respiratory Flashcards
distinct VA / VE / VD
conducting zone: anatomical dead space ventilation (VD = weight x resp rate)
respiratory zone: alveolar ventilation (VA = VE-VD)
pulmonary ventilation: VE = tidal vol x resp rate
function of conducting zone
- carry filter moisten air
- microbial defense
- bronchial epithelial cells have cilia which sweep mucus + infected stuff towards trachea
3 cells in alveolar
type I (thin flat cell tht makes gas exchgange easier) / type II (secrete surfactant) / micrphages destroy microorg
parietal pleural vs visceral pleura vs intrapleural space
visceral pleural directly on top / then parietal pleural/ space btw them
how much is P in intrapulmonary P?
760 mmHg
distinct btw obstructive vs restrictive disease
FEV > bt no change to FVC vs FVC > bt no change to FEV1
FEV1/FVC less than 80% vs FEV1/FVC more than 80%
exhalation issues vs inhalation
what does a spirometer measure?
tidal vol: amnt in / out of lung during normal breathing
inpspiratory reverse vol: max amnt inhaled after normal inhalation
expiratory reserve vol: …exhalaltion
residual vol: amnt remaining in the lungs after max expiration
emphysema
cause: smoking: loose elastic tissue -> loose elastic recoil -> <> compliance
effect: destructed alvolar wall creates large air sac -> poor gas exchange
what do you wanna increase to increase compliance? why?
surfactant / surface tension/ elastic tissue.
surfactant
has a hydrophilic head + hydrophobic tail
balance forve over the liquids in the alveoli
stop lung collapse -> > surface tension -> < compliance
asthama: C & E?
cause: allergen, pollution
effect: airway inflamation -> narrows
pneumothorax: C & E?
cause: punctures int he pleural membranes
since gas moves from H to L, goes towards the intrapleural membrane
effect: no transpul P -> lung collapse
how does nRDS affect premature infant?
poor gas exchange, alveolar collapse ‘ of weak surfactant system
solution: administer it!
pulmonary fibrosis: C & E?
cause: chronically inhaling abestos. coal dust, polution
effect: fribrous scar tissue @ alveoli
due to thick walls, poor gas exchange
5 factors that maximize simple difussion across blood gas barrier
thin membrane, small molecule, high gradient, high SA, hydrophobic
2 ways in which O is transported
- dissolved in blood
- bounded to hemoglobin as oxyhemoglobin (O2 + Hb = HbO2)
inside hemoglobin: 4 heme groups + 4 oxygen groups
function of hemoglobin
pick up O at the lungs via binding to heme group
drop off that O at tissue’s cell
collect cellular waste (CO2) via binding to globiin
drop off that waste at lungs for removal
explain the bohr effect
lowered afinity for bindging to O2
when increase temp, pCO2 but decrease the pH
’ CO2 + H20 eventually makes H+ + HCO3-
lower pH, O2 readily dissoiciate from oxyhemoglobin
How is CO2 transported?
1) Disolved in plasma
2) carbamino form by binding to globin subunits (CO2+ Hb -> HbCO2)
3_ bVicarbonate form
Types of chemoreceptor
Peripheral: aortic arch and carotid body
Central : medulla oblongata
respiratory acidosis vs respiratory alkalosis
too much H+
increase ventilation to breath out CO2
too lil H+
retain CO2 to make it
decrease ventilation
2 causes of anaemia
low production of erythocytes: bone marrow tissue, improper nutr, kidney failure
loss of …: bleeding, hemolytic disease
how to increase the erythopoetin release?
since the stinulus if low PO2,
- anaemia
circulatory / lung disease
high altitude
differentiate inspiration vs expiration in 3 points
ribcage moves up and OUT; external intercoastal contravs vs external intercoastal relaxes
diaphragm moves down => contracts vs diagraphm moves up => relaxes
what is special abt active phase of expiration?
rectus, obliques abdominus and internal intercoastal contracts (to help diagraphm)
how does Boyle’s Law affect inspiration?
since Boyls’s Law states that pressure is inversely proportional to volume,
increasing vol of thoraic cavity in inspiration would decrease intrapul P
how is control achieved through peripheral chemoreceptor?
respiratory centre compares to set point (PO2 = 100 mmHg, PCO2 = 40 mmHg, pH = 7.4)
respiratory muscle increases ventilation and set pojint achieved
PO2, PCO2 & pH all less than set point
peripheral chemoreceptor @ aortic arch & carotid body sends AP to respiratory centre
how did H+ end up activating central chemoreceptor? what is special abt this compared to peripheral chemoreceptor?
CO2 diffuses to the cerebrospinal fluid
-> combines w/ water, makes carbonic acid
-> disassociates into H+ and bicarbonate
H+ activates centre chemoreceptor =? stimulates respiratory centre
vs peripheral, this one only senses pH
compare anaemia vs polycythemia
depressed hematocrit => low PO2 transport
fatigue, muscle wekaness, and breathlessness
elevated hematocrit, thickened blood
_______, production of RBC in bone marrow and _____, ___ hormone stimulates it
to release that hormone, have low/high PO2
enrythpoeisis / enrythropoetin/ peptide
low!
