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Physiology > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What are the main muscles of inspiration?

A
  • Diaphragm - contracts to force abdominal contents downwards, increasing vertical chest dimension
  • External intercostals - bucket handle movement to lift ribs outward and upwards, increasing transverse diameter
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2
Q

What are the accessory muscles of inspiration?

A
  • Scalenes - elevate 1st 2 rib

- SCMs - lift sternum

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3
Q

During quiet breathing, expiration is

A

passive. The elastic lung and chest wall return to their equilibrium positions after being actively expanded during inspiration.

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4
Q

What are the muscles of active expiration?

A
  • muscles of abdominal wall - RA, IO, EO + TA

- Internal intercostals

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5
Q

What are the antiexpansion forces (resistance to inspiration)?

A

Elastance
Tissue resistance (pleural sliding)
Airway resistance

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6
Q

What are the key pressures to consider in respiration?

A

Intraalveolar pressure
Intrapleural pressure
External chest surface pressure (atmospheric)
Transmural pressures - transpulmonary, transthoracic, transrespiratory

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7
Q

How are the transmural pressures calculated?

A

Transmural pressure = P inside vs P outside. Ie:
P Transpulmonary = Palv - Ppl
P Transthoracic = Ppl - Patm
P Transrespiratory = Palv - Patm

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8
Q

What does it mean for a transmural pressure (e.g. transpulmonary pressure) to be positive or negative?

A

The transmural pressure determines if the structure is inflating (+ve) or deflating (-ve)

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9
Q

The inflation and deflation P-V curves are different, this is called

A

Hysteresis - the deflation lung volume is greater than the inflation volume for a given pressure.

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10
Q

What is lung compliance?

A

Compliance is the volume change of the lung per unit pressure change (the slope of the P-V curve = DV/DP).

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11
Q

At what range of expanding pressures is the lung very compliant?

A

In the normal breathing range - pressures -5 to -10 cm H2O.

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12
Q

What is the compliance of the normal human lung?

A

Approx 200 ml/cmH2O. Note that at high expanding pressures the lung is stiffer and compliance is smaller

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13
Q

What pathology reduces lung compliance?

A

Pulmonary fibrosis
Pulmonary oedema
Atelectasis + increased surface tension in the poorly ventilated lung

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14
Q

What processes increases lung compliance?

A

Normal aging lung

Emphysema

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15
Q

What is surface tension?

A

The tension of a surface film of liquid (e.g. H20 in the alveoli), caused by the attraction of the surface layer to the bulk of the fluid (unopposed downwards + inwards attraction), which tends to minimise surface area.

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16
Q

What is the collapsing pressure?

A

It is a measure of the tendency of an alveolus to collapse, proportional to the surface tension and inversely proportional to radius (P= 2T/r)

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17
Q

What does the collapsing pressure equation imply about alveolar stability?

A

The alveolar system is inherently unstable

  • the collapsing pressure is related to the radius, the smaller alveoli will have larger pressure - and tend to empty into larger alveoli
  • hence the larger alveoli will be overventilated, and smaller alveoli underventilated
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18
Q

What problems does surface tension create?

A

1) Tendency of collapse
2) Alveoli become unequal
3) Alveoli become wet (high T pulls transudate)

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19
Q

How is surfactant produced?

A

It is made + stored in Type 2 pneumocytes as lamillar bodies, and then secreted as tubular myelin.

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20
Q

What is surfactant?

A

Dipalmitoyl phosphatidylchloline - A molecule with hydrophobic (2x palmitoyl) + hydrophilic (phosphate, choline + apoproteins) regions.

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21
Q

How does surfactant decrease surface tension?

A

The DPPC molecules insert themselves into the H20 layer, therefore disrupting the unopposed H20 attractions (intermolecular forces - hydrogen bonding) that lead to surface tension.

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22
Q

What is the special defence function of the A+D apoproteins?

A

A+D apoproteins of the DPPC molecule are opsonins - they bind bacteria to facilitate phagocytosis by macrophages

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23
Q

What are the physiological advantages of surfactant?

A

By decreasing surface tension, surfactant:

  • increases lung compliance => reduces WOB
  • Stabilises alveoli (decreases collapsing pressure (P=2T/r) and reduces tendency of smaller alveoli to empty into larger)
  • Keeps alveoli dry (prevents transudation of capillary fluid)
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24
Q

What are the consequences of loss of surfactant? And what is a pathological example of this?

A
  • stiff lungs (low compliance)
  • atelectasis
  • oedema (transudate into alveoli)
    Occurs in neonatal Respiratory Distress Syndrome
25
Q

What is alveolar interdependence?

A

Interdependence refers to the support offered to lung units by those surrounding them, which resists collapse of individual units.

26
Q

CO2 + O2 TRANSPORT

A

-

27
Q

What volume of O2 is delivered to the tissues per minute?

A

250ml/min of O2

28
Q

What volume of CO2 is produced by tissues per minute?

A

200ml/min of CO2

29
Q

GAS DIFFUSION

A

All gases move across the alveolar wall (blood-gas barrier) by passive diffusion

30
Q

What is Fick’s Law?

A

Fick’s Law states that the rate of transfer of a gas through a sheet of tissue is:
proportional to the tissue area, partial pressure gradient and solubility of the gas
inversely proportional to tissue thickness and molecular weight of the gas

31
Q

What are some key features and measurements of the blood-gas interface?

A

Extremely thin - 0.2-0.3 um
Enormous surface area - 50-100m2 - by having 500 million alveoli
So thin that large increases in capillary pressure can damage barrier.

32
Q

What layers does O2 cross when diffusing across the blood-gas barrier from alveolar gas to Hb?

A

surfactant, epithelial cell, interstitium, endothelial cell, plasma, RBC membrane

33
Q

What are some key features of pulmonary capillaries?

A

They form a dense network in the alveolar walls.
Capillary diameter is 7-10 um, just enough for RBC
RBC spends 0.75 s in the capillaries

34
Q

What are key features of the conducting zone?

A
  • Consists of trachea, bronchi, bronchioles to terminal bronchioles (first 16 generations).
  • cartilage in walls
    = anatomic dead space = 150ml
  • blood supply from bronchial circulation (mere fraction of pulmonary circulation)
  • convectional airflow
35
Q

What are key features of the respiratory zone?

A
  • Consists of respiratory bronchioles, alveolar ducts + alveolar sacs (each unit called acinus), gens 17-23
  • smooth muscle walls
  • 2.5-3L volume
  • Gas movement by diffusion
36
Q

What has been shown about regional differences in ventilation?

A

In subjects who inhale radioactive xenon gas, ventilation per unit volume -
lower> upper lung (standing)
posterior > anterior (supine)

37
Q

Explain the helium dilution technique

A

FRC and RV cannot be measured with simple spirometry - to measure FRC, subject is connected to spirometer with known Conc of helium (insoluble in blood).
After some breaths, helium concentration in lung + spirometer equilibrate.

38
Q

What is alveolar ventilation equation and it’s importance?

A

Alveolar ventilation VA = VCO2/PCO2 x K
In normal subjects PACO2 + PaCO2 are identical, so arterial can be used.
VA is inversely proportional to PCO2 - i.e. halving the alveolar ventilation with double PCO2 (assuming constant CO2 production)

39
Q

Which gases are diffusion or perfusion limited?

A

CO - diffusion limited
NO - perfusion limited
O2 - perfusion limited under normal conditions (diffusion limited at altitude)

40
Q

What is the Hb molecule?

A

Hb is a tetramer - each monomer is made up of:
a protoporhyrin ring with central ferrous iron (Fe2+)
globin protein tail

41
Q

Describe the 3 main types of haemoglobin

A

HbA - 2 alpha + 2 Beta chains (Adult)
HbA2 - 2 alpha + 2 delta chains (normal variant present in low levels in adults)
HbF - 2 alpha + 2 gamma (fetal, replaced over first 6 months of life)

42
Q

What is methemoglobin?

A

Normal HbA can have its ferrous ion (Fe2+) oxidised to ferric form (methemoglobin) by various drugs/chemicals - nitrites, sulphonamides, acetanilide.
Congenital deficiency of methemoglobin reductase - imparts oxygen binding/release to tissues

43
Q

How is oxygen carried in the blood?

A

In 2 ways - dissolved O2 + Hb bound

44
Q

Dissolved O2 obeys Henry law, which means that..

A

the amount dissolved is proportional to partial pressure.

For each mmHg PO2, there is 0.003ml O2/100ml blood.

45
Q

So normal arterial blood contains how much dissolved O2?

A

At PaO2 100: 0.003 x 100 = 0.3ml O2/100ml blood

46
Q

How much O2 can 1g Hb bind?

A

1.39 ml / g

47
Q

What is the oxygen carrying capacity of Hb in 100ml arterial blood?

A

If a person has Hb concentration 15 g/100ml
15 x 1.39 = 20.85 ml O2 / 100ml.
(One can then add 0.3 ml dissolved O2 to calculate total O2 concentration in 100ml blood)

48
Q

In general, O2 concentration in the blood is given by..

A

(1.39 x Hb x Sat/100) + (0.003 x PO2)

49
Q

Compare the normal O2 saturations + volumes, in arterial + mixed venous blood.
What is the minute delivery of O2 to tissues (resting state)?

A

Arterial P02 100 mmHg - 97.5% - approx 20ml O2
Venous PO2 40 mmHg - 75% - approx 15ml O2
So 5ml O2 is delivered to tissues / 100ml blood.
If resting CO is 5L/min, 50 x 5 = 250ml O2/min

50
Q

What is positive cooperativity?

A

O2 binding at the Fe2+ site, increases affinity of next site for O2

51
Q

What are the key anchor points on the Oxygen dissociation curve?

A

PO2 100 mmHg => SO2 97%
PO2 40 mmHg => SO2 75%
P50 = 27 mmHg => SO2 50% (useful measure of L or R shift)

52
Q

What are the physiological advantages of the shape of the oxygen dissociation curve?

A

The flat upper portion - falls in PO2 have little effect on SO2
The steep lower portion - peripheral tissues can withdraw large amounts of O2 for only small drop in PO2

53
Q

What factors shift the oxygen dissociation curve to the right?

A 
Right shift (reduced Hb-O2 affinity) is caused by:
Increased H+, PCO2, temperature and 2,3-DPG in RBC
- enhances O2 delivery to metabolically active tissues
54
Q

What factors shift the oxygen dissociation curve to the left?

A 
Left shift (increased Hb-O2 affinity) is caused by:
Decreased 2,3-DPG, HbF
55
Q

What factors alter production of 2,3-DPG?

A

2-3-DPG is produced by RBC in chronic hypoxia - e.g. high altitudes, chronic lung diseaseWIt’s levels are low in stored blood for transfusions

56
Q

What is the effect of carbon monoxide on the oxygen dissociation curve?

A

CO has 240 x more affinity than O2 for Hb - so even a small amount of CO will bind up significant amounts of Hb in the blood.
COHb (carboxyhemoglobin) is not able to carry O2 - hence it will shift the curve downwards
Hb concentration and PO2 will remain normal, but SO2 will be significantly reduced.
COHb also impairs oxygen unloading, so shifts curve left

57
Q

How do anaemia and polycythemia affect the curve?

A

Anaemia - decreased Hb = decreased O2 carrying capacity, curve shifted down
Polycythemia - increased Hb = increased O2 capacity, curve shifted upward

58
Q

What is the Bohr effect?

A

The Bohr effect describes the rightward shift of the oxygen dissociation curve with increased PCO2 - mostly attributable to the rise in H+ - acidic Hb has lower affinity for O2 (favours O2 dissociation + release to tissues)

59
Q

How is CO2 carried in the blood?

A

In 3 forms -

1) Dissolved CO2 (24 x more soluble than O2, 0.067 ml/100ml/mmHg, also obeys Henry law)
2) Bicarbonate HCO3-
3) Carbamino compounds (CarbaminoHb)

Physiology (9 decks)

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