Regulation of Respiration[1]

8/8/2019 Regulation of Respiration[1]

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Dr.Niranjan Murthy H.L

Asst Professor of Physiology

SSMC, Tumkur



Introduction

• Spontaneous respiration due rhythmic

discharge of motor neurons

•Center for rhythmic discharge is inbrainstem

• Respiratory center is influenced by higher

centers, reflexes and internal chemical

changes.





Neural control of breathing

• Voluntary control: located in cerebral

cortex

•Automatic control: pacemaker cells inmedulla

• Final common path: motor neurons of

respiratory muscles

• Reciprocal innervations



Respiratory center

• Several groups of neurons In pons and

medulla

• Groups:-

(i) Pre-Bötzinger complex

(ii) Dorsal & ventral respiratory group

(iii) Pneumotaxic center (iv) Apneustic center



Respiratory pattern generator

Pre-Bötzinger complex:

Small group of coupled pacemaker cells.

Located between nucleus ambiguus andlateral reticular nucleus

Produce rhythmic discharges in phrenic

nerves NK1(substance P) & μ-opioid receptors

5HT4 receptors



Dorsal respiratory group

• Extends most length of medulla in theregion of NTS

• Receives afferents from airways &

chemoreceptors• Thought to be respiratory pattern

generator- rhythmic drive to phrenic N

• Primarily ‘I’ neurons• Lesioning will not abolish automatic

respiratory rhythm





Pneumotaxic centre

4 th Ventricle

Apneustic centre

Dorsal respiratory group

Ventral Respiratory group



Pneumotaxic center

• Medial parabrachial and kölliker-fuse

nuclei of dorsolateral pons

• Normal function is unknown

• Lesioning will prolong respiration and

increase tidal volume

• Limits inspiration• Inhibit neurons of apneustic center



Apneustic center

• Present in lower pons

• Activate inspiratory neurons of medulla

• Inhibited by vagal input and pneumotaxiccenter







Experimental inferences

I. Sec A & Sec D- respiratory centre between

these sections i.e brain stem

II. Sec C- rhythmic respiration with or without

vagus- rhythmically discharging neurons inmedulla; reciprocal innervation; influence by

other parts

III. Sec B- apneustic centre in lower pons; it isinhibited by vagus and pnemotaxic centre



Inspiratory ramp signal

• Inspiratory signals are not instantaneousbursts

• Begins weakly and rises steadily in a ramp

like manner for 2secs.• Ceases abruptly for next 3secs

• Advantage- causes steady increase in

lung volume• Pneumotaxic center controls switch-off

point of ramp signal



VOLUNTARY CONTROL

• Voluntary hyperventilation, breath holding,

etc

• Limited duration

• Via corticospinal tract ending on motor

neurons innervating respiratory muscles



GENESIS OF RESPIRATION

Pneumotaxic center

Apneustic centre

‘E’ NEURONS ‘I’ NEURONS

Respiratory motor neurons

LUNGS

X N

Intercostal N

Phrenic N

(+)

(-)

(-)

(-)

(-)(+)

(+)



Factors affecting respiratory center

1. Chemical stimuli

2. Non-chemical stimuli



Chemical regulation

• PaO2, Pa

CO2and pH

• Chemoreceptors- central and peripheral

• Pulmonary and myocardial

chemoreceptors



Respiratory chemoreceptors

Peripheral chemoreceptors- carotid and

aortic bodies:

• Heymans, 1930



Carotid body

• Located in bifurcation of CCA

• 2mg weight

• 0.04ml/min (2000ml/100gm/min) bloodsupply

• Type I and type II cells (glomus cells)

• Sinus nerve (branch of IX N) is sensory



Stimulus (hypoxia)

O2-sensitive K+ channel inhibited

Reduced K+ efflux

Increased Ca2+ influx

Depolarization

Release of catecholamines

Stimulation of nerve endings via D2receptors



Factors stimulating peripheral

chemoreceptors

(i) Hypoxia

(ii) Vascular stasis

(iii) Asphyxia- lack of O2 and excess of CO2

(iv) Drugs- nicotine, cyanide

(v) Exercise- increased K+ levels



Aortic bodies

• Located in arch of aorta

• 2-4 in number

• Aortic nerve, branch of X N





Central chemoreceptors

• Located 0.2mm from ventral surface of

medulla

• Stimulated by changes in PaCO2

• Stimulation is directly proportional to

change in [H+]

• Present inside blood-brain barrier • Act via respiratory centers



• The central chemoreceptors regulate the respiration

minute to minute.• 80-85% of resting respiratory drive is due to

stimulatory effect of CO2 on central chemoreceptors,

while 15-20% of initial drive is provided by

peripheral chemoreceptors.

• Central chemoreceptors are depressed by hypoxia.

• They are also inhibited by anaesthesia, cyanide and

during sleep.



Pulmonary and coronary

chemoreceptors

• Bezold-zarisch reflex

• Veratradine, nicotine and other alkaloids

• Bradycardia, hypotension and apnoeafollowed by hyperpnoea



Chemical factors affecting

respiration

I. Effect of PO2





II. Effect of PCO2

• Linear relationship till

a limit• At 7% of inspired CO2,

alveolar PCO2

approaches that of

PaCO2 and CO2 narcosis sets in.

• Significance: O2-CO2

mixture• CO2 primarily acts on

centralchemoreceptors



III. Effect of H+ ion concentration:

Acidosis stimulates and alkalosis depresses

respiration

Acts via peripheral chemoreceptors

1. Metabolic acidosis-

diabetes mellitus

renal failure

diarrhoea

starvation

2. Metabolic alkalosis-

severe vomiting due to GI obstruction

3 Respiratory alkalosis



3. Respiratory alkalosis-

voluntary hyperventilation

high altitude

4. Respiratory acidosis-

emphysema

respiratory depressant drugs





Interaction of chemical factors

• PAO2 and PACO2 levels have

additive effect

on ventilation





Effect of CO2on hypoxia & pH

Pulm

on

aryventilation

(l/min)

0

6

10

20

30

40

3040

50

---------------------------------------------------------------

202060 60100

100

pH 7.3 pH 7.4PAO2 (mm Hg)

Resting ventilation

Alveolar PCO2 (mm Hg)

Apnoea point



Breath Holding: voluntary inhibition.

Breaking point

PaCO2 & PaO2

Breath holding is prolonged by hyperventilation,

breathing 100% O2 or removing carotid bodies

Effect of hormones:

Ventilation is increased during luteal phase of

menstruation & during pregnancy.

Activation of estrogen-dependent progesteronereceptors in hypothalamus



Non-chemical regulation

I. Responses mediated by receptors in the

airways & lungs:

Innervated by vagal fibers

Hering-Breuer inflation reflex

Hering-Breuer deflation reflex

Pulmonary chemoreflex

Vagal innervationt l ti ti l



type location stimulus response

Myelinated fibers

Slowly adapting Airway smoothmuscle cells

Lung inflation Shortening of

inspiratory time.

Hering-Breuer

reflexes.Bronchodilation.

Tachycardia.

Rapidly adapting

(irritantreceptors)

Airway epithelial

cells

Lung hyperinflation.

Exogenous &endogenous subs(histamine, PGs)

Hyperpnoea.

Cough.Bronchoconstriction.

Mucus secretion.

Unmyelinated Cfibers

Pulmonary C

fibers

(J receptors)

Bronchial Cfibers

Close to blood

vessels

Lung hyperinflation.

Exogenous &endogenous subs(bradykinin,serotonin)

Apnea followed by

rapid breathing.

Bronchoconstriction.

Hypotension.

Mucus secretion.

1 H i B i fl ti fl



1. Hering-Breuer inflation reflex:

Inflation of lung

Stimulate pulmonary stretch receptors

Vagal afferents to apneustic centre

Inhibition of apneustic centre

Inhibition of inspiration

Prolonged expiration

Significance:

Absent at normal

tidal volume.

Threshold at 1-

1.5lts of tidal

volume.

2 H i B d fl ti fl d



2. Hering-Breuer deflation reflex: decrease

in duration of expiration following marked

deflation of lungs.

3. J-reflex:

Hyperinflation of lungs

Juxtacapillary receptors

Pulmonary C fibers

Reflex apnoea,

followed by tachypnoea,

hypotension and bradycardia



J receptors:• Juxta-pulmonary capillary receptors

• A.S.Paintal, 1955

• May have physiological role in severeexercise

• Role in pathological conditions like

pulmonary congestion, edema, embolusand strong irritants.



II. Responses mediated by proprioceptors:

Increase in rate and depth of respiration; during

exerciseIII. Responses mediated by irritant receptors:

1. Cough reflex- protective; deep inspiration

followed by forced expiration against closedglottis and sudden opening of glottis

2. Sneeze reflex- similar reflex with an open

glottis and expiration through nose

IV Aff t f b t



IV. Afferents from baroreceptors:

Inhibit respiration by inhibition of respiratory

centreAdrenaline Apnoea

V. Afferents from higher centers:

1. Cerebral cortex-Frontal cortex inhibit respiration.

Motor cortex stimulate respiration.

2. Hypothalamus and limbic system:Pain, emotional stimuli

Fever



VI. Respiratory components of visceral reflexes:

1. Deglutition reflex- causes apnea byinhibition of respiratory centre via IX N.

2. Hiccup- spasmodic contraction of diaphragm; closure of glottis duringinspiration

3. Yawning- deep inspiration probably toprevent collapse of alveoli.

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Regulation of Respiration[1]