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Physiology Modules 3-5 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Respiration definition

A

The metabolic respiration of oxygen by cells and the process by which gaseous exchange occurs between an organism and its environment

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2
Q

Upper airway ends at…

A

larynx

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3
Q

Lower airway starts at….

A

trachea

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4
Q

Structures of the chest wall in to out

A

lung, visceral pleura, pleural cavity, parietal pleura, chest wall

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5
Q

What is the pleural cavity filled with?

A

Intrapleural fluid

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6
Q

What lines the surface of the lung?

A

visceral pleura

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7
Q

What does the visceral pleura line?

A

lung

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8
Q

What lines the surface of the chest wall?

A

parietal pleura

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9
Q

What does the parietal pleura line?

A

chest wall

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10
Q

What does the high branching of bronchi cause?

A

Large surface area for gas exchange and therefore greater rate of diffusion and huge number of alveoli respirating

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11
Q

Is the chest wall recoil tendency inwards or outwards?

A

Outwards

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12
Q

Is the lung elastic recoil tendency inwards or outwards?

A

Inwards (collapse)

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13
Q

What is “negative pressure”

A

A suction pressure due to chest wall expansion, increase in pressure of intrapleural fluid and therefore suctions the visceral pleura to expand the lungs

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14
Q

What is “negative pressure”

A

A suction pressure due to opposite recoil forces causing adherence between the two pleura

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15
Q

Pip

A

Intrapleural pressure (relative to Patm) = -4mmHg

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16
Q

Patm

A

Atmospheric pressure at 760mmHg or 1013Pa

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17
Q

Palv

A

Alveolar pressure (relative to Patm) = 0 (same as atmospheric)

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18
Q

Ptp

A

Transpulmonary pressure: pressure difference between alveoli and the pleural cavity (force acting to expand the lungs)

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19
Q

Transpulmonary pressure

A

Force required to expand the lung, determined by the difference between alveolar pressure and elastic recoil of the chest wall
4mmHg (Palv - Pip)

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20
Q

Elastic recoil of chest wall

A

-4mmHg (Pip - Patm)

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21
Q

Alveolar Dead Space

A

Some alveoli are insufficiently perfused and don’t contribute to gas exchange

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22
Q

Physiological Dead Space

A

= anatomical dead space + alveolar dead space

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23
Q

Minute ventilation

A

total tidal volume into the lungs per minute (Tidal volume x frequency of breathing)

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24
Q

What is the approx volume of dead space?

A

150mL

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25
Q

What is the approx tidal volume?

A

500mL

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26
Q

What is the approx volume of alveolar ventilation?

A

350mL

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27
Q

Alveolar ventilation equation

A

(tidal volume - dead space) x frequency of breathing

(500mL - 150mL) x 12/min = 4200mL/min

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28
Q

Alveolar ventilation and dead space when breathing deeply

A

Increased tidal volume and decreased breathing frequency results in increased alveolar ventilation

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29
Q

Alveolar ventilation and dead space when taking short shallow breaths

A

tidal volume only as much as the dead space, so no matter how many breaths are taken nothing reaches the alveoli

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30
Q

Alveolar ventilation and dead space when breathing through a snorkel

A

Dead space increases but tidal volume increases to maintain alveolar ventilation

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31
Q

High compliance

A

Easy to breathe in, hard to breathe out

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32
Q

What happens to breathing if our lungs have low compliance?

A

Hard to breathe in, easy to breathe out

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33
Q

Emphysema

A

destruction of alveoli = decreased elastic recoil and increased compliance, hard to breathe out

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34
Q

Pulmonary fibrosis

A

Restrictive lung disease, stiff alveolar walls = low compliance, hard to breathe in, shallow rapid breaths

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35
Q

Lung compliance and elastic recoil depend on:

A

Elasticity and surface tension at alveoli

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36
Q

Elastic fibres account for ….% of the elastic recoil

A

25%

Resistance to stretching

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37
Q

Surface tension accounts for ….% of the elastic recoil

A

75%

Alveoli want to collapse, but surfactant reduces this surface tension

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38
Q

Surfactant is produced by what type of cells?

A

Type II pneumocytes

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39
Q

Does surfactant increase or decrease lung compliance?

A

Increase: allows easy inspiration by not letting alveoli walls stick together

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40
Q

Respiratory distress syndrome

A

Premature babies cannot synthesise surfactant causing lung collapse and death

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41
Q

Airways resistance is due to:

A

Friction

  1. Viscosity of air
  2. Length of pathway (fixed)
  3. Diametre/radius (varies)
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42
Q

Resistivity proportional to radius?

A

r is proportional to 1/r^4
Therefore:
R = 4r
2R = 16r

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43
Q

lateral/radial traction

A

elastic tissues outside airways linking to surrounding tissue, increasing transpulmonary pressure which pull airways open

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44
Q

chemical factors effecting bronchi radii

A

blockages by mucus or inflammation

Local inflammators like histamine and leukotrienes causing smooth muscle to contract (bronchoconstriction)

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45
Q

neural factors effecting bronchi radii

A

stimulation of parasympathetic nerves to airways

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46
Q

Determinants of airway radius

A

Physical (lateral traction and elastic recoil)
Chemical (inflammation and mucus)
Neural (effecting amount of constriction)

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47
Q

Volume of O2 breathed per minute assuming:
tidal volume = 500mL,
breathing frequency = 8 breaths/min
21% of air is O2

A

840mL entering the alveoli per minute

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48
Q

concentration of O2 in the arteries

A

200ml/L

1000mL total in the 5L of blood

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49
Q

amount of O2 passing into capillaries from alveoli

per minute

A

250mL
840mL into alveoli - 250mL going into blood = 590mL leaving capillaries

(per minute and of the 4000mL breathed in that minute)

could also say 50ml/L

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50
Q

amount of O2 passing from capillaries into tissues

per minute

A

250mL
1000mL of O2 in arteries, 750mL in veins as 250mL of O2 is put into tissues

could also say 50ml/L

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51
Q

Amount of CO2 breathed out per minute

A

200mL

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52
Q

conc of CO2 in the arteries

A

2600mL

520ml/L

53
Q

conc of CO2 in the veins

A

2800mL

540ml/L

54
Q

conc of O2 in the veins

A

750mL

150ml/L

55
Q

Respiratory quotient equation and definition

A

VCO2/VO2

Volume of CO2 breathed out compared to O2 breathed in

56
Q

Respiratory quotient depends on:

A

Depends on the food consumed and metabolised, what macronutrient is being broken down

57
Q

Normal respiratory quotient for a normal mixed diet

A

RQ
= 200mL of CO2 / 250mL of O2
= 0.8

58
Q

Respiratory quotient for carbs

A

0.8

6O2 -> 6CO2

59
Q

Respiratory quotient for fat

A

0.7

60
Q

Boyles Law

A

Increase in volume = decrease in pressure

P1V1 = P2V2

61
Q

Daltons Law

A

Partial pressure of gases

Each individual gas will have its own partial pressure in a space (PO2, PCO2)

62
Q

Sum of partial pressures of gases

A

Two partial pressures will add to a total pressure

63
Q

PO2 in air

A

Partial pressure of O2 in the atmospheric air is 160mmHg (21% of total 760mmHg)

64
Q

Partial pressure equation

A

P = fractional concentration x total pressure

percent of the gas in the total

65
Q

PAO2 (partial pressure of O2 in the alveoli)

A

105mmHg

66
Q

PACO2 (partial pressure of CO2 in the alveoli)

A

40mmHg

67
Q

Factors affecting PAO2 (partial pressure of O2 in the alveoli)

A

Pio2 - How much O2 inspired from the atmosphere
VA - Volume of fresh air getting to alveoli
Vo2 - how much O2 is being used by the body

68
Q

Factors affecting PACO2 (partial pressure of CO2 in the alveoli)

A

Pio2 - almost always 0
VA - Volume of fresh air getting to alveoli
Vo2 - how much CO2 is being produced by the body

69
Q

Henry’s Law

A

The number of O2 molecules entering the liquid is proportional to the Po2 in the gas

70
Q

Diffusion of gases in a liquid (Henrys Law explained)

A

A gas will diffuse into a liquid until an equilibrium is reached
- Rate of diffusion is proportional to the partial pressure

71
Q

PvO2

A

40mmHg

72
Q

PvCO2

A

46mmHg

73
Q

PaO2

A

100mmHg

74
Q

PaCO2

A

40mmHg

75
Q

Factors effecting diffusion

A

Thickness of alveolar walls
Conc/pressure gradient
Surface area
Diffusion coefficient for the gas

76
Q

Fick’s Law of diffusion

A

Rate of diffusion =

(Diffusion constant of gas x surface area x partial pressure of gas) / thickness

77
Q

Pulmonary Oedema

A

Fluid leaks out of the pulmonary capillaries into the interstitial space, reducing the rate of O2 diffusion

78
Q

Interstitial Fibrosis

A

Thickening of the alveolar wall reducing the rate of O2 diffusion

79
Q

Emphysema

A

Destruction of alveolar walls reducing the surface area for diffusion and number of pulmonary capillaries

80
Q

Ventilation/perfusion mismatching

  • lung diseases
  • gravity
A

Emphysema causes blood to go to alveoli that cant undergo gas exchange and bronchitis/asthma causes mucus to block airflow to particular areas of the lung
Gravity causes lower portions of the lung to receive more blood supply

81
Q

Ventilation/perfusion mismatching

  • lung diseases
  • gravity
A

Emphysema causes blood to go to alveoli that cant undergo gas exchange and bronchitis/asthma causes mucus to block airflow to particular areas of the lung
Gravity causes lower portions of the lung to receive more blood supply

82
Q

Minimising ventilation/perfusion mismatching
(constriction)

Diverts blood and airflow to healthy areas of the lung

A

Vasoconstriction of blood vessels to portions of the lung that don’t receive airflow
Bronchoconstriction of bronchioles to decrease airflow to areas not receiving blood

83
Q

Hb dissolves ….mL of O2 for every L of blood

A

197mL by Hb

3mL dissolved into plasma for 200mL total

84
Q

Hb conc in blood

A

150g/L

85
Q

How to find the O2 content (mL of O2/L of blood) =mL/L

A

[Hb] x 1.34 x (%saturated/100)

86
Q

Max amount of O2+Hb in the blood

A

1.34 x [Hb]
1.34 x 150mL O2/L
= 201mL O2/L of blood

87
Q

Each gram of Hb can carry …mL of O2

A

1.34mL

88
Q

Percent O2 saturation

A

= the amount of O2 bound to Hb / maximal capacity of Hb to bind O2
= 98%
= percent saturation of arterial blood

89
Q

Venous blood O2 saturation percent

A

75%

90
Q

Advantage of Steepness of the O2-Hb dissociation curve

A

Large quantities of O2 can be offloaded from Hb with only a small decrease in PO2

91
Q

Advantages of the plateau of the O2-Hb dissociation curve

A

It allows Hb to keep a good O2 saturation even if atmospheric pressure (then Palv and Parterial) fell to 60mmHg (still about 90% saturated) like at a high altitude or if you had a lung disease

92
Q

P50

A

The affinity of Hb for O2 at which Hb is 50% saturated

93
Q

Increased affinity of Hb for O2

A

reduced P50

left shift

94
Q

Reduced P50

A

Increased affinity of Hb for O2
left shift
facilitates loading of O2 on to Hb

95
Q

Decreased affinity of Hb for O2

A

Increased P50

right shift

96
Q

Increased P50

A

Decreased affinity of Hb for O2
right shift
facilitates release of O2 from Hb

97
Q

Bohr Effect

A

Increased release of O2 at high CO2/low pH
Increased P50
Rightwards shift

98
Q

Bohr Effect in lungs vs Haldane in working tissues

A

When we take O2 into the blood, Hb is supposed to carry O2 and very little CO2, therefore low in H+ and blood has a left shift and can bind O2 stronger

When blood reaches working tissue, it has produced CO2 and H+ and caused the curve to shift to the right, meaning Hb doesn’t bind O2 as strongly /less affinity/ lose saturation and will offload the O2 to the working tissue

Shifting of the curve fits intended purpose for where we need O2 offloading

99
Q

Movement of O2 from lungs capillaries

A

O2 moving from atmosphere into alveoli due to the partial pressure gradient between blood and air

O2 dissolves into plasma and Hb soaks up O2 out of solution driving more O2 to dissolve into the plasma
This occurs until the Hb is 98% saturated
Get highest amount of O2 possible in the blood

100
Q

Movement of O2 from capillaries to working tissue

A

The blood transports O2 to the working tissue
PP gradient between tissue and blood drives the offloading of O2 from Hb into the plasma then into the tissue
This is facilitated by the lower binding affinity due to environment - low pH high CO2
At the same time Hb is picking up CO2 from tissues

101
Q

Carbamino haemoglobin (HbCO2)

A

30% of CO2 bound as HbCO2

Binds to the globin in the RBC

102
Q

Bicarbonate (HCO3-)

A

60% of CO2 bound as HCO3-

103
Q

Conversion of CO2 to HCO3-

A

Once in RBC (contains carbonic anhydrase) - the CO2 can be converted into bicarbonate and H+

Reaction between CO2 and water creates 2 osmotically active particles (bicarbonate and H+ ions)

H+ is buffered quickly
HCO3- is osmotically active and carries a negative charge
A build up causes the bicarbonate to move out (down conc gradient) into the plasma, and therefore to maintain electroneutrality and osmolarity, a CL- moves into the RBC and pulls water in with it

As blood cell travels around, we would see it swell as it enters the venous circulation and shrink (lost water) in the arterial circulation

104
Q

Movement of CO2 from blood to lungs

A

When the CO2 comes back to the alveoli, the processes reverse
CO2 comes out of plasma to alveoli down partial pressure difference drive

Drives the dissociation of CO2 off the globin into the plasma then out of capillary
Also reverses the Cl- shift, bicarbonate HCO3- goes back into the RBC, Cl- and water move out and the bicarbonate is converted back to CO2 and then comes back out of RBC and out of plasma to lungs to be breathed out

105
Q

CO2 - blood dissociation curve

A

relationship between the PCO2 of blood and the amount of CO2 in the blood (in all 3 forms)

106
Q

Haldane Effect

A

The effect presence of O2 has on CO2 and H+ (opposite of Bohr)

107
Q

Blood buffers (3)

A

H+ binding to hemoglobin in RBC
Carbonic acid- bicarbonate buffer
H+ binding to other plasma proteins

108
Q

DeoxyHb and blood buffering

A

binds H+ - buffers acid

109
Q

Respiratory acidosis

A

Caused by reduced ventilation (not breathing out CO2 and H+) and increased production of H+

110
Q

Respiratory alkalosis

A

Caused by increased ventilation (breathing out too much CO2 and H+) and decreased production of H+

111
Q

How to fix respiratory acidosis

A

Breathe more

112
Q

What detects respiratory acidosis and alkalosis

A

Chemoreceptors

113
Q

How to fix respiratory alkalosis

A

Breathe deeper/slower into a paper bad to breathe in more CO2 and bring levels back to normal

114
Q

Generation of rhythmic breathing (involuntary control) - where in brain?

A

Medulla oblongata

Neurons in the inspiratory centre also spontaneously discharge to induce muscle contraction to breathe in

115
Q

Inspiratory and Expiratory neurons are R… I…. to stop firing at the same time

A

reciprocally inhibitive

both send inhibitory signals to the opposite centres

116
Q

Forced breathing (voluntary control) - controlled by where in brain? and acts on where?

A

Cerebral cortex - sends inhibitory signals directly to respiratory muscle’s motor neurons in the spinal cord (bypassing the respiratory centres (in medulla oblongata) that act on the expiratory muscles, inspiratory muscles, and diaphragm

Cerebral cortex takes over for medulla oblongata

117
Q

Sensory input in involuntary control of breathing (2 receptors)

A

Mechanoreceptors and chemoreceptors to cause reflex readjustment in response to exercise, irritants and environmental changes

118
Q

Chemo/Mechanoreceptors communicate to the medulla oblongata via the……

A

NTS
Nucleus of Tractus Solitarius
Located in periphery

119
Q

Protective reflexes

A

Sneezing is caused by irritation of the nasal mucosa and stimulates mechanoreceptors

Coughing is caused by irritation of the larynx and stimulates mechanoreceptors

120
Q

Peripheral chemoreceptors

A

Vagus nerve and glossopharyngeal nerve

121
Q

Hypoxia

A

decrease in arterial PO2

122
Q

Hypercapnia

A

increase in arterial PCO2

123
Q

Hypoxia, hypercapnia and acidosis all cause an …

A

increase in ventilation

124
Q

Peripheral chemoreceptors are stimulated by (3):

A

Hypoxia
Hypercapnia
Acidosis

125
Q

Central chemoreceptors are sensitive to:

A

CO2
The concentration of H+ in the brain ECF
- source of H+ is CO2, which can pass the blood-brain barrier and is then converted into H+ and HCO3- and the H+ is then detected and ventilation increases

126
Q

Ventilation is not stimulated until you reach an arterial PO2 of …..mmHg

A

60mmHg

127
Q

A small increase in arterial PCO2 leads to a large increase in ventilation T/F?

A

TRUE

128
Q

Metabolic Alkalosis (increased pH) is caused by:

A

loss of H+

can be caused by sustained vomiting

Physiology Modules 3-5 (7 decks)

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