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Righto, since you asked - BIOLOGIST AT WAR, engineers and techogeeks need not apply! ;)
The control of respiration.....
The respiratory system can be looked at, simply, as a feedback control system. The simplest feedback systems have the following components: output centre, sensors (which feed back to the output centre) and effectors:
1.Output center: brainstem (both medulla and pons), reticular activating system, the thalamus, hypothalamus and cortex (higher influence--behavioral controller).
2.Sensors:
A.lung sensory receptors--stretch receptors the intercostal muscles (internal and external), irritant receptors located in the airway epithelium
B.irritant receptors--activate cough reflexes; respond to irritant chemicals, vapors or particles.
C.chemoreceptors--carotid body oxygen sensors (peripheral) and (central) ventrolateral medullary chemoreceptors.
3. Effectors: diaphragm, intercostal muscles, abdominal muscles, and accessory muscles of respiration
The respiratory control system functions to generate a rhythmic, coordinated series of inspiratory and expiratory events. One respiratory cycle can be divided into three distinct phases:
i) inspiratory phase--there is an increase in firing of motor nerves to the inspiratory muscles and pharyngeal dilator muscles
ii) post-inspiratory phase--a decrease in motor discharge to inspiratory muscles
iii) expiratory phase--during quiet tidal breathing, all neural activity to respiratory muscles is silent. Normal expiration is a passive process and is caused by the relaxation of the inspiratory muscles - this is mainly the intercostals muscles.
Brainstem controller:
Current theories of respiratory control combine groups of brainstem nuclei into inspiratory/expiratory clusters. These nuclei are spatially diverse in the brainstem, however, and there is no single inspiratory or expiratory nucleus, as was once thought.
Medullary Centers:
These are found in the medulla oblongata which forms part an oblong part in the middle of the brainstem (and you thought scientists had no imagination - shame on you ;) )
Dorsal Respiratory Group (DRG) - these upper motor neurons project primarily to the intercostal nerves. The DRG is the primary inspiratory center, and it is thought to control the timing of the respiratory cycle. The DRG is primarily an inspiratory center, and when stimulated in anesthetized animals, can initiate inspiration.
Ventral Respiratory Group (VRG): located ventrally (to the front) in the medulla and is composed of four nuclear complexes. Signals from these nuclei are to inspiratory muscles, pharyngeal/laryngeal muscless and expiratory muscles.
Pons:
The pontine respiratory center (PRC) most likely modifies the firing of medullary respiratory neurons by receiving and integrating afferents from higher brain centers (cortex), then modifying the output of the DRG and VRG.
Behavioral Inputs:
The normal rate and depth of respiration may be dramatically affected by wakefulness/sleep, reflexes (such as swallowing or sneezing), talking, singing, etc. Mood states such as anxiety or depression can also alter the rate and depth of breathing - this is why you will hear sooooo many divers harping on about "visualisation" and relaxation, the more relaxed, the lower the minute ventilation (SAC). You can voluntarily hold your breath or hyperventilate, though not indefinitely, and the limits of voluntary changes in respiration are often determined by blood gas tensions (O2 and CO2).
Sensors:
To this point, we have reviewed the basic neural circuitry involved in generating the respiratory rhythm; now, we will examine the sensors which increase or decrease the drive to breath.
Chemical control:
Since the mid 1800's, the stimulatory effects of hypoxia and hypercapnia on the respiratory system have been known. Chemical sensors, either peripheral chemoreceptors or central chemoreceptors control the ppCO2 (and ppO2) very tightly, by altering minute ventilation. Normally, ppCO2 never varies more than about ±2mmHg
Central chemoreceptors:
The major stimulus for ventilation in humans comes from the central chemoreceptors responding to HCO3-/H+ (CO2 dissolves into the blood to form HCO3- & H+ carbonic acid). The response to ppCO2 is generated in the brainstem on the surface of the medulla. A rise in ppCO2 causes an increase in Ph, which is conveyed to the brain through the carotid arteries. Changes in CSF pH for a given amount of CO2 are far greater than in the blood due to CSF containing far less H+ buffers. Approximately 85% of the respiratory system response to CO2 occurs at the central chemoreceptors; the remaining 15% of the CO2 response originates in the peripheral chemoreceptors
Peripheral Chemoreceptors:
Peripheral sensors that respond to an increase in blood H+ or CO2, or to a decrease in ppO2 and are located at the carotid arteries (carotid bodies) and in the aortic arch. The carotid bodies, however, contribute more to respiratory control than do the aortic arch receptors.
Now, I'm not going to cover all the mechanisms (partly because they are not all known, partly because I got my biology degree in '98 ;) ) but there are also several ways oxygen is release from the blood such as the CSF Bicarbonate Shift (responsible for the partial reversal of hypocapnia seen in response to high-altitude hypoxia), ventilatory response to hypoxia: (detected by the peripheral chemoreceptors when ppO2 decreases below ~ 60mmHg causing inhibition of the central chemoreceptors, Hering-Breur reflex. I'm also not going into mechanical receptors and their effects on respiration (i.e. Pulmonary Stretch Receptors & C-fibres) but will mention the mammalian diving reflex and effects of anticipation
This occurs when diving to or past approximately 5-8m. The mammalian diving reflex consists of bradycardia (slowing of the heart rate) and shunting of the blood from non-essential organs such as the viscera and to the essential organs such as the brain, lungs and heart.
During exercise, alveolar ventilation changes during exercise to match the increased production of CO2 and demand for O2. This matching however appears to occur far faster than is possible simply by changed in blood Ph or ppCO2. The exact mechanism(s) that matches ventilation to the increased production of CO2 is unknown at present and has been thought to result from an increase in body temperature, cortical "anticipation" of exercise, and mechanical inputs from muscle and joint receptors.
Righty ho, I hope that has answered a few questions. A question was recently posed as to whether Nitrox (higher ppO2) would cause a decrease in minute volume. To be honest, I can't see how apart from the diver being more relaxed. I know that pure oxygen does have theraputic uses and did think that it could potentially due to low acidosis levels but was told the following;
"For any given change in blood pH, there is a larger increase in ventilation for respiratory acidosis than metabolic acidosis, since the protons from organic acids (such as lactic acid or ketoacids) do not cross the blood-brain barrier as quickly as CO2; thus, changes in blood H+ concentrations (due to the production of organic acids) are sensed centrally only over a period of hours, even though H+ rapidly stimulates peripheral chemoreceptors."
So okay, there will be a higher ppO2 on Nitrox but due to the mammalian diving reflex and ppO2 being subservient to ppCO2 and glycolysis in the absence of oxidative phosphorylation ruled out, I am afraid Mr. Tierney I can't support your claims - I think it's a mental thing!
A few terms for you, just to sum up.....
Apnea: cessation of respiration, breath holding
Eupnea: normal respiratory rate, rhythm and depth.
Hypocapnea: an increase in minute ventilation causing a reduction in ppCO2.
Hypercapnea: a decrease in minute ventilation causing an increase in ppCO2.
Hyperventilation: refers to an increase in minute ventilation disproportionate to the metabolic production of CO2. (ppCO2 <37mmHg).
Hypoventilation: refers to a decrease in minute ventilation disproportionate to the metabolic production of CO2. (ppCO2 >43mmHg).
Hypoxia: a reduction in oxygen supply to the body tissues
Anoxia: an absence of oxygen
Tachypnea: an increase in respiratory rate.
(Edited by Driftwood at 10:40 am on July 17, 2002)  |