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Applied physiology and pharmacology > Altitude > Flashcards

Altitude Flashcards

1
Q

Patm at sea level?

A

~760mmHg

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2
Q

O2% in atm?

A

21%

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3
Q

PiO2 sea level?

A

160mmHg

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4
Q

What decreases with altitude?

A

Patm

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5
Q

What effect does falling Patm have on O2?

A

O2% stays at 21% BUT PiO2 falls

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6
Q

What is alveolar PO2? Why lower than PiO2?

A

100mmHg at sea level, oxygen has been extracted by pulmonary blood.

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7
Q

What is PaO2 why is it lower than alveolar PO2?

A

Due to a slight ventilation perfusion mismatch (0.8)

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8
Q

Acclimatization vs adaptation?

A

Adaptation due to selection pressure over thousands of years, seen in communities living at high altitude

Acclimatization consists of physiological changes seen in all humans who ascend to altitude

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9
Q

With every 5500m ascent, what happens to PiO2?

A

PiO2 roughly halves.

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10
Q

Why does arterial saturation remain high until 2000m?

A

Due to plateau on oxyhemoglobin dissociation curve.

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11
Q

When does saturation begin to fall significantly?

A

When PO2 falls below 60mmHg at 3000m.

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12
Q

What are the main systems responding to altitude?

A

Respiratory, cardiovascular and endocrine

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13
Q

When will one experience mountain sickness?

A

If one ascends slowly

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14
Q

What are the initial respiratory changes occurring at altitude?

A

Hypoxic stimulation of peripheral arterial chemoreceptors

Resting hyperventilation - to raise PaO2 closer to PiO2,

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15
Q

What is an immediate consequence of hyperventilation?

A

Reduces alveolar and arterial PCO2 - respiratory alkalosis

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16
Q

What is the initial change to the haemoglobin curve?

A

Due to fall in CO2

Shifts haemoglobin curve to the left (reverse Bohr shift) enabling arterial blood to bind to more O2 at a given PO2.

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17
Q

What happens to the haemoglobin curve at moderate to high altitude?

A

Respiratory alkalosis leads to a rise in 2,3BPG (formed during glycolysis in red blood cells). This binds to one of the beta chains of haemoglobin - deoxygenation and a right hand shift in the Bohr curve - improves O2 unloading to tissues.

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18
Q

What limits the respiratory alkalosis?

A

Central chemoreceptors regulate ventilation according to CSF [H+] influenced by both PCO2 and HCO3-.

Reduction of CO2 during ventilation and resultant alkalosis limits ventilation via central chemoreceptors.

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19
Q

How do we acclimatize to hyperventilation? (what was the traditional belief and what is the more modern belief?)

A

Traditionally attributed to correction of the respiratory alkalosis by the kidneys. Metabolic acidosis – renal response more long term (show on davenport diagram – metabolic acidosis).

But inadequate, because normalization of blood and CSF pH lag behind the ventilatory response.

Instead, in the short term, adaptation within both the peripheral and central chemoreceptors thought to contribute

20
Q

Why don’t we think the kidneys are responsible for hyperventilation acclimatisation?

A

Normalization of blood and CSF pH lag behind the ventilatory response.

21
Q

What happens to the chemoreceptors in altitude?

A

Central chemoreceptors become more sensitive to CO2

O2 threshold of the chemoreceptor drive is higher in acclimatized individuals - increased sensitivity of peripheral chemoreceptors.

22
Q

Acclimatization can only be achieved through…

A

hypoxic hypocapnia

23
Q

Response to O2 or CO2 more important for acclimatization?

A

Oxygen

24
Q

How is hypercapnia controlled long term?

A

By the kidneys

25
Q

How is hypercapnia reduced by kidneys?

A

Upregulation of HCO3- loss (type B intercalated cells)

26
Q

How does acetazolamide accelerate acclimatization? (2 ways)

A

Stimulating renal excretion of bicarbonate to counter the alkalosis - this stimulates the respiratory centre to increase the depth and frequency of respiration - speeding up natural acclimatization process.

Shifts equation to left, facilitate loading of molecular CO2 to keep in the tissue (slow down reaction)– keep CO2 high enough around central chemoreceptors to prevent inhibitory drive.

27
Q

What happens in acute mountain sickness?

A

Raised pH and hypocapnia - Cerebral vasoconstriction - decrease in cerebral blood flow - lightheadedness and loss of consciousness.

28
Q

Why do you get acute mountain sickness?

A

Rapid ascent so reduced time to acclimatize

29
Q

What cardiovascular change is required in altitude? Why>

A

Arterial PO2 is low, blood to cell diffusion gradient falls - arteriovenous difference falls. So increase in CO is needed to maintain O2 to tissues

30
Q

How is raised CO brought about in acclimatization?

A

Raised cardiac output is brought about by a resting tachycardia of up to 100 per minute due to the withdrawal of vagal inhibition of the pacemaker.

31
Q

What happens to stroke volume in acclimatization?

A

Stroke volume falls during the first week at altitude and then tends to stabilize.

Acclimatization: After several weeks, CO returns to sea level values but SV remains reduced - chronic elevation in HR to accommodate this.

32
Q

What causes initial fall in SV?

A

The fall in stroke volume is associated with reduction in left ventricular dimensions and filling pressure

33
Q

Why is there reduced filling pressure at altitude?

A

Hypoxic diuretic response

Initial decrease due to increased release of atrial natriuretic peptide and decreased synthesis of aldosterone

Whereas the further reduction of plasma volume occurs without a net loss of body water by a fluid shift from the extracellular to the intracellular compartment.

34
Q

What happens to systemic and pulmonary pressure?

A

Systemic arterial pressure falls while pulmonary arterial pressure rises

35
Q

Why does systemic pressure fall?

A

Hypoxic reduction of peripheral resistance outweighs CO so systemic pressure falls

Hypoxic diuresis

36
Q

How does pulmonary hypertension develop?

A

Pulmonary hypertension develops due to the raised CO and hypoxic pulmonary vasoconstriction.

37
Q

What is the advantage of hypoxic pulmonary vasocontstriction?

A

Redirects blood flow to the upper parts of the lung that are better ventilated (higher V/Q ratio) so helps match perfusion to ventilation in an upright position

38
Q

What happens to blood pressure in acclimatization?

A

Blood pressure and systemic vascular resistance then rise over at least 3 to 4 weeks because of increasing sympathetic activity and reduced tissue hypoxia associated with acclimatization.

39
Q

Is the red blood cell response short or long term?

A

Long term response

40
Q

What happens to RBC in acclimatization?

A

Polycythaemic response: O2 carrying capacity of blood is increased by a rise in haematocrit (up to 65%).

41
Q

What happens at haematocrit >0.65?

A

Chronic mountain sickness (Monge’s disease) can develop leading to reduced mental and physical capacity.

42
Q

What causes polycythaemic response?

A

Rise in RBC due to increased bone marrow erythropoiesis driven by release of erythropoietin (EPO).

43
Q

What is EPO produced by?

A

EPO is produced by interstitial fibroblasts in the kidney in close association with the PCT.

44
Q

Where is EPO produced in pre-natal period?

A

Liver

45
Q

How does EPO act?

A

Binds to EPO receptor on the red cell progenitor surface - differentiation, survival and proliferation of the erythroid cell.

46
Q

What does an increased Hb mean?

A

Increased O2 carrying capacity of the blood.

47
Q

How do EPO secreting cells sense O2?

A

HIF-1alpha accumulates in hypoxia, can bind HIF-1beta to increase transcription.

Applied physiology and pharmacology (18 decks)

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