Respiration Flashcards
What are the functions of the respiratory system? (6)
- Provides oxygen and eliminates carbon dioxide (Homeostatic regulation of blood gases)
- Protects against microbial infection (Filtering action)
- Regulates blood pH (In coordination with the kidneys)
- Contributes to phonation
- Contributes to olfaction
- Is a reservoir for blood
What are the structures that comprise the respiratory system?
- Upper airways
- trachea
- lungs
- muscles of respiration
- rib cage and pleura
- Part of the CNS that regulates respiration
What is the difference between primary bronchi, bronchi,
bronchioles, terminal bronchioles, and respiratory bronchioles
Trachea & primary bronchi:
- C-shape cartilage (Anteriorly)
- Smooth muscle (Posteriorly)
- trachea: 1 branch, primary bronchi: 2 branches
Bronchi:
- Plates of cartilage & smooth muscle
Bronchioles:
- Smooth muscle only
Terminal bronchioles:
- smallest airway without alveoli
- 60,000 branches
Respiratory bronchioles:
- have occasional alveoli
Conducting vs Respiratory zones
Conducting: Trachea, bronchi, bronchioles, and terminal bronchioles
- Leads gas to the gas exchanging region of lungs, “anatomical dead space” (~ 150 mL): NO alveoli, NO gas exchange
Respiratory: Respiratory bronchioles, alveolar ducts, alveolar sacs
- Where gas exchange happens
(It contains alveoli)
Explain generations?
Generations is the increase in branching from the mouth to the alveoli. As the number of generations increase, diameter and length decrease but the number of each structure and the area it covers increases
Alveoli
Tiny, thin-walled, capillary rich sac
- where oxygen and
carbon dioxide exchange - ~500 million alveoli, diameter = ~ 1/3 mm
- ~280 billion capillaries in the lung (At rest they contain 70 mL of blood, 200mL during physical activity). The capillaries surround the alveoli like a net to increase contact and gas exchange
Alveolar cells
slide 14
Type I:
- Covers most of the surface of the alveolar walls.
- Type I cells are a continuous mono-layer of flat epithelial cells
- Do not divide; susceptible to inhaled or aspirated toxins
Type II:
- 7 % of alveolar surface
- Produce SURFACTANT
- progenitor cells: when there is injury to Type I cells, Type II cells can multiply and eventually differentiate into Type I cells
The respiratory membrane - capillaries and gas exchange
- The alveolar walls also contain a dense network of capillaries and a small interstitial space (Connective tissue and interstitial fluids)
- Capillaries are small (7 to 10 µM in diameter), just enough space for a red blood cell to pass
- Each red blood cell spends about 0.75 seconds in the capillary network and during this time probably traverses 2 or 3 alveoli
Transfer of O2 and CO2 occurs by diffusion through the respiratory membrane
- Respiratory membrane is extremely thin (0.2 - 0.5 µM thick); very thin for easy gas exchange
- Can be easily damaged
Steps of respiration and what are they?
- Ventilation: Exchange of air between atmosphere and
alveoli by bulk flow - Exchange of O2 and CO2 between alveolar air and blood in
lung capillaries by DIFFUSION - Transport of O2 and CO2 through pulmonary and systemic circulation by bulk flow
- Exchange of O2 and CO2 between blood in tissue capillaries and cells in tissues by diffusion (periphery tissue)
- Cellular utilization of O2 and production of CO2
How is ventilation produced?
- CNS sends rhythmic excitatory (Respiratory) drive to respiratory muscles
- Respiratory muscles contract rhythmically and in a very organized pattern
- Changes in volume and pressures at the level of the chest and lung occur
- Air flows in and out
Pump Muscles? What are inspiratory and expiratory?
INS: diaphragm, external
intercostals, parasternal intercostals
EXP: internal intercostals, abdominals
Airway Muscles? What are inspiratory and expiratory?
Keep upper airways open
INS: tongue protruders (Genioglossus), alae nasi, muscles around airways (Pharynx, larynx)
- Pharyngeal and laryngeal dilators are inspiratory
EXP: muscles are airways (Pharynx, larynx)
- Pharyngeal and laryngeal constrictors are expiratory
Obstructive sleep apnea
Reduction in upper airway openness during sleep (Snoring, apneas, sleep disturbances)
- This results in a decreased oxygen saturation = daytime sleepiness affecting cognitive function and cardiovascular hypertension
Sleep apnea is caused by:
- Reduction in muscle tone
- Anatomical defects
Accessory Muscles?
INS:Increase inspiration when there is a high metabolic drive
- contribute little to quiet breathing (At rest)
- They contract vigorously during exercise or forced respiration
- sternocleidomastoid: raise the sternum
- scalene: elevate upper ribs
Diaphragm
a dome-shaped muscle which flattens during contraction (INS), abdominal contents are forced down and forward
and rib cage is widened
‒ Increase in volume of the thorax
Inspiratory intercostal muscles
External intercostal muscles: contract and pull ribs upward
increasing the lateral volume of the thorax
‒ Bucket handle motion
Parasternal intercostal muscles: contract and pull sternum forward, increasing anterior posterior dimension of the rib cage
‒ Pump handle motion
Expiratory pump muscles
External oblique, internal oblique, transversus abdominis, rectus abdominis
- Relaxed at rest. Involved in other physiological functions (Coughing, vomiting, defecation, posture)
- Deeper, faster breathing requires active contraction of abdominal & internal intercostal muscles to return
the lung to its resting position (Exercise) - Internal intercostal muscles: Relaxed at rest
- During exercise, internal intercostal muscles pull rib cage down, reducing thoracic volume
Filtering Action / muco-ciliary escalator
The conducting airways are lined by a layer of epithelial cells which comprise mucus-producing (Goblet) cells and ciliated cells
- These cells function in a coordinated fashion to entrap inhaled biological and inert particulates and remove them from the airways
Clearance requires both ciliary and respiratory tract fluids
(Periciliary fluid and mucus)
Ciliated and Goblet cells
Ciliated: Produce periciliary fluid
(SOL LAYER) which allows ciliated cells to move freely
▪ Low viscosity optimal
for ciliary activity (5 µm optimal thickness)
- tips of cilia in gel layer that pushes the entrapped particles in one direction
- ciliated movement is downward
(Nasopharynx), upward (Trachea) to remove particles via esophagus
Goblet: Produce mucus (5 - 10 µm thick GEL LAYER, distributed in patches)
▪ Has a high viscosity and high elastic properties
▪ Traps inhaled materials
Filtering action by macrophages
Mostly present in the alveoli
- Last defense to inhaled particles if muco-ciliary escalator does not capture everything
- Rapidly phagocytize foreign particles and substances as well as cellular debris
- Silica dust and asbestos (very sharp / kill macrophages) → pulmonary fibrosis
Spirometry
Pulmonary function test to determine the amount and the rate of inspired and expired air (measures the volume of air inspired and expired by the lungs)
Lung volumes
- Tidal volume (TV): the volume of air moved IN OR OUT of the respiratory tract during
each ventilatory cycle (0.5L). - Inspiratory Reserve Volume (IRV): Maximum possible inspiration
- Expiratory Reserve Volume (EXV): Maximum
Voluntary Expiration - Residual Volume (RV): the volume of air remaining in the lungs after a Maximal Expiration. RV cannot be measured with a
spirometry test along with FRC and TLC. RV = FRC - ERV.
Lung capacities
Capacities = correspond to the sum of 2 or more lung volumes
5. Vital Capacity (VC): the maximal volume of air that can be forcibly exhaled after a Maximal
Inspiration. VC = TV + IRV + ERV.
6. Inspiratory capacity: the maximal volume of air that can be forcibly inhaled. IC = TV + IRV
7. Functional Residual Capacity (FRC): the volume of air remaining in the lungs at the end of a normal
expiration. FRC = RV + ERV.
8. Total Lung Capacity (TLC) → the volume of air in the lungs at the end of a Maximal Inspiration.
TLC = FRC + TV + IRV = VC + RV
Ventilation
Total/minute ventilation → total amount of air moved into the
respiratory system per minute
- Total/minute ventilation = Tidal volume x respiratory frequency
Alveolar ventilation → amount of air moved into the alveoli per
minute (Alveolar ventilation < minute ventilation). It depends on the anatomical dead space (0.15L).
Anatomical dead space: ~ 1/3 of normal breath is not available for gas exchange
- anatomical dead space is constant regardless of breath size
Effects of breathing pattern on alveolar ventilation
Increased DEPTH of breathing is more effective in increasing
alveolar ventilation than an equivalent increase in breathing RATE
- However, minute ventilation remains the same
FEV1 and FVC
Forced expiratory volume in 1 sec (FEV1):
- A healthy person can normally blow out most of the air from the lungs within one second
Forced vital capacity (FVC): The total amount of air that is blown out in one breath after max inspiration as fast as possible
- (TV + IRV + ERV) ~ VITAL CAPACITY
FEV1/FVC = Proportion of the amount of air that
is blown out in 1 second
Obstructive vs Restrictive spirometry tests determined by FEV1 and FEC
Obstructive: difficulty in exhaling all the air (comes out slowly) from their lungs (shortness of breath)
- due to damage or narrowing of the airways inside the lungs
- abnormally high amount of air may still linger
in the lungs
- Bronchial asthma, chronic
obstructive pulmonary disease,
cystic fibrosis
- FEV1 is significantly reduced, FVC is ~ normal/reduced, FEV1/FVC is reduced
Reduced: lungs are restricted from fully expanding
- due to restrictive lung disease (stiffness of the chest
wall, weak muscles, or damaged nerves) such as lung fibrosis, neuromuscular diseases and scarring of lung tissue
- Reduced vital capacity
- FEV1 is reduced
- FVC is reduced
- FEV1/FVC almost normal
Helium (gas) dilution method (what does it find?)
- Used to find FRC
Helium → insoluble in blood, equilibrates after several breaths - Concentration C2 is measured at the end of an expiratory effort
(V2 = FRC)
V2 = V1(C1 - C2)/C2 - Measures only communicating gas or ventilated lung volume
Before equilibration After equilibration
Ventilation mechanics: static and dynamic properties
Static properties: when no air is flowing (Necessary to maintain lung and chest wall at a certain volume)
- Intrapleural pressure (Pip), transpulmonary pressure (Ptp)
- Static compliance of the lung
- Surface tension of the lung
Dynamic properties: when the lungs are changing volume and air is flowing in and out (Necessary to permit airflow)
- Alveolar pressure (Palv)
- Dynamic lung compliance
- Airway and tissue resistance
Compliance
What is ventilation
exchange of air between the atmosphere and the alveoli (Bulk flow: gas moves from high pressure to low pressure)
Boyle’s Law - How is change in lung volume translated into a change in lung pressure?
for a fixed amount of an ideal gas kept at a fixed temperature, P [Pressure] and V [Volume] are inversely proportional
- when volume decreases, Palv increases (EXP)
- when volume increases, Palv decreases (INS)
P1V1 = P2V2
- change in volume and then in pressure produces airflow
Pressure dynamic required at the alveloi and atmosphere for inpiration and expiration
inspiration: Palv < Patm
expiration: Palv > Patm
At the end of INS and EXP, Patm = Palv; F = 0 (F = ΔP/R)
Structure of pleura
Thin double-layered envelope
▪ Visceral pleura: covers the external surface of the lung
▪ Parietal pleura: covers thoracic wall and superior face of the diaphragm
* Intrapleural fluid (~ 10 mL): reduces friction of lung against thoracic wall during breathing
(Extremely thin, 5 - 35 µm)
Elastic recoil
- Lungs → tendency to collapse due to elastic recoil
- Chest wall → pulls thoracic cage outward due to elastic recoil
- At equilibrium, inward elastic recoil of lungs exactly balances outward elastic recoil of chest wall
- Interaction between lungs and chest wall does not occur by direct attachment but through the intrapleural space
What are the characteristics of intrapleural, alveolar and transpulmonary pressure
Pip: pressure in the pleural cavity that acts as a relative vacuum
- Fluctuates with breathing but it is ALWAYS sub atmospheric
due to the opposing directions of the elastic recoil of lungs and
thoracic cage - If the Pip equals Palv lungs would collapse
Palv: pressure of the air inside the alveoli
- Palv = Patm when no air is flowing
- (Palv - Patm) governs the gas exchange between the lungs and the atmosphere
Ptp: the force responsible for keeping the alveoli open, expressed as the pressure gradient across the alveolar wall
Ptp = Palv - Pip
- Palv should be always > Pip (PTP > 0) in order to maintain the lungs
expanded in the thorax - Ptp is a static parameter which does not cause airflow, but determines lung volume (VL)
How does intrapleural, alveolar and transpulmonary pressure change during inspiration?
Thorax expands → Pip = more sub atmospheric → increase Ptp → the lungs expand → Palv = more sub atmospheric → air flows into the alveoli
- At the end of INS, Pip is at its lowest level, Ptp is at its max, and the change in Palv = 0
How does intrapleural, alveolar and transpulmonary pressure change during expiration?
Factors contributing to airway resistance -
What contributes most?
slide 86-87
flow = ΔP/R
resistive forces:
1. Inertia of RS (negligible)
2. Friction: (1) lung tissue past itself during expansion, (2) lung & chest wall gliding past each other, (3) frictional resistance through airways (80% total airway resistance)
- laminar airflow: gas particles move in a linear fashion and airflow resistance is minimal (small airways distal to terminal bronchioles)
- transitional flow: flow isn’t smooth, requires extra energy to redirect the air through branches/ramifications → increased resistance (bronchial tree)
- turbulent flow: airway radius is large and linear air velocities extremely high → resistance to airflow is the highest (trachea, larynx, pharynx)
IF - intrapleural fluid
RS - respiratory system
Poiseuille’s law in relation to airway resistance
R= 8ηl/πr⁴
- if radius ↓, resistance ↑
- small airways have the highest resistance to the airflow and have laminar flow
- resistance to airflow is highly sensitive to changes in airway radius
- each small airway has a high individal resistance, however numerous terminal bronchioles have a much lower resistance compared to the few large airways
- for airways arranged in series, the resistance is sum of individual resistances
- for airways arranged in parallel, resistance will be given by the inverse of each specific resistance, added together
What is lung compliance? Relate to the pressure volume curve
slide 94
a measure of the elastic properties of the lungs and a measure of how easily lungs can expand
* the magnitude of the change in lung volume produced by a given change in the transpulmonary pressure (slope of pressure-volume curve)
C = ΔVₗ /ΔPₜₚ
What is static and dynamic compliance?
slide 95-96
static compliance represents lung compliance measured during periods of no gas flow (inspiratory/expiratory pause)
dynamic compliance represents pulmonary complicance during periods of gas flow, such as during an inspiration (Pt continuously changing)
* reflects lung stiffness and airway resistance that distending forces must act against
* always < than or = to static lung compliance
* decreases when lung stiffness/airway resistance ↑
Phases of the pressure-volume curve (4)
slide 97-98
- Stable VL (flat): low lung volume, difficult to open an almost completely collapsed airway
- Opening of airways (first curve): first increase in VL - popping open of the proximal airways → expansion and recruitment of others
- Linear expansion of open airways: all airways open → Pip more (-) by chest wall expansion → lungs inflate, increasing VL linearly
- Limit of airway inflation: at high VL lungs compliance decreases
VL - lung volume
Hysterisis
slide 99
defines the difference between the inflation and deflation compliance paths; defines the different behaviour of the inflation and deflation curves in pathological vs physiological conditions
- has to do with the elastic properties of the lung
- a greater pressure is required to open a previously closed or narrowed airway than to keep an open airway from closing
What determines lung compliance
- elastic components of lungs and airway tissue (elastin, collagen)
- surface tension at the air-water interfave within the alveoli
Elastic properties of the lungs - what happens to these properties and lung compliance with age?
- lung elastic behaviour has to do with geometrical arrangements (nylon stockings)
- elastin: weak spring, low tensile strength, extensible
- collagen: strong twine, high tensile strength, inextensible
- with age, elastin & collagen ↓ = lung compliance ↑ (floppy lungs)
How do elastic properties & lung compliance change during emphysema and pulmonary fibrosis?
emphysema: elastin and alveolar wall destruction; ↑ lung compliance (floppy lungs) with much less elastic recoil. Large alveolar spaces compared to healthy lungs
* little changes in Ptp = large changes in LV
pulmonary fibrosis: collagen deposition in alveolar walls (lung injury, silica dust, asbestosis); stiff lungs & ↓ lung compliance
* higher Ptp is necessary to generate changes in LV
Surface tension & it’s affect on alveoli
slide 107, 109
a measure of the attracting forces acting to pull a liquid’s surface molecules together at an air-liquid interface, result of H-bonds
* surface water molecules cover alveolar surface which creates inward recoil → alveolar collapse, like a “belt”
* ↓ volume of compressible gas in alveoli and ↑ it’s pressure
* accounts or 2/3 of elastic recoil of the lungs, decreases lung compliance
LaPlace’s equation - what’s it’s relation to the alveoli
P=2T/r
P - pressure
T - surface tension (constant)
r - radius
- describes equilibrium between tendancy of pressure to expand alveolus and tendancy of surface tension to collapse it
- smaller bubble radius = greater pressure needed to keep bubble inflated
- affected by different sizes of alveolis - small alveoli’s collapse into larger ones in the lungs
Function of surfactant, where it’s made? Most important components (4)?
function: lowers surface tension, stabilizes against collapse
produced by type II alveolar cells
components: phospholipids DPPC, phosphatidyl-choline, apoproteins and calcium ions
DPPC - dipalmitoyl-phosphatidylcholine
How does surfactant affect pressure b/w alveoli of different sizes? How does it affect compliance?
- hydrophobic/hydrophilic properties of surfactant allow it to get into the air-water interface and decrease density of water molecules - makes it easier to expand lungs ↑ LC
- thickness of surfactant is decreases with increased surface area - equalizes pressures between alveoli of different sizes, preventing collapse of small alveoli into larger ones
LC - lung complicane
Regional differences in ventilation in the lungs
Diffusion, partial pressure, solubility of gases
Dalton’s law, Fick’s Law, Henry’s Law
What affects amount of gas dissolved in a liquid
How does the partial pressure of O₂ and CO₂ in the alveoli change with ↑ ventilation and ↑ metabolic rate
Gas exchange between alveoli and blood
ventilation-perfusion relationship
How does the ventilation-perfusion ratio change in a lung?
ventilation-perfusion matching
How is oxygen carried in the blood?
what is hemoglobin, deoxyhemoglobin, oxyhemoglobin
features of oxygen-Hb dissociation curve
hemoglobin saturation/concentration*
Cooperative binding
effect of pH, PCO2, and temperature on oxygen-dissociation curve
How is carbon dioxide carried in the blood
Reactions of CO2 with H2O and hemoglobin
CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3 (IMPORTANT)
Transport of H+ in blood and effect on pH
Respiratory centers in the medulla, sensory and neuromodulator inputs to medulla
Inspiratory and expiratory pathways
chemical control of respiration
peripheral and central chemoreceptors
