1. Oxygen Concentration and Partial Pressure in the Alveoli
The oxygen concentration in the alveoli, and its partial pressure is controlled by:
The rate of absorption of oxygen into the blood
The rate of entry of new oxygen into the lungs by the ventilatory process. Rate of alveolar ventilation.

2. CO2 Concentration and Partial Pressure in the Alveoli
Determined by two factors:
First, the alveolar PCO2 increases directly in proportion to the rate of carbon dioxide excretion
Second, the alveolar PCO2 decreases in inverse proportion to alveolar ventilation.

3. REGULATION OF RESPIRATIONBy
Dr. Mudassar Ali Roomi (MBBS, M.Phil.)
Assist. Prof. Physiology

4. Control of respiration
Two types:
Nervous control of respiration
Chemical control of respiration

5. Control of repiration Components: Sensors Central controller Effectors
gather information
Central controller
integrate signals
Effectors
muscles

6. Respiratory centre Located bilaterally in medulla oblongata and pons.
Composed of
1. Dorsal Respiratory Group (DRG)
2. Ventral Respiratory Group (VRG)
3. Pneumotaxic center
4. Apneustic center

7. Respiratory centre

8. Pre-Botzinger complex (pre-BOTC)
A collection of pace-maker cells at the upper end of Dorsal Respiratory Group (DRG)
Synaptic connection with DRG
Function: Discharges rhythmic respiratory signals

9. Dorsal Respiratory Group (DRG)
Extends most of the length of M. oblongata
LOCATION: Neurons located in nucleus of tractus solitarius and additional neurons in reticular substance of medulla
vagus and glossopharyngeal nerve terminates at Nucleus of tractus solitarius
Both nerves – afferent nerves for resp. signals to center
Pace maker neurons send ramp signals to inspiratory muscles in a Rhythmic fashion

10. Ramp signals controlled by
Pneumotaxic center
Stretch receptors in the lungs
Significance of ramp signals
No gasping
Smooth inflation of lungs
Full cycle of respiration
5 seconds
2sec inspiration
3 sec expiration

11. Fibers from respiratory center (DRG) reach the motor neurons in spinal cord between C3 & C5 to form phrenic nerve
Complete lesion of spinal cord above C3 will stop the breathing
Lesion after C5 will not affect the respiration

12. The Hering-Breuer Inflation Reflex
Muscular portions of the walls of the bronchi and bronchioles throughout the lungs have stretch receptors
Transmit signals through the vagi into the dorsal respiratory group of neurons when the lungs become overstretched.
Switches Off the inspiratory ramp and thus stops further inspiration
These signals affect inspiration in much the same way as signals from the pneumotaxic center
It also increases rate of respiration

13. The Hering-Breuer Inflation Reflex
This reflex is activated when tidal volume increases to more than three times normal
Therefore, this reflex appears to be mainly a protective mechanism for preventing excess lung inflation

14. Lung “J Receptors.”
Location: In the alveolar walls in juxtaposition to the pulmonary capillaries
Stimalation: Stimulated especially when the pulmonary capillaries become engorged with blood or
Example: When pulmonary edema occurs in such conditions as congestive heart failure.
Their excitation may give the person a feeling of dyspnea.

15. Ventral Respiratory Group (VRG)
LOCATION: Ventral part of medulla
Two nuclei
(1) Nucleus Ambiguus rostrally
(2) Nucleus Retroambiguus caudally
Both types of neurons – INSPIRATORY & EXPIRATORY
Center remain inactive during quite breathing
Active only in increased pulmonary ventilation, during which signal from DRG spill over to VRG
Stimulation of accessory inspiratory muscles & expiratory muscles

16. Pneumotaxic Center Location: Upper part of Pons
Function: Switches off Ramp Signal
Controls rate and duration of Inspiratory ramp signals
Strong stimulation may reduce Inspiratory phase to 0.5 sec respiratory rate ↑ to 30 – 40/min
Weak stimulation may ↑ Inspiratory phase to 5sec or more respiratory rate ↓ to 3-5/ min

17. Apneustic Center Located in lower part of pons
Function: Prevent inspiratory neurons from being switched off → prolonged inspiration
Shortens expiration
Such Respiration called – apneusis

18. CHEMICAL CONTROL OF RESPIRATION
Following chemical stimuli stimulate the respiration:
Excess CO2
Excess Hydrogen ion
Decreased Oxygen

19. Central chemosensitive area Peripheral chemoreceptors
Stimulated by CO2 & H+ .Oxygen have no effect
Peripheral chemoreceptors
Stimulated by O2. CO2 & H+ has little effect

20. Location of Chemosenstive area
Located bilaterally beneath the ventral surface of medulla
Hydrogen ions are only the main direct stimulus for these group of neurons

22. Decreased Stimulatory Effect of Carbon Dioxide After the First 1 to 2 Days
CO2 has a potent acute effect on controlling respiratory drive but only a weak chronic effect after a few days of adaptation.
Mechanism of adaptation: Renal readjustment of the hydrogen ion by increasing the blood bicarbonate, which binds with the hydrogen ions in the blood and cerebrospinal fluid to reduce their concentrations

23. Acclimatization of chemoreceptors
Mountain climbers have found that when they ascend a mountain slowly
Over a period of days rather than a period of hours
They breathe much more deeply and therefore can withstand far lower atmospheric oxygen concentrations than when they ascend rapidly

24. The reason is within 2 to 3 days, the respiratory center in the brain stem loses about four fifths of its sensitivity to changes in Pco2 and hydrogen ions.
Therefore, the excess ventilatory blow-off of carbon dioxide that normally would inhibit an increase in respiration fails to occur
Low oxygen can drive the respiratory system to a much higher level of alveolar ventilation than under acute condition
The alveolar ventilation often increases 400 to 500 per cent after 2 to 3 days of low oxygen

25. Peripheral Chemoreceptor
Carotid bodies through
Hering N to Glossopharyngeal N
Aortic Bodies through Vagus N to DRG
Both bodies are supplied by special minute arteries direct from the arterial trunk

26. Stimulation of the Chemoreceptors by Decreased Arterial Oxygen

27. Effect of Carbon Dioxide and Hydrogen Ion Concentration on Chemoreceptor Activity
They have a weak effect but stimulation by way of the peripheral chemoreceptors occurs as much as five times as rapidly as central stimulation

30. Regulation of Respiration During Exercise

31. PERIODIC BREATHING CHEYNE-STOKES BREATHING
An abnormality of respiration
CHEYNE-STOKES BREATHING
is characterized by slowly waxing and waning respiration occurring about every 40 to 60 seconds

32. CHEYNE-STOKES BREATHING
mechanism :
Overbreathes decrease CO2 & increase O2 in pulmonary blood
It takes several seconds before the changed pulmonary blood can be transported to the brain and inhibit the excess ventilation
Overventilated for an extra few seconds.
Therefore, when the overventilated blood finally reaches the brain respiratory center
The center becomes depressed an excessive amount
Then the opposite cycle begins and cycle repeats
CHEYNE-STOKES BREATHING

33. Under normal conditions, this mechanism is highly Damped
But in two conditions it occurs
Long delay occurs for transport of blood from the lungs to the brain seen in severe cardiac failure
Increased negative feedback gain in the respiratory control areas seen in brain damage

34. Biot Breathing / Cluster respiration:
Alternate periods of Respiration & Apnea, but transition of one period to other is abrupt, not gradual.
CAUSES:
Meningitis
Disease affecting medulla.

35. Sleep Apnea Absence of spontaneous breathing Occur during normal sleep
TYPES
Obstructive Sleep Apnea
Central Sleep Apnea

36. Obstructive Sleep Apnea
most commonly occurs in older, obese persons
1. Narrow pharyngeal passage, and relaxation of these muscles during sleep causes the pharynx to completely close so that air cannot flow into the lungs.
2. The snoring proceeds, often becoming louder, and is then interrupted by a long silent period during which no breathing (apnea) occurs.
3. decreases in PO2 and increases in PCO2, which greatly stimulate respiration.
4. This, in turn, causes sudden attempts to breathe, which result in loud snorts and gasps followed by snoring and repeated episodes of apnea.
5. excessive daytime drowsiness as well as other disorders, including increased symphatetic activity

38. Central Sleep Apnea (CSA)
CAUSES:
damage to the central respiratory centers
abnormalities of the respiratory neuromuscular apparatus
Cessation of the ventilatory drive during Sleep
Strokes

39. Treatment of CSA: Respiratory stimulants may be helpful.
Ventilation with CPAP at night is usually necessary.