Lungs

Question 1

conducting zone

Answer 1

-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

Question 2

innervation of smooth muscle in conducting zone

Answer 2

-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

Question 3

respiratory zone

Answer 3

-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

Question 4

total volume normal inspiration

Answer 4

-500mL
-150 in the conducting zone -> no air exchange
-350 in the respiratory zone -> exchange

Question 5

residual air

Answer 5

-stays in the lungs with each expiration
-in conducting zone
-prevent collapse

Question 6

lung volumes - need to know

Answer 6

-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

Question 7

inspiratory capacity

Answer 7

-tidal volume + inspiratory reserve
-3500mL (500+3000)

Question 8

functional residual capacity

Answer 8

-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

Question 9

vital capacity

Answer 9

-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

Question 10

total lung capcity

Answer 10

-vital capacity + residual volume
-5900 (4700+1200)
-inspiratory capacity + functional residual capacity
-everything

Question 11

diffusion capacity

Answer 11

-thickness of membrane - decreases
-restrictive lung disease - hardening of tissue
-

Question 12

FEV1

Answer 12

-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

Question 13

obstructive lung disease

Answer 13

-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

Question 14

restrictive lung disease

Answer 14

-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

Question 15

law of laplace

Answer 15

-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

Question 16

O2 partial pressure

Answer 16

-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

Question 17

pulse ox (o2 saturation) 80

Answer 17

-hemoglobin not binding
-you can still breathe mechanically but nothing is binding -> nothing is being perfused
-PO2 = 40 -> 75% sat
-PO2 = 50 -> 75% sat

Question 18

shift to right

Answer 18

-increase PCO2
-decrease pH
-increase temperature
-increase 2,3 DPG

Question 19

shift to left

Answer 19

-decrease PCO2
-increase pH
-decrease temperature
-decrease 2,3 DPG
-fetal hemoglobin

Question 20

surface area of lung

Answer 20

-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

Question 21

function of respiratory system

Answer 21

-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)

Question 22

alveolar walls

Answer 22

-elastic fibers
-epithelial cells -> type 1 and 2 pneumocytes
-type 2- produce surfactant

Question 23

alveolar macrophages

Answer 23

-phagocytic cells
-fill with debris and migrate to bronchioles -> cilia carry up -> swallowed or coughed

Question 24

regulation of pulmonary blood flow

Answer 24

-altering resistance of pulmonary arterioles via local factors (O2)

Question 25

dead space

Answer 25

-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

Question 26

ventilation perfusion defect

Answer 26

-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

Question 27

physiologic dead space in relation to CO2

Answer 27

-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

Question 28

ventilation rate and alveolar ventilation rate

Answer 28

-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

Question 29

exercise

Answer 29

-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

Question 30

alveolar gas equation

Answer 30

-predicts alveolar O2 based on alveolar CO2 -oxygen concentration -reduce alveolar ventilation -> increase CO2 -> decrease O2 -increase alveolar ventilation -> decrease CO2 -> increase O2

Question 31

inspiration

Answer 31

-increase intrathoracic volume and decreases intrathoracic pressure -> air flows into lungs -asthma, exercise- expiration uses rectus abdominis and inspiratory muscles

Question 32

compliance- boyles law

Answer 32

-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

Question 33

elastance

Answer 33

-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

Question 33

pressure-volume loop

Answer 33

-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

Question 34

transmural pressure

Answer 34

-difference in pressure in alveoli compared to intrapleural space

Question 35

intrapleural pressure

Answer 35

-elastic force of chest wall wants to expand -elastic force of lung wants to collapse -intrapleural space has negative pressure- vacuum

Question 36

pneumothorax

Answer 36

-air enters into intrapleural space -> equals atmospheric pressure = 0 -absence of elastic forces (vacuum) -lung collapse and chest wall springs out

Question 37

emphysema

Answer 37

-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

Question 38

fibrosis

Answer 38

-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

Question 39

neonatal respiratory distress syndrome

Answer 39

-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

Question 40

pressure changes in lungs- dynamic interplay

Answer 40

-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

Question 41

functional residual capacity (FRC)

Answer 41

-equilibrium at functional residual capacity (FRC) -expanding force on chest wall is = to collapsing force on lungs