regulation of respiration[1]
TRANSCRIPT
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Dr.Niranjan Murthy H.L
Asst Professor of Physiology
SSMC, Tumkur
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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.
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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
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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
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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
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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
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Pneumotaxic centre
4 th Ventricle
Apneustic centre
Dorsal respiratory group
Ventral Respiratory group
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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
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Apneustic center
• Present in lower pons
• Activate inspiratory neurons of medulla
• Inhibited by vagal input and pneumotaxiccenter
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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
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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
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VOLUNTARY CONTROL
• Voluntary hyperventilation, breath holding,
etc
• Limited duration
• Via corticospinal tract ending on motor
neurons innervating respiratory muscles
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GENESIS OF RESPIRATION
Pneumotaxic center
Apneustic centre
‘E’ NEURONS ‘I’ NEURONS
Respiratory motor neurons
LUNGS
X N
Intercostal N
Phrenic N
(+)
(-)
(-)
(-)
(-)(+)
(+)
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Factors affecting respiratory center
1. Chemical stimuli
2. Non-chemical stimuli
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Chemical regulation
• PaO2, Pa
CO2and pH
• Chemoreceptors- central and peripheral
• Pulmonary and myocardial
chemoreceptors
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Respiratory chemoreceptors
Peripheral chemoreceptors- carotid and
aortic bodies:
• Heymans, 1930
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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
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Stimulus (hypoxia)
O2-sensitive K+ channel inhibited
Reduced K+ efflux
Increased Ca2+ influx
Depolarization
Release of catecholamines
Stimulation of nerve endings via D2receptors
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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
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Aortic bodies
• Located in arch of aorta
• 2-4 in number
• Aortic nerve, branch of X N
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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
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• 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.
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Pulmonary and coronary
chemoreceptors
• Bezold-zarisch reflex
• Veratradine, nicotine and other alkaloids
• Bradycardia, hypotension and apnoeafollowed by hyperpnoea
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Chemical factors affecting
respiration
I. Effect of PO2
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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
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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
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3. Respiratory alkalosis-
voluntary hyperventilation
high altitude
4. Respiratory acidosis-
emphysema
respiratory depressant drugs
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Interaction of chemical factors
• PAO2 and PACO2 levels have
additive effect
on ventilation
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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
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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
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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
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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
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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
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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
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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.
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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
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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
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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.