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Jess Resp > First Aid Physiology > Flashcards

First Aid Physiology Flashcards

1
Q

What defines a capacity? Define the four capacities and what they are comprised of

A

The sum of 2 or more physiological volumes
1. Inspiratory capacity: Amount of air that can be inspired after a quiet expiration, TV + IRV

  1. Functional residual capacity: volume of air in the lungs after a quiet expiration, ERV + RV
  2. Vital capacity: Amount that can be exhaled after a max inhalation, IRV + TV + ERV
  3. Total lung capacity: volume of air in the lungs after a max inhalation, IRV + TV + ERV + RV
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2
Q

Name and briefly describe the four lung volumes (that aren’t capacities)

A

IRV: the amount of air that can be breathed in after a normal inspiration

TV: air that moves in and out of lung with each quiet breath

ERV: the amount of air that can be breathed out after a normal expiration

RV: air in the lungs after max expiration

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3
Q

Which lung volume cannot be measured using spirometry?

A

RV (as well as any lung capacity including RV)

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4
Q

What comprises physiological dead space?

A

Anatomic dead space (determined by the volume of conducting zone, as it does not participate in gas exchange) + alveolar dead space

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5
Q

Which part of the lung is the largest contributor to alveolar dead space and why?

A

The apex, as

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6
Q

When is physiological dead space approximately equal to anatomic dead space, when might it be greater?

A

Approximately equal in healthy lungs and may be greater in lung diseases with a V/Q defect

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7
Q

How is physiological dead space calculated?

A

Taco, paco, peco, paco
Vd = Vt (Tidal volume) x(PaCO2 - PeCO2/PaCO2)

PaCO2 = arterial pCO2 
PeCO2 = pCO2 expired
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8
Q

What are the normal values for the following

a) TV
b) RR
c) Vd (physiological dead space)

A

a) 500 ml/breath
b) 12-20 breaths/min
c) 150 ml/breath

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9
Q

Define minute and alveolar ventilation, how are they calculated?

A

Minute: total volume of gas entering the lung/min
Ve = Vt X RR

Alveolar: volume of gas reaching the alveoli/min
VA = (Vt-Vd) X RR

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10
Q

Explain elastic recoil

A

It’s the tendency for the lungs to collapse inward and the chest wall to spring outward

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11
Q

When is the respiratory system’s pressure equal to atmospheric pressure and why? What is pulmonary vascular resistance like at this point?

A

At FRC, when the airway and alveolar pressures equal atmospheric pressure and the intrapleural pressure is negative to prevent atelectasis - so the inward pull of the lung is balanced by the outward pull of the chest wall

Pulmonary vascular resistance is at a minimum

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12
Q

What is lung compliance? What is it proportional and inversely proportional to?

A

Lung compliance: change in lung volume for a change in pressure
Proportional: surfactant
Inversely proportional: wall stiffness

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13
Q

Name two conditions that would increase the lung’s compliance and four that would make it decrease

A

Increase: emphysema, ageing
Decrease: ARDS, pneumonia, pulmonary fibrosis and pulmonary edema

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14
Q

What is hysteresis?

A

The difference in the pressure-volume curve during exhalation vs inspiration - as inspiration requires overcoming surfactant

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15
Q

What lung volume isn’t affected by age?

A

Total lung capacity

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16
Q

Name four things that increase and four that decrease with ageing

A

Increase:

  1. Lung compliance (loss of elastic recoil)
  2. RV
  3. V/Q mismatch
  4. A-a gradient

Decrease:

  1. Chest wall compliance
  2. FEV1/FVC
  3. Respiratory muscle strength
  4. Ventilatory response to hypoxia/hypercapnia
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17
Q

What are the structural differences between Hb and myoglobin?

A

Hb: 4 polypeptide chains (2 alpha, 2 betas) - each chain contains a heme group (that surrounds a globin) that has an iron molecule that can reversibly bind O2.
It can exist in two forms
-Deoxygenated form: a low affinity for O2 (easily unload)
-Oxygenated form: a high affinity for O2

Myoglobin: one polypeptide chain with one heme group, has a higher affinity for O2

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18
Q

How many ml of O2 can 1 g of Hb bind?

A

1.34 ml

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19
Q

How does decreased Hb affect O2 content, O2 saturation and PaO2?

What determines O2 delivery to tissues?

A

When Hb content decreases O2 content should also decrease, but O2 saturation and PaO2 won’t change

O2 delivery to tissues = CO X O2 content of blood

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20
Q

What happens to Hb concentration in the following conditions?

a) CO poisoning
b) Anemia
c) polycythemia

A

a) Normal
b) Decreased (less RBCs)
c) increased (more RBCs)

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21
Q

What happens to O2 saturation in the following conditions?

a) CO poisoning
b) Anemia
c) polycythemia

A

a) Decreased (as CO is competing with O2)
b) normal
c) normal

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22
Q

What happens to dissolved O2 or PaO2 in the following conditions?

a) CO poisoning
b) Anemia
c) polycythemia

A

Normal for all

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23
Q

What happens to total O2 content in the following conditions?

a) CO poisoning
b) Anemia
c) polycythemia

A

a) decreased
b) decreased
c) Increased

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24
Q

How is methemoglobin formed and what happens as a result?

A

When Hb changes from its reduced to its oxidized state (Ferrous Fe2+ -> Ferric 3+). Fe3+ doesn’t bind to O2 as readily as Fe2+ and has a higher affinity for cyanide - this result in tissue hypoxia and decreased O2 saturation and O2 content

Nitrites (from the diet or polluted/high-altitude water) and benzocaine can cause this oxidation of iron

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25
Q

How can methemoglobinemia present?

A

Cyanosis and chocolate coloured blood

26
Q

How can methemoglobinemia be treated?

A

Methyl Blue and vitamin C

27
Q

Describe the shape of the oxygen dissociation curve for hemoglobin and myoglobin

A

Hb: sigmoidal shape, as it is a tetrameric molecule whose O2 affinity increases with each subsequent molecule bound

Myoglobin: not sigmoidal as it is monomeric and doesn’t have this positive cooperativity

28
Q

What does it mean for the ODC to shift to the right or left?

A

Right shift: means there’s been a decreased Hb affinity for O2 - so there is more unloading. This increases the amount of oxygen needed to maintain 50% saturation (aka a higher P50)

Left shift: means there’s been increased Hb affinity

29
Q

What happens as a result of a Left shift to the ODC?

A

Decreased unloading of O2 can result in renal hypoxia -> this stimulates the production of EPO/erythropoietin and cause compensatory erythrocytosis

30
Q

Describe the structural and ODC differences in fetal Hb in comparison to adult Hb

A

Fetal Hb has 2 alpha and 2 gamma subunits and a higher affinity for O2 as it has decreased affinity for 2,3 BPG, therefore the ODC shifts left and there is more diffusion of O2 across the placenta

*2,3 BPG decreases Hb’s affinity for O2

31
Q

How do cyanide and CO affect aerobic metabolism and what can it lead to? What specific intervention won’t work to correct this problem?

A

They inhibit aerobic metabolism through inhibition of complex IV (on the ETC)/cytochrome C oxidase leading to an increase in anaerobic metabolism

Supplemental O2 doesn’t work

32
Q

How does cyanide and CO poisoning present?

A

Pink or cherry red skin, seizures and coma

33
Q

What are some sources of cyanide?

A
  1. Byproduct of synthetic product combustion
  2. Ingestion of amygdalin which is a cyanogenic glucoside found in apricot seeds
  3. cyanide
34
Q

What are some sources of CO?

A

car exhaust, gas heaters, odourless gas from fires

35
Q

How can cyanide poisoning be treated?

A
  1. Hydroxocobalamin (binds cyanide to form cyanocobalamin which is excreted renally)
  2. Nitrites (they oxidize Hb to form methemoglobin which binds cyanide to form cyanomethemoglobin which is less toxic)
  3. Sodium thiosulfate (this increases cyanide conversion to thiocyanate which is excreted renally)
36
Q

How is CO treated?

A

100% O2, hyperbaric O2

37
Q

What are the different symptoms of cyanide and CO poisoning?

A

Cyanide: bitter almond breath, CVS collapse

CO: headache, dizziness (and multiple family members may be involved with similar symptoms in the winter)

38
Q

How does CO poisoning classically present on an MRI

A

Bilateral globus pallidus lesions

39
Q

Describe how the ODC changes in CO and cyanide poisoning

A

Cyanide: normal curve

CO: L shift

40
Q

What does a decrease in PAO2 cause and why?

A

Hypoxic pulmonary vasoconstriction that shifts blood away from poorly ventilated alveoli to better-ventilated regions of the lung

41
Q

What increases gas exchange? When does gas (i.e O2, CO2 and N2O) tend to equilibrate?

A

Increased bloodflow

Gases tend to equilibrate early along the length of the capillary

42
Q

What can limit the diffusion of gases so that they don’t equilibrate by the time blood reaches the end of the capillary?

A

O2: emphysema, fibrosis, exercise

CO is “diffusion-limited”

43
Q

What is DLCO

A

The extent that CO passes from air sacs of the lung into the blood

44
Q

What are two consequences of pulmonary hypertension

A

Cor pulmonale and subsequent RVF

45
Q

Name one disease that causes a decrease in the alveolar surface area and an increase in alveolar wall thickness

A

Decreased alveolar SA: emphysema (causes alveoli to rupture resulting in one large air space)

Increased alveolar wall thickness: fibrosis

46
Q

How is pulmonary vascular resistance calculated?

A

PVR = Ppulm - P(l atrium)/CO (or ‘Q’)

Ppulm: pressure in the pulmonary artery
P l atrium: the pulmonary capillary wedge pressure (small catheter inserted into pulmonary arteries to estimate the pressure in the l atria)

47
Q

Name five general scenarios that result in hypoxia

A

*2 COs and 3 ‘emias’

  1. Decreased CO
  2. CO poisoning
  3. Anemia
  4. Ischemia
  5. Hypoxemia
48
Q

Define hypoxemia, when would you see a normal and an increased A-a gradient with it?

A

Hypoxemia: low PaO2

Normal A-a gradient: high altitudes and hyperventilation (i.e due to opioid use, obesity hypoventilation syndrome)

Increased A-a gradient: V/Q mismatch, diffusion limitation (like in fibrosis) and a R-L shunt

49
Q

Where in the lung is there wasted ventilation and wasted perfusion? Where are they both greatest?

A

Wasted ventilation at the apex, wasted perfusion at the base. They’re both greatest at the base (rather than the apex)

50
Q

What drives the V/Q ratio closer to 1?

A

Exercise: this increases the CO which causes more vasodilation at the apical capillaries - this drives the V/Q closer to 1

51
Q

Where do organisms that require O2 thrive in the lung? Name one example

A

The apex, TB

52
Q

What does it mean if the V/Q = 0 and if it = infinity

A

=0: there is an obstruction, like in a R-L shunt where deoxygenated blood does not return to the pulmonary arteries and participate in gas exchange at the pulmonary capillaries.

=infinity: blood flow obstruction

53
Q

How does ischemia affect venous drainage?

A

Impeded arterial blood flow means there will be less venous drainage

54
Q

What are the three forms that CO2 can be transported from the tissues to the lungs and how they form?

A
  1. HCO3- (70%): CO2 combines with water and is converted to carbonic acid via carbonic anhydrase, this then reorganizes to an H+ ion and a bicarbonate molecule (the H+ then joins with Hb and is buffered)
  2. Carbaminohemoglobin (HbCO2): Hb binds to the N-terminus of the globin and favours the deoxygenated form (so there is more O2 unloading)
  3. Dissolved CO2 (in the bloodstream)
55
Q

What defines pathologic dead space?

A

When part of the respiratory zone is ventilated but not perfused (and so cannot contribute to gas exchange)

56
Q

What is the alveolar gas equation?

A

PAO2 = PIO2 - (PaCO2/R)

PIO2: PO2 in inspired air
PaCO2: PCO2 in the pulmonary arteries
R: Respiratory quotient (CO2 produced/O2 consumed)

57
Q

How can functional residual capacity be measured?

A

Helium dilution or body plethysmograph

58
Q

Compare the Haldane and the Bohr effect

A

Bohr effect: CO2 and H+ decrease the affinity of Hb for O2: so there is more unloading in acidic/metabolically active tissue

Haldane: O2 is affecting the affinity of Hb for CO2 and H+: oxygenation of Hb promotes dissociation of H+ from Hb, shifting the equilibrium towards forming more CO2 (H+ binds to bicarbonate to form carbonic acid which dissociates into water and CO2) and thus increasing CO2 delivery back to the lungs!

59
Q

Describe how high altitudes results in ‘altitude sickness’, what is the bodily and respiratory response?

A

Low atmospheric oxygen lowers the PaO2, this increases the ventilation and decreases the PaCO2 -> inducing respiratory alkalosis and altitude sickness

Things that increase: VMEBRH (ME Recommends Beautiful Valley Holidays)

  1. Chronic increase in ventilation
  2. Chronic hypoxia stimulates an increase in EPO -> increases Hct and Hb
  3. Increased 2,3 BPG which binds to Hb causing a right shift in the ODC so that Hb releases more O2
  4. Cellular changes such as an increase in mitochondria
  5. Increased renal excretion of HCO3- to compensate for respiratory alkalosis

Chronic hypoxic pulmonary vasoconstriction results in pulmonary hypertension and RVH

60
Q

What is the metabolic and respiratory response to exercise? What happens to the gas content in the pulmonary arteries and the veins?

A

Increased CO2 production: lowers the ph (lactic acidosis)

Increased O2 consumption: this shifts the ODC to the right (more unloading) and the ventilation rate increases to meet the high O2 demand.

Increased cardiac output: Apical capillaries dilate so there is an increase in pulmonary bloodflow and the V/Q ratio from the apex-base becomes more uniform

No change in PaO2 or PaCO2, but the venous O2 content lowers and CO2 content rises

Jess Resp (20 decks)

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