbon monoxide poisoning (and affect on O2 dissociation curve)
HbCO
Binds to Hb tighter than O2
reduced O2 binding to Hb
LEFT SHIFT = decreased unloading of O2 to tissues; conformational change
saturation
Hb cannot hold more O2, sigmoidal curve flattens
Oxygen movement in lungs and tissues
driven by pressure gradient generated by two different environments
pH change on O2 dissociation curve
RIGHT shift
Oxygen movement at level of respiratory membrane
Po2alv»_space; po2blood
Oxygen movement in peripheral tissue
capillary
peripheral tissue cells consumed dissolved O2
intracellular space –> mitochondria
Temp change on O2 dissociation curve
Favour oxygen unloading
RIGHT shift
PCO2 change on O2 dissociation curve
Favour oxygen unloading
RIGHT shift
Right shift
lower percentage of Hb that has bound oxygen
More unloading of oxygen
higher metabolism
Left shift
less oxygen unloading
cell/body metabolism
2,3-diphosphoglycerate (DPG)
end product of RBC metabolism
RIGHT SHIFT
increase - chronic hypoxia
high altitude, lung disease
Carbon dioxide transport in blood
CO2 is much more soluble in water than oxygen is
Peripheral tissue –> respiratory system
Carbonic anhydrase (CA) Carbonic acid - H2CO3
In RBC
Decrease pH
Catalyzes reaction where CO2 reacts with water
CO2 forms in blood (3)
Dissolved (5%)
Bicarbonate HCO3- (60-65%)
Carbamino compounds (25-30%0
Bicarbonate HCO3-
what does Carbonic acid dissociate into
H2CO3
dissociates into bicarbonate and H+ ions
Chloride Shift
HCO3- (bicarbonate) leaves RBC, stays in plasma
Cl- move into RBC, maintaining electrical neutrality in RBC
Carbamino Groups
CO2 interacts with amino groups in blood proteins
Periphery –> alveolar tissue
Carbaminohemoglobin
Hb + CO2 HbCO2
No enzyme required
T/F - DeoxyHb has higher affinity for CO2
True
High levels of CO2 results in large in increased oxygen unloading
Respiratory Acidosis
hypoventilation
CO2 is produced faster than it is eliminated
decreased PCO2, increased H+
Respiratory alkalosis
Hyperventilation
Co2 is removed faster that it is produced
decrease in both PCO2 and H+
Metabolic acidosis
Increased H+ in blood (independent from PCO2 changes)
Metabolic alkalosis
Decreased H+ in blood
independent from PCO2 changes
Physiological pH
7.4
venous blood is slightly more acidic(7.3)
What buffers the blood
Hb
What controls the automatic rhythm of breathing
Central nervous system
Pontine respiratory group
Dorsal respiratory group
***Ventral respiratory group
What does the medulla do
Initiates breatihing via specialized neurons
What modifies breathing
Higher CNS structures via CNS and input from central and peripheral chemo/mechano receptors
PreBotzinger complex
neurons in ventral respiratory group
Excitatory INSPIRATORY RHYTHMIC ACTIVITY (polysynaptic pathway)
Parafacial respiratory group (pFRG)
active contraction of abdomen muscles
Possible changes that need to accommodate breathing
1
2
3
4
Rhythm of Breathing
Generated in Ventral Resp Group (VRG)
PreBotC and pFRG neurons drive activity in premotor neurons
these excite motoneurons which active rhythmically respiratory muscles
Rhythmic activity is influenced by sensory and neuromodulatory (NT) units organization from different regions within and outside CNS
Neuro-Repiratory Pathways - Inspiration
Neuro-respiratory Pathways - Active Respiration
Control of ventilation by PO2, PCO2, H+
TV and rest rate respond to these changes Hypoxia hypercapnia acidosis INCREASE ventilation, raise PO2, dec CO2
Peripheral Chemoreceptors
Carotid and Aortic bodies
Carotid - baroreceptors
sense hypoxia, sensitive to pH
Carotid bodies
small chemsensitive vascularized high metabolic rate Type 1 - Glomus cell (chemosensitive) Type 2 - Sustentacular cells - support
Glomus cells
Neuron-like characteristics
What stimulates chemoreceptors
Arterial PO2 value below 60 mmHg
Central chemoreceptors
indirectly sense changes in PCO2
Rostral, intermediate, caudal regions of medulla
medullary raphe, hypothalamus
excitatory drive
hypercapnia
too much CO2 in blood
response is mediated dorsal and ventral group (change ventilation)
Lactic acid
reduce blood pH, increase H+ concentration
during exercise
hyperventilation