Lecture 5.2: Altitude and Exercise Flashcards
What is Hypercapnia?
• It is when the concentration of carbon dioxide (CO2) in the bloodstream rises
above a certain level
• Partial pressure of carbon dioxide rises, partial pressure of oxygen falls
What is Hypoxia?
A state in which oxygen is not available in sufficient amounts at the tissue level to maintain adequate homeostasis
What is Persisting Hypercapnia?
• As disease progresses CO2 retained because of inadequate ventilation
• pCO2 now chronically elevated
• Now changes in CSF pH is compensated by the choroid plexus cells retaining
HCO3
• Central chemoreceptors therefore ‘reset’
•Ventilation no longer stimulated
What can Persisting Hypercapnia lead to?
• Normally rises in pCO2 lead to drive to increased ventilation
• Produces breathlessness
• Which, initially may drive ventilation enough to keep pCO2 down and pO2 up
• May even produce hypocapnia
What is Hypocapnia?
Decrease in alveolar and blood carbon dioxide (CO2) levels below the normal reference range of 35 mmHg
Persisting Hypercapnia (from Cerebrospinal Fluid [CSF] pH perspective)
• As disease progresses CO2 retained because of inadequate ventilation
• pCO2 now chronically elevated
• Now changes in CSF pH is compensated by the choroid plexus cells retaining
HCO3-
• Central chemoreceptors therefore ‘reset’
• Ventilation no longer stimulated
What organ compensates systemic acid base balance and how?
• Kidneys
• By retaining HCO3-
Why can excess oxygen lead to Hypercapnia?
• High O2 causes respiratory depression
• Thus decrease in breathing rate
• Thus very high CO2 as hypoventilation
What are the Symptoms of Acute Hypoxia? (5)
• Initially Pleasant Euphoria
• Nausea
• Lack of Coordination
• Unconsciousness
• Death
Acute Exposure to High Altitude: Effects (20,000 and 29,000ft)
• Above 20,000ft acute exposure leads rapidly to
unconsciousness
• Exposure at 29,000ft leads to unconsciousness in 40 sec
What is Acute Hypoxia detected by?
• Acute hypoxia detected by peripheral chemoreceptors
What happens to respiratory control in acute exposure?
• Try to increase breathing
• As ventilation increases pCO2 falls
• CSF becomes alkaline
• Alkaline CSF inhibits central chemoreceptors
• Counteracts hypoxic drive
What happens when hypoxic drive is counteracted?
• System Trapped!
• Breathe More = Die from Alkalosis
• Don’t Breathe More = Die from Hypoxia
• System Gives Up = You Die
Initial Effects of Gradual Exposure
• Mild hypoxia stimulates ventilation enough to raise CSF pH slightly
• Choroid plexus cells respond by exporting HCO3- from CSF
• CSF pH corrected, so hypoxic drive now expressed
• Subject breathes more
Effects of Longer Term Acclimatisation
• Oxygen carrying capacity of blood increased (polycythaemia, 2,3 DPG)
• Cardiac output increased
• Cardiac output directed to vital organs
• Systemic acid/base balance corrected
Oxygen and Carbon Dioxide in Exercise
• In exercise O2 consumption and
CO2 production increased
• Arterial pO2 tends to fall, pCO2 to
rise
• Both easily corrected by breathing
more
Ventilation in Exercise 1 (sudden jump)
• Ventilation rate jumps suddenly as
exercise begins
• Before chemical changes occur
• Neural mechanism anticipating
extra demand
• Stimuli from joint and muscle.
receptors
Ventilation in Exercise 2 (ventilation rate rises slowly to plateau)
• In the plateau phase ventilation
matches exercise
• In moderate exercise pO2 and.
pCO2 normal
• Due to effective chemical control by
central chemoreceptors
Ventilation in Exercise 3 (end of exercise)
• At end of exercise ventilation drops.
abruptly
• Removal of signals from joints etc
• Then gentle decline back to normal
as ‘oxygen debt’ repaid
Ventilation in Strenuous Exercise
• High body temperature and
metabolic production of acid
stimulate breathing more
• Normal subjects hyperventilate in
severe exercise
• So, paradoxically, PaCO2 falls
despite high CO2 production
