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Also see Neurologic Control of Bronchial Smooth Muscle Also see Control of Ventilation - More in depth outline The central nervous system, CNS, consists of the brain and spinal cord. Regulation of breathing is done here. The CNS gets stimuli; it makes a decision based on the data and sends a command along a motor nerve [neuron] to the muscles of ventilation.
The CNS gets stimuli · Chemoreceptors o Central Chemoreceptors: § Because the Central chemoreceptors are located on the surface of the medulla they are in contact with CSF. As C02 diffuses out of the capillaries into the CNS, the C02 undergoes hydrolysis and the build up of H+ triggers increased respirations. § Because the medulla responds to acidosis rather than C02, metabolic acidosis such as seen in keto-acidosis in diabetics will also trigger rapid and deep respirations. § This response is quite sensitive and changes of only 2 mmHg will trigger alteration in the breath rate. § But over time, these central chemoreceptors will become blunted to chronic hypercapnia. § Peripheral Chemoreceptors: located in the carotid artery and in the aorta, these are a group of chemoreceptors that are sensitive to decreased Pa02 [less than 60 mmHg] and increased PaC02 as well as acidosis [must be changes as large as .05 to .1 unit before it responds] § When the central chemoreceptors fail to respond to hypercapnia by increasing the Ve, the peripheral chemoreceptors will respond to hypoxemia. § The chronic hypercapnic person is now breathing off a hypoxic drive.
· Cerebral cortex: o SOB: The high areas of the brain become involved in the breath pattern once the patient become aware he is having difficulties. This awareness is called SOB and it is not just triggered by hypoxemia or hypercapnia, but by sensations caused by increased WOB & fatigue associated with low compliance or increased RAW. o The hypoxic person feels restless and gets frightened and may decide to increase Ve over the automatic increase. o Deliberate alterations: Frequently, the normal rhythm of breathing is interrupted by the higher part of the brain, when the person needs to talk, swim, sing or alter the breathing for other activities. As soon as the cerebral cortex ends its interference in breathing the medulla takes over. Obviously, the cerebral cortex cannot override the compulsions of the lower brain. You might hold your breath until you faint, but as soon as you faint, you will start breathing again. The CNS processes the information Medulla: is a portion of what is called the lower brain. On the surface of the medulla are two areas called the DRG and the VRG. These are collectively responsible for ventilation. There is no main ‘pacemaker’ located for breathing. The center is in the medulla but no specific area is located. During quiet breathing the inspiratory command fire for about 2 seconds then 3 seconds is allowed for exhalation. · Dorsal respiratory group DRG: contain mainly inspiratory neurons. These send motor commands to the phrenic nerve
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Ventral respiratory group VRG: Some inspiratory neurons which
send commands to the chest wall and some expiratory neurons that
send commands to the abdominal wall muscles Pons: the word “pon” means bridge and the pons is a bridge between the higher brain and the medulla. It “translates” complex commands such as “I need to talk, swim, sing” into simple “breath now, hold now” commands. · The pons doesn't regulate regular breathing; rather it modifies the medulla’s output. · Pneumotaxic center: controls the ending of inspiration thus the inspiratory time. Works with the Apneustic center to control the depth of respirations. · Apneustic center: it’s function is ill-defined but when the Apneustic center is isolated, the patient will breath with prolonged inspiratory gasp and few exhalations The CNS sends a command along the neural pathways Spinal cord: the pathways for nerve conduction, both sensation and motor impulses, are along the spinal cord that lies within the protection of the ventricles of the spinal cord.
Sensory nerves: send information to the CNS via a couple of cranial nerves. Vagus nerve: sends data to the medulla about breathing reflexes as well as blood pressure and cardiac activity. Because the vagus nerve is also involved with the larynx, damage can also effect the voice Glossopharyngeal nerves: the sensations of breathing and blood pressure come to the CNS via these cranial nerves Motor nerves: send commands to the muscles or organs Phrenic nerve: The medulla sends breathing commands along the phrenic nerve · A right and a left phrenic nerve runs along the mediastinum to send motor commands to the diaphragms · These exit the spinal cord between C3 and C5. Cutting the spinal cord above C2 will result in complete chest & diaphragmatic muscle paralysis
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The intercostal nerves: these nerves enter the muscle groups
between T2 and T11 and run along the rib cage. Reflexes · The Hering-Breur reflex: stretch receptors in the airways respond to hyperinflation [800-1000 mL] by sending inhibition messages to the CNS · Deflation Reflex: in the presence of sudden lung collapse the response is rapid deep breathing. · Head’s Paradoxical reflex: if the vagus nerve is blocked so that the Hering-Breur reflex is halted, there will be increased Ve. This stops almost immediately and it may be responsible for sighs and for the first breathe at birth. It may also be associated with sighs. · Irritant receptors: o Cholinergic reflex bronchospasm and coughing due to tactile stimulation of the central airways [especially at the carina & other airway bifurcations. o Vago-vagal reflex: tactile stimulation of the upper airways causing reflex bradycardia [such as during suctioning or intubation]
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Abnormal breathing patterns Cheyne-Stokes breathing: Ve ventilation increases until there is a crescendo [or climax] then apnea occurs. · There is a delay between PaC02 in the CNS and PaC02 in the rest of the body frequently due to decreased CO. Blood flow is too slow between these two areas so the brain is still reacting to acidotic CSF while the lower arterial C02 suddenly arrives and causes apnea. · Seen in CHF [low Cardiac Output] and in some brain injuries Theophylline Therapy for Near-Fatal Cheyne-Stokes Respiration: A Case Report Biot’s breathing: due to increased intracranial pressure the apnea comes between times of constant breathing. Apneustic breathing: persistent hyper-ventilation. Due to damage in the pons. Prolonged inspiratory gaps interrupted by exhalations. Phasing is off. Central neurogenic hypoventilation: the CNS is not responding to changes in acid base of the CNS
Central neurogenic hyperventilation:
CNS is responding to abnormal stimuli [because of brain damage] Also see our Breathing Patterns page
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