BRS Physiology Review - Supplemental Flashcards

1
Q

What is the equation for deadspace?

A

VD = VT x ((PACO2-PECO2)/PACO2)

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2
Q

What is the equation for alveolar ventilation?

A

AV = (Tidal volume - deadspace) x RR

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3
Q

What are the most important muscles for inspiration?

A

Diaphragm - contraction pushes abdominal contents downward and increases volume of thoracic cavity

External intercostal muscles - used during exercise

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4
Q

What are the most important muscles for expiration?

A

Expiration is normally passive

During times of exercise, the abdominal muscles and the internal intercostal muscles are used

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5
Q

What is the term for the different curves on a pressure volume graph that inspiration and expiration follow?

A

Hysteresis

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6
Q

What is the equation for LaPlaces law?

A

P = 2T/r

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7
Q

What are more likely to collapse without surfactant small or large alveoli?

A

Small

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8
Q

What will shift the O2 curve to the right?

A

Increased temp

2,3 - DPG

Decreased pH

Increased CO2

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9
Q

Expiratory reserve volume is equal to?

A

VC - Inspiratory capacity

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10
Q

Inspiratory Capacity

A

sum of the tidal volume and IRV (amount you can take in after you inspire tidally)

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11
Q

Functional residual capacity

A

sum of ERV and RV (tidle exire to the complete empty of lungs)

includes RV so it cant be measured by spirometry

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12
Q

Vital capacity/ forced vital capacity (VC/FVC)

A

all but the RV - forced means you are forcing fast flow

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13
Q

Total lung capacity

A

all the air in a lung

includes RV - so can not be measured by spirometry

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14
Q

FEV1/FVC

A

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
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15
Q

muscles of inspiration and expiration

A
  • 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
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16
Q

Complience (and what happens in emphysemia and fibrosis)

A

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
17
Q

Surface tension

A

P= 2T/r

  • this means that smaller alveoli want to colapse more
    *
18
Q

surfactant

A
  • 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)
19
Q

Gas exchange equations

A
  • 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)
20
Q

hemoglobin sat curve shifts

A
  • 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
21
Q

Transport of CO2 in blood

A
  • 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
22
Q
A