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CONTROL OF RESPIRATION b.
DR. REVILLA / NOV. 26, 2015
FINALS: QUIZ #3
BOLD, RED LETTERS: EMPHASIZED DURING LECTURE
BLUE, ITALICIZED: AUDIO
GREEN LETTERS: FROM OT
CARBON DIOXIDE TRANSPORT
 CO2 is transported in three forms:
a. Dissolved Co2
b. Carbamino-Protein Complexes
c. Bicarbonate
 Of the three, CO2 is transported to the RBC primarily as
BICARBONATE (transport is caused by the generation
of Carbonic Acid by the enzyme Carbonic Anhydrase)
 Carbonic Anhydrase Mechanism
 conversion of Carbon Dioxide to Bicarbonate
 Generation of Carbonic Acid→H2 ion release→
formation of Bicarbonate→ released in plasma
 Bicarbonate is negative, therefore the negative ion
inside the RBC when released makes the RBC more
positive (Nagkakaroon ng imbalance doon sa ion
content of RBC)
 To maintain usual concentration inside RBC, Chloride
goes in to replace Bicarbonate (Chloride Shift). The
released Bicarbonate combines again to hydrogen ion in
plasma → released of Co2 to alveolar air (Haldane
Effect)
 Bohr Effect
 Oxygen released to circulation
REGULATION OF RESPIRATION
 Semi-Automatic, rhythmic and voluntary
 Four major sites of ventilatory control:
a. Respiratory control center
b. Central Chemoreceptors
c. Peripheral Chemoreceptors
d. Pulmonary Mechanoreceptors
Respiratory Control Center
 central control of respiration is MEDULLA
Ex. When you hold your breath, as you progress in holding your
breath this sends signal to the respiratory control center and tells
the brain that there is a buildup of CO2 inside, that's why you
need to inhale again and then exhale
1. Dorsal Respiratory group
 Basic control of respiration
 One that is active in the basic rhythm of respiration,
inspiration ramp signal
 Stimulates respiration using two mechanisms:
a. Control of the rate of increase in the ramp
signal
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TRANSCRIBERS: CASTRO, AUSTRIA
physiology
Control of the limiting point at which the ramp
suddenly ceases
Ramp signal- increase inspiration until certain point, then elastic
recoil
*Hering Breuer inflation reflex- for lung deflation
- TLC stimulates the reflex→ Stop breathing in
-if no reflex → possible lung rupture
2. Ventral respiratory group
 inactive during normal quiet breathing because
respiration or expiration is passive and it governed by
recoil mechanism
 activated only during respiratory overdrive ( exercise,
stress, DOB)
 it may contribute inspiration and expiration during
respiratory overdrive
Central Chemoreceptor
 receptors that is sensitive to the effect of different
chemicals of the body
 includes CO2, Oxygen and Hydrogen ion
 Blood Brain Barrier is relatively impermeable to CO2,
therefore, CO2 is the only chemical that can stimulate
central chemoreceptor
 Sensitivity of the brain is to hydrogen/Ph level,
therefore, CO2 when it passes to blood brain barrier
combines with H20→ forms carbonic acid→ release
hydrogen ion →change in ph allows central
chemoreceptor to react→ patient starts to
hyperventilate or hyperventilate
Hydrogen Ion- primary source for neuronal excitation
CO2- has more potent effect since hydrogen ion does not cross
the BBB
 technically the major controller of respiration is CO2,
not O2
 any change in carbon dioxide in the circulation increase
transfer of CO2 in the CSF→ signals chemoreceptors the
degree of acidity → signals the lungs to hyperventilate
→ decrease the CO2→ overdrive→ stimulates ventral
respiratory group
Peripheral Chemoreceptor
 includes carotid and aortic bodies; made out of type 1
glomus cells
 reacts to all pO2, pCO2, Bicarbonate and Hydrogen ion
(pH)
 Oxygen would be the most potent stimulus
 Decrease in paO2 stimulates glomus bodies (carotid and
aortic)
-reason why people has Acclimatization
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Acclimatization C. Juxtaalveolar or "J" Receptors
 when living in high altitudes there decreased  responsible for feeling of dyspnea
atmospheric pressure because barometric pressure is  stimulated when lungs are filled with water
thin → hypoxia→ when prolonged → Acclimazation,
which includes:
IMPLICATIONS
a. Increased Erythropoiesis Exercise
b. Increased in the threshold to hypoxia by  when you exercise you need more oxygen
peripheral chemoreceptors →Hyperventilate → decrease CO2 →Respiratory
Alkalosis, but...
High Altitude Pulmonary Edema (HAPE)  if mild to moderate exercise→ body compensates → no
 experienced on shifting from low to high altitudes; change of pH
decread O2 levels  if heavy exercise→ more muscles involved→ increase
 without acclimazation need of oxygen → lactic acidosis → change in ABG
ex. Climbing mount everest
Athletes: normal: there is adaptation to increase drive
Pulmonary Mechanoreceptors  normal blood gas
A. Chest and Lung Reflexes  pH remains normal
1. Hering Breuer inflation reflex
 Avoid lung rupture due to overinflation Cheyne- Stokes Respiration
 alternate period of Apnea and hyperventilation
*if you inhlale to TLC, the expansion of the lungs stimulate the  seen in patient with Heart Failure and Organic brain
hering breuer reflex and tells the lungs to stop because it is already damage (Stroke)
inflated  recurrent until brain is repaired
 poor prognosis
2. Diving Reflex  How?
 protective reflex when we drown Once CO2 penetrate BBB and circulates to CSF→
damaged brain allows delay in recognition in lack of
* when you dive in deep water, the laryngeal area closes so that CO2 in CSF→ brain interprets it as if there is no CO2→
you do not aspirate Hypoventilation/ Apnea→ CO2 Builds up → Eventually,
brain will recognize increase in CO2→ Hyperventilate →
3. Aspiration Sniff Reflex overshoots → decrease CO2 → Apnea again →Cycle....
 occurs when there is nasal congestion
Sleep Apnea
*it governs swallowing→ closing of epiglottis to protect trachea  usually in obese and short neck
 deposition of fat in hypopharynx→ compression→
B. Sensory Receptors closes as sleep deepens → narrowing of airway causes
1. Irritant Receptors snoring → Apnea → Wakes up
 found in trachea and pharyngeal wall  periods of apnea→ increase in CO2→ periods of
 stimulated when you inhale noxious stimuli→ wakefulness
bronchoconstriction to prevent entry of these  patients do not reach REM stage; experience daytime
substances; COUGHING sleepiness
 A.K.A Rapid Adapting Pulmonary Stretch
Receptors *Obstructive Sleep Apnea (OSA)
 Awake: muscle in hypopharynx overcomes the
2. Slowly Adapting Pulmonary Stretch Receptors pressure created by fat
 in play when patient has disease Asleep: muscles are relaxed. Airway closes slowly as
 Eg. COPD-prevents vast expiration/ inspiration the person goes to sleep→ when air passes in the small
opening causes turbulence which leads to snoring→
*Obstruction→ accumulation of carbon dioxide → stimulates the when person reaches deep sleep, apnea occurs. the CO2
receptors → pursed lip breathing builds up, need to wake up in order to catch his breath
*2 objectives of pursed lip breathing: leading to hypeventilation
 blow of CO2 by prolonging CO2
 Prevent dynamic compression of airways due to slow -Treatment- Continuous positive airway pressure (CPAP) to open
expiration airways

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TRANSCRIBERS: CASTRO, AUSTRIA Page 2 of 2