Lungs Flashcards
conducting zone
-carry air into respiratory system
-nose, nasopharynx, larynx, trachea, bronchi, bronchioles, terminal bronchioles
-warm, humidify, filter air
-trachea, bronchi, and bronchioles has cilia and smooth muscle -> cartilage present in trachea, patchy in bronchi, and absent in bronchioles
-mucus secreting cells present
-filters
-smooth muscle- sympathetic/parasympathetic innervation
innervation of smooth muscle in conducting zone
-sympathetic adrenergic -> beta 2 receptors activated -> relaxation and dilation
-beta 2 activated by epinephrine from adrenal medulla and agonists like isoproterenol, albuterol
-beta 2 agonist- tx asthma
-parasympathetic cholinergic -> activate muscarinic receptors -> contraction and constriction -> resistance increase
-muscarinic antagonist- atropine
respiratory zone
-actual transference of O2
-lined with alveoli
-respiratory bronchioles- transitional (alveoli occasionally bud off here)
-no cilia and little smooth muscle
alveoli- thin, large SA
-300 mil alveoli in each lung
total volume normal inspiration
-500mL
-150 in the conducting zone -> no air exchange
-350 in the respiratory zone -> exchange
residual air
-stays in the lungs with each expiration
-in conducting zone
-prevent collapse
lung volumes - need to know
-inspiratory reserve volume- 3000ml - deep breath in above tidal volume (negative pressure gradient pulls in)
-tidal volume- 500ml- normal breathing in and out (volume in alveoli and airways)
-expiratory reserve volume- forced expiration below tidal volume -1200ml
-residual volume- 1200ml- volume left in lungs after max forced expiration
inspiratory capacity
-tidal volume + inspiratory reserve
-3500mL (500+3000)
functional residual capacity
-residual volume + expiratory reserve volume
-2400mL (1200 + 1200)
-volume remaining in lungs after normal tidal volume is expired
-equilibrium volume of lungs
-measured with helium dilution and body plethysmograph
vital capacity
-full depth inspiration and expiration
-inspiratory capacity + expiratory reserve volume
-4700mL (3500+1200)
-volume that can be expired after maximal inspiration
-increase with body size, male gender
-decreases with age
-forced vital capacity -total volume that can be forcibly expired after maximal inspiration
-FEV1- volume that is forcibly expired in first second
-FEV2- volume that is forcibly expired in 2 seconds
-FEV3- “” normally only takes 3 seconds to complete
total lung capcity
-vital capacity + residual volume
-5900 (4700+1200)
-inspiratory capacity + functional residual capacity
-everything
diffusion capacity
-thickness of membrane - decreases
-restrictive lung disease - hardening of tissue
-
FEV1
-fraction of expiratory volume in 1 second
-%
-what percentage of your lung volume are you able to blow out in 1 second
-70-80% in normal lungs
-lungs have high compliance-> elastic recoil
-FEV1/FVC (fraction of vital capacity expired in 1s) indicate lung disease
-normal - 0.8 -> 80% of vital capacity expired in 1s
obstructive lung disease
-COPD and asthma
-FEV1- 50-60%
-lost compliance to force air out
-increased resistance to expiratory flow
-FEV1 and FVC both reduce but FEV1 reduces more -> decreases FEV1/FVC
restrictive lung disease
-hardened, stiff
-fibrosis
-total volume and expiration is both down proportionally
-less capacity to take air in, doesnt affect the forced expiration as much
-can even be higher FEV1
-FEV1 and FVC decrease but FEV1 decreased less -> FEV1/FVC increases
law of laplace
-effect of alveolar size and surfactant on collapsing pressure
-pressure tending to collapse a alveolus is directly proportional to surface tension and inversely proportional to alveolar radius
-large alveoli- low collapsing pressure -> minimal pressure to keep it open
-smaller alveoli- higher collapsing pressure -> more pressure required to keep it open
-small is good for increased SA for gas exchange but bad for collapsing -> SOLVE THIS WITH SURFACTANT!
-surfactant reduces surface tension -> decreases collapsing pressure
-alveolar collapse- atelectasis
O2 partial pressure
-alveolar air partial pressure O2 of 100
-up until systemic arteries
-systemic capillary beds partial pressure O2 of 40 (drop drive exchange -> CO2 PP barely changes)
-Hmg drops of O2 - hmg disassociation
pulse ox (o2 saturation) 80
-hemoglobin not binding
-you can still breathe mechanically but nothing is binding -> nothing is being perfused
-PO2 = 40 -> 75% sat
-PO2 = 50 -> 75% sat
shift to right
-increase PCO2
-decrease pH
-increase temperature
-increase 2,3 DPG
shift to left
-decrease PCO2
-increase pH
-decrease temperature
-decrease 2,3 DPG
-fetal hemoglobin
surface area of lung
-greater on the back and base
-if person has interstitial pneumonia (fluid in lungs not alveoli) -> lay them supine so greater surface area if freed for breathing
function of respiratory system
-O2 and CO2 exchange between environment and cells
-conducting zone- brings air into and out of lungs -> cilia and smooth muscle
-respiratory zone- gas exchange (alveoli)
alveolar walls
-elastic fibers
-epithelial cells -> type 1 and 2 pneumocytes
-type 2- produce surfactant
alveolar macrophages
-phagocytic cells
-fill with debris and migrate to bronchioles -> cilia carry up -> swallowed or coughed
regulation of pulmonary blood flow
-altering resistance of pulmonary arterioles via local factors (O2)
dead space
-no gas exchange
-anatomic dead space- nose, mouth, trachea, bronchi, bronchioles -> 150ml
-physiological dead space- anatomic dead space +functional dead space in alveoli
-functional dead space- ex. alveoli that is ventilated but no gas exchange
-physiologic and anatomic dead space should be equal -> alveolar ventilation is well matched to perfusion
-physiologic dead space > anatomic -> suggest ventilation/perfusion defect
ventilation perfusion defect
-mismatch of ventilation and perfusion
-this is why some alveoli dont participate in gas exchange (dead space)
-ventilated alveoli that are not perfused by pulmonary capillary blood
-ventilation perfusion defect- increases functional dead space
-ratio of physiologic dead space to tidal volume -> estimate of wasted ventilated (in conducting or nonperfused alveoli)
-ex. pulmonary embolism -> cuts off perfusion -> no ventilation
-in dead space -> alveolar gas composition = humidified inspired air bc no gas exchange
physiologic dead space in relation to CO2
-is physiologic dead space = 0 -> expired CO2 = alveolar CO2 = arteriole CO2
-physiological dead space present -> arteriole CO2 is higher than expiratory
-this is bc some alveolar didnt receive any blood to exchange CO2
-allows us to figure out how much physiological dead space there is
ventilation rate and alveolar ventilation rate
-ventilation rate- air into and of lungs
-alveolar ventilation- accounts for physiologic dead space -> how much air is going into alveoli and being exchanged
-as alveolar ventilation increases -> partial pressure of CO2 reduces
-breath faster -> breath off more CO2
-breath slower -> CO2 expiration reduces
exercise
-produce more CO2 during exercise
-shifts alveolar ventilation x PP CO2 curve to right
-to maintain normal CO2 during exercise -> we need to increase alveolar ventilation rate -> expires more CO2
alveolar gas equation
-predicts alveolar O2 based on alveolar CO2
-oxygen concentration
-reduce alveolar ventilation -> increase CO2 -> decrease O2
-increase alveolar ventilation -> decrease CO2 -> increase O2
inspiration
-increase intrathoracic volume and decreases intrathoracic pressure -> air flows into lungs
-asthma, exercise- expiration uses rectus abdominis and inspiratory muscles
compliance- boyles law
-distensibility
-how volume changes as result of pressure change
-pressure and volume are inverse
-high compliance -> increase volume of lungs with only small increase in pressure
-low compliance -> small increase in volume -> dramatic increase in pressure
elastance
-highly elastic tissue (thick rubber band) -> lower compliance -> harder to stretch it with a volume change -> increase pressure
-nonelastic tissue (thin rubber band) -> higher compliance -> easier to stretch with volume change -> only small increase in pressure
-inverse to elastic properties
pressure-volume loop
-expanding pressure- negative outside pressure that expands lungs
-hysteresis
-start of inspiration compliance is low (due to high surface tension in alveoli) as you continue to inspire compliance increases half way through
-as you inspire alveoli expand and reduce surface tension -> surfactant can come into play -> increases compliance
-once alveoli are full -> compliance decrease
-expiration- compliance is high throughout
transmural pressure
-difference in pressure in alveoli compared to intrapleural space
intrapleural pressure
-elastic force of chest wall wants to expand
-elastic force of lung wants to collapse
-intrapleural space has negative pressure- vacuum
pneumothorax
-air enters into intrapleural space -> equals atmospheric pressure = 0
-absence of elastic forces (vacuum)
-lung collapse and chest wall springs out
emphysema
-increased lung compliance due to loss of elastic fibers
-elastic recoil is decreased
-capacity is high
-this causes decreased alveolar pressure
-breathe at higher lung volumes
-functional residual capacity increases compared to normal
-forced expiration may cause airway collapse -> slow expiration and pursed lip breathing to increase resistance and restore pressure gradients -> prevents airway collapse
fibrosis
-lungs are less compliant
-elasticity is high
-thickening and stiffening of lung tissues
-volume in lung reduces with pressure
-functional residual capacity decreases compared to normal
neonatal respiratory distress syndrome
-surfactant lacking
-more premature -> more likely less surfactant
-without surfactant -> increase surface tension of alveoli -> increase pressure will collapse (atelectasis)
-no perfusion
-hypoxemia
-lung compliance decreased and work of inflation is increased
pressure changes in lungs- dynamic interplay
-rest- alveolar pressure = 0, intrapleural pressure = atmospheric pressure = 0
-inspiration - thorax increase pressure, lungs decrease pressure (-)
-pressure gradient between atmospheric and alveolar -> drives air into alveoli
-ALVEOLAR PRESSURE = 0 = ATMOSPHERIC PRESSURE at end of inspiration
-expiration- alveolar pressure is positive
functional residual capacity (FRC)
-equilibrium at functional residual capacity (FRC)
-expanding force on chest wall is = to collapsing force on lungs
