Central sleep apnea is characterized by a decrease in respiratory motor neurons, leading to repeated episodes of apnea where individuals make no respiratory effort during sleep. The degree of hypercapnia and hypoxemia is less compared to individuals with obstructive sleep apnea (OSA), but the same complications can occur with recurrent and severe central sleep apnea. Cheyne-Stokes ventilation is another abnormal breathing pattern characterized by varying tidal volume and ventilatory frequency. After a period of apnea, tidal volume and respiratory frequency progressively increase and then decrease until apnea recurs. This irregular breathing pattern is seen in individuals with central nervous system diseases, head trauma, and increased intracranial pressure. It can also occur in normal individuals during sleep at high altitudes. The mechanism underlying Cheyne-Stokes respiration is not known, but it may be related to slow blood flow in the brain and overshooting/undershooting ventilatory effort in response to changes in PCO2. Central alveolar hypoventilation, also known as Ondine's curse, is a rare disease where voluntary breathing is intact but abnormalities in automaticity exist. People with central alveolar hypoventilation can only breathe while awake. Mechanical ventilation or bilateral diaphragmatic pacing can be life-saving for these individuals. Apneustic breathing is characterized by sustained periods of inspiration separated by brief periods of exhalation. The mechanism behind this ventilatory pattern involves a loss of inspiratory-inhibitory activities, resulting in an augmentation of the inspiratory drive. Sudden infant death syndrome (SIDS) is the most common cause of death in infants within the first year of life. While the exact cause is unknown, abnormalities in ventilatory control, particularly related to PaCO2, are thought to be involved. Ventilatory control involves the respiratory control center, central chemoreceptors, peripheral chemoreceptors, and pulmonary mechanoreceptors/sensory nerves.
the respiratory motor neurons decreases. Individuals with central sleep apnea have repeated episodes of apnea, during which time they make no respiratory effort, every night (see
Fig. 25.8 ). The degree of hypercapnia and hypoxemia in individuals with central sleep apnea is less than that in individuals with OSA, but the same complications (e.g., polycythemia) can occur when central sleep apnea is recurrent and severe.
Cheyne-Stokes ventilation is another abnormality of breathing that is characterized by varying tidal volume and ventilatory frequency (
Fig. 25.9 ). After a period of apnea, tidal volume and respiratory frequency increase progressively over several breaths, and then they progressively decrease until apnea recurs. This irregular breathing pattern is seen in some individuals with central nervous system diseases, head trauma, and increased intracranial pressure. It is also present on occasion in normal individuals during sleep at high altitude. The mechanism underlying Cheyne-Stokes respiration is not known. In some individuals, it appears to be due to slow blood flow in the brain in association with periods of overshooting and undershooting ventilatory effort in response to changes in PCO2.
Central alveolar hypoventilation, alsoknownasOndine’s curse, isararediseaseinwhichvoluntarybreathingisintactbutabnormalitiesinautomaticityexist.Itisthemostsevereofthecentralsleepapneasyndromes.Asaresult,peoplewithcentralalveolarhypoventilationcanbreatheaslongastheydonotfallasleep.Fortheseindividuals,mechanicalventilationor,morerecently,bilateraldiaphragmaticpacing(similartoacardiacpacemaker)canbelifesaving.
Apneustic breathing is another abnormal breathing pattern that is characterized by sustained periods of inspiration separated by brief periods of exhalation (
Fig. 25.10, C •Fig. 25.9 In Cheyne-Stokes Breathing, Tidal Volume and, as a Consequence, Arterial Blood Gas Levels Wax and Wane. Ingeneral,Cheyne-Stokesbreathingisasignofvasomotorinstability,particularlylowcardiacoutput.PaCO2,partialpressureofarterialcarbondioxide;PaO2,partialpressureofarterialoxygen.
Lung volumeRemove input from cortex, thalamus, and vagus nerves A B Remove sensory input from lungs •Fig. 25.10 Some Patterns of Breathing. A, Normalrateofbreathingisintherangeof12to20breathsperminute.B, Whensensoryinputisremovedfromvariouslungreceptors(mainlystretch),eachbreathingcycleislengthenedandtidalvolumeisincreased,sothatalveolarventilationisnotsignificantlyaffected.C, Wheninputfromthecerebralcortexandthalamusisalsoeliminated,togetherwithvagalblockade,theresultisprolongedinspiratoryactivitybrokenafterseveralsecondsbybriefexpirations(apneusis).
The mechanism underlying this ventilatory pattern appears to be a loss of inspiratory-inhibitory activities that results in augmentation of the inspiratory drive. The pattern sometimes occurs in individuals with central nervous system injury.
Sudden infant death syndrome (SIDS)isthemostcommoncauseofdeathininfantsinthefirstyearoflifeaftertheperinatalperiod.AlthoughthecauseofSIDSisnotknown,abnormalitiesinventilatorycontrol,particularlyin 1.
Ventilatory control is composed of the respiratory control center, central chemoreceptors, peripheral chemoreceptors, and pulmonary mechanoreceptors/ sensory nerves. PaCO2 is the major factor that influences ventilation.
2.