Respiratory System Flashcards
1
Q
general function of respiratory system
A
to obtain O2 for use by the body’s cells, and to eliminate the CO2 the body’s cells produce
2
Q
what is another name for internal respiration
A
cellular respuration
3
Q
describe internal respiration
A
- oxidative phosphorylation
- refers to metabolic processes and carried out within the mitochondria, which use O2 and produce CO2 while deriving energy from nutrient molecules
4
Q
four steps of external respiration
A
- has exchange between the atmosphere and alveoli in the lung
- exchange of O2 and CO2 between air in the alveoli and the blood in the pulmonary capillaries
- Transport of O2 and CO2 by the blood between the lungs and the tissues
- Exchange of O2 and CO2 between the blood in the systematic capillaries and the tissue cells
* respiration occurs now
5
Q
seven secondary functions of the respiratory system
A
- Short term pH regulation
- Enables vocalisation
- Aids in defense againt pathogens in the airways
- Removes, modifies, activates (i.e. angiotensin II), or inactivates (i.e. prostaglandins) various materials passing through the pulmonary circulation
- Eliminates heat and water
- Assists venous return
- Nose is the organ of smell
6
Q
three componenents of upper airways
A
- Nasal cavity
- Oral cavity
- Pharynx (common passageway for respiratory and digestive systems)
7
Q
three componenents of respiratory airways
A
- Larynx
- Conducting zone
- Respiratory zone
8
Q
important point of conduction zone
A
it’s an anatomical dead space
9
Q
why is the conducting zone an anatomical dead space
A
no gases are exchanged even though air is moving through it
10
Q
what does the respiratory zone consist of
A
bronchi, bronchioles and alveoli
11
Q
six structures of the conducting zone
A
- trachea
- primary bronchi
- secondary bronchi
- tertiary bronchi
- bronchioles
- terminal bronchioles
12
Q
dimensions of the trachea
A
2.5 cm diameter, 10 cm long
13
Q
what is the trachea made up of
A
C-shaped bands of cartilage for structural rigidity
14
Q
how many secondary bronchi on the right side
A
3
15
Q
how many secondary bronchi on the left side
A
2
16
Q
bronchiole diameter
A
less than 1mm
17
Q
functions of the conducting zone
A
- Air passageway (150ml volume - dead space)
- Increase air temperature to body temperature
- Humidify air
18
Q
two types of cells in the conducting zone
A
goblet and cilliated
19
Q
important point about bronchiole composition
A
they have no cartilage, thus there is a risk of collapse
to prevent this they have walls of elastic fibres and smooth muscle
20
Q
goblet cell function
A
secrete mucus and traps foreign particles
21
Q
cilliated cell function
A
propel the mucus up the glottis to be swallowed or expelled
22
Q
clinical consideration regarding cilliated cells
A
Smoking stops cilliated cells from working as effectively - thus smokers cough a lot
23
Q
four main structures of respiratory zone
A
- Respiratory bronchioles
- Alveolar ducts
- Alveolar sacs
- Alveoli
24
Q
function of respiratory zone
A
Exchange of gases between air and blood by diffusion
25
what are alveoli
site of gas exchange
26
what is the respiratory membrane made up of
- Alveoli: Type 1 cells and basement membrane
- Capillaries: Endothelial cells and basement membrane
27
how many alveoli per lung
200-500 million
28
comment on blood supply of alveoli
They have a rich blood supply as capillaries form a sheet over each alveolus
29
what is collateral ventilation
alveoli have pores (pore of Kohn) which permit airflow between adjacent alveoli in case one stops working
30
name the three alveoli cell types
- type I alveolar cells
- type II alveolar cells
- alveolar macrophages
31
function of type I alveolar cells
Make up wall of alveoli, single layer epithelial cells
32
function of type II alveolar cells
- Secrete surfactant
- Reduces surface tension in alveolar walls
- Helps prevent alveolar collapse
33
purpose of alveolar macrophages
Remove foreign particles
34
how thick is the respiratory membrane
0.2 microns
35
name the three main pressure considerations
- atmospheric pressure
- intra-alveolar pressure
- intrapleural pressure
36
another name for atmospheric pressure
barometric
37
another name for intra-alveolar pressure
intrapulmonary pressure
38
another name for intrapleural pressure
intrathoracic
39
what is atmospheric pressure at sea level (in mmHg)
760 mmHg
40
what is the relationship between atmospheric pressure and altitude
as altitude increases atmospheric pressure decreases
41
what is intra-alveolar pressure
pressure of air within alveoli in the lungs
42
is intra-alveolar pressure an open or closed system
open
43
what is intra-alveolar pressure during inspiraion
negative - less than atmospheric pressure
44
what is intra-alveolar pressure during expiration
positive - more than atmospheric pressure
45
what drives ventilation
the difference between intra-alveolar pressure (Palv) and atmospheric pressure Patm
46
what is intra-pleural pressure
pressure inside teh pleural sac
47
is intra-pleural pressure an open or closed system
closed
48
what is intrapleural pressure at rest (in mmHg)
756 (-4) mmHg
49
why is intrapleural pressure negative
- due to the elacisity in the lungs and chest wall
- Lungs recoil inward
- Chest walls recoil outwards
- Opposing forces pull on the intrapleural space
- The surface tension of the intrapleural fluids holds the wall and lungs together - this si because H2O molecules are polar and attract eachother
- Sub-atmospheric pressure is due to a vacuum in the pleural cavity
50
what does at rest mean
between breaths - no movement of air
51
how to calculate teh transmural pressure gradient across teh lung wall
the intra-alveolar pressure take away the intrapleural pressure
52
how to calculate the transmural pressure gradient across the thoracic wall
the atmospheric pressure take away the intrapleural pressure
53
what is a pneumothorax
a punctured lung
54
how does a pneumothorax occur
- Occurs when pleural cavity is punctured
- It looses its negative pressure
- The lung then collapses
- The thorax expands
- Only happens to one lung because the pleural sacs are seperate
55
two types of pneumothorax
traumatic and spontaneous
56
explain traumatic pneumothorax
- Puncture wound in chest wall
- Can come about due to a stab wound
57
explain spontaneous pneumothorax
- Caused by a hole in the lung
- Can be caused by emphesma
58
boyle's law
pressure is inversely related to volume in an airtight container (closed system) - therefore, if the volume doubles, the pressure halves
59
mechanics of breathing formula
- R = resistance to airflow - this resistance is related to the radius of airways and mucus
60
two factors determining intra-alveolar pressure
- Quantity of air in alveoli
- Volume of alveoli
61
waht happens to intra-alveolar pressure during inspiration
- Lungs expand - therefore volume of alveolar pressure increases (this requires muscles)
- Palv decreases
- Pressure gradient forces air into the lungs
- Quantity of air in the alveoli rises
- Palv increases
62
what happens to intra-alveolar pressure during expiration
- Lungs recoil - therefore alveolar volume decreases (passive - no muscles required)
- Palv increases
- Pressure gradient forces air out of lungs
- Quantity of air in the alveoli decreases
- Palv decreases
63
what is happening to muscles before inspiration
- External intercostal muscles are relaxed
- Diaphragm is relaxed
64
what are muscles doing during inspiration
- External intercostal muscles contract
- Contraction of external intercostal muscles causes rib elevation, increasing side-to-side dimension of thoracic cavity
- Rib cage becomes elevated
- Elevation of ribs causes sternum to move up and out, increasing front-to-back dimension of thoracic cavity
- Diaphragm contracts
- Lowering of diaphragm upon contraction increases vertical dimension of thoracic cavity
65
what are muscles doing during passive expiration
- Relaxation of external intercostal muscles
- Relaxation of diaphragm
- Return of diaphragm, ribs and sternum to resting position on relaxation of inspiratory muscles restores thoracic cavity to pre-inspiratory size
66
what are muscles doing during active expiration
- Contraction of internal intercostal muscles
- This flattens ribs and sternum, further reducing side-to-side and front-to-back dimensions of thoracic cavity
- Contraction of abdominal muscles
- This causes diaphragm to be pushed upward, further reducing vertical dimension of thoracic cavity
- All of this creates higher air pressure, facilitating increased air flow
67
what are the principle muscles of inspiration
- External intercostals - elevate ribs
- Interchondral part of internal intercostals - elevate ribs
- Diaphragm - domes descend, increasing longitudinal dimension of chest and elevating lower ribs
68
what are teh accessory muscles of inspiration
- Sternocleidomastoid - elevates sternum
- Scalenus (anterior, middle and posterior) - elevate and fix upper ribs
69
why are there no muscles involved in quiet expiration
because it results from passive recoil of lungs
70
what are the muscles involved in active expiration
- Internal intercostals except interchondral part
- Abdominal muscles - depress lower ribs, compress abdominal contents
- Rectus abdominus
- External Oblique
- Internal oblique
- Transversus abdominus
71
two factors affecting pulmonary ventilation
- lung compliance
- airway resitance
72
what is lung compliance
- Ease with which lungs can be stretched
- The less compliant the lungs are, the more work is required to achieve a given degree of inflation
73
what is lung compliance affected by
elasticity and surface tension of lungs
74
what is airway resistance affected by
passive forces, contractile activity of smooth muscle and mucus secretion
75
how much of total energy expenditure does quiet breathing require
3%
76
four times the work of breathing is increased
- When pulmonary compliance is decreased
- When airway resistance is increased
- When elastic recoil is decreased
- When there is a need for increased ventilation
77
what is tidal volume
amount of air moved in and ou in quiet breath
78
tidal volume total
| healthy adult male
500ml
79
what is inspiratory reserve volume
amount of air which can be breathed in at once
80
inspiratory reserve volume total
| healthy adult male
3000ml
81
what is inspiratory capacity
anount of air that fits in lings
82
what is inspiratory capacity total
| healthy adult male
3500ml
83
what is expiratory reserve volume
amount of air that can be breathed out aditionally
84
wah is expiratory reserve volume total
| healthy adult male
1000ml
85
what is residual volume
air left in lungs (cannot be measured by a spirometer)
86
what is residual volume total
| healthy adult male
1200ml
87
what is functional residual capacity
volume after quiet expiration
88
what is funcitional residual capacity total
| healthy adult male
2200ml
89
what is vital capacity
how much air can be breathed out from maximal expiration
90
what is vital capacity total
4500ml
91
what is total lung capacity
total air that can be breathed in or out
92
what is total lung capacity total
| healthy adult male
5700ml
93
pulmonary minute ventilation
total volume of air entering and leaving the respiratory system wach minute
94
minute ventialtion calculations
- Minute ventilation = tidal volume x RR
- Normal rate of respiration = 12 breaths
- Normal tidal volume = 500ml
- Normal minute ventilation = 500ml x 12 breaths/min = 6000ml
95
alveolar minute ventilation
Volume of air exchanged between the atmosphere and the alveoli per minute
96
alveolar minute ventilation calculations
Alveolar ventilation = (tidal volume - dead space) x RR = (500-150)ml x 12 breaths/min = 4200ml
97
which is more important: alveolar or pulmonary minute ventilation
alveolar
98
Which is smaller: alveolar or pulmonary minute ventilation and why
Less than pulmonary ventilation due to anatomical dead space
99
what does CO2 do to increase airflow when there is large blood flow and small airflow
increase in Co2 in area → relaxation of local airway smooth muscle → dilation of local airways → decrease in airway resistance → increase in airflow
100
what does O2 do to decrease blood flow when there is large blood flow and small airflow
decrease in O2 in area → increase in contraction of local pulmonary-arteriolar smooth muscle → constriction of local blood vessels → increase in vascular resistance → decrease in blood flow
101
what does CO2 do to reduce airflow when there is large airflow and small blood flow
decrease of CO2 in area → increase in contraction of local airway smooth muscle → constriction of local airways → increase in airway resistance → decrease in airflow
102
what does O2 do to increase bloodflow when there is large airflow but low blood flow
increase in O2 in area → relaxation of local pulmonary-arteriolar smooth muscle → dilation of local blood vessels → decrease in vascular resistance → increase in blood flow
103
what is ventilation
airflow
104
what is perfusion
blood supple
105
what is the ventilation in L/min at the top of the lung
0.24
106
what is the perfusion in L/min at the top of the lung
0.07
107
what is the ventilation - perfusion ratio at the top of the lung
3.40
108
what is ventilation in L/min at the bottom of the lung
0.82
109
what is perfusion in L/min at the bottom of the lung
1.29
110
what is the ventilation-perfusion ratio at the bottom of the lung
0.63
111
why is perfusion higher than ventilation at the bottom of the lung
because gravity affects perfusion more than ventilation (blood vs air)
112
two main classifications of respiratory diseases
obstructive and restrictuve
113
what occurs in obstructive diseases
- Airway narrowing
- Increased airway resistance
- Reduced flow during expiration
114
three examples of obstructive respiratory diseases
emphysema, chronic bronchitis, asthma
115
explain restrictive respiratory dieases
- Reduced compliance (ease with which we expand the lungs)
- Scar tissue formation
- Fibrosis
116
an example of a restrictive respiratory disease
pulmonary fibrosis
117
four other respiratory conditions
| not classed as restrictive or obstructive
- Diseases impairing diffusion of O2 and CO2
- Neuromuscular disorders
- Inadequate perfusion
- Ventilation-perfusion imbalances
118
explain asthma
- Airway hyper-reactivity
- Reversible airway narrowing
- Muscous thickening
- Smooth muscle constriction by spasms in small airways
- Most common childhood respiratory disease
- When severe, narrowing could be lethal
119
causes of asthma
- Allergens, pollens, animal fur, dust
- Smoking, smog, airborne pollutants
- Changes in air temperature, humidity, pressure
- Exercise
- Emotional stress, anxiety
120
treatment of asthma
bronchodilators, anti-inflammatory. O2
121
is asthma obstructive or restrictive
obstructive
122
explain chronic bronchitis
-Inflammation of airway walls
- Excessive mucous production
- Airway narrowing and coughing (cough does not remove mucous)
- Reversible
123
Causes of chronic bronchitis
- Bacterial and viral infections
- Smoking
- Airborne pollutants
- Chronic irritation (seen in miners)
124
is chronic bronchitis obstructive or restrictive
obstructive
125
explain emphysema
- Irreversible
- Destruction of alveolar walls (collapsing of small airways)
- Enlargement of air spaces
- Primarily distal to terminal bronchioles
- Increased lung compliance via:
- Destruction of elastic fibres
- Excessive release of the enzyme trypsin - macrophages secrete α anti-trypsin to inhibit trypsin, but with chronic irritation trypsin can break alveolar walls
126
causes of emphysema
- Smoking induced inflammation
- Cilia destruction, tar accumulation
- Airborne contaminants
- Genetic - lack of α anti-trypsin production
127
is emphysema obstructive or restrictive
obstructive
128
explain pulmonary fibrosis
- Diffuse Interstitial Lung Disease (DILL) - larger type of diseases
- Results from over 130 disorders
- Reduced elasticity
- Reduced compliance of lung and chest wall
- Increased work of breathing
- Slim patients - breathing takes up a lot of their energy
129
causes of pulmonary fibrosis
- No known cause in 2/3 of cases
- Breathing in asbestos fibres
- Inflammation
- Scar tissue formation
130
is pulmonary fibrosis restrictive or obstructive
restrictive
131
total lung capacity in obstructive dieases
normal or increased
132
total lung capacity in restrictive dieases
decreased
133
residual volume in obstructive diseases
very increased - lungs cannot empty properly
134
residual volume in restrictive dieases
normal or decreased
135
vital capacity in obstructive diseases
decreased
136
vital capacity in restrictive diseases
decreased
137
functional residual capacity in obstructive diseases
inreased
138
functional residual capacity in restrictive diseases
normal or decreased
139
inspiratory capactiy in obstructive diseases
decreased
140
inspiratory capacity in restrictive diseases
very decreased
141
obstructive or restrictive and why
obstructive as FRC is larger than normal as lungs cannot be emptied as fast as they should be
142
obstructive or restrictive
obstructive
143
obstructive or restrictive and why
IRV is much lower than normal - inspiratory effort is compromised which reduced total lung capacity
144
obstructive or restrictive
restrictive
145
what is total pressure of gases
the sum of all partial pressures
146
what does the partial pressure of a gas depend on
- Fractional concentration of the gas
- Total pressure of the gas mixture
147
gas composition of air at 0% humidity
148
composition of gas in air at 100% humidity
149
rate of diffusion formula
Vgas = rate of diffusion
A = surface area (normally between 50 and 100 mm2 in lung)
T = thickness (normally 0.2-0.5µm)
ΔP = pressure difference
D = diffusion constant
150
diffusion constant formula
S = gas solubility
MW = molecular weight
151
gas solubility of CO2
24
152
gas solubility of O2
1
153
molecular weight of CO2
44
154
molecular weight of O2
32
155
how long is capillary transit time (blood in capilary) at rest
0.75 seconds
156
what is equilibration time reduced to during intense exercise
0.25 seconds
157
two things that affect the diffusion process in the lung
- exercise
- thickening of blood-gas barrier
158
what pathology are highly-trained athletes at risk of
Exercise Induced Arterial Hypoxemia (EAIH)
159
What is Pulmonary Oedema
Fluid accumulation in alveoli and/or interstitial space
160
what does pulmonary oedema do
- Impairs diffusion (greater distance from alveoli to blood)
- Leakage in unprotected capillaries
- Increases work of breathing (decreased lung compliance)
- Arterial blood: lower PO2 and higher PCO2
161
causes of pulmonary oedema
- Increased capillary pressure via left heart failure (inability to supply sufficient blood flow)
- Reduced atmospheric pressure at altitude
162
treatment of pulmonary oedema
administering oxygen and diuretics
163
how many mls of oxygen in every litre of arterial blood
200ml
164
what percentage of O2 in blood is dissolved in plasma
1.5%
165
what percentage of oxygen in arterial blood is bound to haemoglobin
98.5%
166
structure of haemoglobin
Four sub-units - each with one haem group and one globin
167
oxyhaemoglobin
Haemoglobin bound to oxygen
168
deoxyhaemoglobin
Unbound haemoglobin
169
function of haemoglobin
to increase oxygen-carrying capability of blood
170
where is haemoglobin found
red blood cells
171
what is the Hemoglobin-Oxygen Dissociation Curve
a graph that displays how easily oxygen is bound and unbound to haemoglobin
172
waht does a shift of the haemoglobin-oxygen dissociative curve to the right indicate
- decreased affinity meaning a higher PO2 is required to achieve a level of oxygen saturation
- Oxygen is unloaded more easily from haemoglobin, making it more available to tissues
173
what does a shift of the haemoglobin-oxygen dissociative curve to the left indicate
- increased affinity meaning a lower PO2 is required to achieve a level of oxygen saturation
- Oxygen is loaded more easily onto haemoglobin
174
what percentage of carbon dioxide is dissolved
10%
175
what percentage of carbond dioxide is bound to haemoglobin
30%
176
what percentage of carbon dioxide is transported in the form of bicarbonate ios
60%
177
carbon dioxide transport formula
178
hypoxia
Insufficient cellular O2
179
hyperoxia
Too much arterial O2 - O2 toxicity
180
hypocapnia
Excess PaCO2
181
hypocapnia
Below normal PaCO2
182
Model of Respiratory Control During Quiet Breathing
sensory input/pons/cortex → central pattern generator (medulla) → inspiratory neurons of DRG and VRG (medulla → breathing rhythm
183
what do chemoreceptors detect
PO2 and PCO2 changes
184
what do pulmonary stretch receptors detect
(Hering-breuer reflex): Inflation and deflation
185
what do irritant receptors detect
Dust and pollutants (trigger coughing/sneezing)
186
two types of chemoreceptor
central and peripheral
187
peripheral chemoreceptor location
- Carotid bodies - near baroreceptors in carotid sinus
- Aortic bodies - aortic arch
188
peripheral chemoreceptor function
- Respond to decreasing PaO2 (less than 60mmHg) - this is crucial when at an altitude
- Respond to increasing PaCO2 and increasing H+ - this provides 20% of respiratory drive
- Aortic bodies (although rarely) respond to decreasing total arterial O2 content - crucial for anaemia and carbon monoxide poisoning
189
central chemoreceptor loaction
medulla
190
central chemoreceptor function
- Directly respond to changes in H+ concentration in the CSF
- Specifically those ions converted from CO2 - not those circulating as they cannot cross the blood-brain barrier
- Therefore they indirectly respond to changes in the PaCO2
- Provide 80% of the respiratory drive
191
effects of arterial O2 on ventilation
- Declining arterial PO2 has little effect on minute ventilation until PO2 drops to less than 60 mmHg
- Response is due to the activation of peripheral chemoreceptors
192
Effects of Arterial CO2 on Ventilation
- Increasing arterial PCO2 has large effects on minute ventilation
- At a PCO2 greater than 90mmHg, coma and death can occur
- Effects are mediated through both central and peripheral chemoreceptors but Co2 must be converted to H+ first
193
Effects of Hypoventilation on Minute Ventilation
increasing PCO2, increasing H+ and decreasing PO2 in arterial blood → chemoreceptors detect and respond → respiratory control centre increases ventilation → negative feedback to step 1
194
Effects of Hyper-ventilation on Minute Ventilation
decreasing PCO2, decreasing H+ increasing PO2 in arterial blood → chemoreceptors detect and respond → respiratory control centre decreases ventilation → negative feedback to step 1
195
arterial pH
7.4
196
how does C2 maintain pH balance
- pH is directly related to H+ ion concentration
- CO2 is a source of H+ ions
197
acidosis
when arterial blood is excessively acidic - pH greater than 7.0
198
what does acidosis cause
- Depresses CNS activity
- Progress to coma and respiratory failure
199
alkalosis
when blood is excessively alkaline or basic
200
what does alkalosis do
- Increases CNS excitability causing uncontrollable muscle seizures and convulsions
- Can lead to death as a result of spasmodic contraction of respiratory muscles
200
bronchiole response to increased PcO2
Dilation (increased ventilation)
201
pulmonary arteriole response to increased PCO2
Weak constriction (decreased perfusion)
202
bronchiole response to decreased PCO2
Constriction (decreased ventilation)
203
Pulmonary arteriole response to decreased PCO2
Weak dilation (increased perfusion)
204
bronchiole response to increased PO2
Weak constriction (decreased ventilation)
205
pulmonary arteriole response to increased PO2
Dilation (increased perfusion)
206
Bronchiole response to decreased PO2
Weak dilation (increased ventilation)
207
pulmonary arteriole response to decreased PO2
Constriction (decreased perfusion)
208
cause of hyperventilation
decreased PaO2 acting on carotid body peripheral chemoreceptors - hypoxic ventilatory drive
209
body's response to hyperventilation
- CO2 clearance increases → blood pH increases → respiratory alkalosis (reduced ventilation)
- To prevent alkalosis: kidneys excrete bicarbonate ions → more acid remains in blood → alkalosis is reversed → pH is normal within 2-3 days
- Ventilation then increases again
- Reason for maintained ventilation is unknown
- Likely increases sensitivity to PaO2
210
what is Polycythaemia
- Increased red blood cell concentration in blood
- Increased haemoglobin content in blood
211
body's repsonse to Polycythaemia
- Decreased PaO2 (hypoxemia) stimulates erythropoietin (EPO) after about 3 hours (the peak is 24-48 hours)
- This comes from the kidney
- It acts in bone marrow
- Stimulate:
- Reticulocyte maturation and release
- Erythropoiesis
- Despite a decrease in PaO2 and thus a decrease in haemoglobin saturation (by the oxygen-haemoglobin dissociation curve) total O2 content may be normal or elevated
212
what causes elevated blood viscosity
Polycythaemia
213
what does elevated blood viscosity cause
- Increase in cardiac work (hypertrophy)
- Uneven blood flow distribution
214
what other adaptations to high altitudes are there
- Improved diffusion capacity via:
- Expanded surface area due to greater lung volume upon inflation
- Increased tissue capillarisation (angiogenesis) - occurs over days
- Endothelial cells release up to 10 times more nitric oxide (NO)
- Reduced skeletal muscle fibre size - occurs over weeks
- In conjunction with increased oxidative capacity and mitochondria numbers
215
symptoms of acute mountain sickness
- Headaches
- Loss of appetite
- Insomnia
- Nausea
- Vomiting
- Dyspnea
216
when is onset of actute mountain sickness symptoms
6-48 hours after ascent
216
when do the most severe sympotoms of acute mountain sickness occur
on days 2 and 3
217
why is acute mountain sickness worse at night
respiratory drive is reduced
218
what does incidence of acute mountain sickness vary by
altitude, rate of ascent and the individual’s susceptibility
219
what percentage of people experience symptoms of acture mountain sickness at elevations of 2,500-3,500 metres
15% but higher in women
220
what percentage of people experience symptoms of acute mountain sickness at elevations of greater than 3,500 metres
75% of individuals at least mild symptoms
221
what causes high altitude pulmonary oedema
pulmonary vasoconstriction (hypoxia)
222
what does high altitude pulmonary oedema lead to
- Fluid accumulation leads to persistent cough, shortness of breath, cyanosis of lips and fingernails and loss of consciousness.
- Could lead to high altitude cerebral oedema (fluid accumulation in cranial cavity)
223
treatment of high altitude pulmonary oedema
descending to lower altitude and supplemental oxygen
224
name four Altitude/Hypoxic Training Strategies to Maximise Sea-Level Performance in Athletes
- *Live high – train high (LHTH or HiHi)*
- *Live (or sleep) high – train low (LHTL or HiLo)*
- *Live low – train high (LLTH or LoHi)*
- *Intermittent hypoxia at rest*
225
describe live high-train high
- Benefit: increase red blood cell volume (>2000m x 3-4 weeks)
- Problem: difficult to train at same volume/intensity as at sea level
- There are few well controlled studies on elite athletes
226
describe live high -train low
- Most effective (altitude: 2100-2800m x 3-4 weeks)
- Problem: logistics and financial
- New modalities: Hypoxic tents (sleeping devices) or even hypoxic living apartments (>2000m x 3 weeks x >12h/day)
227
effects of live low-train high
weak if any
228
effects of intermittent hypoxia at rest
weak if any
229
what happens to gas pressures at depth
- total gas pressure increases
- partial gas pressures increase as well
230
what problems are caused to gas cavities (lung, middle ear) by increasing pressures at depth
- Compression with descent
- Over-expansion with ascent
231
nitrogen solubility at sea level
- N2 is poorly soluble
- Low amounts of dissolved N2 - no adverse effects
232
nitrogen solubility at depth
- Increase in N2 partial pressures → increase in N2 solubility
- This leads to a high amount of N2 being dissolved in blood, influencing ion regulation and excitable cells
233
nitrogen narcosis cause
Increased N2 solubility → reduced neuron excitability → nitrogen narcosis
234
nitrogen narcosis effects at 50m (150 ft)
“Cocktail” effect (euphoria and drowsiness)
235
nitrogen narcosis effects at 50-90m (150 - 300 ft)
- Fatigued and weak
- Loss of coordination
- Clumsiness
236
nitrogen narcosis effects at 100-120m (350 - 400 ft)
Lose consciousness
237
prevention of nitrogen narcosis
- Use N2 free gas
- Substitute helium for N2 because its solubility is ½ that of N2
- 100% O2 is not appropriate due to O2 toxicity
238
how does decompression sickenss occur
- Occurs during rapid ascent and decreasing pressure
- As N2 suddenly becomes less soluble, it comes out of its solution
- These leads to the formation of bubbles (Champagne cork effect)
- Its effects depend on the size and location of the bubbles
239
effects of nitrogen narcosis when it cuases a gas embolus in circulation
- tissue ischaemia
- May be critical in Brain, Coronary or Pulmonary circulations
- Avascular necrosis common in head of femur
240
effects of decompression sickness when it causes bubble formation in the myelin sheath
Compromise nerve conduction (dizziness, paralysis)
241
decompression sickness effects whe it cuases bubble/gas expansion
- Muscle and joints (The Bends): severely painful
- Ear: vestibular disturbances, deafness
- Lung: tissue rupture (airway bursting)
242
decompression sickness prevention
- Slow ascent
- N2 gas replacement
- Exhale during ascent
243
decompression sickness treatment
recompression
