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40 Cards in this Set

  • Front
  • Back
How do you calculate Ventilation?
VE = Br Freq x Tidal Vol

VE = 10 br/min x 500 ml/br
What is the normal minute ventilation rate?
5-7.5 L/min
Approximately normal breathing frequency
10-15 breaths/min
Normal tidal volume
.5 L/breath (500 mL)
Why did end tidal PCo2 go up when Josh breathed in hypercapnic air?
Because he was breathing in more CO2
Why did end tidal PO2 go up when Josh breathed in hypercapnic air?
Because his breathing frequency doubled!
Does PCO2 normally go UP in hyperventilation?
No; but we would call this hyperventilation in terms of O2 because he was breathing at a rate higher than his metabolic demand.
What happened to Josh's minute ventilation (VE) during hypercapnic breathing?
It went up 4X
Why did Josh's Ve go up so much?
Because carotid and medullary chemoreceptors responded to the increased CO2 and consequently increased breathing.
What was Josh's acid status during hypercapnic breathing?
Acute Respiratory Acidosis
Why did Josh's breathing remain elevated for a while even AFTER he stopped inhaling the high CO2?
B/c there was a sustained acidosis in the brain for a few minutes.
How much does pH change for every mm Hg change in Pco2?
0.01 pH for every mm Hg
So if Josh's PCO2 went up from 45 mm Hg to 53 mm Hg, how much did his pH change?
pH went down from 7.4 to 7.32
How is COPD similar to hypercapnic breathing?
How is COPD different from hypercapnia?
Breathing is REDUCED in COPD, not increased.
How does Chronic alveolar hypoventilation as in COPD affect breathing and plasma pH?
-Breathing is not high freq b/c the CO2 chemoreceptors adapt and become less sensitive.
-Kidneys compensate for the low pH by generating more bicarb
What happened to josh's breathing frequency when inspiratory resistance increased?
The time it took to inspire increased, so he adapted by breathing out faster - CO2 went down as a result.
What happened to Josh's breathing freq when both insp and exp resistance increased?
Now expiratory time increased too, so CO2 increased.
If Josh had increased exp and insp resistance for a long time, what would happen?
His chemoreceptors would adjust so that he wouldn't have to keep working so hard to fight the resistance, they would just let his bloodgas levels stay abnormal.
What happens to breathing frequency when inspired O2 is reduced (hypoxic)?
Frequency increased, but only to 22, not as much in hypercapnia.
What happened to Josh's end tidal PCO2 and PO2 during hypoxic breathing?
They both went down.
Why did Josh's end tidal PCO2 go down during hypoxic breathing?
Because he was hyperventilating
Why did Josh's end tidal PO2 go down during hypoxic breathing?
Because he was breathing less O2
Why did it take time for the PetO2 to go down?
Because it took a while to deplete his FRC store of oxygen.
Why did minute ventilations increase so much more dramatically under hypercapnic conditions compared to hypoxemic?
Because CO2 is more important than O2 in regulation of eupneic breathing.
How would you characterize Josh's H+ status during hypoxia?
Low PCO2 bc he was breathing off CO2, his pH was 7.47 - Acute Respiratory Alkalosis
What type of acid base imbalance results during brief periods of hypoxia?
Acute Resp Alkalosis
What is the first phase of blood gas and ventilation changes during chronic hypoxic conditions?
1. Increase ventilation in response to low PO2 (results in low PCO2 as you blow it off)
What is the 2nd phase of blood gas and ventilation changes during chronic hypoxic conditions?
2. Decrease ventilation as the CO2/H+ decrease is sensed by carotid chemoreceptors.
What 2 things contribute to the decrease in ventilation during phase 2 of chronic hypoxia?
-Lower stimulation of carotid chemoreceptors
-Hypoxic brain depression
What is hypoxic brain depression?
The direct depressant effect of hypoxia on the excitability of neurons
What does HBD do?
Decreases the metabolic use of oxygen
What happens during the 3rd phase of chronic hypoxia?
Frequency goes back up as the carotid chemoreceptors are stimulated by once again.
What does phase 3 represent?
The major ventilatory acclimatization mechanism by which adult humans compensate their arterial O2 content when sojourning at high altitude.
What is phase 4?
Attenuation of the carotid chemoreceptors sensitivity to hypoxia - only seen in hi altitude natives or children that move there.
What happens if there is too much HBD?
What is the major control-of-breathing clinical condition in the USA?
Obstructive sleep apnea
How many adults are affected?
What is Congenital central alveolar hypoventilation?
1. Absence of Co2/H+ chemoreceptor sensitivity
2. Absence of O2 chemoreceptor sensitivity
3. Absence of drive to breathe during sleep
What is another name for CCAH?
Central sleep apnea