Respiratory System Flashcards
conducting zone
moves air
-last part is terminal bronchioles
-ciliated bronchial epithelial cells -mucus traps particles and cilia sweeps it out of lungs
alveolar sac
cluster of alveoli
alveolus
inside air filled
blood gas barrier
wrapped in capillaries
type 2 epithelial cell
make up alveolar wall
-produces surfactant
type 1 epithelial cell
most of alveoli wall
-gas exchange
alveolar macrophage
helps keep alveoli free from bacteria and viruses using endocytosis
alveolar ventilation
moving air in and out alveoli
pulmonary ventilation
how much air enters the whole lung
= tidal volume x respiratory rate
tidal volume
amount of air 1 breath during normal breathing
500ml
anatomical dead space VD
conducting zone
every 1lb is 1lm of dead space x resp. rate
alveolar ventilation equation
=(tidal volume x resp. rate) - (body weight x resp. rate)
pleural membranes
2 thin membranes that surrounds lungs
parietal and visceral pleura
P-attached to top of diaphragm and inside ribs
v- attached to lungs
intrapleural space
fluid filled space within the pleural membranes
boyle’s law
increase P, decrease V
vis versa
intrapulmonary P
pressure of air inside lungs
atmospheric P
P in air we breathe
760mmHg
intrapleural P
p in intrapleural space
-always less then intrapulmonary P
pneumothorax
collapsed lung
-transpulmonary P=0
2 ways
puncturing parietal pleura so atm. P fills intrapleural space
puncturing visceral pleura so intrapul. P fills intrapleural space
transpulmonary P
intrapulmonary P - intrapleural P.
-mmHg
-pressure across intrapleural space
-stops collapse
when 0 it has reached equilibrium
lung recoil
elastic tissues causes it to recoil (deflate)
-can promote pneumothorax
-elastin is found in walls of alveoli to promot this
-caused by surface tension
surface tension
h2o attracted to each other b/c of H-bond
too much surface tension in alveolus can cause it to collapse
pulmonary surfactant
-phospholipids so head attracts h20 but tails balances out forces to stop collapse
-lies over air-liquid interface
=decreases surface tension
lung compliance
measure of stretchability of lungs
-lower compliance by too much elastin, too much surface tension
Neonatal Respiratory Distress syndrome
occurs in premature infants
-lack mature surfactant system
>poor lung function, alveolar collapse, hypoxemia
treatment: administer surfactant (bLES)
emphysema
-types of chronic obstructive pulmonary disease
-inhales irritants, damaging alveoli and its wall
- decrease number of available involved in gas exchange decrease o2 in blood
-loss of elastin
increase lung compliance, issue with exhalations
-increase [] of co2 in aveoli
spirometry
measures tidal V, inspiratory pressure V, expiratory pressure V
inspiratory reserve V
how much air a person can inhale forcefully after a normal breath (extra air on top of tidal volume
expiratory reserve V
the amount of air that can be forcefully exhaled after a normal breath
residual volume
air that stays in lung after all breathing
-can’t use spirometry
total lung capacity
Vt + inspiratory reserve V + expiratory reserve V + residual V
=5-6L
vital capacity
max air inhaled and exhaled
Vt + inspiratory reserve V + expiratory reserve V
forced vital capacity
max air inhaled, force air out as quickly as you can
FEV1
measure FEV (forced expiratory volume) in 1 sec
/how much air comes out in 1 sec
obstructive lung diseases
uses spirometry
FEV1/FVC (Forced vital capacity)= normal lung =80%
ex. asthma, emphysema
asthma
narrowing of airways b/c smooth muscle contraction/hyper responsive
-hyper secretion of mucus
thickened + inflamed air way wall
causes: allergens, pollution, cold air, exercise
restrictive lung disease and example
issue with inhaling
-decrease lung compliance
pulmonary fibrosis>less compliant b/c scar tissue on alveoli walls (less stretch and thicker)
partial pressure of o2 (PO2)
how much pressure o2 contributes to total atmospheric pressure
-PO2 of atmosphere air is =160mmHg
partial pressure of CO2
how much pressure co2 contributes to total atmospheric pressure
-0.3mmHg
high elevations
decrease atm. p
o2 % same
less o2 entering alveoli, less o2 in systemic circulation
transporting o2 in blood
plasma (dissolved) and hemoglobin
hemoglobin
4 polypeptide globin (chains)
4 heme (Fe) binds with o2
1 hemoglobin binds with 4 oxygen
carrying co2 in blood
plasma (7%)
RBC (23%) called carbamino transport
RBC/plasma: by using hco3 and enzyme carbonic anhydrase
bicarbonate reaction
co2 + h2o from cytoplasm + carbonic anhydrase >carbonic acid > H and hco3
(high co2 rx to right, high hco3 rx to left
blood leaving pulmonary capillary and going through systemic arteries
-when co2 is leaving the pulmonary capillaries, high hco3, right to L, causes low hco3+ H
-so blood leaving in low hco3 and basic
blood leaving systemic capillary and going through systemic veins
higher co2 in these capillaries, rx to right, causes high hco3 and low pH
negative feedback with blood gases
central and peripheral chemoreceptors detect change in po2, pco2, pH,
-then send AP to respiratory center in medulla oblongata
-diaphragm and intercostals change to restore balance
peripheral chemoreceptors
found in aortic arch and carotid sinus
-monitoring blood flow through systemic arteries
stimulus:
po2 under 100, pco2 higher 40, acidic
central chemoreceptors
-in medulla oblongata
-bathed in cerebrospinal fluid (interstitial fluid)
stimulus: pH change
low pH, high frequency of AP send to respiratory center to increase VA
how do central chemoreceptors work
co2 from brain cap. enters cerebrospinal fluid
-then co2 and h2o from fluid make hco3 and h
-H then increases AP sent and increase alveiolar ventilation
mechanisms to balance pH in blood
- reabsorb hco3 if too acidic
- excrete H if too acidic
3) excrete hco3 if too basic
conserving hco3
-H going in tubule lumen from epithelial cells using Na/H exchanger
-H and hco3 in lumen react to from co2 and h2o
-h2o moves in epithelial cells by h2o channels
and co2 in b/c non-polar
-co2 and h2o make H and hco3 in cells
-hco3 using protein carriers on basolateral membrane to move in blood
-H gets used again in cycle
-happens regardless of pH levels
type A intercalated cells
will activate to secrete H if blood too acidic
-H secretes in tubule using protein carrier with ATP
-then is excreted
-primary active transport
type B intercalated cells
will activate to secrete hco3 if blood too basic
hco3 is secreted using hco3/cl exchanger
-then is excreted
norm blood pH, acidosis and alkalosis
7.4
= less than 7.4
= more than 7.4
respiratory vs metabolic acidosis and alkalosis
-lung function changes alveolar gas exchange
-unrelated to lungs
respiratory acidosis
preventing co2 from being exhaled properly
1. hypoventilation
2. pulmonary fibrosis
3. emphysema
respiratory alkalosis
decrease in PCO2, less H b/c no hco3 reaction
-any condition with overventilation/exhaling of co2
metabolic alkalosis
decrease pco2
-prolonged vomiting -HCl imbalance
metabolic acidosis
increase pco2
-kidney disease- decrease filtration, more H
-prolonged diarrhea- too much hco3 excreted
summary of gas exchange at tissues
-low po2, high co2 in tissue -high po2, low co2 in RBC
-o2 from plasma and hemoglobin enter tissue
-co2 from tissue enters rbc and with h20 makes hco3 and H
summary of gas exchange at alveoli
-high po2, low co2 in alveoli
-low po2, high co2 in rbc
-o2 from alveoli enter rbc and plasma
-co2 from plasma and hemoglobin enter alveoli
-hco3 and H makes h2o and co2 which enters alveoli
oxyhemoglobin dissociation curve
- increase co2, increase temp, decrease pH, graph shift right
-less po2 in cell then less hemoglobin saturation
