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Physiology Hilary > 6. Barometric pressure > Flashcards

6. Barometric pressure Flashcards

1
Q

What does hyperventilation cause?

A

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

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2
Q

What occurs during hyperventilation?

A
  • CO2 clearance increases
  • Blood pH increases
  • Respiratory alkalosis (reduces ventilation)
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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
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4
Q

Polycythaemia

A

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

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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”

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6
Q

What does the effect of decompression sickness depend on?

A

Size and location of bubbles

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7
Q

Decompression sickness effects x 3

A
  • Gas embolus in circulation → tissue ischaemia
  • Bubble formation in the myelin sheath
  • Bubble/Gas expansion
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8
Q

What could bubble formation in the myelin sheath cause?

A

Compromise nerve conduction (dizziness, paralysis)

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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

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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

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11
Q

Prevention of decompression sickness x 3

A
  • Slow ascent - according to prescribed tables
  • Exhale during ascent
  • N2 gas replacement (He)
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12
Q

Treatment for decompression sickness

A

Recompression

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13
Q

What does slow ascent in decompression sickness depend on?

A
  • Depth
  • Time
  • N2 wash-in & wash-out times
  • Tissue types
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14
Q

What occurs in N2 gas replacement in decompression sickness prevention?

A

– Half Solubility of N2

– decreases MW → faster diffusion (and thus washout)

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15
Q

Depth vs duration of submersion diagram

A
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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)
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17
Q

What does elevated blood viscosity during polycythaemia cause?

A
  • ↑ cardiac work (hypertrophy)

* Uneven blood flow distribution

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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
Q

Acute mountain sickness incidence, linked x 3

A
  • 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
Q

What is high altitude pulmonary oedema linked to?

A

To pulmonary vasoconstriction (hypoxia): high [protein] oedema fluid from damaged capillaries.

27
Q

Treatment of high altitude pulmonary oedema

A

Descending to lower altitude and supplemental oxygen.

28
Q

What does fluid accumulation lead to?

A

Persistent cough, shortness of breath, cyanosis of lips & fingernails and loss of consciousness.

29
Q

What could high altitude pulmonary oedema lead to?

A

High altitude cerebral oedema

30
Q

What is high altitude cerebral oedema?

A

Fluid accumulation in

cranial cavity

31
Q

Kilian Jornet x 5 pts

A 
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
Q

Altitude/hypoxic training strategies to maximise altitude performance x 3

A

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
Q

Why does competing within 24 h of arrival at higher altitudes help?

A

No acclimatization, but avoidance of detrimental responses to altitude such as dehydration and sleep disturbances

34
Q

Train and live at altitude (1,500-3,000 m) for at least 2 weeks, what intensity and when will full intensity be reached?

A
  • Initial intensity: 60-70% of sea-level intensity

* Progress to full intensity within 10-14 days

35
Q

Altitude/hypoxic training strategies to maximise sea-level performance

A

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
Q

Nitrogen narcosis at sea level

A
  • N2 is poorly soluble

* Low [N2] dissolved - no adverse effects

37
Q

Nitrogen narcosis at depth x 3 pts

A

• ↑ 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
Q

↑ N2 solubility =

A

Reduced neuron excitability → nitrogen narcosis

39
Q

Nitrogen narcosis at 50m (150 ft) effect

A

“Cocktail” effect (euphoria and drowsiness)

40
Q

Nitrogen narcosis at 50-90m effect x3

A
  • Fatigued and weak
  • Loss of coordination
  • Clumsiness
41
Q

Nitrogen narcosis at 100-120m effect x3

A

Lose consciousness

42
Q

Prevention nitrogen narcosis

A
  • Use N2 free gas
  • Helium substitution (Solubility ½ that of N2)
  • 100% O2 not appropriate (O2 toxicity)
43
Q

When and how much does total pressure increase?

A

1 atmosphere every 10m (33 feet)

44
Q

Problems with total pressure and gas partial pressure increasing under water

A 
• Gas cavities (lung, middle ear)
– Compression with descent
– Over-expansion with ascent
• Behaviour of Gases
– Gas solubility ∝ partial pressure

Physiology Hilary (12 decks)

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