Respiratory System Control Mechanisms PDF

Intro ○ Spontaneous respiration is produced by rhythmic discharge of motor neurons that innervate the respiratory muscles ○ this discharge is totally dependent on nerve impulses from the brain; breathing stops if the spinal cord is transected above the origin of the front of nerves ○ The rhythmic di...

Intro ○ Spontaneous respiration is produced by rhythmic discharge of motor neurons that innervate the respiratory muscles ○ this discharge is totally dependent on nerve impulses from the brain; breathing stops if the spinal cord is transected above the origin of the front of nerves ○ The rhythmic discharges from the brain that produce spontaneous respiration are regulated by alterations in arterial po2, pco2, and H+ concentration, and this chemical control of breathing is supplemented by a number of non-chemical influences. ○ The overall respiration control system thus consists of a network of neurons in cortex and medulla/pons that exert voluntary control and autonomic control respectively. ○ the system addressed the rate of ventilation as environmental conditions change(e.g. from normoxic to hypoxic condition) and arterial po2, pco2, and H+ concentration alter ○ the mechano and chemoreceptors in the system sense the changes in the force/displacement And arterial levels of gases and metabolites, and adjust the rate of ventilation to ensure optimal gas exchange in the lungs neural control of breathing control systems ○ two separate neural mechanisms regulate respiration. one is responsible for voluntary control and the other for autonomic control ○ the voluntary control system is located in the cerebral cortex and sends impulses to the respiratory motor neurons via the corticospinal tracts ○ the autonomic system is driven by a group of pacemaker cells in the medulla impulses from these cells activate motor neurons in the cervical and thoracic spinal cord that innervate inspiratory muscles those in the cervical cord activate the diaphragm via the phrenic nerves, and those in a thoracic spinal cord activate the external intercostal muscles however the impulses also reach the innervation of the internal intercostal muscles and other expiratory muscles the motor neurons to the expiratory muscles are inhibited when those supplying the inspiratory muscles are active and vice versa Although spinal reflexes contribute to this reciprocal innervation, it is due primarily to activity in descending pathways. Impulses in these descending Pathways excite agonists and inhibit antagonists. the one exception to the reciprocal inhibition is a small amount of activity in front of axons for a short period of time after inspiration the function of this post-inspiratory output appears to break the lungs elastic recoil and make respiration smooth Medullary system ○ The main components of the respiratory control pattern generator responsible for autonomic respiration are located in the medulla ○ rhythmic respiration is initiated by a small group of synaptically coupled pacemaker cells in the pre-botzinger complex (preBOTC) on either side of the medulla between the nucleus ambiguus and the lateral reticular nucleus ○ these neurons discharge rhythmically, and they produce rhythmic discharges in front of motor neurons that are abolished by sections between the preBOTC complex and these motor neurons ○ they also contact the hypoglossal nuclei and the tongue is involved in the regulation of Airway resistance Pontine and vagal influences ○ although the rhythmic discharge of medullary neurons concerned with respiration is spontaneous, it is modified by neurons in the pons and afferents in the Vagas from receptors in the airway and lungs ○ an area known as the pneumotaxic center in the medial pair of brachial and KollikerFuse nuclei or the dorsolateral pons contains neurons active during inspiration and neurons active during expiration ○ when this area is damaged, respiration becomes slower and tidal volume greater and when the vagi are also cut in anesthetized animals, there are prolonged inspiratory spasm that resemble breath holding ○ The normal function of the pneumotaxic Center is unknown, but it may play a role in switching between inspiration and expiration. stretching of the lungs during inspiration initiates impulses in afferent pulmonary Vagal fibers ○ These impulses inhibit inspiratory discharge. ○ this is why the depth of Inspirations increases after vagotomy and apneusis develops if the vagi are cut after damage the pneumotaxic center ○ Vagal feedback activity does not alter the rate of Rise of the neural activity in respiratory motor neurons Stimuli affecting the respiratory center ○ Chemical control CO2 (via CSF and brain interstitial fluid H+ concentration) (via carotid and aortic bodies) ○ Non Chemical control Vagal afferents from receptors in the airways and lungs Afferents from the pons, hypothalamus, and limbic systems Afferents from proprioceptors Afferents from baroreceptors: arterial, atrial, ventricular, pulmonary More receptors in the brainstem ○ the chemoreceptors that mediate the hyperventilation produced by increases in arterial pco2 after the Carotid and aortic bodies are denervated are located in the medulla oblongata and consequently are called medullary chemoreceptors ○ they are separate from the dorsal and ventral respiratory neurons and are located on the ventral surface of the medulla ○ recent evidence indicates that additional chemoreceptors are located in the vicinity of the solitary tract nuclei, the Locus Coeruleus, and the hypothalamus ventilatory response to oxygen deficiency ○ when the oxygen content of the inspired air is decreased respiratory minute volume is increased ○ the stimulation is light when the po2 of the inspired air is more than 60 mmhg, and Marked stimulation of respiration occurs only at lower po2 values ○ however any decline in arterial po2 below 100 mmhg produces increased discharge in the nerves from the Carotid and aortic chemoreceptors ○ There are two reasons why this increase in impulse traffic does not increase ventilation to any extent in normal individuals until the po2 is less than 60 mmhg. first because HB is a weaker acid than hbo2 there is a slight decrease in the H+ concentration of the arterial blood when the arterial po2 Falls and hemoglobin becomes less saturated with O2 The fall in age plus concentration tends to inhibit respiration. in addition any increase ventilation that does occur lowers the alveolar pco2 and this also tends to inhibit respiration therefore the stimulatory effects of hypoxia on ventilation are not clearly manifest until they become strong enough to override the counterbalancing inhibitory effects of a decline in arterial H+ concentration and pco2 effects of Sleep ○ respiration is less rigorously controlled during sleep then in the waking state, and brief periods of apnea occur in normal sleeping adults ○ changes in the ventilatory response to hypoxia vary ○ if the pco2 falls during the waking state, various stimuli from proprioceptors and the environment maintain respiration, but during sleep, these stimuli are decrease and a decrease in pco2 can cause apnea ○ during rapid eye movement sleep, breathing is irregular and the CO2 response is highly variable Periodic breathing and disease ○ Cheyenstokes syndrome periodic breathing occurs in various disease States and is often called cheyne stokes respiration It is seen most commonly in patients with heart failure and uremia, but it occurs also in patients with brain disease and during sleep and some normal individuals some of the patients with this respiration have increased sensitivity to CO2 the increase response is apparently due to disruption of neural Pathways that normally inhibit respiration. and these individuals, CO2 causes relative hyperventilation, lowering the arterial pco2 During the resultant apnea, the arterial pco2 again Rises to normal, but the respiratory mechanism again over responds to co2. breathing seizes on a cycle repeats another cause of periodic breathing in patients with cardiac disease is prolongation of the lung to brain circulation time so that it takes longer for changes in arterial gas tensions to affect the respiratory area in the medulla When individuals with slower circulation hyperventilate, they lower the pco2 of the blood in their lungs, but it takes longer than normal for the blood with a low pco2 to reach the brain during this time the pco2 the pulmonary capillary blood continues to be lowered, and when this Blood reaches the brain, the low pco2 inhibits the respiratory area, producing apnea In other words the respiratory control system oscillates because the negative feedback loop from lungs to brain is abnormally long Sleep apnea ○ Episodes of apnea during sleep can be Central and origin due to failure of discharge in the nerve producing respiration, or they can be due to Airway obstruction obstructive sleep apnea ○ apnea can occur at any age and is produced when the pharyngeal muscles relax during sleep. in some cases, failure of the genioglossus muscle to contract during inspiration contributes to the blockage ○ The genioglossus muscles pull the tongue forward and without or weak contraction the tongue can obstruct the airway ○ after several increasingly strong respiratory efforts, the patient wakes up, takes a few normal breaths and falls back to sleep ○ Apneic episodes are most common during REM sleep. When the muscles are most hypnotic ○ the symptoms are loud snoring, morning headaches, fatigue and daytime sleepiness ○ when severe and prolonged, the condition can lead to hypertension and it's complications ○ frequent apneas can lead to numerous brief Awakenings during sleep and to sleepiness during waking hours ○ with this in mind it is not surprising to find that the incidence of motor vehicle accidents and sleep apnea patients is seven times greater than it is in general driving population ○ in addition sleep apnea is associated with many cardiovascular diseases such as hypertension arrhythmia stroke and heart failure