Respiratory Adaptation Flashcards

1
Q

Describe the changes in ventilation in exercise

A
  • Respiratory- resting (12-18), peak exercise (45-60)
  • Tidal volume- resting (0.5L), peak exercise (2.25L)
  • Minute ventilation- resting (6L/min), peak exercise (175L/min)
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2
Q

What are the respiratory responses to exercise?

A
  • Increased rate and depth of ventilation
  • In exercise both oxygen consumption and carbon dioxide production increase
  • To facilitate oxygen delivery & carbon dioxide removal, both respiratory rate and tidal vol increase
  • Respiratory function normally chemically controlled
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3
Q

Describe blood gases in exercise

A
  • Arterial bg unchanged in moderate exercise
  • Ventilation appropriate- adjusted to maintain arterial PaCO2
  • PO2 doesn’t change (drop in arterial pH at high intensity, lactic acid- anaerobic resp, arterial pH drops- acidotic hyperventilation)
  • Maintaining bg by maintaining ventilation
  • Ventilation increases exponentially with exercise
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4
Q

How is respiration controlled in exercise?

A
  • Dorsal respiratory group firing more frequently
  • Peripheral receptors firing within normal ranges
  • Mechano/chemoreceptors in skeletal muscles
  • All involved in fine-tuning to control respiration
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5
Q

Do the lungs limit oxygen?

A
  • Low-to-moderate intensity exercise- pulmonary system is not a limitation
  • Maximal exercise- not thought as limitation in healthy at sea level, may limit in elite endurance athletes, new evidence that resp muscle fatigue occurs at high intesity
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6
Q

What are the effects on respiration?

A
  • Reduced ventilation at same work rate- maybe lower blood lactic acid levels–>less feedback to stimulate breathing
  • Overall- training has little effect on vent capacity
  • Can go longer without becoming acidotic
  • Any given work rate before training- higher vent- comes down to how acidotic at any given rate
  • No direct impact on ventilation
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7
Q

Describe the effect of altitude on respiration

A
  • Atm press drops –> oxygen drops
  • Oxygen ~12kPa, PaO2-~7kPa, respiratory failure occurs at <8kPa
  • Inspired gas less, alveolar gas less, arterial blood less, mixed ve§nous blood is less, extracting relatively more oxygen
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8
Q

What is the interaction between PaO2 and PaCO2?

A
  • When oxygen drops–> vent increases (peripheral receptor firing)- hyprventilation leads to low PCO2
  • Nothing occurs with central chemoreceotors- carbon dioxide drops–> decreased vent
  • Vent increases and slows again as central chemoreceptors try to normalise PaCO2
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9
Q

How does respiratory adaptation occur during ascent to high altitude initially?

A
  • Initially- hypoxic hyperventilation due to peripheral chemoreceptors
  • Leads to lower PaCO2 and respiratory alkalosis (altitude sickness)
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10
Q

Describe the action of the central chemoreceptor

A
  • CSF contains little protein- buffer capacity much less than plams- sensitive pH changes
  • Plasma H+ won’t cross BBB
  • Plasma CO2 does, so CSF pH proportional to PaCO2 (short-term)
  • Settles higher vent than at sea level- not as high as initially
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11
Q

How does respiratory adaptation to occur after 2-3 days at high altitude?

A
  • Respiratory alkalosis and decrease in PaCO2- decreases vent response to low PaO2
  • Hyperventilation decreases and PaO2 falls
  • CSF compensation for alkalosis returns CSF pH to normal after 1-2 days- hypoxic hyperventilation recovers
  • Renal compensation for alkalosis by excreting extra HCO3- takes ~2-3 days
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12
Q

Describe chronic adaptation to altitude

A
  • Regulation of 2 mutually exclusive factos
  • HR decreases, decreased hyperventilation and hypoventilation
  • Increased RBC
  • Over generations- response less pronounced
  • Pulmonary arteries constrict during hypoxia
  • High altitude pulmonary oedema- major vasoconstriction in lungs, fluid leaks out of capillaries
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13
Q

Describe hypoxia and erthropoiesis

A
  • Normally, production of erythropoietin stimulated by tissue hypoxia
  • Erythropoietin- glycoprotein coming from mainly from kidney
  • Increases RBC production in bone marrow and promotes red cell maturation
  • Increases oxygen carrying capacity
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14
Q

How does BPG stabilise deoxy-Hb?

A
  • BPG binds between lysine and histidine residues of β glib chains
  • Oxygenated Hb has a different conformation and prevents binding
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15
Q

Describe BPG and haemoglobin dissociation

A
  • BPG has limited impact on loading

- Reduced BPG increases the saturation

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16
Q

Describe respiratory adaptation under pressure

A
  • Pressure- force applied/ unit area (atm= pressure exerted on all bodies/structures by earth’s atmosphere, sea level- 1atm ~100kPa
  • Pressure under water- every 10m of depth- 1atm/100kPa
  • E.g. diver at depth of 20m- 1atm (sea level) + 2atm (water depth)= 3atm
  • Dissolves more gas and proportional to partial pressure
17
Q

What are the gas laws?

A
  • Boyle’s Law describes relationship between pressure and volume- P1V1 - P2V2
  • Sea level- 30msw
    • Volume quarter of what at sea level
  • More and more gas dissolved deeper down
18
Q

Describe diffusion

A
  • PO2 increases and solubility increases
  • Diffusion based on partial pressure gradients- dissolving more gas increases diffusion to tissues
  • As such, descent tends to push gas into tissues and ascent opposite direction
  • N 4x greater than at sea level
19
Q

What is decompression sickness?

A
  • Abdominal pain, fainting, laboured breathing, cyanosis
  • All N dissolved at pressure- starts to release as gas during ascent- if not slowly- can be fatal
  • Haldane suggested short, shallow dives
  • Caisson’s disease
20
Q

What is decompression theory?

A
  • Body tissue absorbs N at death
  • Each type absorbs N at different rate
  • Slow, staged ascent releases N harmlessly and exhaled
  • Determined by time and depth of dive
  • Ascent without adequate decompression cause N bubble formation in skin and joints
  • Minute-hours presentation
  • On-site treatment oxygen
  • Definitive treatment recompression