Exam 3 - Regulation of Ventilation Flashcards

1
Q

what buffer system is the most important regulator for ventilation?

A

HCO3- buffer system

  • plasma: 75%
  • red cells: 30%
  • interstitial fluid: 90%
  • other cells: 2%
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2
Q

at what pK does the HCO3- buffer system function best and given this, why is it possible that this system is most important in our body, where the pH is 7.4?

A

pK = 6.1
When acid is added to body fluids, [HCO3-] decreases by conversion to H2CO3, which dissociates to H2O + CO2. CO2 is then eliminated by respiration, minimizing the effect of a change in the ratio of HCO3- to CO2 (H-H eq), which minimizes the effect on pH.

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3
Q

what is the CO2 dissociation equation?

A

CO2 + H2O H2CO3 H+ + HCO3-

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4
Q

COPD

A

elasticity of lung is lost -> incomplete exhalation -> retention of CO2 -> pH decreases -> respiratory acidosis -> shift O2 dissociation curve to right -> less Hb-bound O2

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5
Q

hyperventilation

A

CO2 blown off -> pH increases -> respiratory alkalosis

-another sign: paresthesia around mouth or fingers

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6
Q

what is the primary factor in respiratory control?

A

CO2 - when [CO2] decreases, respirations slow and may even temporarily stop -> hypoxia (can cause a seizure)

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7
Q

what is a CPG?

A

central pattern generator - group of neurons capable of rhythmic patterned output in the absence of outside influence or sensory feedback

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8
Q

what is the primary stimulus for inspiration?

A

DRG (dorsal respiratory group)

  • input from central/peripheral chemoreceptors, pulmonary stretch receptors, somatic pain receptors, mechanoreceptors, etc.
  • increased discharge of phrenic n. during inspiration -> recruit more muscles -> increase TV
  • inspiration terminated by CPG too, then expiration passive
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9
Q

ventral respiratory group (VRG)

A

contains inspiratory and expiratory neurons

-inspiratory are mainly to the accessory muscle

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10
Q

which parts of the brainstem are responsible for which parts of respiration?

A

the medulla is capable of sustaining patterned breathing but the pattern can be fine-tuned by neurons in the pons and by feedback via the vagus.

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11
Q

what two brainstem centers function to prevent excessive inhalation?

A
pneumotaxic center (pons) and stretch receptors (vagus) provide negative feedback to the apneustic center (medulla) to prevent excessive inhalation
-cut out either of these, get gasping because too much inhalation
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12
Q

describe chemical control of ventilation

A

concentration changes in CO2 and H+ in CSF (central chemoreceptors) + changes in pH, CO2, and O2 (carotid/aortic bodies)

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13
Q

what is the principal chemical control of ventilation?

A

arterial CO2 acting on central chemoreceptors

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14
Q

describe the response of the carotid/aortic bodies to changes in pH

A

increase their discharge with decrease in pH -> increase ventilation by increasing both rate and TV

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15
Q

when do the carotid bodies become sensitive to O2?

A

only at very low concentrations of O2 - they are primarily sensitive to decrease in pH and increase in CO2

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16
Q

what are the central chemoreceptors exclusively sensitive to?

A

H+ directly and CO2 indirectly:
-BBB poorly permeable to H+, but CO2 can cross, where it is then hydrated into H2CO3, then dissociated to H+ and HCO3- -> acidosis of CSF -> increase TV

17
Q

describe the locations of the central chemoreceptors

A
  • ventral surface of the medulla near cranial nerves VI-X

- no direct contact w/ arterial blood, but bathed in CSF

18
Q

describe the process of adaptation

A

ventilatory response to high PCO2 decreases after hours due to compensatory transport of HCO3- across BBB via anion exchanger w/ Cl- -> then PO2 drive in the periphery becomes major influence on ventilation

19
Q

describe the ventilatory responses to changes in acid-base balance

A
  • if metabolic acidosis, try to compensate w/ respiratory alkalosis (hyperventilation to drop blood H+ by blowing off CO2)
  • if metabolic alkalosis, try to compensate w/ respiratory acidosis (hypoventilation to increase CO2 and H+ back to normal)
20
Q

list some causes of metabolic acidosis

A

hyperchloremic:
- diarrhea
- acetazolamide
- IV hyperalimentation
- interstitial renal disease
- renal tubular acidosis

increased undetermined anion:

  • generalized renal failure
  • DKA
  • alcholic ketoacidosis
  • lactic acidosis
21
Q

list some causes of metabolic alkalosis

A
  • vomiting
  • nasogastric suction
  • diuretics
  • alkali treatment
  • corticoid treatment
  • severe K+ depletion
  • Cl- restriction
22
Q

list some causes of respiratory acidosis

A
  • respiratory failure
    • obstructive lung disease
    • chest wall disease
    • mechanical hypoventilation
  • CNS depression
  • severe pulmonary edema
  • status asthmaticus
  • primary hypoventilation
  • pneumothorax
  • abdominal distension
23
Q

list some causes of respiratory alkalosis

A
  • hyperventilation
  • G(-) sepsis
  • pulmonary emboli
  • pneumonia
  • hepatic failure
  • high altitude
  • severe anemia
24
Q

describe the relationship between alveolar PCO2 and ventilation rate

A

nearly linear, direct relationship

-but when PCO2 of inspired air comes near to alveolar PCO2 (40 mmHg), CO2 elimination becomes difficult

25
Q

explain the mechanism of CO poisoning

A
  • CO binds to Hb with greater affinity than O2 binds Hb
  • also, binding of CO to one of four O2 binding sites on Hb results in retention of O2 at the other sites -> fail to release O2 to tissues

shifts O2 dissociation curve to the left

26
Q

describe 3 non-chemical influences on ventilation

A
  • proprioceptors and stretch receptors - stimulate ventilation in response to physical disturbance (slap, tickle)
  • irritant receptors - chemical/mechanical irritants or histamine/bradykinin in allergic response -> rapid shallow breathing + bronchoconstriction
  • other pulmonary receptors - Hering-Breuer reflex: stretch receptors in vagus inhibit respiration; deflation receptors - rapid, shallow breathing
27
Q

what is the RAS

A

reticular activating system - diffuse network of neurons in midbrain and medulla that contribute to many of the autonomic functions