physiology Flashcards

1
Q

what is internal respiration?

A

the intracellular mechanisms which consumes O2 and produces CO2

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2
Q

what is external respiration?

A

the sequence of events that lead to the exchange of O2 and CO2 between the external environment and the cells of the body
4 stages

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3
Q

what are the stages of external respiration?

A
  1. ventilation - moving gas in and out of the lungs
  2. gas exchange - O2 from alveoli to blood
  3. the binding and transport of gasses in blood stream
  4. gas exchange - O2 from blood to tissues
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4
Q

what are the body systems involved in external respiration?

A
  • respiratory system
  • cardiovascular system
  • haematology system
  • nervous system
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5
Q

definition of ventilation

A

the mechanical process of moving air between the atmosphere and alveolar sacs

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6
Q

boyle’s law

A

as the volume of gas increases, the pressure exerted by the gas decreases

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7
Q

what holds the thoracic wall and the lungs in close opposition?

A
  1. the intrapleural fluid cohesiveness = the water molecules in the intrapleural fluid are attracted to each other and resist being pulled apart. hence the pleural membranes tend to stick together
  2. the negative intrapleural pressure = the SUB-ATMOSPHERIC intrapleural pressure creates a transmural pressure gradient across the lung wall and across the chest wall. so the lungs are forced to expand outwards while the chest is forced to squeeze inwards
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8
Q

what is the equation for transmural pressure gradient across lung wall?

A

Palv - Pip

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9
Q

what is the equation for the transmural pressure gradient across thoracic wall?

A

Patm - Pip

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10
Q

what happens during inspiration?

A
  • active process depending on muscle contraction
  • the volume of the thorax is increased vertically by contraction of the diaphragm, flattening out it’s dome shape
  • the external intercostal muscle contraction lifts the ribs and moves out the sternum - bucket handle mechanism
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11
Q

what does inspiration result in?

A
  • increased size of lungs
  • so intra-alveolar pressure falls because air molecules becomes contained in a larger volume
  • air then enters the lungs down it’s pressure gradient
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12
Q

what happens during expiration?

A
  • passive process
  • chest wall and stretched lungs recoil
  • recoil of lungs make the intra-alveolar pressure rise because air becomes contained in a smaller volume
  • sir then leaves the lungs down it’s concentration gradient
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13
Q

what is pneumothorax?

A
  • air in the pleural space
  • can be spontaneous traumatic or iatrogenic
  • it can abolish transmural pressure gradient leading to lung collapse
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14
Q

what are the signs of pneumothorax?

A
  • symptoms include shortness or breath and chest pain

- physical signs include hyperresonant percussion note and decreased breath sounds

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15
Q

how do lungs recoil during expiration?

A
  • elastic connective tissue in the lungs causes the structure to bounce back into shape
  • alveolar surface tension
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16
Q

what is alveolar surface tension?

A
  • attraction between water molecules at liquid air interface
  • in the alveoli this produces a force which resists the stretching of the lungs
  • if the alveoli were lines with eater along, the surface tension would be too strong so the alveoli would collapse
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17
Q

what does surfactant do?

A

reduces the alveolar surface tension by interspersing between the water molecules lining the alveoli, preventing the smaller alveoli from collapsing

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18
Q

LaPlace’s law

A
P = 2T/r
P = inward directed collapsing pressure
T = surface tension
r = radius of the bubble
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19
Q

respiratory distress syndrome of new born

A
  • premature babies may not have enough pulmonary surfactant
  • this causes respiratory distress syndrome of the new born
  • the baby makes very strenuous inspiratory efforts in an attempt to overcome the high surface tension and inflate the lungs
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20
Q

what is alveolar interdependence?

A
  • helps keep alveoli open
  • in an alveolus starts to collapse, the surrounding alveoli are stretched and then recoil, exerting expanding forces in the collapsing alveolus to open it
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21
Q

what are the forces that keep alveoli open?

A
  • transmural pressure gradient
  • pulmonary surfactant
  • alveolar interdependence
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22
Q

what are the forces promoting alveolar collapse?

A
  • elasticity of stretched lung connective tissue

- alveolar surface tension

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23
Q

what are the major inspiratory muscles?

A
  • diaphragm

- external intercostal muscles

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24
Q

what are the accessory muscles of inspiration?

A
  • (contracts only during forceful inspiration)
  • sternocleidomastoid
  • scalenus
  • pectoral
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25
Q

what are the muscles of active expiration?

A

(contracts only during active expiration)

  • abdominal muscles
  • internal intercostal muscle
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26
Q

tidal volume (TV)

A
  • volume of air entering or leaving lungs during a single breath
  • 0.5L
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27
Q

inspiratory reserve volume (IRV)

A
  • extra volume of air that can be maximally inspired over and above the typical resting tidal volume
  • 3.0L
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28
Q

expiratory reserve volume (ERV)

A
  • extra volume of air that can be actively expired by maximal contraction beyond the normal volume of air after a resting tidal volume
  • 1.0L
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29
Q

Residual volume (RV)

A
  • Minimum volume of air remaining in the lungs even after a maximal expiration
  • 1.2L
  • REST
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30
Q

Inspiratory Capacity (IC)

A

Maximum volume of air that can be inspired at the end of a normal quiet expiration
(IC =IRV + TV)
3.5L

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31
Q

Functional Residual Capacity (FRC)

A

Volume of air in lungs at end of normal passive expiration (FRC = ERV + RV)
2.2L

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32
Q

Forced Vital Capacity (FVC)

A

Maximum volume of air that can be moved out during a single breath following a maximal inspiration (VC = IRV + TV + ERV)
4.5L

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33
Q

Total Lung Capacity (TLC)

A

Total volume of air the lungs can hold
(TLC = VC + RV)
5.7L
- residual volume and lung volume can’t be measured by spirometry

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34
Q

when does residual volume increase?

A

when the elastic recoil of the lungs is lost eg in emphysema

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35
Q

forced vital capacity (FVC)

A

maximum volume that can be forcibly expelled from the lungs following a maximum inspiration

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36
Q

forced expiratory volume in one second (FEV1)

A

volume of air that can be expired during the first second of expiration in an FVC determination

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37
Q

FEV1/FVC ratio

A

FEV1/FVC x 100 = normally more than 70%

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38
Q

equation for airflow

A
F = detlaP/R
F = flow
P = pressure
R = resistance
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39
Q

dynamic airway compression

A
  • pressure applied to alveolus helps push air out of lungs

- pressure applied to airway compresses it

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40
Q

increased airway resistance in in dynamic airway compression

A
  • causes an increase in airway pressure upstream = helps open airways by increasing the driving pressure between the alveolus and airway
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41
Q

dynamic airway compression during active expiration in patients with airway obstruction

A
  • if there is an obstruction eg asthma of COPD, the driving pressure between the alveolus and airway is lost over the obstructed segment
  • this causes a fall in airway pressure along the airway downstream
  • resulting in airway compression by the rising pleural pressure during active expiration
42
Q

peak flow meter

A
  • assesses airway function

- useful in patients with obstructive lung disease eg asthma or COPD

43
Q

pulmonary compliance

A

a measure of effort that has to go into stretching of distending the lungs

44
Q

decreased pulmonary compliance

A
  • decreased by = pulmonary fibrosis, pulmonary oedema, lung collapse, pneumonia, absence of surfactant
  • great change in pressure required to produce a change in volume = causes shortness of breath on exertion
  • may cause a restrictive pattern of lung volumes in spirometry
45
Q

increased pulmonary compliance

A
  • increased if elastic recoil of lungs is lost
  • occurs in emphysema = patients have to work harder to get air out of lungs
  • increases with age
46
Q

when is work of breathing increased?

A
  • when pulmonary compliance is decreased
  • when airway resistance is increased
  • when elastic recoil is decreased
  • when there is a need for increased ventilation
47
Q

pulmonary ventilation (L)

A

= tidal volume x respiratory rate

- volume of air breathed in and out per minute

48
Q

alveolar ventilation

A

(tidal volume - dead space volume) x respiratory rate

- volume of air exchanged between atmosphere and alveoli per minute

49
Q

how to increase pulmonary ventilation

A
  • increase both depth (mainly) and rate of breathing
50
Q

ventilation perfusion

A
  • the rate at which gas and blood flows through the lungs

- average arterial and alveolar partial pressures of O2 are not the same but difference is not significant

51
Q

alveolar dead space

A
  • ventilated alveoli which are not adequately perfused with blood are considered as alveolar dead space = the anatomical dead space + . the alveolar dead space
  • can increase significantly in disease
52
Q

ventilation perfusion match in the lungs

A
  • local control act on smooth muscles of airways and arterioles to match airflow to blood flow
  • accumulation of CO2 in alveoli as a result of increased perfusion decreases airway resistance leading to increased airflow
  • increased in alveolar O2 concentration as a result of increased ventilation causes pulmonary vasodilation which increases blood flow to match larger airflow
53
Q

when is perfusion (rate of blood flow) greater than ventilation (rate of airflow)

A
  • when CO2 increases in an area
  • when O2 decreases in an area
  • dilation of local airways
  • constriction of local blood vessels
  • airflow increase
  • blood flow decreases
54
Q

factors that influence the rate of gas exchange across alveolar membrane

A
  1. partial pressure gradient of O2 and cO2
  2. diffusion coefficient for O2 and CO2
  3. surface area of alveolar membrane
  4. thickness of alveolar membrane
55
Q

dalton’s law of partial pressure

A

the total pressure exerted by a gaseous mixtures = the sum of partial pressures of each individual component in the as mixture

56
Q

partial pressure of gas

A

the pressure that one gas in a mixture of gases would exert if it were the only gas present in the whole volume occupied by the mixture at a given tmie

57
Q

partial pressure of oxygen in alveolar air

A
PAO2 = partial pressure of O2 in alveolar air
PiO2 = partial pressure of O2 in inspired air
PaCO2 = partial pressure of CO2 in arterial blood
PAO2 = PiO2-(PACO2/0.8)
58
Q

what does a large gradient between PAO2 ad PaO2 indicate?

A

problems with gas exchange in the lungs or a right to left shunt in the heart

59
Q

alveoli membrane

A
  • thin walled inflatable sacs
  • function in gas exchange
  • walls consist of a single layer of flattened type 1 alveolar cells
60
Q

henry’s law

A

as we increase partial pressure (gas) the concentration of gas in the liquid phase will decrease proportionally

61
Q

what is the normal kPa of Po2

A

13.3 kPa

62
Q

in which form is most of the O2 travelling through the body?

A
  • bound to haemoglobin

- the other is physically dissolved

63
Q

oxygen binding to haemoglobin

A
  • reversible
  • each Hb molecule has 4 haem groups
  • haemoglobin is fully saturated when it’s carrying it’s maximum O2
64
Q

what is PO2?

A

the primary factor which determines the percentage saturation of haemoglobin with O2

65
Q

oxygen delivery index (DO2I)

A

= CaO2 x Cl

- oxygen delivery to the tissues is a function of oxygen content of arterial blood and the cardiac output

66
Q

oxygen content of arterial blood (CaO2)

A

= 1.34 x [Hb] x SaO2

  • the O2 content of arterial blood is determined by haemoglobin concentration [Hb and the saturation of Hb with O2
  • one gram of Hb carries 1.34ml of Ow when fully saturated
67
Q

what sis oxygen delivery to tissues impaired by?

A
  • respiratory disease = these can decrease arterial PO2 and hence decrease Hb saturation with O2 and O2 content of blood
  • heart failure = this decreases cardiac output
  • anaemia = this decreases Hb concentration and hence decreases O2 content of the blood
68
Q

what does partial pressure of oxygen depend on?

A
  1. total pressure (eg atmospheric pressure)

2. proportion of oxygen in gas mixtures (21% in atmosphere)

69
Q

what is the bohr effect?

A

increased release of O2 by Hb at tissues - sigmoid shifts to the right

70
Q

foetal haemoglobin (HbF)

A
  • higher affinity for O2
  • this allows O2 to transfer from mother to foetus even if the PO2 is low
  • 2 alpha and 2 gamma subunits
71
Q

myoglobin

A
  • present in skeletal and cardiac muscles
  • only one haem group oer myoglobin molecule
  • no cooperative binding of O2
  • hyperbolic dissociation curve
  • releases O2 at very low PO2
  • provides short term storage of O2 for anaerobic conditions
72
Q

what would indicate muscle damage?

A

presence of myoglobin in the blood

73
Q

how is CO2 transported in the blood?

A
  1. as solution
  2. as bicarbonate = formed in the body by carbonic anhydrase and occurs in red blood cells
  3. as carbamino compounds = formed by combination of CO2 with terminal amine groups in blood proteins, reduced Hb can bind more CO2 than HbO2
74
Q

where does CO2 bind to haemoglobin to form carbamino compounds?

A

globin part

75
Q

the haldane effect

A

removing O2 from Hb increases the ability of Hb to pick-up CO2 and CO2 generated H+

76
Q

what happens when Hb picks up O2 at the lungs?

A

it weakens it’s ability to bind CO2 and H+

77
Q

what is neural control of respiration?

A
  • the rhythm: inspiration followed by expiration
  • normal ventilation retained if section above the medulla
  • ventilation ceases if section below the medulla
78
Q

what part of the brain is the major rhythm generator?

A

the medulla

79
Q

what is the breathing rhythm generated by?

A
  • the pre-botzinger complex
  • it displays pacemaker activity
  • located near the upper end of the medullary respiratory centre
80
Q

what gives rise to inspiration?

A
  • rhythm generated by pre-botzinger complex
  • excites dorsal respiratory group neurones (inspiratory)
  • fire in bursts
  • firing leads to contraction of inspiratory muscles = inspiration
  • when firing stops, passive expiration
81
Q

what happens in active expiratory during hyperventilation?

A
  • increased firing of doral neurones excites a second group called ventral respiratory group neurons
  • these excite internal intercostals, abdominals etc
    = forceful expiration
82
Q

in normal quiet breathing, do ventral neurones activate expiratory muscles?

A

No

83
Q

what do neurones in the pons do?

A
  • modify the rhythm generated in the medulla

-

84
Q

what does the pneumotaxic centre (PC) do?

A
  • stimulation of it terminates inspiration
  • PC stimulated when dorsal respiratory neurones fire
    = inspiration inhibited
85
Q

what would happen without PC?

A

breathing is prolonged inspiratory gasps with brief expiration = apneusis

86
Q

what is the apneustic centre?

A
  • impulses from these neurones excite inspiratory area of medulla = prolonging inspiration
87
Q

what are respirator centres influenced by?

A

stimuli received from:

  • higher brain centres eg cerebral cortex
  • stretch receptors in walls of bronchi (hering-breur reflex)
  • joint receptors -stimulated by joint movement
  • baroreceptors - increased ventilatory rate in response to decreased blood pressure
  • centreal chemoreceptors
  • peripheral chemoreceptors
88
Q

examples of involuntary modifications of breathing

A
  • pulmonary stretch receptors hering-breur reflex
  • joint receptors reflex in exercise
  • stimulation of respiratory centre by temperature, adrenaline, or impulses from cerebral cortex
  • cough reflex
89
Q

what are pulmonary stretch receptors?

A
  • activated during inspiration, afferent discharge inhibits inspiration - hering-breur reflex
  • unlikely to switch off inspiration during normal respiratory cycle
90
Q

what are joint receptors?

A
  • impulses from moving limbs reflexly increase breathing

- probably contribute to the increase ventilation during exercise

91
Q

factors that increase ventilation during exercise

A
  • reflexes originating from body movement
  • adrenaline release
  • impulses from the cerebral cortex
  • increase in body temperature
  • later: accumulation of CO2 and H+ generated by active muscles
92
Q

what is the cough reflex?

A
  • helps clear airway of dust/dirt
  • activated by irritation of airways or tight airways
  • centre in the medulla
93
Q

what does afferent discharge stimulate?

A
  • short intake of breath
  • closure of larynx
  • contraction of abdominal muscles
  • opening of the larynx and expulsion of air at high speed
94
Q

what is chemical control of respiration?

A
  • example of negative feedback control system
  • controlled variables are blood gas tensions, esp CO2
  • chemoreceptors sense the valves of gas tensions
95
Q

what are peripheral chemoreceptors?

A

they sense tension of O2 and CO2 and H+ in the blood

96
Q

what are central chemoreceptors?

A
  • situated near surface of medulla of brainstem
  • respond to H+ of the cerebrospinal fluid (CSF)
  • CSF os separated from the blood by the blood-brain barrier relatively impermeable to H+ and HCO3-, CO2 diffuses readily
  • CSF contains less proteins than blood ad hence is less buffered than blood
97
Q

what is the hypoxic drive of respiration?

A
  • the effect is all via peripheral chemoreceptors
  • stimulated only when arterial PO2 falls to low levels
  • is not important in normal respiration
  • may become important in patients with chronic CO2 retention
  • important at high altitudes
98
Q

what is hypoxia at high altitudes caused by?

A
  • decreased partial pressure of inspired oxygen (PiO2)
99
Q

what are the chronic adaptions to high altitude hypoxia?

A
  • RBC increased
  • 2,3 BPG increased
  • number of capillaries increased
  • number of mitochondria increased
  • kidneys conserve acid so arterial pH decreases
100
Q

what is the H+ drive of respiration?

A
  • effect is via peripheral chemoreceptors
  • H+ doesnt readily cross the BBB
  • peripheral chemoreceptors play a role in adjusting for acidosis caused by the addition of non-carbonic acid H+ to the blood
  • their stimulation by H+ causes hyperventilation and increases elimination of CO2 from the body
  • important in the acid-base balance