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