Respiratory System Physiology Flashcards
types of epithelium in the lungs
columnar epithelium —> stratified epithelium with mucosy material that traps small particles in microns
what types of particles get through the layers?
silica, bugs, and bacteria that are too small to be trapped go through the air space
functions of lung
-gas exchange- take in O2 for body to function and exhale CO2
-filter inspired air
-defends against inhaled particles
-immunological surveillance- lung is exposed to the outside environment
-peptide processing- produce and process peptides that regulate functions
what do we need to do to breathe?
-breathing is automatic but we can induce it consciously
-breathing center in brainstem and regulates ventilation
-circulation is automatic- transport O2 to the tissues and the CO2 away
-respiration is automatic and affected by the environment
breathing: the steps
-respiration is regulated by CO2 levels in the blood and is affected by low O2 levels but the primary is CO2 levels
-stimulus to start breathing
-lungs expand/muscle contracts and muscles are in the ribcage (intercostal muscle) and diaphragm (men use diaphragm more than women) —> creates negative pressure in chest and expands lung
-air comes in (higher in O2 than CO2)
-gets carried to alveoli and O2 gets diffused to capillaries
-O2 gets picked up by hemoglobin and CO2 will diffuse to alveolar space and when you exhale it gets removed
-pulmonary veins carry oxygen rich blood and carried to left ventricle and CO2 gets carried to lungs
-exhaled air with oxygen and CO2 goes out
-process begins again
anatomy
-respiratory bronchiole (last airway)- in the beginning they are lined by ciliated columnar epithelium then it flattens to cuboidal then flat
-in the alveolar duct you have flat epithelia, which branches into alveolar sacs that contain alveoli —> increases surface area
-capillaries are lined with endothelial cells that have a permeable cytoplasm and junctions between them
-permeability varies depending on conditions like if there is inflammation in the cytoplasm, the permeability will increase
how many cell types line aveolar spaces?
two types
type I pneumocytes
-flat cells in the cytoplasm that are difficult to see under a microscope and the nuclei are small
-basement membrane underneath
type II pneumocytes
-bigger and plumper so they are easier to spot and they produce surfactant, which decreases the tension of surfaces to keep them open
-basement membrane underneath
what are the layers air goes through?
air and cells travel through the cytoplasm —> basement membrane —> cytoplasm —> capillary space
what do macrophages do?
-air spaces have macrophages to clean up
-if one macrophage can’t do it, a bunch of them will fuse together to create one big macrophage
what are the types of giant cells?
osteoclasts, langerhan cells, and foreign body giant cells
arteriole wall
-airways, air spaces, and alveoli
-alveoli are composed of the alveolar wall, capillaries, and flat big cells called type I and type II pneumocytes
what do clinicians do for premature babies who do not produce enough surfactant?
-inject surfactant into them
-they can also give steroids to accelerate maturation of cells and supplemental O2 but have to be careful not to give too much O2 since that can be toxic
how does air travel from the terminal bronchioles?
respiratory bronchioles (lined by ciliated columnar epithelium) —> alveolar duct —> atrium —> alveolar sac (flat)
how do we decide to breathe?
central controller (brain stem) gives output to effectors (respiratory muscles), which send to sensors (chemoreceptors and stretch receptors) and they will give input back to the brainstem to increase/decrease breathing
central chemoreceptors
-from the capillaries, CO2, H+, and HCO3 will diffuse from the blood-brain barrier to the extracellular fluid and the chemoreceptors will react to the CO2 and pH environment
-receptors are located near the ventral surface of the medulla
-sensitive to the CO2 in the blood but not the O2
-chemoreceptors are based in CSF —> CO2 to get across to ECF then CSF to drop pH
CO2 and O2 stimulate ventilation
-as CO2 levels increase, they stimulate ventilation and the level of ventilation depends on the amount of O2 in the air
-in the presence of hypoxia, move in more air to get the same amount of O2 when there is less O2 in the air
-low pH can also mean that there is more CO2 in the blood
peripheral chemoreceptors
-located in the carotid and aortic bodies
-respond to decreased arterial PO2 and increased PCO2 and H+
-rapidly responding
-only receptors that respond to decreased arterial PCO2
-these will kick when you have high altitude or hypoxia since the central chemoreceptors are more sensitive to CO2
ventilatory response to hypoxia
-only the peripheral chemoreceptors are involved (not in the brain)
-there is neglible control during normoxic conditions
-control becomes important in chronic hypoxic situations like the Himalaya and long-term hypoxemia caused by chronic lung disease —> want to move in more air to get the same amount of O2
-brain allows you to have high CO2 and people need hypoxic drive to breathe
how do we move air into lungs?
-lung has airways and air spaces
-bronchus- areas with cartilage
-bronchioles- areas without cartilage
-peripheral lung has few bronchi
-terminal bronchioles split into respiratory bronchioles and into alveoli
how many layers are there to airways?
-23 levels
-go 16 branching to get to the terminal bronchiole
-go 6 or 7 levels of branching, each airway branches into 2-3 branches
-no respiration in the conduction zone —> dead space volume that is 150 mls vs the volume of the alveolar region being 2.5-3 liters
what does the space in airways do?
-does not participate in respiration
-conducts the air to alveolar space for respiration
-called the dead space
physiological dead space
-anatomical dead space- fairly constant and spans up to level 16
-alveolar dead space- varies and spans levels 17-19
-these together make up the physiological dead space
cross section and airway generation
at level 16 the terminal bronchioles end and you see the exponential increase in the airway generation
-increase in cross-sectional area of the airways is due to the number of airways increasing —> past level 16 there are more branches that come off
airway resistance
-resistance changes depending on the size of the airways
-highest at 5th generation airways then decreases at terminal bronchiole
-in the beginning, the resistance goes up since the trachea gets smaller then as you divide further you have a decrease in resistance so very low in small airways since they tent up and there are so many that the air has many choices
why does resistance decrease as lung volume increases?
-large airways with a lot of cartilage don’t change much
-small airways have smooth muscle and elastic tissue that pulls them to a certain size but not more —> decreases resistance since the airways are pulled open
-elastic fibers in alveolar walls help keep them open but they are larger than airways
-negative pressure opens up capillaries
-breathe in dense gas, increase resistance
bronchial smooth muscle
-bronchial smooth muscle is controlled by the autonomic nervous system —> the stimulation of beta-adrenergic receptors causes bronchodilation
-in diseases where these malfunction like asthma or small airway disease —> airways contract and small glands make mucus so the thick mucus makes the airways narrower
how do you treat asthma?
-relaxing the muscle and filtering mucus
-taking steroids to reduce inflammation
total lung volume
6 liters
tidal volume
-certain amount of volume that moves into and out of the lungs during a breath
-1/12 of the total volume
crude way of measuring someone’s chest
-have patient breathe in and out and use tape measure to measure the circumference
-people with emphysema have barrel chests and use their diaphragm to breathe
expiratory reserve volume
extra air above normal that can be exhaled during forceful exhalation
what is minute ventilation?
respiratory rate * tidal volume
Ex. the tidal volume is 500 ml and frequency is 15 1/min —> minute ventilation is 7500 ml/min and of the 7500, 5250 is used for alveolar ventilation
tidal volume
dead space + alveolar volume
pulmonary capillary blood + pulmonary blood flow
blood in pulmonary capillary is 70 ml amd pulmonary blood flow is 5000 ml/min —> push through the whole volume in one minute
what are lungs covered by?
mesothelioma (pleura) with mesothelial lining and mesothelial cells are flat cells
what does the mesothelium do?
provides a slippery, non-adhesive and protective surface that allows the pleura that covers the chest wall and the chest to slide together with virtuospace
pneumothorax
-puncture chest wall/lung —> air will go from inside to outside and virtuospace increases
-negative pressure during inhalation is absent and the lung collapses
-if someone has a pneumothorax from a gunshot wound or knife, do not remove the object that is causing it so that the space can remain partially closed
CT scan of pneumothorax
-in the CT scan, you see a big, black space which is air
-you have to suck the air out or inject something to make the surfaces stick together
spontaneous pneumothorax
typically happens in young men who are tall and skinny and lack collagen
surfactant
-reduces surface tension
-produced by type II pneumocytes
-reduces lung compliance if it is absent and can cause pulmonary edema
how can lack of surfactant lead to pulmonary edema?
-it causes the alveoli to close or not open properly —> abnormal gas exchange
-lack of surfactant can lead to RDS, which can lead to pulmonary edema
pulmonary circulation
-gas has to go from air to the lung
-pleura has systemic arteries, veins, lymphatics, and interlobular septa where the veins and lymphatic channels run to collect venous blood from the alveoli
-pulmonary arteries are running with airways and carrying venous blood to right heart
-systemic arteries are small and they provide enough oxygen to keep the tissue viable
alveoli radiograph
-dark structures are red blood cells
-cross section through capillary and alveolar wall
-one alveolus
-alveoli is very thin @ 0.2-0.3 microns
-enormous surface area of 50-100 m^2
-very thin and can be easily damaged —> too much pressure to get air into lungs like on a ventilator with positive pressure and overextend the lung
alveolus: sheet of blood
-holes are little spaces between cells where cellular components go through
-output of right heart goes to lung with lower pressures and into pulmonary arteries
-diameters of capillaries is 7-10 microns
-blood spends ~0.75 seconds in capillaries
-capillary segments are so short it seems like a sheet of blood
vessels on the bronchus
-some lymphatic channels in the airway walls but most run with arteries and veins
-see lymphatic channels in disease processes or increased pressure in the venous system
-sometimes tumors get into lymphatic channels and you can see the channels that way
-pulmonary artery branches off the bronchus —> goes to capillaries along alveoli —> drain into pulmonary veins
pulmonary vs systemic circulation pressures
-pressure in aorta of LV is 120/80 and as you go down to the capillary bed it becomes 30 then 20 and 10 in venous system
-osmotic pressure in blood —> normally the fluid doesn’t ooze out of capillary to tissue
-in the right heart you go up the right atrium and the pressure is 2 and the left heart results in 25/15 then decreases to 8 in the pulmonary veins
—> pulmonary circulation has much lower pressures than the systemic circulation (makes sense since pumping blood out to the whole body and not just the lungs)
-pulmonary artery- only artery in the body that carries deoxygenated blood (low pressure system)
what is pulmonary hypertension?
-narrowing of lumen in the arteries
-walls thicken and the fibrin in the arteries narrows them and leads to hypertension high V/Q
-arteries get big and pop out with pink smooth muscle fibrosis and the walls are bigger
how do we increase blood flow in the pulmonary circulation?
-increase in blood vessels or bigger ones (proliferated vessels don’t go away and can affect gas exchange but the widening of the vessels is reversible)
-increase in venous pressure due to obstruction can back up pressure to lungs —> creates chronic congestion and proliferation of capillaries
why do more blood vessels affect gas exchange?
the heart must pump more blood through the additional vessels
lung volumes vs pulmonary vessels
-when you breathe in, the blood vessels dilate a little but arterioles have a muscular wall and won’t be affected by negative pressure —> capillaries will dilate a little
-as the lung volume grows, capillaries open up a little and resistance decreases
-as the lung volume continues to grow, resistance grows too b/c the extra alveolar vessels dilate and capillaries thin out
-optimal condition and change in either direction results in increased resistance
-as you breathe in resistance to blood flow decreases in the extra-alveolar vessels and increases in capillaries for U-shaped curve
ventilation and circulation
unobstructed air flow will result in gas exchange in the alveolar spaces where venous blood is oxygenated and arterial blood is present in pulmonary venous system
discrepancy between perfusion and ventilation (V/Q mismatch)
-disruptions to air flow or blood supply decreasing or right to left shunt —> arterial blood less oxygenized
Ex. air volume is 4 liters/min and blood volume is 5 so ratio is air volume/blood volume —> 0.8 (normal) BUT of air volume goes down and blood volume is less or if blood volume increases
high V/Q mismatch
-results in dead space and inadequate perfusion and adequate ventilation
-V/Q > 0.8 (blood volume decreases or air volume increases)
Ex. pulmonary embolism since the blood clot blocks flow in vessels
low V/Q mismatch
-adequate perfusion and inadequate ventilation
-V/Q < 0.8 (increase in blood volume or decrease in air volume)
Ex. obstruction in airways, tumors, fluids, or toxic gases
right-to-left shunt
-occurs when blood flows from the right side of the heart to the left, causing oxygen-poor blood to bypass the lungs and return directly to the body
-normal ventilation but you have a capillary that never sees an alveolar unit so it can’t pick up oxygen —> blood is shunting away from lung
gas exchange
-O2 diffusion on the x-axis is time in the capillary and in normal O2 diffusion at the alveolar level
-curve flattens to the right, which signals abnormal condition and grossly abnormal is when the line is flatter (may take a full 0.75 of a second to pick up O2 before the RBC leaves capillary)
-some have grossly abnormal lungs they can’t pick up enough O2 before the RBC leaves —> even if you gave them enough O2, you couldn’t get to high enough threshold
O2 transport: how to determine how much O2 is in the blood?
cardiac output * arterial O2 content
arterial O2 content
dissolved O2 + Hb-bound O2
what is Hb-bound O2?
O2 that is available for oxygenation of tissues
how can Hb-O2 be found?
1.39 ml O2 * Hb (mg/ml) * (Hb sat/100)
-Hb can greatly change your O2-carrying content
-as O2 grows so does the hemoglobin saturation but exponentially
-Hb concentration affects O2 content and saturation —> in male it is 13-15 and 10 is low but functional so you start transfusing @ 6 or 7 but don’t want to transfuse before that
-more Hb you have, the less you require O2 saturation
shifts in oxyhemoglobin dissociation curve
-lower body temp shifts the curve to the left so you need less O2 to get same saturation
-higher body temp shifts the curve to the right
Ex. when you have a fever you’re good for awhile but eventually it will require more O2
-increased pH levels, higher capnia, and DPG can shift levels to the right —> high PCO2 the further the curve goes to the right since you need more O2 in the air space for same saturation
-lower body temp the hemoglobin holds on to the oxygen
gas concentrations in different compartments
-in arterial blood we lose O2 and venous blood has fairly constant level of PCO2 and it dramatically increases during inspiration
-higher PCO2 concentration in alveoli —> greater respiratory volume and increases inspiration
-% of saturation –> higher saturation means a lower level of ventilation for oxygen
-O2 is highest in the air, lower in lungs, less in arterioles, and you lose it in the tissues and CO2 is the highest
inspiration (inhalation)
air flowing into the lungs
expiration (exhalation)
air leaving the lungs
lung diseases
airway disease, vascular disease, and parenchymal disease
emphysema
-obstructive lung disease where the lung volume increases and alveolar tissue gets destroyed —> spaces increase and total surface decreases
-V/Q > 0.8 since there is a decrease in surface from the alveolar tissue being destroyed and the elasticity decreasing —> decrease in blood flow
-overinflated lung with loss of elasticity and small airways narrow down —> respiration not as efficient
fibrosis
-caused by a buildup of scar tissue, which leads to constricted airways and mucus buildup in air spaces,
-alveoli are destroyed and the airways are obstructed by fibrosis
-prevents gas exchange and volume of lung shrinks
-diffusion goes down
-in a normal lung, the alveoli are uniform
-low V/Q < 0.8 since the ventilation is disrupted
terminal bronchiole in a normal lung
-lymphocytes and macrophages
-air spaces don’t have macrophages
asthma
-large airway with cartilage
-submosal salivary glands that become hyperplastic and secrete mucus into air spaces and bulge out
—> leads to smaller arteries and contraction of the airways
-low V/Q mismatch since adequate profusion and inadequate ventilation
-use bronchodilators to treat them
-airways that have less cartilage, the smooth muscle will be where cartilage is and gets hypertrophic
-smaller bronchiole and the smooth muscle is not prominent
what comprises COPD?
emphysema and chronic bronchitis
rhinitis
inflammation of the mucosa in the nose —> can block off the openings of the sphenoid, maxillary sinuses, and nasolacrimal —> causes headache by environment in bony sinuses doesn’t equal the external environment
pulmonary hypertension with thrombo-embolis
-fibroblats grow in the lumen
-increases the blood flow
-higher blood pressure
-high V/Q since the profusion is inadequate but the ventilation is adequate
-can be treated with anti-coagulation therapy
CT scans of normal vs emphysema
-little black holes of variable size, which represent air and the destruction of brachia
-black pigment is macrophages in interstitial fluid
-spaces are bigger or smaller in emphysema and classification is based on these spaces
interstitial fibrosis
-when lungs become fibrotic and shrink —> they become rubbery and hard
-spaces with mucus and lined with respiratory epithelium
-airway epithelium replaces alveolar epithelium —> hinders breathing
-cystic spaces are filled with pink material or mucus —> no respiration occurs
-decreased V/Q since the profusion is adequate with inadequate ventilation —> air flow is compromised since the airways are surrounded by fibrosis and cannot expand
restrictive lung disease
collagen is rigid and lung cannot expand —> air flow is decreased and the total lung capacity decreases
residual lung volume
amount of air left in lung at the end of full expiration
Ex. people with asthma are closing earlier and trapping more air —> impedes ability to breathe
pleural space
-causes negative pressure (chest wall wanting to expand while lungs want to collapse)
-fluid between visceral and parietal pleura
pleural pressure
alveolar pressure - lung pressure
normal V/Q relationship
-V is the ventilation and Q is the profusion
-each lung unit can have a slightly different V/Q relationship but under normal circumstances very uniform ventilation
