BRS Physiology Review - Supplemental Flashcards
What is the equation for deadspace?
VD = VT x ((PACO2-PECO2)/PACO2)
What is the equation for alveolar ventilation?
AV = (Tidal volume - deadspace) x RR
What are the most important muscles for inspiration?
Diaphragm - contraction pushes abdominal contents downward and increases volume of thoracic cavity
External intercostal muscles - used during exercise
What are the most important muscles for expiration?
Expiration is normally passive
During times of exercise, the abdominal muscles and the internal intercostal muscles are used
What is the term for the different curves on a pressure volume graph that inspiration and expiration follow?
Hysteresis
What is the equation for LaPlaces law?
P = 2T/r
What are more likely to collapse without surfactant small or large alveoli?
Small
What will shift the O2 curve to the right?
Increased temp
2,3 - DPG
Decreased pH
Increased CO2
Expiratory reserve volume is equal to?
VC - Inspiratory capacity
Inspiratory Capacity
sum of the tidal volume and IRV (amount you can take in after you inspire tidally)
Functional residual capacity
sum of ERV and RV (tidle exire to the complete empty of lungs)
includes RV so it cant be measured by spirometry
Vital capacity/ forced vital capacity (VC/FVC)
all but the RV - forced means you are forcing fast flow
Total lung capacity
all the air in a lung
includes RV - so can not be measured by spirometry
FEV1/FVC
normal = .8
- in obstructive disease (asthma, COPD) both are reduced but FEV1 is reduced more so the fraction decreases
- in restrictive lung diseases (fibrosis) they both decrease but FEV1 is reduced the same or less so the fraction stays the same or increases
muscles of inspiration and expiration
- diaphram is most important - moves down
- external intercostals and accessory muscles
- not used for normal quiet breathing - used during exarcise
- expiration muscles
- normal expiration is passive - elasticity of the lungs
- abdominals - increase abdominal cav pressure pushing the diaphram up
- internal intercostals - pulls ribs down and in
Complience (and what happens in emphysemia and fibrosis)
C= V/P - change in volume per change in pressure - slope of pressure volume curve
- in emphysema lung C is increased - the patients FRC (where chest wall expansion and lung colapse are balanced when lungs are at atmospheric P) increases because the lungs arent as elastic - this leads to barrel chestedness
- in patients with fibrosis lung C is decreased the FRC moves down
Surface tension
P= 2T/r
- this means that smaller alveoli want to colapse more
*
surfactant
- reduces surface tension of alveoli - secreted by type 2 pneumocytes
- consists primarily of phsopholipid dipalmitoylphosphatidylcholine (DPPC)
- not produced in great quantities until 35 months of gestation
- a lectin:sphingomyelin ratio greater than 2:1 in amniotic fluid reflects mature levels of surfactant
- Neonatal respiratory distress syndrome can occur in early born infants (not enough surfactant) - atelectasis, difficulty reinflating lungs (decreased complience) and hypoxemia (decreased V/Q)
Gas exchange equations
- Dissolved O2 = PO2 X Solubility (solu = .003)
- Vx(dot) = Dl X (change in pressure)
- Dl increases: exarcise because there are more open capilaries = increased surface area
- Dl decreases: in emphysema (decreased SA) and in fibrosis and pulm edema (increased diffusion distance)
hemoglobin sat curve shifts
- shift Right - when affinity of hemoglobin for O2 is decreased
- increase in PCO2 or decrease in pH - helps unload O2 at exarcising muscles
- increase in temperature
- increase in 2,3-DPG - binds to the beta chain of deoxy hemoglobin and stabilizes the deoxy form
- shift left - when affinity of hem for O2 is increased
- mirror image of the abouve right shift
- HbF - doesnt bind DPG as strongly
- CO poisoning
Transport of CO2 in blood
- carbonic anhydrase cats CO2+H2O -> H2CO3 - this occurs inside RBCs
- HCO3 leaves the cell in exchange for Cl
- the H+ from the conversion of H2CO3 to HCO3 is buffered by deoxy hemeoglobin (this also cuases oxy hemoglobin to release O2
- in the lungs the opposite happens - HCO3 goes into RBCs (exchange Cl) and recombine with H+ to form H2CO3 which decomposes to H2O and CO2