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38 Cards in this Set

  • Front
  • Back
What happens to breathing during muscular exercise?
It increases - hyperpnea results.
What is the temporal response pattern of alveolar ventilation at the onset of exercise?
It sharply increases within seconds of exercise onset, then slowly increases to a steady state.
How soon after exercise onset does alveolar ventilation reach the steady state?
90 sec
So what does that tell us about the signal for hyperpnea?
It has both a fast and slow component.
What is the effect of exercise on alveolar and arterial blood gases?
Homeostasis is maintained until about 60% of maximal exercise capacity.
So what do we know is NOT the signal for hyperpnea during exercise?
Increased stimulation of Carotid or intracranial chemoreceptors - they would kick in initially.
What is observed at about 60% of maximal exercise capacity?
-Lactic Acidosis
-Hyperventilation
What is the relationship between metabolic rate and alveolar ventilation during exercise?
Because homeostasis is maintained up to 60% max, VA is increasing in proportion to metabolic rate increase. After that, the increase exceeds the increase in metabolic rate.
How do we know that the ventilatory response is not central command-dependent?
It is not different when the stimulus is voluntary versus electrically induced.
Is the ventilatory response to electrically induced exercise different in normal vs paraplegics?
No; so we see it is also not critically dependent on spinal afferents.
If oxygen content in room air is increased to 40% will it affect alveolar ventilation?
No; PaCO2 will remain 40 even though PaO2 doubles (100-200)
Will the same increase in O2 content affect breathing in a severe COPD patient?
Yes; PaCO2 will increase from 65 to 70.
What likely causes the increase in alveolar CO2 in hyperoxic conditions for a COPD patient?
The increase in alveolar O2, resulting in reduced carotid chemoreceptor activity
For a resting patient with abnormal ventilation:
PaCO2 = 30 (below normal)
PaO2 = 110 (above normal)
pH = 7.5
What has happened to alveolar ventilation and CO2 ventilation?
Both are above normal - indicated by the hypocapnia.
What is driving the hyperventilation in this patient?
Emotional stress or brain lesions
Why does H+ concentration need to be maintained at such a narrow range?
Because acid affects protein function.
How does suboptimal protein function affect neurons?
Excess acid = decreased excitability

Deficient acid = increased excitability
What is an acid?
Compound that donates H
What is a base?
Compound that accepts H
What is Physical-chemical buffering?
The ability of a compound in solution to minimize the change in H+ in the solution when a strong acid or base are added.
What are the primary buffers in ECF?
-Bicarb
-Phosphoric acid
-Proteins
What are the primary buffers in ICF?
-Phosphoric acid
-Proteins
How can you distinguish whether an acidosis is metabolic or respiratory?
By looking at the PCO2; if Elevated = respiratory
Decrsed = metabolic
What is the isohydric principle?
The fact that when acid balance is disrupted, all buffers will be altered.
What are the 2 determinants of the hydrogen ion buffering capacity of a buffer pair within a solution?
1. Amt of buffer pair in solution
2. pK of buffer pair relative to the pH of the solution
What happens when pH = pK?
There are equal amts of hydrogen ion, acid, and base.
When are conditions optimal for buffering?
When pH = pK
What is physiologic buffering?
Processes in the body that alter the amount of physical-chemical buffers.
2 Ways by which plasma [H+] is regulated:
1. Transmembrane exchange
2. Pulmonary ventilation
What is transmembrane exchange?
Buffering of ECF by moving Na or K from cells in exchange for H.
2 main sites of bicarb production:
-Kidney
-Brain
When does the brain make lactic acid?
To buffer a respiratory alkalosis
How does the kidney respond when tissues produce excess acid?
it regenerates bicarb by producing ammonia.
What will increase in urine during a severe metabolic acidosis?
Ammonium chloride
What is the role of the BBB in regulating brain [H+]?
It prevents acid from entering the brain.
During systemic metabolic acidosis how much does CSF [H+] increase?
Only 10% of the increase in blood [H+].
Can the blood brain barrier buffer a respiratory acidosis or alkalosis? Why/why not?
no; b/c CO2 can easily diffuse across it.
How does the brain respond to a resp acidosis or alkalosis?
Acid: increases NH3 production
Alk: increases lactic acid production
-Glial cells produce both