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Physiology for Anaesthetists > Altitude > Flashcards

Altitude Flashcards

1
Q

What level of elevation defines ‘altitude’?

A

2500 m

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2
Q

Above what altitude is long term habitation impossible.

A

6000 m

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3
Q

Above what altitude would acute exposure lead to loss of consciousness

A

5500 m

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4
Q

What’s Everests peak altitude

A

8848 m

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5
Q

How many people live at altitudes pf more than 2500 m

A

100 million

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6
Q

List the problems associated with increasing altitude

A
  1. Barometric pressure declines exponentially
  2. Temp declines 1 deg C every 150 m
  3. Reduced relative humidity (fluid loss)
  4. Increased solar radiation (reduces cloud cover)
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7
Q

What’s Dalton’s law. Give the equation for PAO2

A

Dalton’s law states that the total pressure of a mixture of gases is equal to the sum of the partial pressures of the gases in the mixture.

Therefore,

PAO2 = PB x FiO2

So as PB decreases with altitude, PaO2 decreases too.

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8
Q

How is the PaO2 affected by altitude

A

Alveolar gas equation
PA = FIO2 (PB - PH20) - PaCO2/R

Reduced alveolar PAO2 leads to hypoxic hypoxia

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9
Q

How is saturated vapour pressure changed by altitude?

A

It remains unchanged –> 6.3 kPa at 37 deg C

PA = FIO2 (PB - PH20) - PaCO2/R
PH20 - saturated vapour pressure of water is unchanged at altitude 6.3 kPa. Therefore it has a relatively greater effect at altitude.

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10
Q

At what altitude are physiological changes observed? Why do physiological changes not occur below this altitude. And which systems are involved

A

> 2500
At this altitude the PaO2 falls below 8 kPa which is the THRESHOLD FOR ACTIVATION of the PERIPHERAL CHEMORECEPTORS

RSP, CVS, Haem, Renal

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11
Q

Summarise the acute and chronic physiological response to altitude

A

Acute adaptation aims to increase PaO2 by hyperventilation and is limited by respiratory alkalosis.

Chronic adaptation permits hyperventilation as the kidneys correct the pH disturbance.

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12
Q

What is the ‘Braking effect’ with regard to the acute physiological response to altitude?

A

Peripheral chemoreceptors sense PaO2 < 8 kPa
–> hyperventilation

Hyperventilation –>

  1. Low PaCO2
  2. High pH

Low PaCO2 sensed by central chemoreceptors
–> Limits hyperventilation

High pH sensed by carotid bodies
–> Limits hyperventilation

This limitation on hyperventilation by the central and peripheral chemoreceptors is known as the braking effect

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13
Q

What is the mechanism for chronic physiological adaptation to altitude, i.e. what removes the braking effect

A

Previously thought:
–> Over a few days, kidneys excrete excess HCO3- reducing alkalosis and permitting more hyperventilation to compensate for low PaO2.

Now:
–> recent studies show that braking effect is decreased before renal HCO3- excretion begins. So now it is believed that the CSF HCO3- is reduced by another mechanism not yet elucidated.

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14
Q

Is there a diffusion limitation at altitude? Describe the mechanism.

A

Under certain circumstances: with exercise and/or High Altitude Pulmonary Edema

Exercise reduces transit of blood past alveoli. As O2 conc gradient is lower, O2 diffusion may not complete prior to RBC completing pass of alveoli.

HAPE –> Increased interstitial fluid thickens the alveolar-capillary barrier.

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15
Q

Summarise the acute and chronic RESP response to altitude

A

Low PaO2 < 8.0 –> peripheral chemoreceptor driven hyperventilation + respiratory alkalosis. Low PaCO2 (central chemoreceptors) + High pH (peripheral chemoreceptors) –> braking effect on hyperventilation.

Over time, first BBB (unknown mechanism) and then kidneys excrete additional HCO3- to mitigate the braking effect and allow for further hyperventilation and chronic adaptation to altitude (low PaO2)

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16
Q

Summarise the CVS response to altitude

A
  1. Increased HR (SNS response to low PaO@)
  2. Reduced plasma volume (Hct increases 20%)
    - -> low PaO2 –> SNS –> Increase CO and increased GFR (pressure diuresis)
    - -> Hyperventilation + Reduced relative humidity –> increased insensible losses.
  3. Increased myocardial work
    - -> Increased blood viscosity (Hct 0.6) increases LV work
  4. Hypoxic Pulmonary Vasoconstriction
    - -> HAPE (Hydrostatic Pressure increased)
    - -> Acute RHF
17
Q

What are the mechanisms for reduced plasma volume at altitude

A

Low PaO2 –> SNS –> increased CO –> increased GFR and RPP –> Pressure diuresis

Also

Hyperventilation combined with reduced relative humidity at altitude increases insensible fluid losses from lungs.

18
Q

Describe the changes to the oxygen haemoglobin dissociation curve that occur at altitude

A

Initially
P50 shifts to the left due to respiratory alkalosis

Thereafter, (over 7 days)
RBC’s produce increased 2.3 DPG returning P50 rightward

19
Q

How is the red cell mass affected by altitude

A

Chronic hypoxia at altitude (over hours) kidney responds by increasing EPO secretion stimulating bone marrow to produce erythrocytes

20
Q

How does the VTE risk differ at altitude

A

Thrombosis is more likely at altitude due to increased blood viscosity and hypoxic platelet activation

21
Q

Describe and classify the body’s response to chronic exposure to a cold environment

A

Heat conservation

  1. Peripheral vasoconstriction
  2. Decreased sweating
  3. Behavioural change (clothing)

Heat production

  1. Increased BMR
  2. Shivering
  3. Increased brown fat activity

All heat generating mechanism consume O2 at a time of relative hypoxeamia

22
Q

Summarise the haematological changes to altitude

A
  1. OHDC P50 initially left from resp. alk and then right RBCs make more 2.3 DPG (7 days)
  2. EPO from kidney to low PaO2 – hours
  3. Increased thrombosis risk (viscosity and plt activation with low PaO2)
23
Q

Define acute high-altitude illness

A

Maladaptive physiological response to high altitude, occurring in unacclimatised individuals who ascend too quickly

24
Q

Define and describe the three high altitude syndromes?

A

Acute Mountain Sickness (AMS)
- Headache +
—> Nausea / Dizziness / Anorexia / Insomnia
Rx: Remain at same altitude 3 - 4 days

High Altitude Cerebral Edema (HACE)
- Headache +
---> Ataxia / Severe Cognitive Impairment 
(Can result in seizures / coma / death)
Rx: Descent

High Altitude Pulmonary Edema (HAPE)
- Exertional dyspnoea and persistent dry cough
–> then haemoptysis and orthopnoea
–> Most serious accounting for most mortality
Rx: Descent

25
Q

Describe the treatment of high altitude illness

A

Definitive treatment = DESCENT

Other treatments buy time

  1. Supplemental O2
  2. Hyperbaric chamber (Gamow bag) (simulates descent)
  3. Pharmacological Rx
    - -> Acetazolamide
    - -> Dexamethasone
    - -> Nifedipine
26
Q

What is the name of the portable pressure bag that simulates descent used for high altitude illness

A

Gamow bag

27
Q

Vaporizers are calibrated at sea level. How does this influence their use at hospitals located 2000 - 3000 m above sea level

A

It does not. Saturated Vapour Pressure is independent of Barometric Pressure. Therefore the SVP above the volatile agent liquid is unchanged. Alveolar partial pressure of volatile agent remains the same at altitude.

28
Q

How does the function of flowmeters differ at altitude and how should the use be adjusted>

A

Flowmeters underread at altitude due to reduced gas density. However, since the number of molecules (e.g. O2) is what matters and not the volume of gas, flowmeters can be used as normal

29
Q

How does altitude affect the function of Venturi Masks

A

At altitude they deliver a slightly higher percentage of O2 than at sea level

30
Q

How are the cuff pressures within ETTs and LMAs affected by altitude

A

Rapid ascent during aeromedical transfer of a critically ill patient can result in significant increase in cuff pressures of ETTs and LMAs

31
Q

Summarise the pathophysiology of AMS and HACE

A

AMS:
Hypoxaemia –> cerebral vasodilation –> activation of trigeminal vascular system (like in migraine) –> headache and nausea.

Hypoxaemia –> cerebral vasodilation –> increase brain volume –> Increase ICP (Monroe Kelly) –> headache

If this does not resolve –> HACE

HACE
Prolonged increased cerebral vasodilation + ICP –> Cascade of oedema formation
1. Intracellular (cytotoxic) oedema
2. Extracellular (ionic) oedema
3. Vasogenic oedema with protein extravasation
4. Loss of BBB integrity –> red cells and microhaemorrhages

32
Q

Summarise the pathophysiology of HAPE

A

HAPE (Strong genetic role)

Maladaptive response to hypobaric hypoxia

  1. SNS activation –> increase CO
  2. HPV - uneven
  3. Inadequate NO + too much endothelin
  4. Inadequate alveolar fluid clearance

–> accumulation of extravascular fluid in alveolar spaces –> impair gas exchange

High PMAP + Uneven HPV –> regional overperfusion –> patchy pulmonary oedema

Physiology for Anaesthetists (61 decks)

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