Oxygen Concentration and Partial Pressure in the Alveoli

REGULATION OF RESPIRATION

Oxygen Concentration and PartialPressure 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.

CO2 Concentration and PartialPressure in the Alveoli

Determined by two factors:First, the alveolar PCO2 increases directly in proportion to the rate of carbon dioxide excretionSecond, the alveolar PCO2 decreases in inverse proportion to alveolar ventilation.

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

Control of respirationTwo types: Nervous control of respirationChemical control of respirationControl of repirationComponents: Sensorsgather informationCentral controllerintegrate signalsEffectorsmuscles

Respiratory centreLocated bilaterally in medulla oblongata and pons. Composed of1. Dorsal Respiratory Group (DRG)

2. Ventral Respiratory Group (VRG)

3. Pneumotaxic center

4. Apneustic center

Respiratory centrePre-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

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

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 seconds2sec inspiration 3 sec expiration

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

The Hering-Breuer Inflation ReflexMuscular 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

The Hering-Breuer Inflation ReflexThis 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

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.

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

Pneumotaxic CenterLocation: 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

Apneustic CenterLocated in lower part of pons

Function: Prevent inspiratory neurons from being switched off prolonged inspiration

Shortens expiration

Such Respiration called apneusis

CHEMICAL CONTROL OF RESPIRATIONFollowing chemical stimuli stimulate the respiration:

Excess CO2

Excess Hydrogen ion

Decreased Oxygen

Central chemosensitive areaStimulated by CO2 & H+ .Oxygen have no effect Peripheral chemoreceptorsStimulated by O2. CO2 & H+ has little effect

Location of Chemosenstive areaLocated bilaterally beneath the ventral surface of medulla

Hydrogen ions are only the main direct stimulus for these group of neurons

Decreased Stimulatory Effect of Carbon Dioxide After the First 1 to 2 DaysCO2 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 concentrationsAcclimatization of chemoreceptorsMountain 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 rapidlyThe 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 oxygenPeripheral ChemoreceptorCarotid bodies through Hering N to Glossopharyngeal NAortic Bodies through Vagus N to DRG Both bodies are supplied by special minute arteries direct from the arterial trunk

Stimulation of the Chemoreceptors by Decreased Arterial Oxygen

Effect of Carbon Dioxide and Hydrogen Ion Concentration onChemoreceptor ActivityThey have a weak effect but stimulation by way of the peripheral chemoreceptors occurs as much as five times as rapidly as central stimulation

Regulation of Respiration During Exercise

PERIODIC BREATHINGAn abnormality of respiration

CHEYNE-STOKES BREATHINGis characterized by slowly waxing and waning respiration occurring about every 40 to 60 secondsCHEYNE-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

Under normal conditions, this mechanism is highly Damped

But in two conditions it occursLong delay occurs for transport of blood from the lungs to the brain seen in severe cardiac failureIncreased negative feedback gain in the respiratory control areas seen in brain damageBiot Breathing / Cluster respiration:Alternate periods of Respiration & Apnea, but transition of one period to other is abrupt, not gradual.CAUSES:MeningitisDisease affecting medulla.Sleep ApneaAbsence of spontaneous breathingOccur during normal sleep

TYPESObstructive Sleep ApneaCentral Sleep Apnea

Obstructive Sleep Apnea

most commonly occurs in older, obese persons1. 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

Central Sleep Apnea (CSA)

CAUSES:

damage to the central respiratory centers abnormalities of the respiratory neuromuscular apparatusCessation of the ventilatory drive during SleepStrokesTreatment of CSA:Respiratory stimulants may be helpful.Ventilation with CPAP at night is usually necessary.