ch 22 respiratory system p2 Flashcards
respiratory volumes
amount of air that can be pushed into and out of lungs during ventilation
tidal volume
normal volume of air that moves into and out of lungs during normal breathing, 500 mL air
IRV inspiratory reserve volume
amount of air that can be inspired forcibly past tidal volume. 2100-3000 mL air breathe in until iu can’t
ERV expiratory reserve volume
amount of air that can be forced from lungs after normal tidal volume expiration 1000-1200 mL air
force air out until u can’t
RV residual reserve
amount of air left in lungs after forced expiration 1200 mL
can the lungs be void of all air
no, lungs can never be empty of air- even in dead
respiratory capacities
sum of two or more respiratory volumes.
inspiratory capacity IC
total amount of air that can be inspired after normal tidal volume expiration, how much air we can force in after we breathe out
IC=
TV plus IRV
functional residual capacity FRC
amount of air remaining in lungs after normal tidal volume expiration,
FRC=
RV plus ERV
vital capacity
total amount of exchangeable air
VC=
TV + IRV + ERV
what volume does not contribute to vital capacity
residual volume, it never leaves the lungs so it can’t contribute
total lung. capacity TLC
the total amount of air the lungs can hold after maximum inhalation, 6 L
TLC =
IRV + TV + ERV + RV
deadspace
air that fills conducting zone, but never contribute to gas exchange
anatomical dead space
150 mL air
what is the total volume used for gas exchange
350 mL for the exchange (500 from TV - dead space 150 mL)
alveolar dead space
air reaches alveoli but no gas exchange occurs. due to localized damage or alveoli collapse. ex smoking damage or mucus blockage temporary
total dead space
anatomical dead + alveolar dead, all non useful volumes
daltons law of partial pressure
total pressure exerted by a mixture of gases is sum of pressures exerted independently by each gas in the mixture
daltons law for dummies
total atm pressure = pressure of different gases that make up the air we breathe
how much N and O air in the air we breathe
N 79
O 20.9
rest is CO2 and water vapor
partial pressure
each individual gas in the mixture, PP of each gas is independent of the other no influence
why is partial pressure important
if we know the PP of each gas, we can see pressure gradients which drive diffuion into and out of blood
henrys law
gas will dissolve in liquid proportional to its partial pressure.
more PP = (henrys law)
more gas dissolved in liquid
gases dissolve best in liquid under what conditions of pressure, tem, and solubility
pressure- high
temp- low
solubility- high
is the PP of O2 greater in alveolar space as a gas or in blood as liquid? would O2 move into or out of the blood as liquid
PP more as gas, alveolar space. gas goes out into space, in the body CO2 leaves and diffuses from blood to lungs to become O2. O2 foes into blood as liquid
gas exchange occurs in
alveoli
3 factors which affect rate at which gas exchange occurs between alveoli and capillaries
PP gradients and gas solubility, thickness and surface area of respiratory membrane, ventilation perfusion coupling
PP gradients and gas solubility alveoli
alveoli pressure > lung capillary pressure. O2 moves from alveoli into vblood
what direction does CO2 move
CO2 moves from blood to lungs, equal amounts CO2 and O2 exchanged.
thickness and surface area of respiratory membrane
respiratory membrane is so thin, gas exchange occurs fast. more SA more gas that can exchange, and alveolar SA is huuuuge
ventilation perfusion coupling
optimal gas exchange results from equal amounts of gas reaching alveoli and blood supply to pulmonary capillaries
perfusion is
blood flow thorough vessels
influence of PO2 on perfusion
occurs at lungs, local PO2 low and local arterioles to those alveoli constrict
why do local arterioles to those alveoli constrict when PO2 Is low
less blood to capillary where lungs don’t have O2, redirect blood flow to optimize O2 exchange. ensures it is good O2 intake
what happen when local pO2 is high n why
local arterioles to those alveoli dilate, to flush blood and capillaries with more O2, blood intake is more
influence of PCO2 on ventilation
local PCO2 high makes bronchioles dilate so CO2 eliminated faster and affects blood pH, PCO2 levels low they all constrict (usually to dispose of CO2 bc basic
alveolar gas is composed of
mostly CO2 and water vapors.
why is atm gas different from alveolar gas
gas exchange occurs in alveoli so O2 diffuses into blood and CO2 to alveoli.
conducting passages humidify air creating water vapor
mixture of air in alveoli inspiration brings new gases in, but reserve volume wit leftover air still exists
internal respiration
gas exchange that occurs in body tissues
PCO2 in tissues > PCO2 in blood, what direction does CO2 travel
high to low, opposite of lungs. CO2 enters blood tho
PO2 in blood > PO2 in tissueswhat direction does O2 travel
cellular respiration moves blood to body tissues and O2 leaves blood
what can be said about PP and diffusion gradients between internal and external respiration
external is high to low pressure in blood, internal is high to low in tissues
oxygen is transported usually by
Hb, 4 O2 per 1 Hb. first O2 bind makes rest go go go
why is it helpful for first O2 molecule to begin the unloading of the next 3 in Hb
1 heme bind 4 O2, 1 O2 facilitates other 3 so O2 more readily binds and the process is faster and Easier
arterial blood is how saturated
98%
venous blood is how saturated
75%
why is venous blood not 0% saturated
venous blood is not completely deoxygenated, more than half the heme still bound, 75% is our reserve. ensures blood circulation before hypoxia happens.
CO2 ways to transport
dissolved in plasma, bound to Hb, as bicarbonate ions in plasma.
CO2 when bound to Hb
doesn’t bind heme, binds amino acids of globulin
why do we not want CO2 to bind Heme or Fe
ensures fast and easy pickup so O2 and CO2 don’t have to compete w each other for transport spot
bicarbonate ions in plasma with CO2 transport
most important, CO2 diffuses Into erythrocyte comb9nes with water to make carbonic acid. splits to form H+ and HCO3- (bicarb) THIS REACTION CAUSES FREE H+ TO RELEASE IN BLOOD PLASMA SO CO2 INFLUENCES BLOOD PH
what will release when CO2 goes to bicarbonate
H+, buffered by RBC and maintains the pH of blood
respiratory acidosis
too much CO2 so pH decreases. slow, shallow breathing
respiratory alkalosis
too little CO2, pH increases, rapid deep breathing
medullary respiratory center
two areas that set normal respiratory rhythm
ventral respiratory group, VRG
neurons fire during inspiration and expiration, but do NOT fire at same time.
dorsal respiratory group (DRG)
integrates info fro, other structures and delivers to VRG
pontine respiratory center PRC
interacts with medullary respiratory centers to smooth respiratory patterns in pons. transports from inspiration to expiration.
what does the CNS measure to determine breathing rate and depth
CO2 (most potent and closely controlled) and PO2 of arterial blood
hypercapnia , what happens to blood pH and how does CNS change breathing rate to correct it
increase In PCO2 levels of blood, pH more acidic drops down.
too much CO2, H+ ions will cause blood pH to drop and chemoreceptors say HEY inc the breath rate and don’t notice a lot (person won’t) can hyperventilate to make it go down bc breathing in own CO2
hypocapnia
decrease in PCO2 levels of blood, pH more basic and alkalosis, slows breath rate and depth, so pH will balance out
PO2 of arterial blood
not much infleunce as CO2, venous blood reservoir is there so body can use it. if its a lot dropped, respiratory centers stimulated and ventilation inc
COPD
group of conditions characterized by the physiological inability to expel air from lungs. irreversible, coughing hard to breathe q
emphysema
type of COPD, permanent enlargement of alveoli and eventual destruction of their walls. lungs lose elasticity. bronchioles collapse and traps air in alveoli. leads to barrel chest bc ribs expand due t excess inside. damages pulmonary capillaries
chronic bronchitis
chronic production of excess mucous due to inhaled irritants. lower respiratory passages enflamed over time and fibrous (scar tissue) so ventilation decreases. mucous won’t leave lungs, easy to get infection bc bacteria breeds in mucous
asthma
temporary bronchospasm attacks with symptom free periods. allergic asthma most common, inflammation caused by IgE antibodies. no real cure but can be treated
Tuberculosis
bacterial disease spread by inhaled air, 33% of world infected but usually not active, can spread past lungs, bad cough with fever and sweats as well as weight loss
sleep apnea
temporary cessation of breathing during sleep
must wake up during sleep, due to lack of gas exchange. 30x per hour even, leads to fatigue as well as heart disease and strokw
obstructive esleep apnea
upper air ways collapse during sleep. muscles associated with pharynx relax, airway closes. men common more. obesity worse. CPAP helps to make continuous airway response
central sleep apnea
resp centers of brain slack during sleep so breathing rate not maintained. hard to treat.
