Exam 3 - Regulation of Ventilation Flashcards
what buffer system is the most important regulator for ventilation?
HCO3- buffer system
- plasma: 75%
- red cells: 30%
- interstitial fluid: 90%
- other cells: 2%
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?
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.
what is the CO2 dissociation equation?
CO2 + H2O H2CO3 H+ + HCO3-
COPD
elasticity of lung is lost -> incomplete exhalation -> retention of CO2 -> pH decreases -> respiratory acidosis -> shift O2 dissociation curve to right -> less Hb-bound O2
hyperventilation
CO2 blown off -> pH increases -> respiratory alkalosis
-another sign: paresthesia around mouth or fingers
what is the primary factor in respiratory control?
CO2 - when [CO2] decreases, respirations slow and may even temporarily stop -> hypoxia (can cause a seizure)
what is a CPG?
central pattern generator - group of neurons capable of rhythmic patterned output in the absence of outside influence or sensory feedback
what is the primary stimulus for inspiration?
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
ventral respiratory group (VRG)
contains inspiratory and expiratory neurons
-inspiratory are mainly to the accessory muscle
which parts of the brainstem are responsible for which parts of respiration?
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.
what two brainstem centers function to prevent excessive inhalation?
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
describe chemical control of ventilation
concentration changes in CO2 and H+ in CSF (central chemoreceptors) + changes in pH, CO2, and O2 (carotid/aortic bodies)
what is the principal chemical control of ventilation?
arterial CO2 acting on central chemoreceptors
describe the response of the carotid/aortic bodies to changes in pH
increase their discharge with decrease in pH -> increase ventilation by increasing both rate and TV
when do the carotid bodies become sensitive to O2?
only at very low concentrations of O2 - they are primarily sensitive to decrease in pH and increase in CO2
what are the central chemoreceptors exclusively sensitive to?
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
describe the locations of the central chemoreceptors
- ventral surface of the medulla near cranial nerves VI-X
- no direct contact w/ arterial blood, but bathed in CSF
describe the process of adaptation
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
describe the ventilatory responses to changes in acid-base balance
- 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)
list some causes of metabolic acidosis
hyperchloremic:
- diarrhea
- acetazolamide
- IV hyperalimentation
- interstitial renal disease
- renal tubular acidosis
increased undetermined anion:
- generalized renal failure
- DKA
- alcholic ketoacidosis
- lactic acidosis
list some causes of metabolic alkalosis
- vomiting
- nasogastric suction
- diuretics
- alkali treatment
- corticoid treatment
- severe K+ depletion
- Cl- restriction
list some causes of respiratory acidosis
- respiratory failure
- obstructive lung disease
- chest wall disease
- mechanical hypoventilation
- CNS depression
- severe pulmonary edema
- status asthmaticus
- primary hypoventilation
- pneumothorax
- abdominal distension
list some causes of respiratory alkalosis
- hyperventilation
- G(-) sepsis
- pulmonary emboli
- pneumonia
- hepatic failure
- high altitude
- severe anemia
describe the relationship between alveolar PCO2 and ventilation rate
nearly linear, direct relationship
-but when PCO2 of inspired air comes near to alveolar PCO2 (40 mmHg), CO2 elimination becomes difficult
explain the mechanism of CO poisoning
- 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
describe 3 non-chemical influences on ventilation
- 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
what is the RAS
reticular activating system - diffuse network of neurons in midbrain and medulla that contribute to many of the autonomic functions
