Respiratory system Flashcards
What is the main function of the respiratory system?
Provide oxygen and eliminate CO2
What are secondary functions of the respiratory system?
-microbial protection
-regulation of blood pH
-phonation (sound production)
-olfaction (smell)
-blood reservoir
What structures make up the RS?
-Upper airways (nasal, pharynx, larynx)
-Trachea
-Lungs
-Muscles of respiration
-Rib cage and pleura
-parts of CNS
what is the order from trachea to bronchi?
Trachea–> primary bronchus–> bronchi
–>bronchioles—>alveoli
What is the structure/function of the Trachea?
the trachea has a C shaped cartilage on the anterior and smooth muscle in the posterior
-this allows support from the cartilage and elasticity from muscle
-its function is to allow air passage to and from the lungs
What is the structure and function of the Bronchi?
The bronchi have plates of cartilage and smooth muscle; they don’t have a C shape like the trachea in order to allow for greater expansion
what is the structure of the bronchioles?
Smooth muscle only
What is the conducting zone?
a region in the lungs where air moves from the external environment into the internal
-there is NO gas exchange here
What is the respiratory zone?
An area where gas exchange happens
what is the structure of alveoli?
tiny, thin walled, capillary rich sac that exchanged O2 and CO2
What kinds of cells are present in alveloi?
Type 1: Don’t divide and are susceptible to toxins
Type 2 alveolar cells: produce SURFACTANT which is important prevents alveoli from collapsing
-can differentiate into type 1 cells
What do the alveolar walls contain?
Dense network of capillaries and small interstitial space
Where does diffusion of O2 and CO2 occur inside the capillaries?
respiratory membrane
-extremely thin and easily damaged
What are the steps involved in respiration?
1) VENTILATION- exchange of air between atmosphere and alveoli
2) EXCHANGE of O2 and CO2 between alveolar air and blood in capillaries
3) TRANSPORT of O2/CO2 through pulmonary and systemic circulation
4) EXCHANGE of O2/CO2 between blood in tissue capillaries and cells in tissues
5) UTILIZATION of O2 and production of CO2 in cells
What ways is airflow produced?
What 3 kinds of respiratory muscles are there?
1) Pump muscles
INSPIRATORY- diaphragm, external intercostals, parasternal intercostals
EXPIRATORY- abdominals, internal intercostal
2) Airway muscles
INSPIRATORY-tongue protruders (genioglossus), alae nasi, pharynx, larynx
EXPIRATORY-pharynx, larynx,
3) Accessory muscles
INSPIRATORY- sternocleidomastoid, scalene, pectoralis
What differs from expiratory vs inspiratory muscles?
https://youtu.be/6bkjJWBBnCo?si=nA7_PnvDg3om1x2t
What is the difference in movement between the external intercostals and parasternal intercostals for inspiration?
External- contract and pull ribs UP in a bucket handle motion
-increases volume of thorax
Internal-contract and pull sternum forward in pump handle motion
What abdominal muscles are involved in expiration? and what are characteristics of them?
External oblique
Internal oblique
Rectus abdominis
Transverse abdominis
These muscles are relaxed at rest and are involved in other physiological functions (coughing. vomiting, posture)
What is the function of the internal intercostals for expiration?
They are relaxed at rest and push the rib cage down when contracted to push out as much air as possible
What muscles are involved in inspiration?
what muscles are involved in expiration?
What is the function of the accessory inspiratory muscles?
They are relaxed at rest and contract vigorously during exercise or forced respiration
scalenes- elevate upper ribs
sternocleidomastoid- raises sternum
pectoralis- contribute to quiet breathing at rest (elevate ribs)
What happens to the muscles during inspiration at rest vs when forced?
What happens to the muscles during expiration at rest vs when forced?
What muscles help open the upper airways?
-tongue protruders
-alae nasi
-pharyngeal and laryngeal dilators (inspiratory)
-pharyngeal and laryngeal constrictors (expiratory)
what is obstructive sleep apnea?
Expansion of chest wall but air doesn’t enter because upper airways are blocked; signals are still sent for contraction but exchange of air doesn’t occur
-can cause brain damage and CVS issues
What 2 cells make up the epithelial layer in the conducting airways? how do they differ?
1) goblet cells
- produce mucus that trap inhaled particles
- cilia makes contact with mucus to move
-too much mucus fluid will cause cilia to slip while too little mucus won’t allow for cilia to adhere to move the mucus
2) ciliated cells
-produce periciliary fluid (sol layer) with low viscosity that is optimal for ciliary activity
What is the last defense to inhaled particles in the alveoli?
Macrophages
What device converts airflow rates into electronic signals?
Electronic spirometer
https://youtu.be/WIBhxAG3os0?si=w32k0pj6iO3K0rfg
What is tidal volume (TV)?
volume of air moved in or out of the respiratory tract during each cycle (breath)
what is inspiratory reserve volume (IRV)
the additional volume of air that can be forcibly inhaled after normal inspiration
-maximum possible inspiration
what is expiratory reserve volume (ERV)?
the additional volume of air that can be forcibly exhaled after normal expiration
-maximum voluntary expiration
what is residual volume (RV)?
volume of air remaining in the lungs after maximal expiration
-cannot be measured with a spirometry test
-RV = FRC - ERV
what is vital capacity (VC)?
maximum volume of air forcibly exhaled after maximal inspiration
VC = TV + IRV + ERV
what is inspiration capacity (IC) ?
the maximal volume of air that can be forcibly inhaled
IC = TV + IRV
what is functional residual capacity (FRC)?
volume of air remaining in lungs at the end of a normal expiration
FRC = RV + ERV
what is total lung capacity (TLC)?
volume of air remaining in lungs at the end of a maximal inspiration
TLC = FRC + TV + IRV = VC + RV
How is total ventilation calculated (minute ventilation)?
tidal volume x frequency (L/min)
What is alveolar ventilation? what does it depend on?
The amount of air moved into the alveoli (respiratory zone) per minute
-depends on the anatomical dead space
-alveolar ventilation < minute ventilation
what effect does breathing pattern have on alveolar ventilation?
breathing shallow + fast there will be no alveolar ventilation because the air doesn’t make it to the respiratory zone
breathing deep + slow increases alveolar ventilation due to increase in air going into the respiratory zone
-increasing DEPTH is more effective than increasing RATE of breath in increasing alveolar ventilation
What is FEV1?
it is the forced expiratory volume in the first second
-healthy people can blow most of the air out of their lungs in the first second
What is FVC?
forced vital capacity is the total amount of air that is blown out in one breath after max inspiration as fast as possible
(TV + IRV +ERV)
What does FEV1 / FVC represent?
it is the proportion of air that is blown out in one second ~80%
What are the 3 main respiratory patterns?
Normal, obstructive and restrictive
what is an obstructive respiratory pattern?
shortness in breath due to difficulty in exhaling all the air from the lungs
-air lingers in lungs
-damage to lungs or narrowing of airways
-exhalation is slower than normal
-FEV1 is reduced
-FVC is ~normal / reduced
-FEV1/FVC is reduced (<0.7)
what is a restrictive respiratory pattern?
inability to fully fill lungs with air due to restriction in lungs from fully expanding
-caused by stiffness in chest wall, weak muscles, or nerve damage
-ALS, lung fibrosis
-reduced vital capacity
-FEV1 reduced
-FVC reduced
-FEV1 / FVC ~normal
What lung volumes and capacities are unable to be measured by a spirometry test?
residual volume
- resulting in the inability to measure functional residual capacity and total lung capacity
HOw does the helium dilution method work?
Within the lungs, the helium blends with the pre-existing air, serving as a mixing chamber.
By evaluating the shift in helium concentration, one can accurately determine the patient’s functional residual capacity (FRC).
From this data, it’s then possible to calculate both the residual volume and the total lung capacity (TLC).
https://youtu.be/4nQApZ8Q0XM?si=u8IO_FhxGS6du8bi
What 2 mechanical properties of ventilation?
static; when no air is flowing
-maintain lung and chest wall at a certain volume
-intrapleural pressure (Pip/ Ptp) and transpulmonary pressure
-surface tension
-static compliance
dynamic; when lungs change in volume and air is flowing in/out (permits airflow)
-alveolar pressure (Palv)
-dynamic lung compliance
-airway and tissue resistance
what is ventilation?
movement of air between the atmosphere and the alveoli (bulk-flow of gas from high to low pressure)
what does boyles law state?
Pressure and volume are inversely proportional for a fixed amount of gas at a fixed T
how does air move in regards to pressure?
What is the air movement at the end and beginning of inspiration/expiration?
there is no air flow due to lack of pressure difference
what pressures are of concern in regards to airflow?
pressure of the alveoli and the atmosphere
what occurs when the pressure of the alveoli < pressure of the atmosphere?
air moves towards the alveoli
what occurs when the pressure of the alveoli > pressure of the atmosphere?
air moves towards the atmosphere
What pressures are responsible for moving air in/out of the lungs?
1) intrapleural pressure (Pip)
2) alveolar pressure (Palv)
3) transpulmonary pressure (Ptp)
what 2 layers of tissue encase the pleural sac
Parietal pleura(Outer layer)
-attaches to thoracic wall; lines inside wall
Visceral pleura(inside layer)
-wraps around lungs to protect and isolate it
What is intrapleural fluid?
fluid that reduces friction of lungs against the thoracic wall during breathing
What interaction determines the lung volume?
the interaction between the lungs and the thoracic cage
what is elastic recoil?
a tendency for lungs to collapse following inflation
what is intrapleural pressure?
the pressure within the pleural cavity; always subatmospheric due to opposing direction of elastic recoil of lungs and thoracic cage
-relative vacuum
-if Pip = Palv the lungs would collapse
https://youtu.be/OvMxXIkw_BE?si=y1DJya3uxxk51diV
what is alveolar pressure?
the pressure inside the alveoli
Palv = atmospheric pressure when glottis is open and no air flows in/out of lungs
explain the change in volume in pressure during one breath
https://youtu.be/s1QFW1aSh5Q?si=6ToUO3mavmYCnMqQ
what are the 3 types of airflow resistance patterns?
laminar-little energy in airflow resistance; small airways distal to terminal bronchioles
transitional-extra energy needed to produce vortices; higher resistance
-through most of the bronchial tree
turbulent-resistance of airflow the highest; occurs in large airways (trachea, larynx, pharynx)
what does resistance largely depend on?
radius of the airway
what does poiseuille’s law state?
do larger or smaller airways experience higher resistance?
each small airway has a high individual resistance however since they are aligned parallelly they have a much lower aggregated resistance
R in series = R1 + R2 + R3…
R in parallel= 1/R1 + 1/R2 + 1/R3….
what is lung compliance?
a measure of the elastic properties of the lungs; how easily the lungs expand
what is static compliance?
lung compliance during periods of no gas flow
-determined by the P/V slope when measured at FRC
what is dynamic compliance?
pulmonary compliance during periods of gas flow
-reflects lung stiffness and airway resistance; compliance falls when either increase
what determines lung compliance?
Elastic components and airway tissues (localized in alveolar walls and around vessels / bronchi)
-elastin; like strong twine,high tensile strength inextensible
-collagen; like a weak spring, low tensile strength, extensible
Surface tension at the air-water interface within the alveoli
what is hysteresis?
defines the difference between the inflation and deflation compliance paths
-it exists because a greater pressure difference is required to open a previously closed airway rather then to keep an open airway from closing
what is emphysema?
the destruction of elastin and alveolar walls resulting in increased compliance of the lungs (floppy lungs)
-decreased elastic recoil; little change in PTP, large change in lung volume
what is pulmonary fibrosis?
collagen deposition in the alveolar walls resulting in lung stiffness or a reduction in lung compliance
what is alveolar surface tension?
a cohesive force where water molecules at the surface of a liquid-gas interface are attracted to the water molecules within the liquid mass
how does surface tension affect lung compliance?
surface tension decreases the volume of compressible gas inside the alveoli and increases its pressure
https://youtu.be/7ZMweT5o3Io?si=si6cQbr7CFka9OD9
what properties allow surfactant to decrease tension?
hydrophobic/philic properties decreases water density3
how does surfactant minimize the collapse of smaller alveoli into larger ones?
the thickness of surfactant decreases as SA increases so tension increases as the size of alveolar diameter increases
-this allows equalization of pressure between alveoli of different sizes
True or False:
Premature babies lack surfactant
True- premature infants lack surfactant and lung compliance decreases leading to increased work to breathe
how is pressure different throughout the lungs?
how is gas exchanged through capillaries?
DIFFUSION
what does Ficks law state?
the rate of transfer of gas through a sheet of tissue / unit time is proportional to the tissue area and the difference in gas partial pressure
-it is inversely proportional to the thickness
What does henry’s law state?
Does a gas always contribute to partial pressure?
no, only a gas dissolved in a solution will contribute to the partial pressure
how does partial pressure of CO2 and O2 change from inspired air to alveolar air?
CO2 goes from nearly 0 to 40mmHg
O2 drops ~1/3
is the pressure of air greater in the air or in the alveoli? why?
greater in the air due to humidity of air, loss of O2 in blood diffusion, mixing of inspired air with alveolar air
what determines PO2?
-PO2 in atmosphere
-Alveolar ventilation
-respiratory frequency
-Metabolic rate
-Perfusion
what determines PCO2?
-PCO2 atmosphere
-Alveolar ventilation
-Metabolic rate
-Perfusion
What effect on PO2 / PCO2 does increasing alveolar ventilation have?
increases alveolar PO2
decreases alveolar PCO2 (more similar to air ~0)
What effect on PO2 / PCO2 does increasing metabolic rate (O2 consumption / CO2 production) have?
decreases alveolar PO2
increases PCO2
what is a marker of healthy gas exchange between alveoli and blood?
blood gases reaching equilibrium quickly on their way through the lungs
what is perfusion of the lungs?
passage of fluid / blood through circulatory / lymphatic system to tissues
what is the relationship between ventilation and perfusion?
https://youtu.be/UKsOLb5XWa0?si=tljDHKE1B_15uuL3
What occurs with ventilated alveoli that lack perfusion?
dead space; air is not taken up by blood due to lack of circulation of new blood through the capillary system
What occurs with alveoli that have perfusion but no ventilation?
a shunt; a portion of the blood doesn’t get oxygenated and goes back to arterial blood
where is ventilation greatest? why?
it is greatest near the base of the lungs due to gravity
-alveoli start more deflated so they are able to expand more
True or false:
ventilation-perfusion relationship is uniform throughout a healthy lung
False. blood flow and alveolar ventilation are reduced in the apical lung
What 2 forms is O2 carried in/
-dissolved (2%)
-With hemoglobin (98%)
O2 solubility is low so it gets bound to hemoglobin
(3mL O2/L blood vs 197mL O2/ L blood with hemoglobin)
How many O2 molecules can Hb bind to? what is each for called for bound O2 vs non bound O2?
Up to four O2 molecules
-deoxyhemoglobin (no O2)
-oxyhemoglobin (O2 bound)
Why is the O2 dissociation curve sigmoidal?
As each O2 molecule binds, the affinity of O2 to Hb increases
-also sensitive to pH PCO2 and Temp
https://youtu.be/r-16hB76Ark?si=pjZPWy2U6-DLEZno
what is Hb saturation?
the percentage of available Hb binding sites that have O2 attached
Hb saturation of arterial blood is 100mmHg PO2 is 97.5%
Hb saturation of mixed venous blood with 40mmHg PO2 is 75%
what determines Hb saturation?
-Arterial PO2 (main)
-Cooperative binding
What does the plateau of the curve signify? what pressure does it contain?
The plateau shows that the saturation stays high over a wide range of alveolar PO2; 60-100mmHg
-this provides a safety factor incase pressure decreases, it will still allow for saturation if Hb
What is the significance of the steep portion? what pressure does it contain?
the steep portion shows that large amounts of O2 are unloading within a small change in pressure; 40-60mmHg
-75% of O2 saturation of Hb at 40 mmHg
-PO2 must still remain high in capillaries to drive diffusion
What is the significance of the very steep portion? what pressure does it contain?
Changes in metabolic rate will increase / decrease PO2; 10-40mmHg
How does the curve shift in response to changes in [Hb]?
how is O2 moved into the lungs and tissues?
pressure gradients dictate the movement of O2
-O2 dissolves briefly into plasma before binding to Hb or being released into tissues
https://youtu.be/WXOBJEXxNEo?si=fhJO9AciX_DCchWB
what factors affect the Hb-O2 dissociation curve ?
ph, Temp and Pco2
shift to right- REDUCTION in affinity of O2 to Hb = more unloading
shift to left-INCREASED affinity of O2 to Hb = less unloading
What three forms transport CO2 in the blood?
Carried in 3 forms:
1) dissolved (5%)
2) HCO3- (60-65%)
3) Carbamino compounds (25-30%)
CO2 has high solubility; 26.8mL /L of blood at 40mmHg
how is CO2 transported ?
https://youtu.be/VgpNSdWvrno?si=zWNHsJFvbZooqRnl
How does CO2 help with unloading of O2?
deoxyHb has much high affinity for CO2 compared to OxyHb-CO2 helps to unload O2 from Hb at the tissues due to their competition for binding sites
what happens to the H+ released as a bi-product from HCO3- dissociation? Why is this needed?
majority gets bound to Hb; higher affinity for deoxyHb
-this helps to buffer the production of H+ in tissues / capillaries making the pH in the blood (7.4) slightly less acidic than in the venous blood (7.3)
What are the different types of respiratory and metabolic acidosis / alkalosis?
Respiratory acidosis- increased [H+] (increased Pco2 )
metabolic acidosis- increased [H+] independent from changes in Pco2
Respiratory alkalosis- decreased [H+] from decreased Pco2
metabolic alkalosis- decreased [H+] independent of Pco2 changes
where is the rhythm of breathing established?
In the CNS
-initiated in the medulla
what initiates breathing and what modifies it?
Initiated by: special neurons in the medulla
Modified by: higher structures of CNS
-central/peripheral chemoreceptors
-mechanoreceptors in lungs / chest walls
What are the 3 respiratory groups that help establish the automatic rhythm for contraction of respiratory muscles?
What neurons in the ventral respiratory group generate excitatory inspiratory rhythmic activity?
The prebotzinger complex (PreBotC)
What neurons generate active excitatory expiratory rhythmic activity?
The lateral parafacial (pFL)
what changes cause the neuronal networks to adjust the breathing rhythm?
The neuronal networks can generate their own activity; however, many factors affect the length and intensity
what is the effect of depressed preBotC neurons? what is a common cause?
Activity may be depressed by drugs (anesthetics and opioids/ fentanyl)
This leads to respiratory depression and eventually death for respiratory arrest
-naloxone can reverse opioid effects
How is ventilation controlled by [Po2], [Pco2] and [H+]?
-Chemical control
-Peripheral and central chemoreceptors
what are peripheral chemoreceptors?
receptors located in the carotid and aortic bodies that detect Po2 levels
https://youtu.be/1STBUJyyeYg?si=nPxcxp1tiy9-iKxB
what are carotid bodies?
very small chemosensitive structures that detect Po2 levels in the capillaries. They are highly vascularized and have a high metabolic rate
what are the chemosensitive cells in carotid bodies called? what is their structure and function?
Type 1 or glomus cells
-Neuron-like with voltage gated ion channels that trigger AP
-They release NT when stimulated to control the firing of sensory nerve endings
-sensitive to Po2, Pco2 and pH
what are type 2 cells in carotid bodies and what is their function?
They are sustentacular cells and they act as support in the Carotid bodies
what is the primary stimulus for peripheral chemoreceptors?
A decrease in arterial Po2
-low Po2 will increase firing rate for glomus cells
what level does stimulation of peripheral chemoreceptors occur at?
Arterial Po2 values below 60mmHg
-ventilation is stable between Po2 60-120mmHg
explain how the response to hypoxia is mediated by peripheral chemoreceptors
how are ventilation changes in arterial Pco2 different from ventilation changes in Po2?
PCO2 is more tightly controlled so smaller changes in Pco2 result in more dramatic changes in ventilation
What are central chemoreceptors?
specialized neurons located near the medulla
https://youtu.be/1STBUJyyeYg?si=nPxcxp1tiy9-iKxB
explain how the response to hypercapnia is mediated by peripheral chemoreceptors
explain the respiratory response to metabolic acidosis?
explain the chemical control of ventilation when:
1) arterial Po2 decreases
2) arterial Po2 increases
3) production of non-CO2 acids increases
