Respiratory Flashcards

(128 cards)

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
What is the approx tidal volume?
500mL
26
What is the approx volume of alveolar ventilation?
350mL
27
Alveolar ventilation equation
(tidal volume - dead space) x frequency of breathing | (500mL - 150mL) x 12/min = 4200mL/min
28
Alveolar ventilation and dead space when breathing deeply
Increased tidal volume and decreased breathing frequency results in increased alveolar ventilation
29
Alveolar ventilation and dead space when taking short shallow breaths
tidal volume only as much as the dead space, so no matter how many breaths are taken nothing reaches the alveoli
30
Alveolar ventilation and dead space when breathing through a snorkel
Dead space increases but tidal volume increases to maintain alveolar ventilation
31
High compliance
Easy to breathe in, hard to breathe out
32
What happens to breathing if our lungs have low compliance?
Hard to breathe in, easy to breathe out
33
Emphysema
destruction of alveoli = decreased elastic recoil and increased compliance, hard to breathe out
34
Pulmonary fibrosis
Restrictive lung disease, stiff alveolar walls = low compliance, hard to breathe in, shallow rapid breaths
35
Lung compliance and elastic recoil depend on:
Elasticity and surface tension at alveoli
36
Elastic fibres account for ....% of the elastic recoil
25% | Resistance to stretching
37
Surface tension accounts for ....% of the elastic recoil
75% | Alveoli want to collapse, but surfactant reduces this surface tension
38
Surfactant is produced by what type of cells?
Type II pneumocytes
39
Does surfactant increase or decrease lung compliance?
Increase: allows easy inspiration by not letting alveoli walls stick together
40
Respiratory distress syndrome
Premature babies cannot synthesise surfactant causing lung collapse and death
41
Airways resistance is due to:
Friction 1. Viscosity of air 2. Length of pathway (fixed) 3. Diametre/radius (varies)
42
Resistivity proportional to radius?
r is proportional to 1/r^4 Therefore: R = 4r 2R = 16r
43
lateral/radial traction
elastic tissues outside airways linking to surrounding tissue, increasing transpulmonary pressure which pull airways open
44
chemical factors effecting bronchi radii
blockages by mucus or inflammation | Local inflammators like histamine and leukotrienes causing smooth muscle to contract (bronchoconstriction)
45
neural factors effecting bronchi radii
stimulation of parasympathetic nerves to airways
46
Determinants of airway radius
Physical (lateral traction and elastic recoil) Chemical (inflammation and mucus) Neural (effecting amount of constriction)
47
Volume of O2 breathed per minute assuming: tidal volume = 500mL, breathing frequency = 8 breaths/min 21% of air is O2
840mL entering the alveoli per minute
48
concentration of O2 in the arteries
200ml/L | 1000mL total in the 5L of blood
49
amount of O2 passing into capillaries from alveoli | per minute
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
50
amount of O2 passing from capillaries into tissues | per minute
250mL 1000mL of O2 in arteries, 750mL in veins as 250mL of O2 is put into tissues could also say 50ml/L
51
Amount of CO2 breathed out per minute
200mL
52
conc of CO2 in the arteries
2600mL | 520ml/L
53
conc of CO2 in the veins
2800mL | 540ml/L
54
conc of O2 in the veins
750mL | 150ml/L
55
Respiratory quotient equation and definition
VCO2/VO2 | Volume of CO2 breathed out compared to O2 breathed in
56
Respiratory quotient depends on:
Depends on the food consumed and metabolised, what macronutrient is being broken down
57
Normal respiratory quotient for a normal mixed diet
RQ = 200mL of CO2 / 250mL of O2 = 0.8
58
Respiratory quotient for carbs
0.8 | 6O2 -> 6CO2
59
Respiratory quotient for fat
0.7
60
Boyles Law
Increase in volume = decrease in pressure P1V1 = P2V2
61
Daltons Law
Partial pressure of gases | Each individual gas will have its own partial pressure in a space (PO2, PCO2)
62
Sum of partial pressures of gases
Two partial pressures will add to a total pressure
63
PO2 in air
Partial pressure of O2 in the atmospheric air is 160mmHg (21% of total 760mmHg)
64
Partial pressure equation
P = fractional concentration x total pressure | percent of the gas in the total
65
PAO2 (partial pressure of O2 in the alveoli)
105mmHg
66
PACO2 (partial pressure of CO2 in the alveoli)
40mmHg
67
Factors affecting PAO2 (partial pressure of O2 in the alveoli)
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
Factors affecting PACO2 (partial pressure of CO2 in the alveoli)
Pio2 - almost always 0 VA - Volume of fresh air getting to alveoli Vo2 - how much CO2 is being produced by the body
69
Henry's Law
The number of O2 molecules entering the liquid is proportional to the Po2 in the gas
70
Diffusion of gases in a liquid (Henrys Law explained)
A gas will diffuse into a liquid until an equilibrium is reached - Rate of diffusion is proportional to the partial pressure
71
PvO2
40mmHg
72
PvCO2
46mmHg
73
PaO2
100mmHg
74
PaCO2
40mmHg
75
Factors effecting diffusion
Thickness of alveolar walls Conc/pressure gradient Surface area Diffusion coefficient for the gas
76
Fick's Law of diffusion
Rate of diffusion = | (Diffusion constant of gas x surface area x partial pressure of gas) / thickness
77
Pulmonary Oedema
Fluid leaks out of the pulmonary capillaries into the interstitial space, reducing the rate of O2 diffusion
78
Interstitial Fibrosis
Thickening of the alveolar wall reducing the rate of O2 diffusion
79
Emphysema
Destruction of alveolar walls reducing the surface area for diffusion and number of pulmonary capillaries
80
Ventilation/perfusion mismatching - lung diseases - gravity
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
Ventilation/perfusion mismatching - lung diseases - gravity
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
Minimising ventilation/perfusion mismatching (constriction) Diverts blood and airflow to healthy areas of the lung
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
Hb dissolves ....mL of O2 for every L of blood
197mL by Hb | 3mL dissolved into plasma for 200mL total
84
Hb conc in blood
150g/L
85
How to find the O2 content (mL of O2/L of blood) =mL/L
[Hb] x 1.34 x (%saturated/100)
86
Max amount of O2+Hb in the blood
1.34 x [Hb] 1.34 x 150mL O2/L = 201mL O2/L of blood
87
Each gram of Hb can carry ...mL of O2
1.34mL
88
Percent O2 saturation
= the amount of O2 bound to Hb / maximal capacity of Hb to bind O2 = 98% = percent saturation of arterial blood
89
Venous blood O2 saturation percent
75%
90
Advantage of Steepness of the O2-Hb dissociation curve
Large quantities of O2 can be offloaded from Hb with only a small decrease in PO2
91
Advantages of the plateau of the O2-Hb dissociation curve
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
P50
The affinity of Hb for O2 at which Hb is 50% saturated
93
Increased affinity of Hb for O2
reduced P50 | left shift
94
Reduced P50
Increased affinity of Hb for O2 left shift facilitates loading of O2 on to Hb
95
Decreased affinity of Hb for O2
Increased P50 | right shift
96
Increased P50
Decreased affinity of Hb for O2 right shift facilitates release of O2 from Hb
97
Bohr Effect
Increased release of O2 at high CO2/low pH Increased P50 Rightwards shift
98
Bohr Effect in lungs vs Haldane in working tissues
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
Movement of O2 from lungs capillaries
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
Movement of O2 from capillaries to working tissue
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
Carbamino haemoglobin (HbCO2)
30% of CO2 bound as HbCO2 | Binds to the globin in the RBC
102
Bicarbonate (HCO3-)
60% of CO2 bound as HCO3-
103
Conversion of CO2 to HCO3-
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
Movement of CO2 from blood to lungs
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
CO2 - blood dissociation curve
relationship between the PCO2 of blood and the amount of CO2 in the blood (in all 3 forms)
106
Haldane Effect
The effect presence of O2 has on CO2 and H+ (opposite of Bohr)
107
Blood buffers (3)
H+ binding to hemoglobin in RBC Carbonic acid- bicarbonate buffer H+ binding to other plasma proteins
108
DeoxyHb and blood buffering
binds H+ - buffers acid
109
Respiratory acidosis
Caused by reduced ventilation (not breathing out CO2 and H+) and increased production of H+
110
Respiratory alkalosis
Caused by increased ventilation (breathing out too much CO2 and H+) and decreased production of H+
111
How to fix respiratory acidosis
Breathe more
112
What detects respiratory acidosis and alkalosis
Chemoreceptors
113
How to fix respiratory alkalosis
Breathe deeper/slower into a paper bad to breathe in more CO2 and bring levels back to normal
114
Generation of rhythmic breathing (involuntary control) - where in brain?
Medulla oblongata Neurons in the inspiratory centre also spontaneously discharge to induce muscle contraction to breathe in
115
Inspiratory and Expiratory neurons are R... I.... to stop firing at the same time
reciprocally inhibitive | both send inhibitory signals to the opposite centres
116
Forced breathing (voluntary control) - controlled by where in brain? and acts on where?
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
Sensory input in involuntary control of breathing (2 receptors)
Mechanoreceptors and chemoreceptors to cause reflex readjustment in response to exercise, irritants and environmental changes
118
Chemo/Mechanoreceptors communicate to the medulla oblongata via the......
NTS Nucleus of Tractus Solitarius Located in periphery
119
Protective reflexes
Sneezing is caused by irritation of the nasal mucosa and stimulates mechanoreceptors Coughing is caused by irritation of the larynx and stimulates mechanoreceptors
120
Peripheral chemoreceptors
Vagus nerve and glossopharyngeal nerve
121
Hypoxia
decrease in arterial PO2
122
Hypercapnia
increase in arterial PCO2
123
Hypoxia, hypercapnia and acidosis all cause an ...
increase in ventilation
124
Peripheral chemoreceptors are stimulated by (3):
Hypoxia Hypercapnia Acidosis
125
Central chemoreceptors are sensitive to:
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
Ventilation is not stimulated until you reach an arterial PO2 of .....mmHg
60mmHg
127
A small increase in arterial PCO2 leads to a large increase in ventilation T/F?
TRUE
128
Metabolic Alkalosis (increased pH) is caused by:
loss of H+ | can be caused by sustained vomiting