Regulation of respiration - medicinebau.com · Regulation of respiration “Ramp” is controlled by 2 ways: a- control the rate of increment of “ramp” signals. during heavy respiration,

Regulation of respiration

Nervous system:

Normally adjusts the rate of alv. vent. almost exactly to the demands of the body so that arterial PO2 & PCO2 are hardly altered even during respir. Stress (exercise)


Respiratory centre:

neurons in the medulla oblongata and pons of the brain stem

divided into:

1- dorsal respiratory group

2- ventral respiratory group

3- pneumotaxic centre

4- apneustic center & pre-Botzinger complex


Dorsal respiratory group:

extends through most of the length of the medulla

sensory termination of vagal & glossopharyngeal nerves then transmit sensory signals into the respiratory centre

signals received from:

1- peripheral chemoreceptors

2- various receptors in the lungs


Rhythmical inspiratory discharge from the dorsal group

basic respiratory rhythm is generated in the dorsal group (pre-potzinger complex)

this group still emits repetitive bursts of inspiratory neuronal action potentials even if:

a- all the peripheral nerves entering the medulla are cut

b- the medulla is sectioned from above or below


Inspiratory “ramp” signals :

inspiratory signals to the diaphragm are not instantaneous bursts of action potentials

normally the signal begins weak and increases steadily in a ramp manner for 2 secs. after that the signal ceases for 3 secs. this causes steady increase in lungs volume and not inspiratory gasps


“Ramp” is controlled by 2 ways:

a- control the rate of increment of “ramp” signals.

during heavy respiration, “ramp” increases rapidly and fills the lungs

b- control the limiting point at which the ramp suddenly ceases.

early cease shorter inspiration shorter expiration increased frequency


Pneumotaxic centre:

located dorsally in the nucleus parabrachialis of the upper pons

transmits signals to the inspiratory center

controls the “switch off” point of the inspiratory ramp controlling the duration of the filling phase

when weak filling takes 5 secs.

when strong filling lasts for 0.5 sec.

so the respiratory cycle varies 3-40 breaths/min


Ventral group:

located in each side of the medulla 5mm lateral & anterior to the dorsal group

functions:

1- inactive during normal quite resp.

2- not involved in the basic rhythmical oscillation

3- provides extra resp. drive when ventilation is

more than normal

4- contributes in both inspiration & respiration


The Hering-Breuer inflation reflux:

sensory signals from the lungs help in controlling respiration

stretch receptors that are found in the muscular portion of the bronchi & bronchioles send their signals with the vagus to the dorsal group these signals are:

a- sent when the lungs are overstretched

b- have similar effect to that of the pneumotaxic centre

c- activated when T.V is larger than 1.5L/breath


Chemical control

In order to control [O2], [CO2], [H+] in tissues

Control by CO2 & H+:

the chemosensitive respiratory centre is not affected directly by [CO2] .

located 0.2mm beneath the surface of the ventral medulla

highly sensitive to changes in blood PCO2 or [H+]


Control by CO2 & H+:

H+ is likely the primary stimulus for these receptors

H+ cannot cross the blood-brain barrier so changes in blood [H+] wont affect these receptors

instead an increment in blood PCO2 will indirectly activate these receptors

when [CO2] ↑ in blood ↑ in CSF

CO2+H2O Carbonic acid bicarbonate + H+


Effect of CO2 on chemosensitive neurons:

the excitation effects peaks the 1st hours after the increment in blood [CO2]

after 2 days the effect is decreased because of:

a- renal adjustment of [H+].

b- increased bicarbonate ions that enter the CSF and bind to H+


O2 effect:

virtually no direct effect on respiratory centre because:

1- change of PO2 from 60mmHg to 100mmHg has no effect on the amount of [O2] because of Hb buffering

2- [CO2] in blood & tissue is inversely proportional to the ventilation rate

so evolution has made CO2 the major controller instead of O2


Peripheral chemoreceptors:

special nervous chemical receptors for detecting changes in O2 in blood & tissues, and to less extent changes in CO2 & H+

carotid bodies (through glossopharyngeal) & aortic bodies (through vagus) to the dorsal group

the blood flow supplying these bodies is 20x their weight each minute so the % of removed O2 from the blood flow is virtually zero

those bodies are exposed to arterial blood not venous blood


Peripheral chemoreceptors:

are stimulated by ↓ [O2], and the range of sensitivity is between 30-60 mmHg (a range in which Hb saturation decreases rapidly)


Effect of CO2 & H+ :

↑ [CO2], [H+] excite receptors ↑respiration

both have 7x more effect on the central receptors than on the peripheral receptors but 5x as rapid on the peripheral ones.

Effect of O2:

low [O2] excites peripheral receptors “glomus cells” that synapse directly or indirectly with nerve endings.

low PO2 and normal [CO2], [H+] will drive the ventilatory process quite strongly


Acclimatization “Chronic breathing of low O2”: Mountain climbers ascend slowly over a period of days causing deep breathing and withstanding low PO2

because after 2 days 4/5th of the sensitivity of receptors to CO2 an H+ is lost

so low [O2] ↑ventilation by 400% whereas acute exposure of low [O2] will only ↑ventilation by 70%


Regulation during exercise:

In exercise O2 consumption and CO2 formation is increased 20x

the ventilation is increased so PO2, PCO2 and pH remain Normal

when the brain sends its signals to the muscles it also send collateral signals to the brain stem to increase ventilation even before exercise

then chemical factors play a significant role to maintain [O2],[CO2]


Other factors affecting respiration:

1- voluntary control : for short period of times

2- irritant receptors: stimulated by many incidents coughing & sneezing

3- J receptor in alveolar walls lead to edema where the patient has dyspnea

4- brain edema causes res. centre depression

5- anesthesia & narcotic overdose depresses res. centre (halothane, morphine, pentobarbital)


Periodic “Chyne-Stokes” breathing :

person over-breathes ↑[O2],↓[CO2] after seconds these [ ] are sensed by the resp. centre inhibition of excess ventilation opposite cycle begins ↓[O2],↑[CO2] after seconds these [ ] are sensed by the resp. centre the person is again over-breathing


Periodic “Chyne-Stokes” breathing :

this cycle doesn’t occur normally but can be seen in these conditions:

1- increased neg. feedback gain in resp. control areas change in [CO2], [H+] causes further great change in ventilation “brain-damage”

2- long delay in transporting blood from the lungs to the brain “severe or chronic heart failure,


Sleep apnea:

episodes of apnea lasting for 10 secs. Or more, occurring 300-500 times/night

Obstructive sleep apnea:

during sleep the pharynx is relaxed, in some individuals this may lead to complete closure snoring & labored breathing apnea↓O2,↑CO2 stimulation of resp. center sudden snorts and gasps

1- elderly, obese, nasal ostruction, large tongue, enlarged tonsils 2- Sudden infant death syndrome (SIDS): exaggerated case of sleep apnea, premature baby, smoker pregnant mother

Treatment of obstructive sleep apnea

1-Surgery uvulopalatopharyngoplasty (remove excess fat at back of throat , tonsils, tracheostomy)

2-Continous positive airway pressure CPAP

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Regulation of respiration - medicinebau.com · Regulation of respiration “Ramp” is controlled by 2 ways: a- control the rate of increment of “ramp” signals. during heavy respiration,