Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Cardiorespiratory CC > Physiology of high altitude > Flashcards

Physiology of high altitude Flashcards

1
Q

Partial pressure O2 at high altitudes

A

Less

“driving force” to attach O2 to haemoglobin less

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Blood in lungs at high altitudes

A

Less saturated with O2

–> pulmonary hypoxia + hypoxaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Ventilation is mainly regulated by

A

PaCO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

PaCO2 at altitude

A

Kept constant by body

BUT body becomes hypoxic because of lower partial pressure of O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Hypoxic drive

A

Hypoxic drive cannot overcome inhibition by hypercapnic drive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Physiological effects of ascent to altitude are due to

A

Hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Physiological effects at high altitude

A

Low partial pressure of O2 + resulting hypoxaemia will stimulate increased ventilation via hypoxia detectors in carotid bodies
BUT hypoxia-driven ventilation response partially antagonised by more powerful depression of ventilation caused by excess blow off of CO2
–> alkalosis at central chemoreceptors
–> then inhibit the increase in resp. drive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Ventilatory response at high altitude

A

Inadequate to cope with the low pO2 and a degree of hypoxaemia + hypoxia results

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Hypoxic drive from carotid bodies

A

Weak

Normally only becomes significant at PO2 below about 60mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hypoxic drive significance

A

Only significant in low pO2 together with high pCO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Rapid ascent to 2000m+

A

Stimulates SNS
Increased resting HR + CO
Mildly increased BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Rapid ascent 2000m+ after minutes of exposure

A

PO2 in alveoli is low, so pulmonary circulation reacts to hypoxia with vasoconstriction
–> worsens hypoxaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pulmonary resistance rapid ascent 2000m+

A

Increases

–> mild pulmonary arterial hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Acclimatisation

A

Adapting to high altitude

Initial pulmonary arterial hypertension wears off + hypoxia disappears

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Acclimatisation from sea level –> 2000m

A

Rapid

Day or two

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Acclimatisation from sea level –> 2000-6000m

A

Occur in people without respiratory disease

May take few weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Fully acclimatised climbers at 6000m

A

Feel well
Reasonable appetites
Sleep normally
Capable of carrying loads of 20-25kg on easy ground

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Above 7000m

A

Significant hypoxia
Tiredness + lethargy increases
Continuous exercise impossible
Climbing easy slopes painstaking + breathless

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Above 7500m

A

Death zone
Even acclimatised climbers have severe hypoxia + can only remain 2 or 3 days
–> after that body’s major symptoms will have severe physiological damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Mechanism of Acclimatisation

A

Metabolic acidosis caused by retention of acid + increased excretion of bicarbonate in kidneys
Increase in erythrocyte number
Reduced pulmonary vascular resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Acclimatisation MOA

A

Low pO2 in inspired air increases rate + depth of breathing
BUT blows off excess CO2 + produces respiratory alkalosis
–> high pH inhibits central chemoreceptors
–> decreased breathing
–> hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Acclimatisation MOA Pt 2 (kidneys)

A

Kidneys respond to hypoxaemia by increasing bicarbonate excretion
Decreased excretion of acid
–> metabolic acidosis
Metabolic acidosis counteracts the respiratory alkalosis
–> restores pH to normal
Drive to central chemoreceptors restored –> sustained increase in rate and depth of breathing to restore normoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Hypoxia during acclimatisation

A

Stimulates interstitial cells in kidney to raise EPO

–> increases haematocrit –> increases O2 carrying capacity of blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Haematocrit maximum

A

Functional limit to max haematocrit
Increased haematocrit = increased blood viscosity
Higher viscosity –> higher pulmonary vascular resistance –> pulmonary arterial hypertension + right sided heart failure

25
Pulmonary vascular resistance during acclimatisation
Pulmonary vascular resistance falls Partially due to reduced hypoxic vasoconstriction response Partly due to collateral circulations opening up between pulmonary arteries + veins
26
Increased synthesis of NO in pulmonary endothelium
Causes collateral circulations to open up between pulmonary arteries + veins
27
Acute Mountain Sickness
First sign that something is wrong
28
High Altitude Cerebral oedema
Can follow is AMS untreated Serious neurological condition Fatal if not treated
29
High Altitude Pulmonary Oedema
Equally serious to HACE | Can follow on from AMS
30
AMS signs + symptoms
``` Headache Poor sleep Tiredness Loss of appetite, nausea, vomiting Dizziness ``` All scored 0-3 for severity of symptoms --> need score of >3 for AMS diagnosis Like symptoms of hangover
31
1500-2000m rapid ascent from sea level AMS
Unlikely in most individuals | Mild illness
32
2500m rapid ascent from sea level AMS
1 in 5 people have symptoms if ascend within a day | Most ppl will acclimatise within a day or so
33
5000m rapid ascent from sea level AMS
Everyone temporarily ill if ascend within few hours to 5000m (e.g. plane) Acclimatisation can take several days or more
34
AMS Treatment Mild
Rest | No further ascent
35
AMS Treatment Severe
Immediate descent O2 Acetazolamide 250mg (3x day) Dexamethasone 4mg (4x daily) oral or IV
36
AMS Prevention
Slow ascent- <300m per day over 3000m Avoid unnecessary exercise Acetazolamide 250mg 2x day at start of climb
37
Acetazolamide (Diamox)
Carbonic anhydrase inhibitor
38
Carbonic anhydrase
In proximal tubule of kidney | Vital for renal reabsorption of bicarbonate
39
Acetazolamide MOA
Inhibits CA activity Increases bicarbonate excretion --> metabolic acidosis Compensates for the respiratory alkalosis caused by the hyperventilation at altitude
40
Acetazolamide MOA compared to normal
Kidneys produce metabolic acidosis anyway as part of acclimatisation --> Diamox speeds up process
41
Bicarbonate reabsorption Pt 1
CO2 diffuses from blood into proximal tubule cells Converted into carbonic acid (H2CO3) by Carbonic Anhydrase A inside the cells H2CO3 --> H+ and HCO3- Protons formed are ejected into tubular lumen by a Na+/H+ exchange ATPase --> sodium reabsorbed from tubular fluid + protons ejected into it --> bicarbonate collects in cell
42
Bicarbonate reabsorption Pt 2
Excreted protons react with bicarbonate which has been filtered by glomerulus The two ions are converted to CO2 + water by CA lining the tubule CO2 diffuses back into tubule cell where converted back into carbonic acid (H2CO3) --> bicarbonate is reabsorbed from tubule into tubular cells
43
Bicarbonate reabsorption part 3
CO2 that has diffused back into cell then converted back to H2CO3 by CA inside tubular cells H2CO3 --> H+ and HCO3- Protons pumped out to continue the reabsorption cycle HCO3- transferred from tubular cells back into blood
44
Acetazolamide
Conversion of HCO3- to CO2 in lumen is blocked | --> filtered bicarbonate is lost in urine
45
CA blocked inside cell
CO2 from blood can't be converted to HCO3- - -> no H+ available for the Na+/H+ ATP-ase - -> protons not pumped into urine + Na+ not reabsorbed - -> Na+ excreted in urine instead of H+
46
Acetazolamide net effect
Bicarbonate + Na+ lost in urine Urine becomes alkaline Blood becomes more acid
47
High levels of acetazolamide
Also inhibit CA in erythrocytes Blocks transport of CO2 from tissues --> lungs --> decreases loss of CO2 in lungs --> counteracts excessive loss of CO2 from body by hyperventilation
48
High altitude cerebral oedma (HACE) Symptoms
``` Can follow AMS if AMS left untreated Ataxia Nausea/vomiting Hallucination or disorientation Confusion Reduced conscious level Coma ```
49
HACE MOA
In hypoxaemia, supply of ATP in nerve cells decreases + sodium pumps run down Sodium leaks into nerve cell --> pulls water with it + brain swells Raises ICP + blocks cerebral veins Cerebral circulation fails, hypoxia gets worse + neurones die (starved of O2 + squished)
50
HACE treatment
Descend immediately Acetazolamide (reduces formation of CSF so decreases ICP) O2 Dexamethasone 8mg then 4mg 4x day orally or IV (prevents brain swelling) Hyperbaric chamber
51
High altitude pulmonary oedema (HAPE) sings + symptoms
``` Dyspnoea Reduced exercise tolerance Dry cough Blood stained sputum Crackles on chest ausculation ```
52
HAPE MOA
Hypoxic pulmonary vasoconstriction normally decreases with acclimatization --> if doesn't occur, pulmonary arterial hypertension can develop Raised arterial + capillary pressure --> fluid leaving blood + entering alveoli --> worsens already compromised gas exchange --> increases hypoxia + constriction --> VISCIOUS CYCLE
53
HAPE treatment
Descend immediately Sit patient upright O2 Nifedipine (Ca channel blocker) 20mg 4x day Hyperbaric chamber Viagra (inhibits altitude-induced hypoxaemia + pulmonary hypertension)
54
Nifedipine
Blocks constriction of pulmonary arteries | --> reduces PAH
55
Hyperbaric chamber
Increases partial pressure of O2 to improve oxygenation of blood Reduces hypoxic vasoconstriction
56
Viagra
Slows down breakdown of cyclic GMP, which is the vasodilator produced by NO Increases cGMP levels relaxes pulmonary arteries, stops PAH + improves O2 oxygenation
57
Pulmonary hypoxic vasoconstriction
Due to lack of NO being released from pulmonary endothelium
58
HACE + HAPE symptoms
``` HACE= AMS with CNS symptoms HAPE= AMS with pulmonary symptoms ```

Cardiorespiratory CC (34 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions