6. Barometric pressure Flashcards

1
Q

What does hyperventilation cause?

A

Cause: decrease PaO2 acting on carotid body peripheral chemoreceptors (ie: hypoxic ventilatory drive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What occurs during hyperventilation?

A
  • CO2 clearance increases
  • Blood pH increases
  • Respiratory alkalosis (reduces ventilation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What occurs to prevent alkalosis?

A
  • Kidney excrete bicarbonate ions
  • More acid remains in the blood
  • Alkalosis is reversed
  • pH normal within 2-3 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Polycythaemia

A

Increased:
• RBC concentration in blood
• Hb content in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

When does decompression sickness occur and what happens?

A

During rapid ascent & ↓ pressure
• N2 less soluble, N2 comes out of solution
– Bubble formation - “Champagne Cork Effect”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does the effect of decompression sickness depend on?

A

Size and location of bubbles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Decompression sickness effects x 3

A
  • Gas embolus in circulation → tissue ischaemia
  • Bubble formation in the myelin sheath
  • Bubble/Gas expansion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What could bubble formation in the myelin sheath cause?

A

Compromise nerve conduction (dizziness, paralysis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Effect of gas embolus in circulation

A

May be critical in Brain, Coronary or Pulmonary circulations

Avascular necrosis common in head of femur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Effect of bubble/gas expansion

A

Muscle and joints (The Bends): severely painful
Ear: vestibular disturbances, deafness
Lung: tissue rupture (airway bursting)
→ increased bubble dispersal and multiple emboli
→ catastrophic if not fatal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Prevention of decompression sickness x 3

A
  • Slow ascent - according to prescribed tables
  • Exhale during ascent
  • N2 gas replacement (He)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Treatment for decompression sickness

A

Recompression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does slow ascent in decompression sickness depend on?

A
  • Depth
  • Time
  • N2 wash-in & wash-out times
  • Tissue types
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What occurs in N2 gas replacement in decompression sickness prevention?

A

– Half Solubility of N2

– decreases MW → faster diffusion (and thus washout)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Depth vs duration of submersion diagram

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why does RBC concentration increase during polycythaemia?

A
As the ↓ PaO2 (hypoxemia) stimulates erythropoietin (EPO) after ~3h (peak 24-48h)
• From kidney
• Acts on bone marrow
• Stimulates
– Reticulocyte maturation and release
– Synthesis (erythropoiesis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does elevated blood viscosity during polycythaemia cause?

A
  • ↑ cardiac work (hypertrophy)

* Uneven blood flow distribution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Example of groups with adapted polycythaemia.

A

Peruvian Andes residents (4,572 m)
• PaO2 = 45mmHg; Hb saturation = 81%
• [Hb] increased from 15 to 19.8 g/100ml

19
Q

Adaptation to altitude x 7

A
  • Polycythaemia
  • Hyperventilation
  • Right shifted O2-Hb dissociation curve (moderate altitudes)
  • Left shifted O2-Hb dissociation curve (high altitudes)
  • Improved diffusion capacity
  • Endothelial cells release up to 10 times more nitric oxide (NO)
  • Reduced skeletal muscle fibre size (weeks)
20
Q

What does a right shifted O2-Hb dissociation curve (moderate altitudes) help with for adaptations to altitude.

A
  • Better unloading at tissue level (possible loading limitation)
  • Caused by ­ [2,3-DPG]
21
Q

What does a left shifted O2-Hb dissociation curve (high altitudes) help with for adaptations to altitude.

A
  • Better loading at the pulmonary capillaries

* Caused by respiratory alkalosis

22
Q

What does improved diffusion capacity occur via in adaptations to altitude.

A
  • Expanded surface area via greater lung volume on inflation

* Increased tissue capillarisation (angiogenesis) (days)

23
Q

What is• Reduced skeletal muscle fibre size (weeks) in altitude adaptation in conjunction with?

A

With increased oxidative capacity & mitochondria

numbers

24
Q

Symptoms of acute mountain sickness

A
  • Headaches, Loss of appetite & Insomnia, Nausea, Vomiting, Dyspnea (difficult breathing)
  • Begin from 6 to 48 h after arrival to altitude (most severe days 2 and 3)
25
Acute mountain sickness incidence, linked x 3
* Elevations 2,500–3,500 m: incidence ~15% (higher in women) * Maybe linked to low ventilatory response to hypoxia * Physical conditioning little protection against effect of hypoxia
26
What is high altitude pulmonary oedema linked to?
To pulmonary vasoconstriction (hypoxia): high [protein] oedema fluid from damaged capillaries.
27
Treatment of high altitude pulmonary oedema
Descending to lower altitude and supplemental oxygen.
28
What does fluid accumulation lead to?
Persistent cough, shortness of breath, cyanosis of lips & fingernails and loss of consciousness.
29
What could high altitude pulmonary oedema lead to?
High altitude cerebral oedema
30
What is high altitude cerebral oedema?
Fluid accumulation in | cranial cavity
31
Kilian Jornet x 5 pts
``` Climbed Everest twice (May 2017) • Without artificial O2 • In a single climb (each ascent) • New speed record (first ascent) • Both ascents within a week!! ```
32
Altitude/hypoxic training strategies to maximise altitude performance x 3
a) Compete within 24 h of arrival at higher altitudes b) Train and live at altitude (1,500-3,000 m) for at least 2 weeks c) For team sports requiring considerable endurance • Intense aerobic training at sea level to reach high VO2max values • So, at altitude they will perform at lower relative intensities
33
Why does competing within 24 h of arrival at higher altitudes help?
No acclimatization, but avoidance of detrimental responses to altitude such as dehydration and sleep disturbances
34
Train and live at altitude (1,500-3,000 m) for at least 2 weeks, what intensity and when will full intensity be reached?
* Initial intensity: 60-70% of sea-level intensity | * Progress to full intensity within 10-14 days
35
Altitude/hypoxic training strategies to maximise sea-level performance
a) Live high – train high (LHTH or HiHi) b) Live (or sleep) high – train low (LHTL or HiLo) c) Live low – train high (LLTH or LoHi) d) Intermittent hypoxia at rest
36
Nitrogen narcosis at sea level
* N2 is poorly soluble | * Low [N2] dissolved - no adverse effects
37
Nitrogen narcosis at depth x 3 pts
• ↑ N2 partial pressures → ↑ N2 solubility • High [N2] dissolved in blood, and – Fatty substances (membranes) – Influences ion regulation and therefore excitable cells: e.g. neurons • ↑ Depth, ↑ [N2] dissolved
38
↑ N2 solubility =
Reduced neuron excitability → nitrogen narcosis
39
Nitrogen narcosis at 50m (150 ft) effect
“Cocktail” effect (euphoria and drowsiness)
40
Nitrogen narcosis at 50-90m effect x3
* Fatigued and weak * Loss of coordination * Clumsiness
41
Nitrogen narcosis at 100-120m effect x3
Lose consciousness
42
Prevention nitrogen narcosis
* Use N2 free gas * Helium substitution (Solubility ½ that of N2) * 100% O2 not appropriate (O2 toxicity)
43
When and how much does total pressure increase?
1 atmosphere every 10m (33 feet)
44
Problems with total pressure and gas partial pressure increasing under water
``` • Gas cavities (lung, middle ear) – Compression with descent – Over-expansion with ascent • Behaviour of Gases – Gas solubility ∝ partial pressure ```