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YEAR 2 - Applied Physiology & Pharmacology > 53. Physiological Challenges > Flashcards

53. Physiological Challenges Flashcards

1
Q

What are some different measures for metabolic rate?

[IMPORTANT]

A
  • O2 consumption
  • CO2 production
  • Combined heat and work output
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2
Q

What is exercise?

A

The voluntary exertion of muscles.

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3
Q

In exercise, what do we use as a typical indicator of metabolic rate?

A

Oxygen consumption

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4
Q

What is the symbol for oxygen consumption?

A

VO2

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5
Q

What is the basal oxygen consumption?

[IMPORTANT]

A

250ml/min (at STP)

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6
Q

Under what conditions is basal oxygen consumption quoted?

A
  • Morning
  • Lying down
  • Fasted
  • Neutral temperature (no shivering or sweating)
  • Body temperature 37*C
  • No exciting thought
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7
Q

For a normal mixed diet, how much energy is each ml of oxygen consumed associated with?

A

20J

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8
Q

Estimate the power dissipation of the body under basal conditions.

A
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9
Q

How does power dissipated by the body change from the basal state to doing mild exercise (stepping up on a box repeteadly)?

A

Oxygen consumption rises hugely, so the power dissipated does also.

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10
Q

Describe how you can calculate the efficiency of exercise, such as climbing stairs.

[EXTRA]

A
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11
Q

Draw a graph of useful energy output against total energy expended for different intensities of exercise.

[EXTRA?]

A
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12
Q

When doing some exercise experiments, only expired gas is collected. How can oxygen consumption be determined from this?

A
  • We assume nitrogen balance, so that the amount of oxygen breathed in is the same as the amount breathed out
  • This allows us to know how much air is being breathed in and therefore how much oxygen is being breathed in
  • By measuring the expired oxygen, the consumption can be calculated
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13
Q

What type of exercise has a mechanical efficiency of 0?

[EXTRA]

A

Isometric

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14
Q

What are the ATP yields per molecule of:

  • Glucose (aerobic)
  • Glucose (anaerobic)
  • Fatty acids

[IMPORTANT]

A
  • Glucose (aerobic) -> 36-39 ATP/molecule
  • Glucose (anaerobic) -> 2-3 ATP/molecule
  • Fatty acids -> 16 ATP/CH2CH2 unit
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15
Q

Draw a graph to show how the usage of different fuel sources changes over time in exercise.

A
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16
Q

Draw the process of actin-myosin cross-bridge cycling.

A
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17
Q

What is the respiratory quotient?

[IMPORTANT]

A
  • The ratio of CO2 produced to O2 consumed
  • RQ = CO2 eliminated / O2 consumed
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18
Q

Compare the respiratory quotient for pure carbohydrate metabolism and pure lipid metabolism.

[IMPORTANT]

A
  • Carbohydrate -> RQ = 1
  • Lipid -> RQ = 0.7
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19
Q

How do the ratio of carbohydrate to lipid usage and the respiratory quotient change during prolonged exercise?

[IMPORTANT]

A
  • At first, carbohydrates provide most of the energy, meaning the RQ is closer to 1
  • As time goes on, lipids provide progressively more of the energy, meaning the RQ is closer to 0.7
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20
Q

State the total amount of energy stored in these energy stores:

  • ATP
  • Creatine phosphate
  • Glycogen
  • Lipid
A
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21
Q

Write an equation for the oxygen concentration of arterial blood.

A
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22
Q

Write an equation for the oxygen concentration of venous blood.

A
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23
Q

Write an equation for the oxygen consumption of the body.

A
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24
Q

How much does oxygen consumption increase by during exercise?

A

It can increase up to 12-fold, from 250ml/min to 3000ml/min.

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25
Q

Oxygen consumption rises up to 12-fold in exercise. How is this increased consumption emabled by the cardiovascular system?

A
  • 4 times increase due to 4 times increase in cardiac output
  • 3 times increase due to 3 times as much oxygen being extracted from venous blood

(Note: SaO2 cannot be increased because arterial blood is almost completely saturated already)

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26
Q

Draw a graph to show how extraction of oxygen from venous blood increases during exercise.

A

Venous saturation must drop from around 0.73 to around 0.25.

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27
Q

How much does cardiac output increase during exercise?

A

4 times

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28
Q

How much blood flow is there to muscles during exercise?

A

It is a rise of 20-fold (compared to just a 4-fold increase in cardiac output).

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29
Q

Draw a graph to show how blood flow to different parts of the body changes during exercise.

A
  • Muscles -> Increases
  • Heart and brain -> Around constant
  • Viscera -> Decreases
  • Skin -> Depends on need for heat loss
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30
Q

Describe how much oxygen consumption of muscle changes during exercise and how this is achieved.

A

VO2​ increases about 40-fold due to:

  • Blood flow increases 20-fold due to:
    • 4-fold increase in blood velocity
    • 5-fold increase in number of capillaries open
  • Oxygen extraction from blood doubles

4 x 5 x 2 = 20

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31
Q

How do heart rate and stroke volume change between rest and exercise?

A

Heart rate:

  • Increases linearly
  • Increase from around 70 to 190bpm

Stroke volume:

  • Plateaus at around 1/3rd VO2
  • Increase from around 70 to 100ml
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32
Q

State the relationship between cardiac output and blood pressure.

[IMPORTANT FOR ESSAY]

A

BP = CO x SVR

(Note that blood pressure here ignores venous pressure because it is so small, but this induces some error. So could consider it as the difference in blood pressure, really.)

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33
Q

During exercise, cardiac output must increase. Describe how the cardiovascular system accomodates this increase.

[IMPORTANT FOR ESSAYS]

A

BP = CO x SVR

  • Blood pressure increases are quite small (which is sort of intuitive)
  • Therefore, the body must accomodate most of the increase in BP by decreasing the systemic vascular resistance
  • This is done mostly by dilation of arterioles supplying muscles and other respiring tissues
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34
Q

How does systemic vascular resistance change during exercise?

A

It decreases.

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35
Q

If systemic vascular resistance falls during exercise, how is blood pressure maintained?

A
  • Systemic vascular resistance falls in exercise due to vasodilatation in active skeletal muscles
  • Blood pressure is maintained at normal or elevated levels during exercise by increasing cardiac output (CO) and increasing sympathetic vasomotor tone as exercise intensity increases.

In other words, skeletal muscle arterioles vasodilate, but the rest of the system vasoconstricts.

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36
Q

Compare how blood pressure changes during static and dynamic exercise.

[EXTRA]

A
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37
Q

How much does ventilation increase by during exercise?

A

12-fold (in proportion to increased oxygen consumption)

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38
Q

Write an equation for the components that define ventilation.

A

Ventilation = Tidal volume x Respiratory rate

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39
Q

Describe how ventilation changes with exercise.

A
  • Ventilation increases pretty linearly with oxygen consumption up until a ‘break point’ where the ventilation increases rapidly (1st graph)
  • This increase is mostly due to tidal volume at first (2nd graph), and then due to respiratory rate (3rd graph)
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40
Q

Is gas exchange in the lungs diffusion or perfusion limited?

A
  • At rest, it is perfusion limited due to the large excess area of lungs
  • During exercise, the lungs may become diffusion limited at times
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41
Q

What are two examples of humoral changes during exercise?

A
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42
Q

Summarise the effects of rising adrenaline during exercise.

A
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43
Q

During exercise, extracellular potassium can reach levels that would be otherwise dangerous at rest. Why is it not dangerous during exercise?

A

The adrenaline protects the heart from dysrhythmias.

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44
Q

Draw how lactate levels change with exercise in trained, untrained and heart failure patients.

A
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45
Q

What effects does lactate have?

A
  • It contributes to the pain and fatigue seen during exercise
  • It makes the blood more acidic -> This means that the anaerobic threshold at which lactate starts being produced is often associated with the ‘breaking point’ of ventilation, where the ventilation rapidly increases
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46
Q

What are some factors that may limit exercise (i.e. what limits oxygen consumption)?

[EXTRA]

A
  • Total body haemoglobin
  • Heart size
  • Flow rates in ventilation are lower than maximally possible
  • Has to be diffusion gradient for oxygen to diffuse into lungs (so cannot extract too much oxygen from the venous blood)
  • Heart rate

In general, in healthy people it is the cardiovascular system that limits exercise, not the respiratory system.

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47
Q

Give some evidence for how total body haemoglobin can limit exercise.

[EXTRA]

A

(Astrand, 1952):

  • Compared the maximum oxygen consumption in individuals with their total body haemoglobin
  • A roughly proportional relationship was seen
  • The thinking behind this was that a larger total body haemoglobin is associated with a higher volume of blood, which is associated with a higher cardiac output
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48
Q

Give some evidence for how the size of the heart may limit exercise.

[EXTRA]

A

(Hammond, 1992):

  • Operated on two groups of sheep, cutting the pericardium of one group (since the pericardium limits the size of the heart)
  • The group with the cut pericardium showed an increased cardiac output upon follow up, while the control group showed a small decrease
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49
Q

Draw an inspiratory-expiratory flow loop for:

  • At rest
  • During exercise
  • Maximal inspiration and expiration
A

Note how the exercise loop is not as large as the maximal loop, suggesting that it may be ventilation that is the limiting factor occasionally. However, it is usually cardiovascular factors that are limiting, not ventilation.

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50
Q

How does maximum heart rate change with age?

A
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51
Q

Give a summary of the factors that can limit exercise.

[EXTRA]

A
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52
Q

What factors change the most in athletes that allow them to perform better?

A

Most of all, stroke volume.

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53
Q

Give some experimental evidence showing how an athlete’s heart adapts to exercise.

A

(Scharhag, 2002):

  • Compared 21 male athletes with untrained controls
  • Scans showed that heart volume and wall thickness were increased in the athletes
  • The athletes also had a 62% larger VO2 max
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54
Q

What part of the brain controls ventilation?

A

Medulla

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55
Q

Give a summary of the control of ventilation.

[IMPORTANT]

A

The medulla, which controls ventilation, receives input from:

  • Voluntary inputs
  • Stretch receptors in the lungs
  • Chemoreceptors:
    • Central (in medulla) -> Respond to PaCO2 mostly
    • Peripheral -> Respond to PaO2 mostly

Muscle spindles in thoracic wall also lead to spinal reflexes that affect ventilation.

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56
Q

Draw graphs to show how blood oxygen and carbon dioxide affect ventilation. How does exercise fit onto these?

A

These curves are at rest. You can see that, during exercise, the carbon dioxide and oxygen do not change much, but the ventilation does, which implies that something else must be at play during exercise!

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57
Q

At the central and peripheral chemoreceptors important in maintaining correct ventilation at rest and during exercise?

A
  • At rest, they are important
  • However, during exercise, blood oxygen and carbon dioxide do not change much, while ventilation must increase, meaning that they cannot be the only signals
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58
Q

Describe the different stages of breathing during exercise.

A
  • Phase 1 -> Rapid increase in breathing within seconds of starting the exercise
  • Phase 2 -> More slow increase in breathing later
  • Phase 3 -> Plateau in breathing
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59
Q

What are some hypotheses for why the ventilation increases rapidly at the very start of exercise (phase 1)?

A
  • Central command -> This would allow a faster response since there is no need to wait for feedback. Learning plays a major role in this
  • Peripheral chemoreceptors:
    • Mean PaCO2 does not change majorly, but there are oscillations in PaCO2, which increase during exercise. Chemoreceptors could detect this increased oscillation.
    • Lactate, potassium and adrenaline all stimulate peripheral chemoreceptors.
  • Reflex feedback from muscle ‘work receptors’ via the spinal cord (experiments in dogs suggest this is the case, but experiments in paraplegics suggest it is not)

After these fast responses, the feedback mechanisms, such as from the peripheral chemoreceptors, can also assist in ventilation control.

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60
Q

Summary control of heart rate.

[IMPORTANT]

A
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61
Q

What are the main parasympathetic and sympathetic nerves that supply the heart?

A
  • Parasympathetic -> Vagus
  • Sympathetic -> Superior, middle and inferior cardiac nerves
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62
Q

Describe an experiment to show the relative importance of the different factors that control heart rate.

A

(Donald, 1968):

  • Exercised 4 groups of greyhounds: 2 with all heart innervation removed and 2 with beta blockade due to propranolol
  • The heart rate increased more slowly in the black line on the right graph than the left graph, showing that circulating catecholamines work more slowly
  • The heart rate was slightly lower in the red graph on the left than the black line, which is due to partial blockage of the noradrenaline by propranolol
  • The red line on the right was flat due to complete blockage by propranolol
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63
Q

Draw a graph to show how the heart rate changes with exercise.

A

The phases are called phases 1, 2 and 3, just like with ventilation changes.

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64
Q

What are some hypotheses for why the heart rate increases rapidly at the very start of exercise (phase 1)?

A
  • Central command -> This would allow a faster response since there is no need to wait for feedback. Learning plays a major role in this
  • Feedback from muscles from ‘work receptors’ -> Potassium and H+ are probably sensed

After these fast responses, the feedback mechanisms, such as from the peripheral chemoreceptors and the baroreflex, can also assist in ventilation control.

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65
Q

What type of receptors are muscle ‘work receptors’?

A

Chemoreceptors

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66
Q

Give some experimental evidence for the importance of muscle ‘work receptors’ during exercise.

A

(Rowell, 1976):

  • A cuff was used to trap metabolites in the thighs after exercise
  • This showed that the trapped metabolites maintained blood pressure and (to a lesser extent) heart rate after exercise, but not ventilation
  • Release of occlusion showed a spike in all three, due to stimulation the peripheral chemoreceptors, etc.
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67
Q

Compare the control of muscle blood flow at rest and during exercise.

[IMPORTANT]

A

At rest:

  • Mostly controlled by sympathetic vasoconstrictor nerves
  • Blood flow is normally 30ml/kg/min, but can go as low as 6ml/kg/min when there is haemorrhage

During exercise:

  • Mostly due to local metabolic vasodilation (increases flow up to 20 times)
  • Not certain which factors produce this vasodilation, but could include: K+, H+, ADP and low PO2
  • Flow to muscle is also increased by vasoconstriction of blood vessels supplying other tissues, such as voscreal organs
  • Adrenaline also increases vasodilation by acting on beta-2 receptors
  • The ‘muscle pump’ -> Contraction of muscles pushes blood through the veins
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68
Q

Describe the limitation of exercise at altitude.

A
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69
Q

What are some symptoms of disease related to exercise?

A
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70
Q

Give some clinical relevance relating to treating exercise capacity in heart failure.

[EXTRA]

A

(Ponikowski, 2015):

  • Showed that iron supplementation was beneficial to heart failure patients, even without any anaemia
  • Supplementing iron was shown to improve the distance the patient could walk in 6 minutes
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71
Q

Give an example of a rare disease relating to exercise.

[EXTRA]

A

McArdles’ disease: Patients cannot break down glycogen and become easily fatigued

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72
Q

What are some of the challenges of being at high altitude?

A
  • Temperature
  • Humidity
  • Solar radiation
  • Remoteness
  • Hypoxia
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73
Q

Draw a graph to show how PO2 changes with altitude.

A

(Peacock, 1998)

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74
Q

Draw a graph of how PO2 changes along the airways (from the air to the venous blood) at both sea level and 5800m.

A

(Peacock, 1998)

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75
Q

Describe the changes in physiological measurements that are seen in the first 7 days after a person rises to high altitude.

A
  • Breathing increases so the alveolar partial pressure of CO2 decreases
  • Heart rate increases
  • Red blood cell production increases
  • Systolic pulmonary blood pressure increases
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76
Q

Summarise the control of ventilation.

A
  • Peripheral chemoreceptors (carotid body) -> Samples arterial blood for decreases in PO2 or to a lesser extent increases in pH and PCO2
  • Central chemoreceptors (medullary) -> Sample CSF pH, which is dependent on blood PCO2 and HCO3-

These communicate with medullary respiratory neurons, which control breathing.

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77
Q

Compare the carotid sinus and carotid body.

A
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78
Q

Which chemoreceptors respond to hypoxia?

A

Mostly the carotid body (peripheral).

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79
Q

Which chemoreceptors respond to hypercapnia?

A

Central chemoreceptors (medullary)

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80
Q

Describe and explain the ventilatory response to altitude.

A

Assuming that there is a sudden change of altitude:

  • PO2 drops and this hypoxia drives hyperventilation via the carotid bodies
  • This increases PO2 and decreases PCO2
  • The fall in PCO2 leads to alkalosis, which reduces ventilation via reduced stimulation of the central chemoreceptors
  • This leads to a balance between hypoxia and hypocapnia
  • Over several days, acclimatisation occurs, causing a shift towards hyperventilation
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81
Q

How does acclimatisation to high altitudes via hyperventilation happen?

A

It could be either by:

  • Reduced inhibition of ventilation by hypocapnia
  • Increased stimulation of ventilation by hypoxia

We are not sure about the balance of these two.

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82
Q

Draw a graph of ventilation against PCO2 and show how this graph changes during acclimatisation at high altitude.

A
  • Parallel shift of line to the left (shown on the left graph)
    • This is due to increased sensitivity of the central chemoreceptors to PCO2
    • This change in sensitivity may be due to prolonged alkalinisation of the body as PCO2 falls
    • The result is increased ventilation
  • Increased slope of the line (shown on the right graph)
    • This is due to an increase in the sensitivity of the peripheral chemoreceptors to PO2
    • The result is increased ventilation

(Remember that this change only occurs over a few days as the body acclimatises to high altitude)

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83
Q

Give some experimental evidence for the two types of shift that occur to the ventilation against PCO2 graph at altitude.

[EXTRA]

A

(Kellogg, 1963):

  • Saw that the graph shifted to the left AND increased in slope
  • Therefore, both types of shift occur
84
Q

At high altitudes, is there hypocapnia or hypercapnia?

A

Hypocapnia

85
Q

Give evidence for the importance of each of these mechanisms in acclimatisation to high altitude:

  • Increased sensitivity of the central chemoreceptors to PCO2 (leading to a shift to the left on the ventilation-PCO2 graph)
  • Increased sensitivity of the peripheral chemoreceptors to PO2 (leading to an increased slope on the ventilation-PCO2 graph)

[EXTRA]

A

Evidence that peripheral chemoreceptors detecting PO2 is important:

  • (Howard, 1995) -> Varied PO2 without changing PCO2. It turns out that there is a large increase in ventilation upon hypoxia when PCO2 is kept constant.
  • (Bisgard, 1986) -> Altered the blood supply to a goat’s brain so that the peripheral chemoreceptors can be independently perfused. Induced hypoxia at the carotid bodies but not at the central chemoreceptors. It turns out that ventilation increases when only the peripheral chemoreceptors are hypoxic.

Evidence that central chemoreceptors detecting PCO2 is important:

  • (Ren, 1999) -> Asked patients to hyperventilate while keeping their PO2 constant. In patients where PCO2 was allowed to drop, the line shifted to the left. In patients where CO2 was supplied to keep PCO2 constant, the line did not shift.
86
Q

What may underlie the shift of the ventilation against PCO2 graph during acclimatisation to high altitude?

A
  • It may be reduced CSF bicarbonate.
  • This can be explained this way:
    • At high altitude, there is hyperventilation
    • This leads to falls in PCO2 in the body (respiratory alkalosis)
    • The kidneys excrete increased amounts of bicarbonate to compensate for this
    • So there are low levels of bicarbonate in the blood and CSF
87
Q

Summarise the main hypothesis as to why CSF bicarbonate falls during acclimatisation to high altitudes. Why is this important?

A

There are 3 main hypothesis:

  • Renal compensation
    • At high altitude, there is hyperventilation
    • This leads to falls in PCO2 in the body (respiratory alkalosis)
    • The kidneys excrete increased amounts of bicarbonate to compensate for this
    • There is redistribution of bicarbonate from the CSF
  • Active transport out of the CSF (not fully believed)
    • At high altitude, there is hyperventilation, leading to respiratory alkalosis
    • As pH of the CSF fluid falls, bicarbonate is actively transported out of it
  • Lactacidosis
    • At high altitudes, there is cerebral tissue hypoxia
    • This leads to acidosis, which is buffered using bicarbonate
88
Q

What is renal adaptation to high altitude?

[IMPORTANT especially as summary]

A
  • When the body hyperventilates and leads to respiratory alkalosis, the kidneys excrete increased amounts of bicarbonate to recover.
  • This leads to drops in CSF bicarbonate, which leads to increased sensitivity of the central chemoreceptors to PCO2
  • This leads to adaptation to high altitude by hyperventilation
89
Q

Which is the more important mechanism in acclimatisation to high altitudes and why:

  • Increased sensitivity of the central chemoreceptors to PCO2 (leading to a shift to the left on the ventilation-PCO2 graph)
  • Increased sensitivity of the peripheral chemoreceptors to PO2 (leading to an increased slope on the ventilation-PCO2 graph)
A
  • Increased sensitivity of the peripheral chemoreceptors to PO2 is likely to be the first response that kicks in, responsible for most of the acclimatisation
  • Increased sensitivity of the central chemoreceptors to PCO2 is likely to be slower because it relies on the kidneys excreting bicarbonate in order for CSF bicarbonate to fall
90
Q

What drug may be taken to prepare for mountain climbing?

[IMPORTANT]

A
  • Acetazolamide (a carbonic anhydrase inhibitor)
  • It increases renal bicarbonate loss
  • Therefore, it gives a head start to acclimatisation to high altitudes since renal excretion of bicarbonate is required for central chemoreceptor adaptation and it is usually slow
91
Q

What is acute mountain sickness?

[IMPORTANT]

A
  • Sickness that occurs during an ascent, typically before you acclimatise
  • Risk factors include:
    • Speed of ascent
    • Final altitude
    • Individual predisposition
  • Defined as headache and Lake Louise Score >3, in setting of recent ascent
92
Q

What may underlie altitude sickness?

A

A small degree of cerebral oedema.

93
Q

What is high altitude cerebral oedema (HACE)? What are the causes, symptoms and treatment?

[IMPORTANT]

A
  • Severe swelling of the brain due to fluid
  • Causes:
    • Hypoxia leads to increased cerebral blood flow, increased cerebral blood volume and increased permeability of the BBB
  • Symptoms:
    • Headache, malaise, ataxia, confusion and coma
  • Treatment:
    • Descent
    • Decompression
    • Oxygen
    • Dexamethasone [IMPORTANT]
94
Q

Describe how breathing during sleep at high altitude happens.

[EXTRA]

A
  • There is periodic (Cheyne Stokes) breathing
  • This is where there are short bursts of fast, intense ventilation and then periods of very little ventilation
  • This is due to instability of the breathing system caused by its high gain
95
Q

What happens to pulmonary arterial pressure at high altitudes?

A

It increases due to vasoconstriction.

96
Q

Why does pulmonary vasoconstriction occur and is it always helpful?

A
  • It occurs in hypoxic areas of the lungs
  • This preserves flow to better oxygenated parts of the lungs, optimising ventilation/perfusion matching
  • This is useful when it is local (e.g. in pneumonia) but it is harmful when it is widespread (e.g. at altitude)
97
Q

What is high altitude pulmonary oedema (HAPE)? What are the causes, symptoms and treatment?

[IMPORTANT]

A
  • Severe swelling of the lungs due to fluid accumulation
  • Causes:
    • Widespread pulmonary vasoconstriction upon ascent to high altitudes
    • Strong individual predisposition
    • Leading cause of death at high altitudes
  • Symptoms:
    • Dry cough, then pink frothy sputum and progressive hypoxia
  • Treatment:
    • Descent
    • Oxygen
    • Nifedipine [IMPORTANT] -> Calcium channel blocker that reduces vasoconstriction
98
Q

What drugs can be used to treat high altitude sickness, high altitude cerebral oedema and high altitude pulmonary oedema? How do they work?

[IMPORTANT[

A
  • Altitude sickness -> Acetazolamide:
    • This is a carbonic anhydrase inhibitor
    • It increases renal bicarbonate loss
    • Therefore, it gives a head start to acclimatisation to high altitudes since renal excretion of bicarbonate is required for central chemoreceptor adaptation and it is usually slow
  • High altitude cerebral oedema -> Dexamethasone:
    • This is a steroid
    • It acts to decrease inflammation and thus it prevents oedema, but the exact mechanism of action is not known
  • High altitude pulmonary oedema -> Nifedipine
    • This is a calcium channel blocker, quite specific to the lungs
    • It acts to decrease vasoconstriction of the lungs, which prevents oedema
99
Q

What can make high altitude pulmonary oedema (HAPE) particularly bad?

A

Stress failure -> This is when uneven vasoconstriction can lead to very high pressures in certain capillaries, so that the pressure becomes high enough to damage them.

100
Q

What is HPV?

A

Hypoxic pulmonary vasoconstriction

101
Q

How does high altitude affect haemoglobin levels affected by altitude?

A

High altitude leads to high levels of haemoglobin.

102
Q

Draw a graph of how arterial PO2, arterial oxygen saturation, haemoglobin saturation and arterial oxygen content change with altitude.

A
103
Q

At high altitudes, is arterial PCO2 low or high?

A

Much lower than normal

104
Q

What things can cause the haemoglobin dissociation curve to shift to the right?

A
  • Increased [H+]
  • Increased PCO2
  • 2-3DPG
  • Temperature
105
Q

What is the Bohr effect and how is it relevant at high altitudes?

[IMPORTANT]

A
  • At high altitudes, the low PCO2 in the blood and atmosphere causes the haemoglobin dissociation curve to shift to the left
  • This makes it easier for haemoglobin to pick up oxygen, but it also makes it more difficult for oxygen to dissociate from haemoglobin at tissues
106
Q

Describe what is unusual about gas exchange in the lungs at high altitudes.

A
  • Usually, at sea level, arterial and alveolar PO2 are very similar
  • However, at high altitudes, the arterial blood has lower PO2 than the alevoli
  • This is due to diffusion limitation in the lungs, which results from a smaller diffusion gradient
107
Q

What does HIF stand for?

A

Hypoxia inducible factor

108
Q

What is HIF?

A

It is a transcription factor that regulates many genes in hypoxia.

109
Q

Describe the synthesis and breakdown of HIF.

A
  • HIF is continuously being produced
  • In the presence of oxygen and iron, HIF is broken down
  • When there is no oxygen, HIF cannot be broken down so it accumulates and leads to gene transcription
110
Q

What is the archetypal gene regulated by HIF?

[IMPORTANT]

A
  • Erythropoietin (EPO)
  • Thus, creation of RBCs is increased during hypoxia
111
Q

What is polycythemia?

A

A condition where there is an increased number of RBCs.

112
Q

What can cause polycythemia?

A

HIF upregulation (or other changes in the HIF pathway), which leads to increased EPO production and thus RBC production.

113
Q

Give an example of a polythemia and the physiological changes that are seen.

A
  • Chuvash polythemia
  • Upregulation of HIF pathways not only causes erythropoiesis, but also mimics cardiorespiratory effects of high altitude (hyperventilation and increased pulmonary arterial pressure)
114
Q

How does polycythemia affect oxygen delivery to tissues?

A

Polycythemia slows blood flow, which decreases oxygen delivery to tissues.

115
Q

Is hypoxic pulmonary vasoconstriction useful at high altitudes? What is the evidence for this?

A
  • No, it is not, and it can be dangerous
  • (Petousi, 2014) found that Tibetans (a high-altitude population) had reduced HPV in response to altitude compare to Han Chinese (a low-altitude population)
116
Q

What may underlie Tibetans’ reduced HPV in response to altitude?

A
  • Differences in expression of genes within the HIF-pathways.
  • These HIF differences also underlie different haemoglobin concentrations in these populations.
117
Q

What is chronic mountain sickness?

[EXTRA]

A
118
Q

What equation can be used to understand all of the physiological changes at altitude?

[EXTRA]

A
  • The alveolar gas equation
  • You can understand the changes by remembering that Patm decreases, PH20 stays the same and PaCO2 increases slightly.
  • This means that the PAO2 greatly falls and therefore haemoglobin saturation falls too. CO and ventilation can be increased to compensate.
  • Ventilation decreases PaCO2, which helps.
119
Q

Aside from EPO-mediated haemoglobin synthesis, how can haemoglobin concentration be increased at altitude?

A

ADH levels decrease, so blood volume decreases and thus [Hb] increases.

120
Q

What are the usual physiological parameters and the variation seen in each?

A

NB The parameters for core body temperature are very tight, and there is a good reason for this!

121
Q

How many compartments do we consider the body to have in temperature regulation?

A
  • Two compartment system:
    • The core (brain, thoracic and abdominal compartments containing the heat producing organs)
      • This region is held at ~37.0+/- 0.5*C
    • The peripheral shell (this is cooler and allows for regulation of temperature)
  • Communication between the two compartments is achieved via the circulation as blood is allowed to move between the two compartments, and can do so in either direction
122
Q

What are some normal variations in body temperature?

A
  • Circadian rhythms
    • Daily variations in body temperature occur, +/-0.5*C
    • Minimum occurs in the early hours of the morning, peak in the late afternoon
  • Menstrual cycle
    • Rise of +1*C is seen following ovulation
123
Q

Why is body temperature so tightly regulated?

A
  • To provide optimal conditions for cellular enzymatic reactions
    • When body temperature exceeds 42*C, cellular proteins are damaged
    • If the temperature drops, these enzymes and proteins become less efficient/effective
    • Energy expenditure falls 13% for every 1*C drop in core temperature (as drop in body temperature results in decreased enzymatic rates)
124
Q

What is a homeotherm?

A
  • This is an organism that maintains a constant body temperature through metabolic processes
    • This body temperature is often above that of the surrounding temperature
    • Humans are homeotherms
125
Q

What are the challenges against body temperature regulation?

A
  • External conditions can vary greatly and cause some challenge
    • Environmental conditions mean that external temperatures can vary by more than 100°C
    • The highest temperature recorded was 56.7°C in Death Valley, California
    • The lowest temperature recorded was -89.2°C at Vostok Station in Antarctica
  • Internal changes in temperature in response to changes in metabolism
    • This can range from something as simple as eating to exercise
126
Q

What is the thermoneutral zone?

A
  • This is the temperature range over which there is no ‘active’ temperature gain or loss
    • This means that the surrounding temperature is pretty well matched with our typical heat generation
    • If temperature drops below this zone, we start to increase heat production to maintain homeostasis
    • If the temperature increases above the thermoneutral zone, we begin to actively dissipate heat and begin cooler temperature-seeking behaviours
127
Q

What is the thermoneutral zone for humans?

A
  • Naked = 25-30*C
  • Light clothing = 18-22*C
    • Affects heat loss from the body therefore reduces the range
128
Q

Approximately how much of daily energy expenditure is accounted for by basal metabolism?

A

~60%

129
Q

What is Kleiber’s law?

[EXTRA]

A
  • ‘For the vast majority of animals, an animal’s metabolic rate scales to the 3/4 power of the animal’s mass’
    • I.e. if q0 is the animal’s metabolic rate, and M the mass, then Kleiber’s law states that q0 =~M3/4
    • Essentially, larger animal = larger metabolic rate
  • Named after Max Kleiber, Swiss agricultural biologist
  • There is still some argument over the exact value of the power, with some claiming it to be 2/3, but the constant is relatively arbitrary
130
Q

How does most of the energy generated from food end up?

A
  • Most eventually ends up as heat
  • Metabolic reactions are frequently inefficient, and so end up releasing the byproduct of heat
131
Q

How do we measure the energy in food?

[EXTRA]

A
  • In calories
    • One calorie is the energy required to heat 1g of water by 1*C
    • The Calorie (or kilocalorie) is 1000 calories
132
Q

What is the average energy requirements of 70kg man at rest?

[EXTRA]

A
  • Average 70kg man at rest will use 1650 kcal/day
133
Q

What hormones affect BMR?

A
  • Thyroid hormone
  • Testosterone
  • Growth hormone
134
Q

What is the largest variable for heat production?

A

Physical exercise

  • ~7% of daily energy expenditure is due to ‘non-exercise’ activity (e.g. fidgeting, non-specific exercise, muscle tone required for holding posture)
  • As exercise increases/becomes more significant, there is a rapid increase in energy expenditure requirements
135
Q

How does thyroid hormone (thyroxine) affect BMR?

A
  • Thyroid hormones (thyroxine) can raise BMR to 50-100% above normal
  • Total loss of thyroxine will decrease BMR to 40-60% of normal levels

[EXTRA]

  • Adaptation of the thyroid gland is seen in people living in different geographical locations
  • People living in arctic regions have a BMR 10-20% above those in tropical regions, allowing an increased generation of heat to deal with the colder environment
136
Q

What is brown adipose tissue (BAT)? How does it generate heat?

A
  • Adipose tissue rich in mitochondria
  • Also contain the uncoupling protein 1 (UCP-1)
  • Heat is generated through the dissipation of the proton gradient across the inner mitochondrial membrane via UCP-1
  • Role in adults is a topic of ongoing research (particularly in isolating treatments for obesity) but it has been shown to play a vital role in neonatal thermogenesis (as neonates are unable to shiver)
    • Found primarily between the shoulder blades and around the kidneys
137
Q

How does testosterone affect BMR?

A

~10-50% increase in BMR

138
Q

When is brown adipose tissue (BAT) activated? Through what mechanisms is this achieved?

A
  • BAT is activated in resposne to low temperatures
  • Stimulation occurs via the release of noradrenaline from the sympathetic nervous system
  • Activation acts via multiple transcription factors, including PGC1alpha and the PPARs to increase mitochondrial proliferation and fatty acid metabolism
    • PPARs = peroxisome proliferation activated receptor
139
Q

What are the 4 heat loss mechanisms?

A
140
Q

How does growth hormone affect BMR?

A

~15-20% increase in BMR

141
Q

What law is used to describe heat losses due to radiation?

A

Stefan-Boltzmann law

  • Emissivity is the measure of a material’s effective ability to emit and absorb thermal radiation, black objects have a high emissivity, white objects do not
  • NB That the temperature difference between the object and the environment is to the power of 4, therefore has a large effect on the equation
    • Also note that energy can only be lost from the body via radiation if the temperature gradient favours energy loss to the surroundings (i.e. they are cooler than the body)
    • If the surrounding temperature increases to exceed that of the body, radiation will occur in the other direction/heat is transferred to the body
142
Q

What is the effect of food on body temperature?

A
  • Thermogenic
  • Heat is generated as a byproduct of the chemical reactions including digestion, absorption and storage
    • NB That the actual temperature of the food will also have an effect (e.g. food is often hot, and so will warm you up that way regardless)
143
Q

How does the content of the meal affect changes in BMR?

A
  • Fat/carbohydrate meals cause BMR to increase by ~4%
  • Protein heavy meals can raise BMR up to 30% (hence the meat sweats due to raised body temp after raised BMR)
144
Q

What is thermogenesis?

A

The process of heat generation in warm-blooded animals (and some plants). Includes the actions of shivering and brown adipose tissue in animals.

145
Q

What is core body temperature?

A

Between 36.1-37.8*C in normal physiological parameters

NB that this can differ from the peripheral temperature, which is (understandably) cooler

146
Q

What is radiative heat loss?

A

This is heat loss due to the emission of a spectrum of electromagnetic radiation due to an object’s temperature. Requires a thermal gradient.

147
Q

What is convection?

A
  • This is the removal of heat from the body by air currents (also liquids)
  • Initial loss is through conduction of heat to the surrounding air, causing these particles to gain heat, become less dense and rise, introducing new, cooler air to the skin and then transferring energy to the surroundings
  • Requires a thermal gradient
148
Q

What is magnitude of heat loss via convection dependent on?

A
  • Magnitude is dependent on the movement of air over the surface of the body
  • Conductive heat loss ∝ √wind velocity
    • Wind = greater movement of particles around the body, therefore windy conditions remove warmed particles from around the body/replacing them with cold particles
      • This increases heat loss
  • This explains wind chill
  • Rate is also heavily affected by clothing trapping air close to the skin, as this prevents the warmed air from moving away from the body
    • [EXTRA] Convection works on all fluids, therefore this is a principle that contributes partly in the function of wetsuits (traps warmed layer of water around the body to limit conductive and convective heat losses)
149
Q

What is conduction?

A

The transfer of heat through direct contact with objects. Requires a thermal gradient.

150
Q

Draw a diagram summarising the inputs and outputs of temperature regulation at the CNS.

A
151
Q

When is conduction most and least relevant?

A
  • Conduction has very little effect on heat loss in air as air is a poor conductor
  • Water is 25x better at conducting heat, therefore conduction is significantly more important
    • Immersion in 10*C water can lead to death in ~2 hours
    • Wet suits work by preventing conduction losses as air bubbles in the material act as poor conductors
152
Q

What is evaporation?

A

This is the conversion of water from a liquid to a gas - energy is required to overcome the latent heat of vaporisation

153
Q

What is the latent heat of vaporisation?

A

This is the amount of energy required to convert one unit (e.g. mol or kg) of liquid into a gas

For water, this value is 538kcal/kg

154
Q

What are typical daily water losses in sweat? How much does this contribute to energy expenditure?

A

600-700ml/day, contributing 16-19 kcal/hour of heat loss

155
Q

At what temperatures can a naked person in dry air maintain a ‘normal’ core body temperature?

A

Between approx. 12*C and 54*C (this is larger than the range for the thermoneutral zone as heat loss and gain processes are considered)

156
Q

What is the equation for body heat?

A

Body heat = Metabolic Heat Production +/- Conductive, Convective and Radiant Heat Exchange - Evaporative Heat Loss

157
Q

How can heat be lost in high environmental temperatures?

A
  • The only way is through evaporative losses
    • Other processes require a temperature gradient (going from high to low temps) and so will actually cause heat gain if the surroundings are too warm
    • This means that sweating and evaporative heat loss become key at high temperatures
158
Q

What are arterio-venous shunts?

A
  • These are methods of allowing a separation between nutritional and thermoregulatory blood flow
    • These vessels bypass the capillaries and can increase or decrease blood flow to the periphery to facilitate or limit heat loss respectively
  • Flow through shunts can be ‘on’ or ‘off’
  • Blood flow through the shunts can be 100-fold greater than nutritional requirements
  • Shunts are controlled by centrally mediated alpha-1 adrenergic receptors
    • Although this is augmented by local alpha-2 adrenergic receptors in the periphery
159
Q

How are changes in temperature sensed?

A
  • Primarily through nervous feedback systems from the periphery to the CNS
  • Centre in the brain: temperature regulating centers in the hypothalamus
160
Q

What is the key centre for temperature regulation in the brain?

A

Hypothalamus is area through which almost all temperature regulating mechanisms work

161
Q

What is the ‘thermostat’ for the body?

A
  • The preoptic and anterior hypothalamus operates as the body’s thermostat
    • This part of the brain has greater sensitivity to heat than to cold
162
Q

Where are the peripheral temperature sensors located and what are they more sensitive to?

A
  • Spinal cord, abdominal viscera and great veins (deep body sensors)
  • Skin
  • Greater sensitivity to cold than hot
163
Q

How can heat loss be increased without the presence of a thermal gradient?

A

Through sweat production and its subsequent evaporation facilitates heat loss from the body, particularly in hot conditions

164
Q

How can sweat production be increased? What properties does this secretion have?

A
  • Sweat production can be increased by cholinergic sympathetic nerve fibres
  • The glands can also be stimulated by adrenaline/noradrenaline, e.g. during exercise to increase heat dissipation
  • This elicits the secretion of a primary fluid into the sweat duct
    • This fluid has a composition similar to that of plasma, just without plasma proteins
    • As regulation/reabsorption occurs along the tubule, if the demand for secretion increases and therefore the transit time decreases, then the time over which this secretion can be modified is rapidly decreased
165
Q

Are the following more sensitive to hot or cold stimuli?

  1. Preoptic and Anterior Hypothalamus
  2. Peripheral temperature receptors
A
  1. Hot
  2. Cold
166
Q

How do peripheral temperature receptors respond to changes in temperature?

A
  • They alter their discharge frequency
    • Sensors are rapidly adapting/will rapidly adapt to new static levels
    • This means that they are bad at sensing absolute temperature, but are very good at sensing changes in temperature
167
Q

What is a simple test to show the adaptive nature of peripheral temperature receptors?

[EXTRA]

A
  • Two bowls of water, one quite warm (35-40*C), the other very cold (add ice, ~0*C)
  • Put a hand in each boel and leave it there for 3-4 mins, then put the hand into a bowl of water at room temperature
  • Hand in ice water thinks that the bowl of room temperature water is really hot, hand in bowl of warmer water thinks that room temperature bowl is very cold
    • This shows that the change in temperature has shaped the response, not the actual temperature, or else the hands would experience the same sensation
168
Q

What is the function of the posterior hypothalamus in relation to temperature regulation?

A
  • This part of the brain collates and combines the signals from the peripheral sensors and from the central sensors (in the anterior hypothalamus)
  • This leads to control over the heat-conserving and heat-producing reactions of the body
169
Q

Overall, how are heat losses from the body minimised?

A
  • Uncontrolled losses from the core are minimised using insulation
    • Therefore a layer of fat is seen around the core to produce this insulation and to minimise heat loss from fluctuations in the core body temperature
  • Flow of heat from the core to the shell is also controlled through regulating blood flow
170
Q

What effect do the arterial and venous systems have on temperature regulation?

A
  • These systems control the flow of heat from the core to the shell
  • Arteries flow in one direction, carrying warm blood from the core, in close proximity to veins flowing in the other direction, carrying cooler blood from the periphery
    • This allows the arteries to warm up blood returning to the core in the veins, therefore minimising heat loss at the periphery through maximising heat transfer between the warm arteries and cooler veins
    • This also has the added benefit of warming the veins to prevent them from taking too much heat away from the viscera
  • Overall, this minimises heat loss from the core
171
Q

How much can heat production be increased by through shivering?

A

~200%

172
Q

What is the temperature range within which humans can sensibly control their body temperature?

A
  • When naked: ~12*C to ~54*C
  • When this range is exceeded, other methods of regulating core body temperature must be found
    • Using clothing, this range can be extended somewhat, and it is easier to deal with colder temperatures in this way
173
Q

What is the comparison between shivering and exercise in terms of energy production?

A
  • Shivering can increase heat production by approx 200%, but this is small compared to exercise-induced increases which can be >10 fold
  • This leads to shivering and exercise-seeking behaviours in cold conditions
174
Q

When can shivering not occur?

A

In newborn infants - this makes them far more susceptible to the cold and they instead rely upon the action of BAT

175
Q

What is shivering?

A
  • Rapid (~50Hz) and unsynchronised muscular activity
    • This results in ATP cross-bridge cycling to facilitate contraction and production of heat as a byproduct of the metabolic reaction
  • Shivering is likely to result from a feedback oscillation of the muscle spindle stretch reflex mechanism
  • Random oscillation is overlaid on a centrally controlled 4-8 cycle/min of ‘waxing and waning’
    • E.g. shivering cycles between more and less severe bouts
176
Q

Where is the need for shivering signalled from? Where is this signal translated?

A
  • Posterior hypothalamus signals the need for shivering after collating inputs from peripheral receptors and central receptors (anterior and preoptic hypothalamus)
  • This signal is translated to the anterior motor neurons
177
Q

What is frostbite?

A
  • Severe form of hypothermia
  • Occurs when surface areas (commonly on peripheral parts of the body) freeze and there is formation of ice crystals
  • Commonly affects the hands, feet and ear lobes
  • If extensive formation of ice crystals occurs, this can lead to cell death
    • Therefore gangrene often follows thawing
  • Surgical removal of affected areas is necessary
178
Q

What are the differences in sweat composition when comparing light and heavy stimulation of sweat secretion?

A
  • With light stimulation, almost all of the Na+ and Cl- is reabsorbed (along with a lot of water) as the secretions travel along the duct
    • This leads to a concentrated solution made up of urea, lactic acid and potassium
  • With heavy stimulation, large volumes of sweat are produced
    • This results in poor reabsorption of NaCl and increased fluid loss (due to the subsequently less concentrated liquid secreted)
179
Q

How much sweat can be produced by trained athletes?

A

2 litres/hour

180
Q

What happens when the set point for body temperature is raised during infection?

A
  • Individuals feel ‘cold’ despite core body temperature being above the normal level
    • This results in the recruitment of normal physiological responses to being cold, such as shivering
  • Upon restoration of a normal set-point, individuals experience a febrile ‘rush’ or ‘crisis’ where the body tries to restore a normal core temperature through sweating and vasodilation
    • This is seen at the end of illness, but there is also some evidence to suggest that this occurs cyclically throughout fever (bouts of breaking and shivering)
181
Q

What is the effect of hot climates on sweat production?

A
  • Over 1-6 weeks of exposure to a hot climate, sweat production is upregulated
  • In response to the increased loss of NaCl caused by this change, the body also upregulates aldosterone secretion to increased Na+ reabsorption
182
Q

Where do behavioural changes in response to temperature originate from?

A

Cerebral cortex provides the necessary inputs

183
Q

What are the behavioural changes in response to hot and cold for radiation?

A
  • Alter the balance with external sources of radiation
    • If too hot: alter clothing to change emissivity of the individual
    • If too cold: find an alternate source of radiation, e.g. sit in front of a fire/lie out in the sun
184
Q

What are the behavioural changes in response to hot and cold for conduction?

A
  • Control with clothing where possible
    • E.g. if hot, will remove layers, if cold, will put them on
    • Remember that air is a poor conductor, so trapping layers of air close to the skin can act as insulation
    • Cold individuals will avoid getting clothes wet, as this will increase conduction
185
Q

What are the behavioural changes in response to hot and cold for convection?

A
  • Convection can be controlled using clothing and flow of air over the skin
    • E.g. if hot, increasing air flow will aid heat losses via convection - this can be achieved using a fan
    • If cold, individuals will try and find shelter/get out of the wind
186
Q

What are the behavioural changes in response to hot and cold for evaporation?

A
  • If hot, can spray/douse themselves with water
    • This will have the same effect as sweating and facilitate transfer of energy to the surroundings through the evaporation of this added water off of the skin
187
Q

How can we measure body temperature?

[EXTRA?]

A
  • There are many methods, all give slightly different values depending on how close you can actually get to the body temperature
  • Tympanic membrane or nasopharyngeal sites can give readings relatively close to that of the central body temperature, but can be uncomfortable and risk damage
  • Rectal thermometers are more peripheral and therefore give a lower reading but can perhaps be tolerated for a longer time
188
Q

What core body temperature is hyperthermia classified as?

A
  • Core body temperature >38.3*C
  • Classified as severe once the temperature reaches 40*C (heat stroke = >40.6*C)
189
Q

What core body temperature is hypothermia classified as?

A
  • Core body temperature <35*C
190
Q

What is hypothermia?

A
  • This is where continued exposure to cold temperatures causes the core body temperature to drop below 35*C
  • Energy expenditure falls 13% for every 1*C drop in core temperature
  • Loss of consciousness occurs at core body temp of 30*C
191
Q

What are the cardiac changes seen in hypothermia?

A
  • Changes can be seen on the ECG, including bradycardia and prolongation of the PR and QT intervals
  • Ventricular fibrillation occurs at 28*C
192
Q

Which groups of people are most susceptible to hypothermia?

[EXTRA]

A
  • Neonates are particularly susceptible due to reduced behavioural adaptations possible (e.g. cannot put on clothes or move) and have a greater SA:Vol ratio than adults
    • They also cannot shiver, but do have BAT for thermogenesis
  • The elderly are also susceptible due to potentially reduced mobility and less efficient thermoregulatory mechanisms
    • Lessened mobility also makes them less able to move for heat generation and also slows the process to find and put on clothes
193
Q

What are some potential benefits from hypothermia?

[EXTRA]

A
  • Recovery from cold injury
    • Anna Båagneholm survived a skiing accident that left her trapped in freezing water under a layer of ice for 80 minutes
    • Took her >2 hours to get to the hospital, core body temp. so low that doctors thought she was dead
    • One doctor believed that the low temp may have saved her/prevented ischaemic damage, so slowly brought her temperature back up
    • Restarted her heart and she somehow survived
    • https://www.youtube.com/watch?v=jLr15BBBtrc
  • Deliberate hypothermia
    • Used in neurosurgery while on extracorporeal (‘out of body’) circulation to allow circulation to be stopped for ~15 minutes without incurring ischaemic injury to tissue
      • Due to reduction of metabolic rate, damage by active enzymes within the ischaemic tissue is reduced
    • Cold cardioplegia – cooling heart with cold solution high in potassium to reduce metabolism and depolarize membrane to prevent cardiac excitation allows cardiac surgery for around an hour without ischemic damage
194
Q

What is the effect of infection on temperature regulation?

A
  • Infection can lead to an elevation of the core body temperature set point, and therefore hyperthermia
  • This is caused either through the direct action of proteins/ protein breakdown products/lipopolysaccharide toxins released from bacterial cells (pyrogens) or by their action on macrophages, leukocytes and lymphocytes
    • This causes the release of cytokines (IL-1 and IL-6)
  • These pyrogens act to elevate prostaglandin E2 synthesis in the hypothalamus (this raises the set point)
195
Q

What molecule causes the set point of body temperature to be raised in the hypothalamus?

A
  • Prostaglandin E2 (PGE2)
  • Acts on E2 receptors in the anterior hypothalamus to raise the set point of body temperature
196
Q

What are antipyretics?

A
  • Drugs that act to reduce the elevated set point
  • Examples include:
    • Acetaminophen (paracetamol)
    • Aspirin and other NSAIDs
197
Q

How are antipyretics thought to work?

A
  • Principally through their inhibition of the enzyme cyclooxygenase (COX), preventing the synthesis of inflammatory prostaglandins (including PGE2)
  • Recent studies on the mechanism of action have revealed effects independent of COX inhibition as well
198
Q

What are the effects of continued exposure to high environmental temperatures?

[EXTRA]

A
  • Heat exhaustion
  • Heat stroke
199
Q

What is heat exhaustion?

A
  • AKA heat syncope
  • Occurs due to hypovolaemia following excessive sweating
  • Symptoms include hyperthermia, excessive sweating, dizziness, nausea, headache
200
Q

What is heat stroke?

[EXTRA]

A
  • This is where body temperature >40.6*C
  • Thermoregulatory mechanisms fail at this point, causing the patient to become dizzy and confused
  • Loss of consciousness follows rapidly, then death
  • Treatment involves rapidly reducing body temperature
    • There is some disagreement over whether cold or cool water should be used
    • Cold water can induce vasoconstriction and shivering, which will instead elevate temperature
201
Q

What is malignant hyperthermia (MHS)?

[EXTRA]

A
  • Malignant hyperthermia is a pathological state where body temperature is overwhelmed by heat production
    • It is often fatal
    • Caused by drugs include the muscle relaxant suxamethonium and volatile anaesthetics including halothane
    • This is very rare (1 case per 100,000 in adult general anaesthetics)
    • Can be caused by mutations in ryanodine receptor 1 (RYR1), inherited in an AR fashion
    • Dantrolene is the reversal agent for MHS caused by anaesthetic agents, and so will be found in the collection of all anaesthetists
    • Some individuals with this condition can occasionally enter malignant hyperthermia after extreme exercise or heat stroke, as the condition is caused by over-activation of skeletal muscle and its contraction, causing excessive heat release
202
Q

What is piloerection?

A
  • Erection or ‘bristling’ of hairs along the body due to the involuntary contraction of erector pili muscles at the base of the hair follicles
  • This is a reflexive response to cold, shock or fear, mediated by the sympathetic nervous system
  • Thought to trap a layer of air close to the surface of the skin, providing some small amount of insulation, and also raises water on the hairs away from the skin
203
Q

What is the effect of burn injuries on thermoregulation?

A
  • Burns cause cell damage and a hypermetabolic state
    • This is characterised by increased energy expenditure and increased muscle protein catabolism, which can lead to a hyperthermia of sorts
  • If there is extensive skin loss, however, hypothermia can occur as the skin is essential for many energy- and heat-preserving behaviours
    • With increased energy expenditure, more heat will be lost and so burns can rapidly lead to hypothermia
204
Q

How do arterial baroreceptors influence ventilation?

A
  • Stimulation of the arterial baroreceptors inhibits respiration and this has been demonstrated experimentally either by applying pressure to an isolated carotid sinus or by stimulation of the carotid sinus nerve (which contains both baroreceptor and chemoreceptor afferents).
  • However, this is a controversial effect that is not well defined.
205
Q

Give an example of a cardiovascular change that happens at altitude.

A
  • Hypoxia inducible factor (HIF) stimulates erythropoiesis via transcription of EPO. The result of this is increased haematocrit, which is contributed to by increased urination.
  • Along with increases in capillary density, this means that it is easier to oxygenate the blood in the lungs and deliver sufficient oxygen to respiring tissues.

YEAR 2 - Applied Physiology & Pharmacology (11 decks)

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