Week 10 Flashcards

1
Q

Respiratory control center

A

Breathing originates from a central pattern generator in the brainstem (medulla and pons)

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2
Q

How can CPG be divided?

A
  1. Sites that generate breathing rhythm
  2. Downstream sites that form the motor pattern and synapse with efferent motor neurons
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3
Q

Central Rhythm generator

A

Rhythmic groups of neurons that area active during inspiration (prebotC), post-inspiration (PiCo), and expiration (pF)

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4
Q

Ventral Respiratory Group

A

Includes the central rhythm generator and the motor pattern generators neurons
- Controls the activity of respiratory muscles

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5
Q

Pontine respiratory group

A

Modulates output from the ventral respiratory group

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6
Q

What nerves innervate the respiratory muscles?

A
  • Diaphragm: phrenic nerve
  • External intercostals: External intercostal nerves
  • Internal Intercostals: Internal intercostal nerves
  • Airway muscles are also controlled by the CPG via cranial nerves
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7
Q

Sensory input to central pattern generators

A
  • Peripheral sensory receptors send afferent information to the NTS in the dorsal medulla
  • Interneurons connect sensory afferents in the NTS to the ventral respiratory group and thus modulate its output
  • Also have central chemoreceptors in the medulla that modulate VRG output
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8
Q

Hypoxic Ventilatory Response

A
  • Reductions in arterial PO2 lead to an increase in ventilation
  • Small declines in PO2 below normal arterial values can be fully corrected by increasing ventilation
  • Larger declines in arterial PO2 cannot be fully compensated, but the increase in ventilation reduces the magnitude of PO2 decline
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9
Q

Peripheral O2 Chemoreceptors

A
  • Primary O2 chemoreceptors are located in the carotid bodies, but the aortic bodies also play a role in the HVR
  • Afferent neurons form synapse with interneurons in the NTS, which transmit the sensory information to the central pattern generator
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10
Q

How do the carotid bodies become activated and send AP

A
  1. Not well understood sensor in membrane of the carotid body glomus cell activated by decrease in PO2
  2. Closing on K+ channels
  3. Depolarization (K+ can’t leave)
  4. Opening of voltage-gated Ca2+ channels
  5. Vesicles release ACh and ATP
  6. Increase AP frequency
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11
Q

How will reducing blood haemoglobin concentration affect the hypoxic ventilatory response

A
  • No change
  • Corotid bodies sense partial pressure
  • decrease in partial pressure drives O2 into cell - decrease in PO2 = decrease in O2 t cell
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12
Q

Ventilatory Response to CO2/H+

A
  • Increase in arterial PCO2 or decrease in pH lead to increase in ventilation
  • Breathing is more sensitive to changes in PCO2 than PO2 in air breathing vertebrates
  • Response results from both peripheral and central chemoreceptors
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13
Q

Central CO2/H+ chemoreceptors

A
  • Central Chemoreceptors in the medulla sense CO2 and H+ cerebral spinal fluid, which are related via the carbonic anhydrase reaction
  • CO2 can cross the blood-brain barrier, but H+ cannot, so arterial CO2 is also sensed by these receptors
  • Central receptors contribute more than peripheral chemoreceptors to the ventilatory response to arterial CO2, but only peripheral chemoreceptors respond to changes in arterial pH
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14
Q

How is a decrease in both PO2 and PCO2 accounted for by alveolar ventilation

A

At a given PCO2, the greater the PO2 the less ventilation will occur in compensation
- A decrease in pH will shift the curves to the left to increase ventilation at a given PCO2 and PO2 value

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15
Q

How will the hypoxic ventilatory response affect arterial CO2?

A
  • Decreases in PO2 cause subsequent decreases in PCO2
  • Increases in PO2 causes increases in PCO2 due to decrease in alveolar ventilation
  • Implies a restrained response to hypoxia - can’t exhale too much CO2 (prominent Vasodilator)
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16
Q

How will experimentally maintaining arterial PCO2 affect the hypoxic ventilatory response?

A
  • Result in a more pronounced homeostatic response
  • Effectors regulate more than 1 variable leading to trade off in homeostatic regulation under normal conditions
17
Q

How does ventilation respond to increased metabolism?

A

Strong positive correlation between increases in metabolism and increased ventilation

18
Q

What 3 factors are responsible for the changes in ventilation in response to an increase in metabolism

A
  1. Central Command
    - Produces initial overshooting for ventilation causing reduction in pCO2
  2. Feedback form active tissues
    - Activated as ventilation reaches peak as mitochondrial mechanisms take time to kick in
  3. Feedback from chemoreceptors
    - Activated second in response to changes in arterial partial pressures
19
Q

Ventilation-Perfusion Relationships

A

Reductions in V/Q lead to large decreases in the partial pressure of O2 in the alveoli, but increases in V/Q lead to only modest increases in alveolar PO2
- This is true across entire lungs and for individual alveoli

20
Q

Ventilation-Perfusion Inequality

A
  • Regional variation in ventilation between lung regions or between alveoli affects the overall effectiveness of gas exchange
  • Having the same ventilation ratio across all alveoli is more effective for gas exchange than having some under-ventilated and some over-ventilated
21
Q

How is the distribution of ventilation and prefusion examined

A

By quantifying the proportion of ventilation or blood flow across a range of V/Q ratios
- in healthy individuals the distributions are tightly centered at 1 (most of the ventilation and blood flow is well matched)

22
Q

How does emphysema affect the distribution of ventilation and perfusion

A

Causes bimodal distribution in perfusion with smaller lump on smaller ratio and main lump shifted slightly right

23
Q

Mechanisms of Ventilation-perfusion Matching

A
  • Pulmonary arterioles constrict in response to low partial pressure of O2
  • Vasoconstriction increases vascular resistance and reduces local blood flow in flavor of other lung regions with higher PO2
24
Q

Global Hypoxia in Lung disease

A
  • Chronic vasoconstriction throughout the entire lungs leads to hypertrophic remodeling that increases arterial wall thickness
  • Contributes to hypoxic pulmonary hypertension
  • HPH can lead to edema and increases workload on the RV, leading to RV hypertrophy and in sever cases RV failure and death