L32, L33 – Control of Breathing Flashcards Preview

MBBS I CPRS > L32, L33 – Control of Breathing > Flashcards

Flashcards in L32, L33 – Control of Breathing Deck (100):

What are 3 basic elements in respiratory control system?

Central controller - brain
Effectors - respiratory muscles


Name the motor centers and coordinating centers.

Motor centers: Inspiratory center & Expiratory center

Coordinating centers: Pneumotaxic center and Apneustic center


Where are motor centers?

medulla oblongata


Where are coordinating centers?


1. Pneumotaxic center (upper pons)

2. Apneustic center (middle and lower pons)


Roles of motor centers?

primary regulation:
1. Inspiratory center: for inspiration
2. Expiratory center: for expiration


Roles of coordinating centers?

modifies level / pattern of breathing:

1. Pneumotaxic center: quickens transition from inspiration to expiration (shorten inspiratory phase > increase breathing frequency)

2. Apneustic center: Inhibits transition from inspiration to expiration > prolong inspiratory phase


What are the 2 neural pathways for control of breathing?

Vagal feedback (Hering Breur Reflex)

Pneumotaxic feedback


What is Neurogenic control of breathing?

Maintain regular, rhythmic
breathing pattern


What neural pathways are stimulated in Inspiration?

Inspiration = Active process

Lung stretch receptor > Stimulate Apneustic centre > Stimulate Inspiratory centre > Inhibit Expiratory centre & Stimulate Lung inspiration (via spinal cord)


What neural pathways are stimulated in Expiration? (2 components- vagal and pneumotaxic feedback)

Passive process

1) Stop discharge of Inspiratory centre:
Lung stretch receptors from lung inspiration inhibit Apneustic centre > decrease stimulation to inspiratory centre via VAGAL FEEDBACK

2) For Passive lung deflation
Inspiratory centre then stimulates Pneumotaxic center > Inhibit Apneustic center> decrease stimulation to Inspiratory centre via PNEUMOTAXIC FEEDBACK

inspiratory muscles relax > passive lung deflation


During lung inspiration, what center is stimulated?

Expiratory center via vagal nerves


During lung expiration, what center is stimulated?

Inspiratory center AND Apneustic center


What is the neural pathway to begin inspiration after expiration?

Lung expiration > Stretch receptors stimulate
1) Inspiratory center
2) Apneustic center > Stimulate Inspiratory center

> both pathways Stimulate Lung Inspiration via spinal cord


Relationship between Higher centers and Pneumotaxic centers?

Stimulate or Inhibit


Deduce the change in breathing if the neural organisation is cut at: Cut between higher centers and pneumotaxic center?

breathe normally


Deduce the change in breathing if the neural organisation is cut at: Cut between pneumotaxic center and apneustic center?

still have vagal feedback between lung Inspiration stretch receptors and apneustic center > breathe normally


Deduce the change in breathing if the neural organisation is cut at: Cut between apneustic center and inspiratory/expiratory centers? e.g.Vagotomy

Cut link between Apnuestic center and Inspiratory center > change in breathing pattern


Deduce the change in breathing if the neural organisation is cut at: Cut between inspiratory/expiratory centers and lungs ? (e.g. spinal cord or vagus cut)

no breathing > die


What receptor type is most important in chemical / metabolic control of breathing (minute to minute control) ?

 Chemoreceptors


What are the two types of chemoreceptors?

1. Peripheral chemoreceptors

2. Central chemoreceptors


Name locations of the 2 types of chemoreceptors?

Peripheral chemoreceptors:
 Aortic arch
 Carotid body (at bifurcation of common carotid artery)

Central chemoreceptors:
 In medulla oblongata, close to motor centers


Explain action of Peripheral chemoreceptors on increasing ventilation?

Increase chemo-sensitive cell activity

Stimulated by:
Decrease pO2, pH, blood flow

Increase pCO2, temperature, drugs

Increase ventilation by increasing frequency and Tidal volume


Explain action of Peripheral chemoreceptors on decreasing ventilation?

Decrease chemo-sensitive cell activity

Stimulated by:
Increase pO2, pH, blood flow

Decrease pCO2, temperature, drugs

Decrease ventilation by decreasing frequency and Tidal volume


Explain action of Central chemoreceptors on decreasing ventilation?

Exactly the same as peripheral chemoreceptor
except the action of pO2

Decrease chemo-sensitive cell activity

Stimulated by:
Increase pH, blood flow

Decrease pCO2, temperature, drugs

Decrease ventilation by decreasing frequency and Tidal volume


Explain action of Central chemoreceptors on Increasing ventilation?

Exactly the same as peripheral receptor except action of pO2

Increase chemo-sensitive cell activity

Stimulated by:
Decrease pH, blood flow

Increase pCO2, temperature, drugs

Increase ventilation by increasing frequency and Tidal volume


What is the main difference between peripheral and central chemoreceptors in their stimulation?

PO2 has effect only in peripheral but not in central chemoreceptors


Why does PO2 has effect only in peripheral but not in central chemoreceptors?

Brain cell activity is not sensitive to oxygen level due to depressive effect.

otherwise hypoxia suppresses central chemoreceptor activity, cannot react to compensate low O2


Are baroreceptors normally employed for control of breathing?



What are baroreceptors? Where are they located depending on function??

mechanical receptors in CVS

 Carotid sinus, aortic arch: high blood pressure
 Pulmonary artery, great veins: low blood pressure


What do the different baroreceptors detect/ monitor?

High BP baroreceptors @ Carotid sinus, aortic arch > monitor systemic arterial pressure

Low BP baroreceptors @ Pulmonary artery, great veins> monitor pulmonary arterial and venous pressure


Explain the action of systemic arterial pressure on ventilation.

Increase BP > Decrease ventilation

Decrease BP > Increase ventilation


Explain the action of Pulmonary arterial pressure on ventilation.

Increase pulmonary arterial or venous pressure > Increase ventilation

Decrease pulmonary arterial or venous pressure > Decrease ventilation


How does Left Heart failure cause change to Ventilation?

2 pathways:

1) LHF cause decrease systemic pressure > stimulate baroreceptors at carotid sinus/ aortic arch > Increase Ventilation

2) LHF cause blood congestion in pulmonary circulation (or RHF cause increase venous pressure) > increase pulmonary arterial pressure >Increase ventilation


Effect of breathing on venous return?

Inspiration changes pleural pressure >

negative thoracic pressure and positive abdominal pressure > distend vena cava and increase lumen diameter > acts as RESPIRATORY PUMP on venous return to propel blood > increase venous return


Aortic arch has which receptors?

High BP baroreceptors and peripheral chemoreceptors


Where are thermoreceptors located?

 Central (hypothalamus)
 Peripheral (skin)


Explain action of thermoreceptors on ventilation?

Increase Temp. > Increase ventilation

Decrease temp > decrease ventilation


How does fever OR exercise change ventilation?

Increase temp.> increase ventilation
 Remove CO2, take in O2
 Remove heat to the environment


Where are Ergoreceptors?

in muscles


How do ergoreceptors stimulate change in ventilation?

Increase muscle contraction (e.g. exercise) > detected by ergoreceptors > stimulate increase in ventilation > prepare for metabolic change in muscle


Name the 3 types of pulmonary receptors.

1. Irritant receptors
2. Stretch receptors
3. Type J receptors
(juxtapulmonary capillary)


name location of the three pulmonary receptors.

Irritant = Epithelium of airways

Stretch = Smooth muscles of airways

Type J = juxtapulmonary capillary in alveolar wall


What are irritant receptors' action on breathing?

rapid, shallow breathing pattern in Lung and airway diseases


What are stretch receptors' action on breathing?

Maintain regular breathing pattern by Vagal feedback neurological control


What are Type J receptors' action on breathing?

Rapid, shallow breathing pattern in lung diseases


What are the stimuli of irritant receptors?

Chemical and mechanical irritations (Pneumothorax, Pulmonary congestion, Asthma)


What are the stimuli of stretch receptors?

Δ lung volume (e.g. inflation,

Δ transpulmonary pressure
(TPP increase = lung size increase)


What are the stimuli of Type J receptors?

Increase Interstitial volume
Chemical injury
Pathological conditions (e.g. fibrosis, emphysema)


What are the changes in ventilation in irritant receptor and Type J receptor activation?

Rapid, shallow breathing, increased ventilation by:

Increase frequency
Decrease tidal volume


What system compensates for airway obstruction diseases?

Gamma system

Act on muscle spindles (intercostalis, diaphragm) > increase muscle contraction to overcome muscle elongation caused by airway obstruction


What and Where are the upper airway receptors?

Upper airway receptors = irritant receptors in nose, nasopharynx, larynx


What is the function of upper airway receptors?

Mechanical or chemical irritation > receptor stimulate Sneezing, coughing, bronchoconstriction

prevents further entry of foreign substances / irritants into system


What blood gas regulates ventilation?


regulate concentration of CO2 throughout the body


What is the slope of Ventilation / PACO2 graph?

Response coefficient to PACO2


How does response coef. change at Low PACO2?

Lower (<40 mmHg) : Response coef. > 0
Ventilation is INDEPENDENT of PCO2


How is PACO2 controlled during sleep?

At low PACO2 during sleep (e.g. sleep apnea):

Higher brain centers activate tonic discharge, WAKEFULLNESS DRIVE, to PREVENT BREATHING CESSATION


How does response coef. change at Normal PACO2?

High response coef.
(3 L/min/mmHg)


How does response coef. change at High PACO2?

Response ceof. decreases (flatter slope)


What is the effect of very high PACO2 on ventilation?

Central depression (brain sensitive to PCO2 so brain activity becomes depressed)

Ventilation decrease to zero > death


Can CO2 in blood directly stimulate CO2?

No, has to diffuse to receptor and then dissociate for H+ to act on receptors


Acute CO2 inhalation:
Compare the speed of action between CO2 in blood and in CSF on stimulating receptors? Why?

In blood (within a second)

In CSF (latency = 20-30 seconds; steady response in 5-10 min)

In CSF, CO2 has to cross blood-brain-barrier, takes time


Acute CO2 inhalation:
Compare the responses induced by blood CO2 vs CSF CO2 on receptors?

Blood CO2 on peripheral chemoreceptors induces smaller response than CSF CO2 on central chemoreceptors


Acute CO2 inhalation:
Why is amplitude of peripheral chemoreceptor response lower than central chemoreceptor response?

PROTEIN BUFFERS IN BLOOD buffer the increase in H+ from CO2, so ventilatory change is lower > (1/3) of total response

No protein buffers in CSF > (2/3) of total response


Chronic CO2 inhalation:
Explain pathway for compensation to restore normal pH

Chronic CO2 inhalation (e.g. obstructive lung disease) > respiratory acidosis > pH drop compensated by increased HCO3- production > more HCO3- in blood and CSF


How does HCO3- concentration change ventilation?

More HCO3- = more H+ buffered = less H+ reach chemoreceptors (peripheral or central) = decrease stimulation of increase ventilation


Where is HCO3- in blood and CSF circulation produced? What is the overall effect of HCO3- production on ventilation?

HCO3 in blood : made by kidneys, affect peripheral chemoreceptors

HCO3 in CSF: made by Choroid plexus and brain cells, affect central chemoreceptors

More HCO3 in blood and CSF = LESS VENTILATION


What is the effect of raised CSF HCO3- over long time on chemoreceptors response to pCO2 change?

reset, acclimatize central chemoreceptors towards a higher PCO2 level > CO2 less stimulatory on pH/ need more CO2 to induce change in ventilation

CO2 no longer acts as a potent ventilator stimulus (e.g. in COPD patients)


How is acclimatization to low pCO2 in CSF achieved? (not the effect of prolonged low pCO2)

Decrease CSF HCO3-
Reset central chemoreceptors to lower pCO2

Lack of O2 becomes important ventilator stimulus


How does PAO2 affect ventilation?

Only at lower than 60mmHg > stimulate Ventilation

Normal O2 levels does not affect ventilation


Why does PAO2 only affect ventilation at lower than 60mmHg?

Sigmoid shape of O2 dissociation curve > decreasing PAO2 only
stimulate when PAO2 < 60 mmHg
60 mmHg = intersection of steep and flat sections of O2 dissociation curve


What is the response coefficient of ventilation to O2? Why is it so low?

low response coefficient (0.25 L/min/mmHg) compared to CO2: 3 L/min/mmHg

Braking effects of accompanying hypocapnia
(at low pCO2 and high pO2, effect of CO2 on ventilation decreases to zero)


Is pO2 important in physiological control of ventilation then?



Explain the action of Hypoxia in blood on ventilation?

Low pO2 > chemoreceptors stimulated > initially ventilation increases > Due to accompanying decrease in pCO2 and H+ (braking effect of accompanying hypocapnia) > LESSEN INITIAL INCREASE in Ventilation


Explain the action of accompanying hypocapnia (after hypoxia) on CSF.

Low pCO2 > decrease H+ to stimulate central chemoreceptors > Lessen initial increase in ventilation

Overall, acute hypoxia causes small increase in ventilation


How is prolonged hypoxia compensated?

Hypoxia induces respiratory alkalosis:

Compensate by decrease HCO3- in blood and CSF > increase H+ stimulation on chemoreceptors > gradual increase ventilation


Explain acclimatization to low PCO2 (e.g. high altitude).

Decrease CSF HCO3- > reset central chemoreceptros to lower PCO2 threshold > pCO2 becomes more stimulatory to ventilation > increase ventilation in low CO2 environment > further increase in ventilation


In summary what gas controls ventilation in normal vs COPD patients?

Normal = CO2
COPD = chronic hypercapnia = O2


Is ventilation more sensitive to CO2 or pH change?

less sensitive to pH change than to PCO2 change (probably due to braking effect of hypocapnia)


How does pH change ventilation?

Lower pH = increase ventilation

Higher pH = decrease ventilation


Summarize the effect of respiratory acidosis/ acute hypercapnia on ventilation

In blood: increase CO2 = increase H+ > due to buffer effect on peripheral chemoreceptors is 1/3 of total response

In CSF: more H+ > no buffer means effect on central chemoreceptors is 2/3 total response

Overal tremendous increase in ventilation


Summarize the effect of metabolic acidosis/ acute hypoxia on ventilation.

In blood: accumulation of non-CO2 acid > increase ventilation via peripheral chemoreceptors > accompanying hypocapnia and decrease in H+ cause braking effect > lessen initial increase in ventilation

In CSF: Hypoxia cause accompanying hypocapnia > decrease CO2 and H+ cause braking effect on central chemoreceptors > Lessen initial increase in ventilation

Overall small increase in ventilation


Overall, ventilation response to respiratory acidosis is higher or lower than response to metabolic acidosis?

Respiratory acidosis response is higher (Response to hypercapnia is much larger than response to hypoxia/ accompnaying hypercapnia)


How does Hypercapnia change the response coef. to O2 lack?

Increase Co2 = decrease O2 lack threshold = increase response coef. to O2 lack > easier to initiate response to change in pO2 at high pCO2


How does Hypoxia change response coef. to CO2?

Low pO2 > decrease CO2 threshold > Increase response coef. to CO2 (accompanying hypocapnia)


How does CO2 response coef. change with pH?

Decrease in pH (e.g. prolong hypercapnia) causes decrease in CO2 threshold but the response coef. remains the same


How can ventilation be depressed in sleep via wakefullness drive?

Inhibit higher centers to stimulate medullary centers by Wakefullness Drive

(During wake- tonic discharge from ascending reticular formation to brain stem and midbrain stimulate medullary centers)


How can ventilatory response be changed to cause depressed ventilation in sleep?

Depress O2 and CO2 ventilatory responses + shift CO2 response curve to right = harder to stimulate


How can upper airway lead to depressed ventilation in sleep?

Sleep > depressed tonic activity in upper airway muscles > tongue fall back > upper airway obstruction


Control of breathing:
During non-REM sleep? (4 stages)

Stage 1 & 2 = control by wakefullness drive and metabolic

Stage 3 & 4 = control by metabolic only


REM sleep control of breathing? (tonic and phasic)

Tonic = Wakefulness drive and metabolic

Phasic = Behavioral


Awake control of breathing?

Rest = wakefulness drive and metabolic

Activity = behavioral


Compare the breathing patterns of stages of non REM sleep?

Stage 1 & 2 = periodic

Stage 3 & 4 = regular


Compare breathing pattern of REM sleep?

Tonic = regular

Phasic = irregular


Compare breathing pattern of awake ?

At rest = regular

Exercise = irregular


Periodic breathing occurs in Stage 1 & 2 (light) of Non-REM sleep. (** ask first **)

(await questions)


What is sleep apnea?

Pathological condition
Periods of apnea (10-90sec) recurring AT LEAST 11 times per sleeping hour

(<5-10 episodes per sleeping hour is normal)


What are the 3 types of sleep apnea?

 Central apnea (loss of ventilatory effort: Decreased drive from brain; or Skeletal muscles do not contract)

 Obstructive apnea (upper airway obstruction)

 Mixed apnea (central + obstructive) – more common


What are some consequences of sleep apnea?

1) Snoring (partial upper airway obstruction)

2) Daytime sleepiness (interrupted sleep at night >need to compensate)

3) polycythemia, pulmonary constriction, right heart failure

4) systemic hypertension


Explain polycythemia and how pulmonary constriction can lead to RHF in sleep apnea?

1) Hypoxia > produce erythropoietin > polycythemia (more RBC) > blood more viscous and harder to pump

2) Repeated hypoxic episodes > pulmonary constriction > increase resistance

Right Heart hypertrophy > Failure


How can sleep apnea cause systemic hypertension?

Frequent cerebral arousals > repeated sympathetic activation > higher BP

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