Respiration 7 Flashcards
Where is breathing established?
Initiated in medulla
- Modified by higher structures - Modified by sensory input from pns (chemoreceptors, chest wall, mechanoreceptors in the lungs) etc.
Kind of like that of the heart!
What are the different types of peripheral receptors?
Peripheral chemoreceptors (o2 decrease, co2 increase, ph decrease in blood)
Central chemoreceptors (co2 increase, pH decrease in co2)
Hering-Breuer reflex (stretch receptors in lungs)
Proprioceptors
Touch receptors
What are the DRG and VRG? Other areas?
Dorsal respiratory group: inspiratory neurons
- Drive diaphragm - Get input from peripheral chemorecptors and Mechanoreceptors
Ventral respiratory group: mainly expiratory
- Silent during quiet breathing - Drive expiratory muscles that are recruited
Other areas:
Pons: regions in pons modify VRG/DRG.
- Apneustic center: sustained inspiration, sudden expiration
- Pneumotaxic center: stop inspiration. Leads to apneusis.
Medulla generates rhyth, but it’s influenced above by PONS or CORTEX or below from peripheral feedback.
How does info get to muscles of respiration?
Phrenic nerve: c3,4,5 supply motor output to diaphragm
Intercostal nerves exit thoracic and lumpar to supply intercostal and abdominal msucle s
Cranial nerves: supply upper airway dilator muscles motor input
What are feedforward and feedbackwards?
Forward: Pons, higher brain regions, motor cortex (voluntary through corticospinal tract)
Automatic through ventrolateral tract
Feedback (negative)
- chemoreceptors and mechanoreceptors
What’s the Hering Breur reflex?
- Prevent overinflation
- Lungs breath the appropriate amount, then brain starts expiring
Mediated by vagus nerve
- Lungs breath the appropriate amount, then brain starts expiring
Works in animals and newborns but not big ppl
- our lungs would have to fill too much
What are central chemorecpetors?
Central Chemoreceptors
- Below medulla
- Stimulated by changes in Pco2 in aterial blood
○ 40mm Hg is normal
This is primary regulatory of breathing
Medulla sees this partial pressure and keeps it there.
If this pco2 is increased (holding breath?)
- Co2 diffuses into brain increases co2 levels in brain exracellular fluid. Becomes carbonic acid. (cause it goes into hydrogen ion)
- This is what the chemoreceptors sense.
- Sends info to medulla
- Changes rhythm of breathing to increase breathing.
- NEGATIVE FEEDBACK SYSTEM.
If this pco2 is decreased (hyperventilate)
® Same pathway but it would do the opposite thing, reduce H+ and increase in co2.
® Decrease ventilation.
If pco2 is VERY VERY HIGH (unusual or disease)
- Inhibits medulla and can’t breathe anymore
This will increase peripheral chemoreceptor.
What is peripheral chemoreceptor?
Peripheral chemoreceptors
- Carotid and aortic bodies
“taste blood” mainly p02 and a little pco2 and arterial pH
Quickly, direct input to the structures
Separate from baroreceptors. Not stretch receptors. But in simliar location.
Carried via glossopharyngeal (CB)nerve and vagus nerve (AB) *****
What is the key oxygen receptor?
We regulate co2 in the blood. We don’t “regulate” o2.
Arterial 02 levels have to go way way low (disease/altitude)
Peripheral chemoreceptors detect low 02 and tell them to get more in (hypoxia).
Decrease po2, increase in alveolar ventilation, correct it to normal level.
- We overventilate alveoli to make up for co2 and keep it normal
NEGATIVE FEEDBACK LOOP; the opposite is true too.
Drop in o2 results in hyperventilation
- Lower co2 below normal (below 40)
Raise 02 above normal (hyperoxia)
How do we sense arterial plasma pH?
- Detect PH or H ions.
- Regulates acid when its non carbon dioxide.
Detect increase in H or decrease in pH
- Send that info to medulla - Raise ventilation - Decrease arterial pco2 - Reduce arterial co2 hydrogen ions - Correct for high acid.
Increase in pH in blood, hydrogen ion can’t penetrate BBB.
- Can’t influence central chemoreceptor.
- The NON CO2 ONE IS SENSED BY PERIPHERAL CHEMORECEPTORS.
- The co2 can cross the BBB, so that’s why it can access the chemoreceptors.
True with any bicarbonate: if you have too basic - decrease ventilation to correct
NEGATIVE FEEDBACK LOOK.
Response is also hyperventiation for acidity: overventilate alveoli (lower co2 and increase o2 both below/above regular levels)
- Alkylosis has opposite effect.
- *ventilation is depedent on both peripheral and central chemoreceptors but the timing is different**
- Central does most of it (80%)
Central: responds to changes in co2 in arterial blood
Only peripheral does oxygen
pH only in the blood: peripheral
pH away from the blood: central
Whats congenital central hypoventilation syndrome?
Voluntary control doesn’t work during sleep in Ondine’s curse. Congenital central hypoventilation syndrome.
Some patients : inability to sense co2 and oxygen!!!!
That is the reason for some of them.
what are examples of when when acid gets into blood/
lactic acid example
diabetic ketoacidosis (kussmaul breathing)
Ventilatory response to acid is hyperventilation to reduce co2 and increase o2 beyond normal levels.
(since co2 makes H+ ions it all works out in the wash)
To basic stuff is the opposite effect.
