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
what are the muscles of active expiration?
(contracts only during active expiration) - abdominal muscles - internal intercostal muscle
26
tidal volume (TV)
- volume of air entering or leaving lungs during a single breath - 0.5L
27
inspiratory reserve volume (IRV)
- extra volume of air that can be maximally inspired over and above the typical resting tidal volume - 3.0L
28
expiratory reserve volume (ERV)
- 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
29
Residual volume (RV)
- Minimum volume of air remaining in the lungs even after a maximal expiration - 1.2L - REST
30
Inspiratory Capacity (IC)
Maximum volume of air that can be inspired at the end of a normal quiet expiration (IC =IRV + TV) 3.5L
31
Functional Residual Capacity (FRC)
Volume of air in lungs at end of normal passive expiration (FRC = ERV + RV) 2.2L
32
Forced Vital Capacity (FVC)
Maximum volume of air that can be moved out during a single breath following a maximal inspiration (VC = IRV + TV + ERV) 4.5L
33
Total Lung Capacity (TLC)
Total volume of air the lungs can hold (TLC = VC + RV) 5.7L - residual volume and lung volume can't be measured by spirometry
34
when does residual volume increase?
when the elastic recoil of the lungs is lost eg in emphysema
35
forced vital capacity (FVC)
maximum volume that can be forcibly expelled from the lungs following a maximum inspiration
36
forced expiratory volume in one second (FEV1)
volume of air that can be expired during the first second of expiration in an FVC determination
37
FEV1/FVC ratio
FEV1/FVC x 100 = normally more than 70%
38
equation for airflow
``` F = detlaP/R F = flow P = pressure R = resistance ```
39
dynamic airway compression
- pressure applied to alveolus helps push air out of lungs | - pressure applied to airway compresses it
40
increased airway resistance in in dynamic airway compression
- causes an increase in airway pressure upstream = helps open airways by increasing the driving pressure between the alveolus and airway
41
dynamic airway compression during active expiration in patients with airway obstruction
- 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
peak flow meter
- assesses airway function | - useful in patients with obstructive lung disease eg asthma or COPD
43
pulmonary compliance
a measure of effort that has to go into stretching of distending the lungs
44
decreased pulmonary compliance
- 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
increased pulmonary compliance
- 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
when is work of breathing increased?
- when pulmonary compliance is decreased - when airway resistance is increased - when elastic recoil is decreased - when there is a need for increased ventilation
47
pulmonary ventilation (L)
= tidal volume x respiratory rate | - volume of air breathed in and out per minute
48
alveolar ventilation
(tidal volume - dead space volume) x respiratory rate | - volume of air exchanged between atmosphere and alveoli per minute
49
how to increase pulmonary ventilation
- increase both depth (mainly) and rate of breathing
50
ventilation perfusion
- 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
alveolar dead space
- 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
ventilation perfusion match in the lungs
- 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
when is perfusion (rate of blood flow) greater than ventilation (rate of airflow)
- 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
factors that influence the rate of gas exchange across alveolar membrane
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
dalton's law of partial pressure
the total pressure exerted by a gaseous mixtures = the sum of partial pressures of each individual component in the as mixture
56
partial pressure of gas
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
partial pressure of oxygen in alveolar air
``` 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
what does a large gradient between PAO2 ad PaO2 indicate?
problems with gas exchange in the lungs or a right to left shunt in the heart
59
alveoli membrane
- thin walled inflatable sacs - function in gas exchange - walls consist of a single layer of flattened type 1 alveolar cells
60
henry's law
as we increase partial pressure (gas) the concentration of gas in the liquid phase will decrease proportionally
61
what is the normal kPa of Po2
13.3 kPa
62
in which form is most of the O2 travelling through the body?
- bound to haemoglobin | - the other is physically dissolved
63
oxygen binding to haemoglobin
- reversible - each Hb molecule has 4 haem groups - haemoglobin is fully saturated when it's carrying it's maximum O2
64
what is PO2?
the primary factor which determines the percentage saturation of haemoglobin with O2
65
oxygen delivery index (DO2I)
= CaO2 x Cl | - oxygen delivery to the tissues is a function of oxygen content of arterial blood and the cardiac output
66
oxygen content of arterial blood (CaO2)
= 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
what sis oxygen delivery to tissues impaired by?
- 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
what does partial pressure of oxygen depend on?
1. total pressure (eg atmospheric pressure) | 2. proportion of oxygen in gas mixtures (21% in atmosphere)
69
what is the bohr effect?
increased release of O2 by Hb at tissues - sigmoid shifts to the right
70
foetal haemoglobin (HbF)
- 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
myoglobin
- 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
what would indicate muscle damage?
presence of myoglobin in the blood
73
how is CO2 transported in the blood?
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
where does CO2 bind to haemoglobin to form carbamino compounds?
globin part
75
the haldane effect
removing O2 from Hb increases the ability of Hb to pick-up CO2 and CO2 generated H+
76
what happens when Hb picks up O2 at the lungs?
it weakens it's ability to bind CO2 and H+
77
what is neural control of respiration?
- the rhythm: inspiration followed by expiration - normal ventilation retained if section above the medulla - ventilation ceases if section below the medulla
78
what part of the brain is the major rhythm generator?
the medulla
79
what is the breathing rhythm generated by?
- the pre-botzinger complex - it displays pacemaker activity - located near the upper end of the medullary respiratory centre
80
what gives rise to inspiration?
- 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
what happens in active expiratory during hyperventilation?
- increased firing of doral neurones excites a second group called ventral respiratory group neurons - these excite internal intercostals, abdominals etc = forceful expiration
82
in normal quiet breathing, do ventral neurones activate expiratory muscles?
No
83
what do neurones in the pons do?
- modify the rhythm generated in the medulla | -
84
what does the pneumotaxic centre (PC) do?
- stimulation of it terminates inspiration - PC stimulated when dorsal respiratory neurones fire = inspiration inhibited
85
what would happen without PC?
breathing is prolonged inspiratory gasps with brief expiration = apneusis
86
what is the apneustic centre?
- impulses from these neurones excite inspiratory area of medulla = prolonging inspiration
87
what are respirator centres influenced by?
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
examples of involuntary modifications of breathing
- 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
what are pulmonary stretch receptors?
- activated during inspiration, afferent discharge inhibits inspiration - hering-breur reflex - unlikely to switch off inspiration during normal respiratory cycle
90
what are joint receptors?
- impulses from moving limbs reflexly increase breathing | - probably contribute to the increase ventilation during exercise
91
factors that increase ventilation during exercise
- 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
what is the cough reflex?
- helps clear airway of dust/dirt - activated by irritation of airways or tight airways - centre in the medulla
93
what does afferent discharge stimulate?
- short intake of breath - closure of larynx - contraction of abdominal muscles - opening of the larynx and expulsion of air at high speed
94
what is chemical control of respiration?
- example of negative feedback control system - controlled variables are blood gas tensions, esp CO2 - chemoreceptors sense the valves of gas tensions
95
what are peripheral chemoreceptors?
they sense tension of O2 and CO2 and H+ in the blood
96
what are central chemoreceptors?
- 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
what is the hypoxic drive of respiration?
- 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
what is hypoxia at high altitudes caused by?
- decreased partial pressure of inspired oxygen (PiO2)
99
what are the chronic adaptions to high altitude hypoxia?
- RBC increased - 2,3 BPG increased - number of capillaries increased - number of mitochondria increased - kidneys conserve acid so arterial pH decreases
100
what is the H+ drive of respiration?
- 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