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Physiology: References & Stats > Extreme Phys > Flashcards

Extreme Phys Flashcards

1
Q

What is microgravity?

A

Loss of standard gravity vector over long periods of time

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2
Q

What is the Karman line?

A

Line (100km) above which aerodynamic lift is not possible (without a rocket)

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3
Q

What is the difference between US and international law demarkation lines for space?

A

US line - 50 miles/ 81km

International line - 150km

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4
Q

Is there still gravity in space?

A

Yes, especially when we get close to a big body

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5
Q

Why do astronauts feel weightlessness if there is gravity?

A

Experience of free falling around the Earth, never hitting it

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6
Q

What is touch temperature in space?

A

40 degrees C = design

49 degrees C = momentary

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7
Q

What are space station ‘deadspots’?

A

Where astronauts are forbidden to sleep

Oxygen flow is reduced meaning that sleeping there increases risk of hypercapnia

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8
Q

Why are effective filtration and ventilation required on space stations?

A
  • Off-gassing from non-metallic substances
  • Particles don’t settle with limited gravity
  • Radiation modified by-products
  • Human ‘micro-waste’ (hair, skin, gas etc.)
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9
Q

What are the most important factors to consider with radiation?

A

Time
Distance
Shielding

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10
Q

What are the requirements of normal gas exchange?

A
  • Efficiently functioning lungs & chest bellows
  • Effective pulmonary circulation
  • Heart pumping capacity
  • Effective vasculature network
  • Adequate haemoglobin concentration in blood
  • Control mechanisms to regulate gas tensions and pH.
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11
Q

Describe the three types of skeletal muscle fibre.

A

Slow twitch - type I
Fast twitch:
Type IIa - fast oxidative
Type IIb - fast glycolytic

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12
Q

What is shunted blood?

A

Blood that enters the arterial system without going through ventilated areas of the lung.
This depresses pO2

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13
Q

During exercise, what are the stimuli for respiration?

A

‘Very complicated and not fully understood’

  • Central command (feed forward)
  • Feedback from muscle (afferent)
  • Humoral
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14
Q

What do studies say about breathing changes during exercise?

A

Eldridge et al. 1981 - change initiated before movement in exercise (cats given curare to inhibit muscle, but respiratory rate could still increase)

Adrian et al. 1997 - Neural feedback; group III and IV afferents in cats showed increase firing with exercise

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15
Q

What is the function of an ‘expiratory exchange ratio’?

A

Indicator of fuel being used at any one time during exercise
6 molecules of oxygen needed for aerobic respiration (6 molecules of glucose produced = 1:1)
A ratio of less than 1 means you’re using fat.

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16
Q

Describe oxygen kinetics during exercise.

A

Phase I - cardiodynamic
Phase II - primary/ fast
Phase III- steady state
The traditional view was that steady state is always achieved.

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17
Q

What is the ‘anaerobic threshold’?

A

Lowest exercise intensity at which lactic acid starts to accumulate in the muscle

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18
Q

Define ‘onset of blood lactate accumulation’.

A

Workload the blood lactate rises above 4mmol/L

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19
Q

What changes would you expect to see above the anaerobic threshold?

A
  • Reduced endurance
  • Disproportionate increase in VE
  • Oxygen kinetics slow (never hits steady state)
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20
Q

Why does oxygen consumption increase during exercise?

A
  • Progressive vasodilation of local muscle units
  • Acidemia shifting oxyhemoglobin dissociation curve to the right -> unloading oxygen from Hb
  • Oxygen cost of converting lactate to glycogen in the liver
  • Increased catecholamine levels
  • Increased recruitment of glycolytic fibres
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21
Q

What are the functions of the cardiovascular system during exercise?

A
  • Supply metabolic requirements of the muscle
  • Dissipate heat
  • Maintain requirements of other organs
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22
Q

What are the general cardiovascular responses to exercise?

A
  • Skeletal muscle blood flow increase (exceeding cardiac output)
  • Cardiac output has to increase (by about 600ml/min) to compensate for the increased muscle blood flow
  • Heart rate, blood pressure and total peripheral resistance increase
  • Competing influence between muscle and central nervous system for oxygen.
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23
Q

What are the cardiovascular responses to isometric exercise?

A

Decreased stroke volume due to:

  • Increased vascular resistance
  • Increased sympathetic drive
  • Increased diastolic, systolic and mean arterial blood pressure
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24
Q

What are the cardiovascular responses to dynamic exercise?

A
  • Increased stroke volume from increased sympathetic drive and atrial filling (venous return from muscle pump)
  • Increased systolic blood pressure and mean arterial pressure
  • Decreased/ unchanged diastolic blood pressure
  • Decreased vascular resistance from active muscle vasodilatation.
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25
Q

What is the difference between isometric and dynamic exercise with respect to total peripheral resistance?

A

Isometric exercise has a much larger increase in total peripheral resistance than dynamic exercise

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26
Q

What are the differences between isometric and dynamic exercise with respect to flow and resistance?

A

Dynamic = increased flow, decreased resistance

Isometric = decreased flow, increased resistance

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27
Q

What changes in vascular tone can occur during exercise?

A

Vasoconstriction - angiotensin II and adrenaline

Vasodilation- nitric oxide, adenosine, potassium, phosphate, ATP/ ADP

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28
Q

What did Rowell and Sherrif discover about blood pressure (BP) changes during exercise?

A

The more effort you invest in exercise, the greater the increase in BP.

Subjects asked to hold 25% of their force, then with neuromuscular blocker (more effort meant their BP increased)
N.B. Isometric conditions

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29
Q

What is the ‘pressor’ reflex?

A

Circulatory occlusion showed that trapped metabolites were responsible for increasing blood pressure during exercise - Alam & Smirk

Chemoreceptor afferent to BP during exercise - Bull et al.

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30
Q

What is driving the pressor reflex during exercise?

A

Group III afferents - respond to chemical and mechanical stimuli; firing declines with force

Group IV afferents- fire after sustained contraction

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31
Q

What happens to baroreceptors during exercise?

A

They defend a new set point during exercise- baroreceptor resetting

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32
Q

What factors limit VO2 max?

A

Skeletal muscle
Mitochondria
Capillary density
Cardiac output

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33
Q

Why does VO2 max differ between individuals?

A

Individuals have different:

  • Normalisation to body weight
  • Fat free mass
  • Muscle mass
  • Genetics
  • Ages (aerobic power, cardiac output, heart rate and muscle mass decrease)
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34
Q

Why does VO2 max differ between tests?

A

Running activates bigger muscle mass than cycling

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35
Q

What is oxygen debt?

A

Lag in oxygen uptake; difference between total oxygen consumed during exercise and total that would have been consumed had steady state been reached

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36
Q

Why is there a prolonged recovery period during heavier aerobic exercise?

A

Required to:

  • Re-synthesise ATP and CP
  • Re-synthesise glycogen
  • Oxidise lactate
  • Regulate increased heat produced during exercise
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37
Q

Why is it impossible to accurately calculate the oxygen deficit during extreme exercise?

A

You don’t reach steady state

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38
Q

What is the difference between acclimation and acclimatisation?

A

Acclimation - stabilising baseline stats to laboratory conditions; short term

Acclimatisation - move someone to a different environment. To perform well, an individual needs some degree of acclimatisation; long term

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39
Q

How much does temperature decrease with altitude?

A

2 degrees Celsius with 1000ft inclines

Reference = -20 degrees C at 18000 ft.

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40
Q

What are the potential consequences of sudden depressurisation at 40000 feet?

A 
Decompression sickness
Hypoxia
Cold
Altitude illness 
Ebullism
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41
Q

What are the circulatory consequences of bed-rest?

A
  • Decreased erythrocyte & plasma volume -> decreased blood volume
  • Decreased central venous pressure (therefore decreased stroke volume)
  • Decreased parasympathetic baseline
  • The only thing that increases is resting heart rate
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42
Q

What is acceleration atelectasis?

A

Alveolar walls are held together by surface tension and remain collapsed on return to 1Gz
Caused by distal airway absorption of alveolar oxygen (which becomes the rate limiting gas if there’s no nitrogen)

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43
Q

What are the controllable factors that affect G tolerance?

A

Hydration
Nutrition
Fatigue
Anti G-Suit

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44
Q

What are the risks associated with positive pressure breathing for G protection?

A

Ear pain
Ear and sinus blocks
Pneumothorax
Air embolism

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45
Q

How does decreased temperature affect the oxygen dissociation curve?

A

Shifts curve to the left

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46
Q

Where are the baroreceptors located?

A

Carotid sinus

Aortic arch

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47
Q

Where are central chemoreceptors located?

A

Medullary neurons

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48
Q

Where are peripheral chemoreceptors located?

A

Carotid & aortic bodies

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49
Q

According to Roiz de Sa, what are the three different patterns of cold acclimatisation?

A

Habituation
Metabolic acclimatisation
Insulative acclimatisation

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50
Q

Compare heat acclimatisation to cold acclimatisation

A

Physiological adjustments to chronic cold exposure are:

  • Less pronounced
  • Slower to develop
  • Less reproducible
  • Less practical (for thermal strain relief, body temperature defence and thermal injury prevention)
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51
Q

How much greater is the thermal capacity of water compared to air?

A

70 times

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52
Q

How much insulation is un-perfused muscle able to provide during resting cold exposure?

A

85% of the limb insulation

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53
Q

Why is exercise in cold water futile for thermogenesis?

A

Un-perfused muscle acts as an insulator; contraction increases muscle perfusion which makes it lose its insulatory potential

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54
Q

How does gender affect outcomes with respect to cold water immersion?

A

Tikuisis et al - compared to men of comparable age and weight, women generally have:

  • Greater body fat content
  • Thicker sub-cutaneous fat layer
  • Less muscle mass
  • Higher surface area: mass ratio
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55
Q

How does age affect cold acclimatisation?

A

People older than 60 have poorer outcomes with cold exposure due to:

  • Decline in physical fitness (reducing heat production capacity before fatigue)
  • Blunted thermal sensitivity
  • Blunted behavioural response to cold
  • Lower surface area to mass ratio compared to children (decreasing rate of cooling for cold water immersion)
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56
Q

What is the predominant metabolic substrate that shivering relies on?

A

Lipid

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57
Q

How does hypoglycaemia affect thermoregulation in cold?

A

Increases peripheral vasodilation
Impaired shivering (500W thermogenesis) mediated through the central nervous system; 50% reduction in glucose can abolish shivering
Impaired shivering rate via declining peripheral carbohydrate stores.

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58
Q

What type of environment poses the greatest risk for developing hypothermia?

A

Cold
Wet
Windy

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59
Q

How does cold weather clothing protect against hypothermia?

A
  • Inner layer wicks moisture (e.g. sweat) to other layers where it can evaporate.
  • Middle layer insulates
  • Outer layer repels wind and rain
  • Trapped air between the layers insulate, reducing heat loss
  • Mittens reduce heat loss (smaller surface area: mass ratio of fingers when together)
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60
Q

What is the likely cause of cold-induced diuresis?

A

Redistribution of body fluids from periphery to central circulation after peripheral vasoconstriction.

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61
Q

Where is frostbite most common and why?

A

Exposed skin (e.g. nose, ears, cheeks, wrists) - temperature can fall faster where there’s no insulation

Hands and feet - peripheral vasoconstriction lowers tissue temperatures

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62
Q

What is contact frostbite?

A

Rapid heat loss due to touching cold objects (like highly conductive metal/ stone) with bare skin

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63
Q

How does wind exacerbate heat loss?

A

Facilitates convective heat loss and reduces insulate value of clothing

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64
Q

What is the ‘wind chill temperature index’?

A

Estimate of the cooling power of the environment (how quickly it can make an object cool to its temperature) by integrating wind speed and air temperature

Things to note:

  • No real consensus on it
  • Can’t be used to predict hypothermia
  • Cannot freeze water if ambient temp is below zero
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65
Q

What happens with simultaneous hypothermia and hypothermia-induced acidosis?

A

The oxygen dissociation curve shifts to the LEFT

Acidosis does shift the curve to the right but only by 1/3 of the effect hypothermia has

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66
Q

What happens to blood pH during hypothermia?

A

Lactic acidosis due to:

  • Decreased spontaneous respiratory activity
  • Shivering
  • Peripheral vasoconstriction -> local tissue hypoxia
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67
Q

At what temperature does it become advantageous to exercise?

A

25 degrees C

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68
Q

How does trauma compromise thermoregulation?

A

Anything breaking the skin increases heat loss

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69
Q

By what factor does thermogenesis increase with exercise compared to when at rest?

A

15-20

70
Q

What are the primary factors that lead to exertion heat stroke?

A

Strenuous exercise in a hot-humid environment
Lack of heat acclimatisation
Poor physical fitness

71
Q

How is hyperthermia caused?

A

Anything that generates more metabolic heat than the body can remove.

72
Q

What are the cardiac effects of hyperthermia?

A

Reductions in:

  • Cardiac output
  • Oxygen delivery to tissues
  • Vascular transport of heat from deep tissues to skin

Increases in:

  • Core temperature
  • Tissue hypoxia
  • Metabolic acidosis
  • Organ dysfunction

Reversible with body cooling.

73
Q

Why are hyperthermic patients pale rather than flushed?

A

They’re vasoconstricting which means that heat cannot be expelled

74
Q

What is it about being bipedal that sets humans at an advantage to other animals?

A
  • Greater energy efficiency while upright
  • Reduced solar radiation exposure
  • Less metabolic heat generation
  • More wind and convective flow (cooling the brain)
  • Bipedality allows for brain growth

We’ve evolved to run long distances while efficiently thermoregulating

75
Q

Why is hyperthermia a problem?

A
  • Above critical reaction level, cells experience ATP depletion
  • When stores can’t be replenished -> loss of membrane and ion channel function
  • Cells also start to denature, fail and malfunction

Extrapolate this to organs and entire organisms and the result is catastrophic

76
Q

How does heat generation vary across individuals?

A

Mass- bigger people have higher heat content, generation and buffers because of their larger mass

77
Q

What is the difference between thermoregulation in humans and other mammals?

A

Mammal:

  • Brain cooling- rete mirabile
  • Pant
  • Behavioural- sit in the shade

Human:

  • Whole body cooling- sweat production
  • Behavioural - removing clothes
78
Q

What are the four main ways of losing heat?

A

Radiation
Evaporation
Conduction
Convection

79
Q

What is the difference between radiation and evaporation?

A

Radiation - heat surrounding gas molecules

Evaporation - heating water molecules on a surface (e.g. skin); converting them from liquid to gas

80
Q

What is the difference between conduction and convection?

A

Conduction- transferring heat onto nearby surfaces (e.g. clothing)

Convection - mass movement of heat from one place to another via gas or liquid molecules

81
Q

What is thermal comfort dependent on?

A

Skin temperature

82
Q

How does the hypothalamus manage changes in core temperature?

A

Sending efferents to capillaries -> vasodilation

Increasing heart rate to divert cardiac output to the skin

83
Q

What happens in conditions where the body can’t compensate for crazy increases in temperature?

A

Heart rate becomes supra-maximal to increase cardiac output for the sake of heat diversion
There will be a point where cardiac output can’t divert anymore heat -> drop in blood pressure -> collapse

84
Q

How does cardiac output diversion change between states of rest and exercise?

A

Rest - 1/5th cardiac output is diverted to the skin

Exercise - competition between skin for thermoregulation and muscle for contraction

85
Q

Why is an individual at greater risk of incapacitation when performing exercise in a hot environment?

A

Competition between skin and muscle for limited cardiac output.

  • For survival, the skin has to win -> lack of blood flow (therefore oxygen) to the muscle -> build up of lactic acid and inability for muscle to contract further.
  • Blood pressure has to drop if blood volume is being shunted to the skin surface
  • Collapse will happen to help get rid of heat faster (by reducing thermogenesis)
86
Q

Why does heart rate increase with increased sweat production?

A

To increase blood flow to the skin

87
Q

Is there a difference between sweating for individuals of different masses?

A

Not really; most of the anastomoses for sweat glands are outside of the fat layer (so the insulate layer in individuals with more fat can quite easily be bypassed)

88
Q

Why do individuals with more fat generally find it harder to give off heat?

A

Reduced fitness - determines how efficiently one can divert their cardiac output to the skin
Larger body mass - storing more heat

89
Q

What is a human evolution for sweating?

A
  • Long upper limbs- massive counter cooling system as a result of larger surface area
  • Movement of arms during exercise allows for loss of heat via convection
90
Q

What is trot gallop speed?

A

The gait humans can maintain for hours while thermoregulating.

91
Q

How does clothing impede thermoregulation?

A

Sweat has to evaporate from the skin surface (not clothing) for an individual to lose heat
Clothes create a microenvironment that reduces the differential across the thermoregulatory gradient (trapping heat)

92
Q

What is wet bulb globe temperature?

A

A way of predicting human thermal stress in a given environment (70% of which comes from air’s water content)

93
Q

With respect to hydration, how does physiological fluid shift occur?

A

As a result of rate of delta change.

Rapid delta change -> fluid shift

94
Q

What is the difference between unacclimatised and acclimatised sports players?

A

Unacclimatised:

  • Predominant use of carbohydrates
  • Severe heat stress stimulus (adrenals produce pheochromocytoma levels of catecholamines)

Acclimatised:

  • Better at using other fuel sources
  • Reduced adrenal response
  • Lower heart rate and core temperature at same workload
95
Q

What are heat shock proteins?

A

Human stress proteins that are unregulated in stress

Stabilise cells, protecting them from damage (DNA unwinding and denaturing)

96
Q

What are the different kinds of heat illness?

A

Heat syncope
Heat cramps
Heat exhaustion
Heat stroke

97
Q

What is the difference between heat syncope and heat stroke?

A

Heat syncope - peripheral pooling from gravity -> poor venous return -> fainting
Quick recovery here because being horizontal, cerebral blood flow normalises

Heat stroke - mimics stroke; severe CNS dysfunction.

98
Q

What is the difference between heat cramps and heat exhaustion?

A

Heat cramps - neuromuscular dysfunction

Heat exhaustion - severe fatigue in trying to maintain core temperature; end up becoming sodium/ water deleted.

99
Q

One common sign of heat disorders is the onset of chills and goosebumps… why is this?

A

The symptoms don’t make any sense, which is indicative of CNS dysfunction.
The brainstem doesn’t like being hot, yet that’s what’s happening.

100
Q

What are common examples of organ/ symptom pathology from heat illness?

A
  • Loss of higher cortical function
  • Cerebellar dysfunction
  • Massive leukocytosis
101
Q

What is malignant hyperthermia?

A

Disorder at calcium handling at sarcoplasmic reticulum within smooth muscle -> death
When exposed to significant stress, their RY1 receptors stop functioning correctly.

102
Q

Is there a link between exertion heat illness, failure of sarcoplasmic handling and genetics?

A

Muscle cellular processes probably don’t recover for a long time
Patients are metabolically inefficient, requiring longer time periods to recover
Muscle break down damages sarcoplasmic reticulum pathways
This can also happen if you take certain medications before performing exercise.

103
Q

What problems would individuals experience with immediate cold exposure?

A
  • Loss of fine motor function
  • Decreased nerve conduction
  • Decreased muscle power (3% for every degree drop in temperature)
104
Q

Are we more sensitive to cold or heat?

A

Cold - we have 3-10 times as many receptors

105
Q

Outline thermoregulation during hypothermia

A

Receptor afferents -> lateral parabrachial nucleus -> median preoptic nucleus -> dorsal- medial hypothalamus -> rostral raphae pallidus nuclei (rRPa)
The rRPa then sends effectors to skeletal muscle, skin blood vessels and brown adipose tissue

106
Q

Why does the Hunting phenomenon/ Lewis reaction exist?

A

To maintain skin temperature about the constant level
Reducing risk of cold injury
Improving manual dexterity with cold induced vasodilation

107
Q

What are the secondary causes of hypothermia?

A
  • Anything that impairs thermoregulation (e.g. trauma wrecks the skin and accelerates heat loss)
  • CNS failure
108
Q

What are the causes of reduced thermogenesis?

A
  • Endocrinological failure: diabetic/ alcoholic ketoacidosis, hypothyroidism and hypoadrenalism
  • Insufficient fuel: malnutrition, hypoglycaemia
  • Extremes of age
  • Physical exertion/ exhaustion
109
Q

What are signs/ symptoms of hypothermia at 35-37 degrees C?

A
  • Shivering; during sleep, basal metabolic rate decreases, therefore you’re as cold as you’re going to get (making this worse)
  • Onset of mild confusion and disorientation
  • Muscles become stiff and difficult to use
110
Q

What are signs/ symptoms of hypothermia at 33-35 degrees C?

A
  • Shivering increases in violence, becomes uncontrollable
  • Increases amnesia, confusion etc. (‘switch off’ phenomenon)
  • Inability to maintain airway (via cold-induced bronchoconstriction)
111
Q

What are signs/ symptoms of hypothermia at less than 33 degrees C?

A
  • Shivering stops
  • Muscle rigidity
  • Cardiac arrhythmia
  • Loss of consciousness (stupor)
  • Bradycardia & poor pulse pressure

This is the reason why patients aren’t dead until they’re warm and dead.

112
Q

What is the ‘afterdrop’?

A
  • Consequence of rewarming too fast
  • Continued fall in body temperature after rewarming has started
  • Initially thought to be the cause of post-rescue collapse
  • Now thought to be the reversal of the thermoregulation gradient

It also happens if you try to aggressively cool hyperthermic patients

113
Q

Outline the different types of rewarming

A

Passive - removal from environment
Active external - heated objects, water, blankets
Active core - lavages, heated IV fluids

114
Q

How do you treat hypothermic patients?

A
  • From core out - cardio-pulmonary bypass
  • Reduce environmental cold exposure
  • Remove wet clothing
  • Lie patient on insulative surface
  • Cover with blankets
115
Q

Why is it more advantageous to use fat as a fuel than glycogen?

A

Fat is released in the long term and is stored so more sustainable in cold environments.

116
Q

What is the biggest problem an individual will encounter when exercising in the cold?

A

Dehydration due to:

  • Lack of fluids/ inhaling cold dry air
  • Cold diuresis
  • Perspiration
  • Overheating
117
Q

What is disseminated intravascular coagulation?

A

Formation of clots and then those clots dissolve; exhaustion of all the clotting factors increases risk of haemorrhage
Characterised by trauma, acidosis and coagulopathy

118
Q

What are the effects of hypothermic on the cardiovascular system?

A
  • Decreased stroke volume
  • Electrophysiological abnormalities
  • Depressed myocardial contractility
119
Q

How does hypothermia affect oxygen transport?

A
  • Oxygen consumption via shivering
  • Haemorrhage compromises VO2 increase (reduced oxygen delivery)
  • Left shift in oxygen dissociation curve
  • Peripheral vasoconstriction can worsen the already anaerobic metabolism
120
Q

How does hypothermia affect coagulation?

A
  • Perpetuated coagulopathy
  • Thromocytopenia
  • PT and PTT prolonged
  • Increased fibrinolytic activity
121
Q

Why are cyclists, skiers, mountaineers and climbers at the highest risk of peripheral cold injuries?

A

Cyclists and skiers - high windflow from speed of movement

Mountaineers and climbers - entering colder environments

122
Q

How does freezing cold injury occur?

A

We’re 60-70% water and that freezes at 0…
Skin has to freeze at about -0.5 degrees C (freezing point increased by antifreeze agents in the blood)
Ice crystal formation within cytoplasm results in cell bursting

123
Q

Outline the elements of a extravehicular motility unit (EMU = spacesuit)

A

Garments:

  • Maximum absorption
  • Liquid cooling and ventilation

Communication system:

  • EMU electrical harness
  • Communications carrier assembly

Bulk:

  • Bottom bit = lower torso assembly
  • Top bit = hard upper torso

Extras:
In-suit drink bag
Primary life support system
Secondary oxygen pack

124
Q

What are some of the requirements of a spacesuit?

A
  • Pressurised volume
  • Breathable atmosphere
  • Thermal control
  • Communication
  • Reusability
  • Fire safety
  • Reliability
125
Q

What is the sustained max G for each axis?

A 
X= 4
Y= 1
Z= 0.5
126
Q

What is the nature of galactic/ cosmic radiation?

A

High energy

High mass particles

127
Q

What does ‘Q’ mean in respect to space?

A

Q= ability of energetic particles to cause biological damage

This is a function of linear energy transfer

128
Q

What are the consequences of high solar activity?

A
  • Solar energetic particle acceleration in coronal flares

- Shock waves driven by coronal mass ejections

129
Q

What are the acute effects of space exposure?

A
  • Vertebral column decompression
  • Weight loss
  • Neurovestibular conflict
  • Loss of hydrostatic gradient
  • Dynamic oscillation of blood pressure
  • Fluid redistribution
  • Decreased central venous pressure
  • Micro ocular syndrome; visual impairment and intracranial pressure
  • Space anaemia
130
Q

How can you psychologically stimulate hyper-emesis?

A

Sickness in a specific circumstance

Association of circumstance and related stimuli to emesis

131
Q

What is the most accepted motion sickness theory?

A

Sensory conflict
Proprioceptors are all experiencing something though this is not what the neuronal store of expected signals (internal model) is expecting -> unexpected sensory inputs -> sickness

132
Q

How is urine output affected in space?

A
  • Motion sickness elevates ADH -> decreased output
  • Decreased sympathetic output to kidneys -> increased output
  • Decreased RAAS -> decreased sodium -> increased output

Studies report little- no diuresis

133
Q

What is the pathogenesis of space anaemia?

A
  • Loss of hydrostatic pressure means upward shift of fluid
  • Upper body congestion ultimately results in decreased fluid excretion -> 20% decrease in plasma volume
  • Haemoconcentration
  • To compensate, erythropoiesis is down regulated -> loss of red blood cells.
134
Q

What cardiothoracic changes occur with space exposure?

A
  • Lung becomes shorter & wider
  • Decreased abdominal girth, increased compliance
  • Heart muscle stretches out and becomes engorged -> stroke volume increases by 30-50%
135
Q

Give examples of acute cardiovascular changes in space

A
  • Stroke volume initially increases then decreases to slightly higher than what it would be at 1Gz after a week
  • Increased left ventricular diameter but after 48 hours it decreases to close to/ below expected size at 1Gz
  • Initial spike in heart rate decreases towards 1Gz levels
  • Cardiac output returns towards 1Gz levels but may remain 5-10% higher in some individuals
136
Q

Why does central venous pressure increase with space exposure?

A

Weight of all the tissue around the heart disappears with microgravity
Abdominal compartment pressure equilibrates (similar to inspiratory effect)
Heart chambers are stretched, allowing for increased atrial filling and therefore stroke volume.

137
Q

Define Starling’s Law

A

Force of contraction is proportional to end-diastolic length
Therefore if you increase stretch (end-diastolic length) with atrial filling you’ll increase stroke volume (via force of contraction)

138
Q

What are the acute respiratory effects of space exposure?

A

Increased blood goes into the lungs from capillary blood volume

Decreases in:

  • Tidal volume
  • Residual volume
  • Vital capacity
  • Total lung capacity
139
Q

Besides atrophy, how do muscle fibres change with chronic space exposure?

A

Nature of force and duration of activity performed in space dictates the types of new fibres recruited.

  • Improved local abdominal endurance
  • Extensor/ flexor (agonist/ antagonist) relationship is compromised
140
Q

What are the chronic cardiovascular effects from space exposure?

A
  • Decreased left ventricular mass
  • Reduced heart muscle size and myocardial contractility -> reduced force output/ stroke volume-> reduced cardiac output
  • Reduced plasma volume and red blood cell mass
  • Altered heart rate and oxygen uptake
141
Q

Why is exercise capability reduced with chronic space exposure?

A
  • Reduced blood volume
  • Motion sickness
  • VO2 max decreases
  • Bio-mechanical nature of exercise is different to on Earth (requires some degree of technical skill)
142
Q

Define orthostatic tolerance

A

The ability to resist effects caused by erect (upright) posture

143
Q

Why is there increased risk of kidney stones with chronic space exposure?

A
  • Increased urinary excretion of calcium, phosphate and sodium
  • Fluid redistribution and decreased fluid intake
  • Concentrated urine
  • Muscle atrophy
144
Q

What are the potential causes of space induced orthostatic intolerance?

A
  • Resetting of baroreceptors/ degraded blood pressure stimulus
  • Atrophy of lean leg tissue (increasing their compliance)
  • Fluid redistribution -> hypovolemia
  • Cardiovascular remodelling
  • Inadequate humoral response
145
Q

Why might astronauts suffer lower back pain after a 6 month mission?

A

Stretch of ligaments and tissue surrounding vertebrae
Atrophy of local lumbopelvic muscles
Reduction in spine axial (stabiliser) and appendicular (mobiliser) muscles.

146
Q

What effect does chronic space exposure have on the immune system?

A
  • Psychosocial stress - stressful conditions, isolation from family and friends
  • Heavy workloads
  • Cosmic radiation
  • Reactivation of latent viruses
  • Confined environment increases risk of spreading illness
  • Reduced immunoglobulin production
  • Increased cortisol and neutrophil count
147
Q

Outline the consequences of chronic space exposure.

A
  • Muscle atrophy
  • Bone demineralisation- particularly weight-bearing
  • Cardiovascular de-conditioning
  • Cartilage de-conditioning
  • Kidney stones
  • Orthostatic intolerance
  • Neuromuscular impairment
  • Sleep disturbance
  • Lower back pain
  • Compromised immune system
148
Q

What are countermeasures for muscular atrophy?

A

Myoelectrostimulation

Interim resistant exercise device (IRED)

149
Q

What are countermeasures for neurovestibular conflict?

A

Minimisation of fast head movement

Drugs:

  • Scopedex
  • Phenergan
  • Stugeron
150
Q

What are countermeasures for cardiovascular deconditioning?

A

Aerobic fitness
Cycle ergometry
Treadmill

151
Q

What are countermeasures for space induced orthostatic intolerance?

A
  • Endurance training
  • Lower body negative pressure suits
  • Pre-orbit fluid loading
  • Anti-gravity trousers/ bladders
152
Q

What are countermeasures for bone demineralisation?

A
  • Impulse stimulation and vibration devices
  • Walking (12 miles/ day at 4mph)
  • Elasticated load suits (e.g. pengvin, gravity loading skinsuit)

Drugs:

  • Bisphosphonate
  • Zoledronic acid
  • Fosamax
153
Q

What are the types of countermeasures to radiation?

A

Protectors- shielding to limit tissue injury
Modulators - increase baseline resistance to radiation
Mitigators - reduce effects of tissue injury after exposure

Treatment:

  • Amiforsyine (radical scavenger)
  • Filgrastin and pegfilgrastim (augment leukocyte production)
154
Q

What are the causes of hypoxia at altitude?

A
  • Ascending without supplemental oxygen
  • Failed oxygen delivery system
  • Loss of cabin pressurisation
155
Q

Outline the different types of hypoxia

A

Hypoxic- environmental cause
Anaemic - poor carrying capacity of Hb
Ischaemic- stagnant circulation reduces oxygen delivery
Histotoxic- tissue can’t use the delivered oxygen

156
Q

Outline the four stages of hypoxia

A
  1. Indifferent (0-10000ft) - heart rate and respiratory rate increase, impaired performance at new tasks
  2. Compensatory (10-15) - few symptoms besides a headache and difficulty performing skill based tasks
  3. Disturbance (15-20) - loss of critical judgement and willpower, euphoria
  4. Critical (>20000) - personality changes, muscular incoordination, cyanosis… -> death
157
Q

Describe reasons for oxygen saturation becoming disproportionate to arterial oxygen tension

A

Oxygen system fails.

  • The subject hyperventilates to keep oxygen levels up.
  • This blows off CO2, causing alkalosis and shifting oxyhemoglobin dissociation curve to the left.
158
Q

Why is oxygen tension lower in blood compared to air?

A
  • Water vapour from air is mixed with oxygen
  • Oxygen gets diluted with respired gas during gas exchange
  • Greater V/Q mismatch at sea level; shunt further decreases oxygen tension
  • Oxygen extracted by tissues is a function of supply and metabolism
159
Q

What is pulmonary capillary diffusion limitation?

A

Exercise exaggerates hypoxaemia
It takes longer for oxygen tension to equilibrate with exercise when transient time decreases with increased cardiac output and the oxygen cascade has smaller pressure differentials.

160
Q

Why does the hypoxic ventilatory response occur?

A
  • To maintain oxygen saturation
  • Allows for greater intake and utilisation of oxygen

Dissociation curve shifts to the left with decreased temperature and increased pH - oxygen saturation stops being a good measure of arterial oxygen tension

161
Q

What is the relevance of the alveolar gas equation?

A

At altitude, barometric pressure drops

The only thing you can do to balance out arterial oxygen tension is increase fractional inspired oxygen.

162
Q

What is ebullism?

A

Pressure drops enough (at over 63000ft) for body fluids to evaporate
At this point, tendon sheaths would start separating

163
Q

What effect does hypoxia have on the oxygen cascade?

A

It completely flattens it

Flattening the oxygen cascade means reduction of the driving pressures facilitating oxygen delivery to tissues

164
Q

What are the normal partial pressures of oxygen and carbon dioxide in the blood?

A

Oxygen- 10-13kPa

Carbon dioxide- 4-6kPa

165
Q

Summarise acclimatisation at altitude

A

Respiratory - increased rate (hypoxic response) and tidal volume
Cardiovascular - heart rate and cardiac output increases
Circulatory - Hb mass and concentration increases

166
Q

How is sleep disturbed at high altitude?

A

Oscillation between REM sleep and non-REM every 90 mins

Apnoea - hypercapnia sends afferents to the brain - arousal and increased ventilatory rate

167
Q

How is the cardiovascular system affected at altitude?

A
  • Sympathetic nervous system increases chronotropy and ionotropy.
  • Decreased stroke volume (reasons unknown; possibly hypovolemia)
  • Pulmonary artery pressure increases
168
Q

How is the circulatory system affected at altitude?

A
  • Blood flow decreases in small and medium blood vessels
  • Decreased plasma volume -> haemoconcentration
  • Mitochondria protein levels decrease
169
Q

What is the role of HIF1 alpha at altitude?

A

Accumulates in hypoxia
Alongside HIF1 beta, it looks for responsive gene elements and makes genes that help when there is little- no oxygen around

170
Q

Outline the different altitude illnesses

A

Acute mountain sickness - self-terminating syndrome (symptoms => hungover)

High altitude cerebral oedema - brain is swelling (symptoms => drunk)

High altitude pulmonary oedema- exaggerated hypoxic pulmonary vasoconstriction, (symptoms: shortness of breath, pink frothy sputum, fatigue)

171
Q

Describe the treatments for the various altitude illnesses

A

Acute mountain sickness - Acetazolamide (carbonic anhydrase inhibitor- causes metabolic acidosis)

High altitude cerebral oedema:

  • Immediate descent
  • Dexamethasone- steroid reduces swelling

High altitude pulmonary oedema:
- Nifedipine- reduces pulmonary artery pressure
- Dexamethasone and sildenafil (never use these together)
High flow oxygen

172
Q

Why is gravity different to every other type of acceleration?

A

Force due to gravity acts in the same direction as the acceleration

Physiology: References & Stats (4 decks)

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