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13 Cards in this Set

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What are the (4) CNS centers involved in the control of cyclic breathing?
Cerebrum - voluntary control
Medulla oblongata - DRG & VRG generate basic rhythmic pattern of breathing
Emotional responses - Limbic system & hypothalamus (anxiety, rage, fear)
Pons - apneustic & pneumotaxic centers can modulate basic pattern of medulla but are not essential (historical)
What are (3) receptors which influence breathing frequency and the neural pathways utilized?
Pulmonary stretch receptors:
~Fire in proportionate response to transmural pressure & continue to fire w/ continued stretch
~Stimulate the inspiratory off-switch neurons which turn off the central inspiratory activity

Irritant Receptors:
~Respond to touch or noxious substances (smoke, particles, histamines, serotonins, prostaglandins, inflammation, edema)
~Stimulates central inspiratory activity producing a cough or gasp
J receptors:
~Juxtapulmonary capillary receptors (C-fiber endings)
~Alveolar C-fibers fire in response to lung injury, overinflation, edema, embolism..but NOT sensitive to inflammatory mediators
~Bronchial C-fibers fire w/ inflammatory mediators
~Stimulate rapid shallow breathing, bronchoconstriction, airway secretion & cardiovascular depression (hypotension & bradycardia)
Which chemoreceptors are sensitive to PCO2 and thus pH?

How does PCO2 equate to either a rise or decline in pH within the CSF?
Central chemoreceptors located on the medulla respond to changes in PCO2 and pH of CSF.

The blood brain barrier is permeable to O2 & CO2. CO2 crosses the BBB and dissociates into HCO3- + H+ which results in a decrease in pH (acidosis), signaling the central chemoreceptors to increase breathing
Which chemoreceptors are sensitive to primarily PO2, however respond in a limited capacity to PCO2 & pH?
Peripheral chemoreceptors on carotid and aortic bodies detect PO2 changes primarily.

Which cranial nerve carries the carotid bodies afferent fibers?

Which cranial nerve carries the aortic bodies afferent fibers?
Carotid bodies afferent fibers feed the CNS via the glossopharyngeal nerves

Aortic bodies afferent fibers feed the CNS via the vagus nerves
What cell type within the carotid and aortic bodies sense ↓PO2?

How do these cells respond to ↓PO2?
The Glomus cell also reacts to a ↓pH, causing what type of response?
The carotid bodies are sensitive to PO2, however pH and PCO2 can affect their activity. Arrange the following conditions from least to greatest carotid body activity:

A) ↓PO2
B) ↓PO2, ↑H+, ↑PCO2
C) ↓PO2, ↓H+, ↓PCO2
C, A, B

A) ↓PO2 = ↑↑ activity
B) ↓PO2, ↑H+, ↑PCO2 = ↑↑↑ activity
C) ↓PO2, ↓H+, ↓PCO2 = ↑ activity
A patient w/ COPD is expected to have:

A) hypoxemia & hypercapnia
B) hypoxemia but not necessarily hypercapnia
C) hypercapnia but not necessarily hypoxemia
D) not necessarily either hypercapnia or hypoxemia
B) hypoxemia but not necessarily hypercapnia

COPD causes a V/Q mismatch and thus hypoxemia. The body increases alveolar ventilation which reduces PCO2 but not very good at increasing PO2 and thus prevents hypercapnia.
In a patient w/ compensated COPD, what is the primary ventilatory drive?
A patient w/ compensated COPD will be experiencing hypoxemia yet hypercapnia will NOT be present as they have compensated for pH. Thus the kidneys correct the blood imbalance while the choroid plexus restores the CSF pH.

In turn, chronic hypoxemia such as w/ compensated COPD, the ventilatory drive is by PO2 and peripheral chemoreceptors (glomus cells).
A patient w/ compensated COPD has been admitted to your ER. Why do you give 40% O2 rather than 100% O2 to help this patient?
The only thing keeping this patient alive is the hypoxia which is stimulating the peripheral chemoreceptors through the ↓PO2 and thus increasing their breathing. High fractional O2 will decrease the only ventilatory drive they have.
ALSO...
The hypoxic vasoconstriction within the lungs will also be lost, further exacerbating the V/Q mismatch.
What are the immediate changes that take place during exposure to high altitude hypoxia?
Hypoxemia stimulates ventilation through peripheral chemoreceptors.
Increased ventilation decreases PCO2 which stimulates the central chemoreceptors to increase ventilation and produces respiratory alkalosis.
Pulmonary vascular resistance increases to try and fix the V/Q mismatch.
Erythropoeitin increases to also help the decreased amount of O2.
Know the immediate and 2-3 week acclimation that takes place during exposure to high altitudes.
High altitude acclimation after 72hrs will increase 2,3 DPG. This increase will cause the O2 saturation curve to shift which way?

Does this promote offloading or uploading of O2?
2,3 DPG causes a right shift of the O2 saturation curve which promotes offloading of O2.