oxygen concentration and partial pressure in the alveoli
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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 - PowerPoint PPT PresentationTRANSCRIPT
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.