SLEE5102 Sleep Medicine (Doc)

Added on -2020-02-19

| SLEE5102| 22 pages| 6414 words| 243 views

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Running head: SLEEP MEDICINESLEEP MEDICINEName of the StudentName of the universityAuthor’s note
1SLEEP MEDICINESLEE5102 : SLEEP DISORDERED BREATHINGASSIGNMENT 1 (10%)Q1. Outline the mechanics of breathing (inspiration and expiration) including the musclesinvolved; what impact does sleep have on this process?The process of breathing is the action of inhaling and exhaling out air, which is due to thepressure changes within the thorax, in comparison to the atmosphere. In the breathing process,the volume of the thoracic cavity changes from time to time1. The change in volume results inthe change in pressure, the air flows from a higher region of pressure to the lower region, whichresults in an equilibrium .This whole mechanism, is coordinated by the part of the brain calledmedulla oblongata. The rhythmic cycle of the breathing begins in the medulla oblongata. Themedulla contains several respiratory related neurons that design the ventral and the dorsalrespiratory groups 1. Respiratory control is generated in the brainstem. The respiratory pumpconsists of the chest wall (ribs), intercoastal muscles and the diaphragm 1,3. During respiration, the diaphragm is the most important muscle which is a dome shaped muscleseparating the abdomen and the chest cavity and is innervated by phrenic nerves 1,3 .There aretwo processes involved in breathing, inspiration and expiration. The intercostals and thediaphragm muscles contract during inspiration which shortens and flattens the diaphragm,moving it down wards3. The space inside the chest cavity increases due this mechanism, whichcauses the thoracic pressure to decrease below the atmospheric pressure 3. This is also associatedwith the loss of its dome shape, hence increasing the intrathoracic volume. There are some accessory muscles present in the neck region such as the sternocleidomastoid andscalene muscles which play an important role in the process of inspiration by an elevation in the
2SLEEP MEDICINEfirst two ribs and the sternum 3,4 . The accessory muscles are attached to the rib cage and possessthe potential to generate the breathing action. The muscles are joined to the two upper ribs, thetop of the sternum. At one end it is joined to the clavicle and at the other end it is joined with themastoid process which is the part of the cervical vertebra. When the accessory muscles showcontraction during the inspiration, the chests is elevated (3,4). These muscles are normally usedby the body when the person is having a thoraco-pulmonary disorder, when there is effortrequired in breathing. The other accessory muscle required in the process of forced inspiration isserratus anterior, pectoralis major, pectoralis minor. The muscles helps in expanding the volumeof the thoracic cavity and helps in exhalation4 . The contraction of the accessory muscles alongwith this process leads to an increased flow and negative intrapleural pressure 5. Additionally the intercoastal muscles also help to increase the volume of the chest cavity. Whenyou inhale, the muscles contract and pulls up the rib cage in an up and down motion thus assistsin breathing. These muscles can also increase the intrathoracic volume by stabilizing andelevating the ribs and increasing the anterioposterior diameter of the thorax1,3. The nervesconnected to the brain causes breathing muscles to contract only when they are intact. In someback and neck injuries, the spinal chord can be severely damaged causing to end the NSconnection between the muscles and brain causing death unless patient is artificially ventilated2 .During expiration, the diaphragm relaxes and moves back up and the chest wall and lungelasticity expels air out of the lungs3. Expiration is a passive process, the relaxation of thediaphragm and the intercoastal muscles leads to the reduction in size of the thoracic cavity whichincreases the internal pressure which forces the air out of the lungs. This occurs when the
3SLEEP MEDICINEimpulse in the inspiratory nerves suddenly ceases. There when a person is at rest, no effort isneeded to breathe out. However at the time of exercise, the intrathoracic pressure changes due tothe contraction of the external and the abdominal intercoastal muscles. It gives rise to thenegative pleural pressure along with an increased alveolar pressure. Lung and the chest volumethen decrease as air flows out into the atmosphere causing lung recoil pressure to fall until a newequilibrium reaches at its functional residual capacity (FRC) 2.Furthermore, the muscles like the internal oblique muscles, rectus abdominis and the transversusabdominis also assist in expiration by the contraction and compression of the abdominalcompartment, which helps to increase the internal pressure. The following pressure increases andeventually tend to push the diaphragm up, which causes an increase in the pressure and thusexpiration. The other accessory muscles that are involved in the forces expiration process isquadrates lumborum, serratus posterior inferior, latissimus dorsi, anterior abdominal wallmuscles 1,3. The quadrates lumborum muscles help the diaphragm in inhalation. It fixes the 12thrib in relation to the pull of the diaphragm. The anterior wall muscles help to compress the lowerportion of the thorax, increasing the pressure in the intra abdomen. The serratus posterior inferiorand the latissimus dorsi helps to depress the ribs and thus leads to forced expiration 1,3.Finally the respiratory mechanism during the sleep is measured by the metabolic demand,whereas the respiratory drive is controlled by a respiratory generator located in the brainstem 3.The respiratory system is regulated by central and the peripheral chemoreceptor and mechanoreceptors that provide negative feedback to maintain ventilation5. There are several physiologicalimpacts sleep has on the respiratory system. During NREM sleep, airway resistance increases by
4SLEEP MEDICINEapproximately 230% 6. The reflex dilator response of the upper airway is jeopardized during thesleep and as a result the mechanical load ventilatory response can be absent. The oxygen level inthe body reduces during the sleep and the response to hypercapnia and hypoxia is depressed bythe sleep2. Sleeps triggers upper –airway hypotonia, which results in the decreased response tothe negative pressure. According to Mortimore and Douglas 1996, the response of the upperairway is improved in the patients with sleep apnea hypopnea syndrome (SAHS). Moreover,patients with BMi<30, FRC decreases from the wake state to sleep in the supine position by_0.2-0.5 L2,3. Postulated mechanisms for the sleep related decline in FRC include alteredrespiratory timing from the CRG, reduced chest wall and lung compliance, accumulated intrathoracic blood volume, and relative hypotonic of the diaphragm 3.Sleep changes in the pharyngeal dilator muscle tone resulting in the increased resistance of theupper airways and the collapsibility contributes to hypoventilation3. During NREM, airwayresistance increases by about 230% from the retro-epiglottic region 3. The resistance increasesdue to the decrease in the tonic activity of the pharyngeal dilator muscles of the upper airways.As a result the esophageal pressure swings during the sleep6. Whereas during REM sleep, upperairways resistance tends to be the highest due to the atonia of the pharyngeal dilator muscles andthe partial collapse of the airways 3,6. In saying that, this is only evident in some studies not all.Rib cage contributes to ventilator increases during NREM sleep3. During breathing, this isdetected by increased amplitude of the EMG. During sleep stages, the diaphragm activity slightlyrises or remains unchanged and the abdominal muscle activity tends to slightly rise7. Incomparison to REM sleep, the intercostals muscle activity and the rib cage contribution to
5SLEEP MEDICINErespiration decreases 3. This is due to the fact that alpha motor neuron drive undergoes an REMrelated supraspinal inhibition. The fusimotor function is also depressed3. The diaphragmaticactivity increases during the REM sleep and breathing is completely dependent on the diagramduring REM6. This decrease in the activity of the intercoastal muscles causes hypoventilation inpatients having borderline pulmonary function. Q.2 Explain the roles of the central and the peripheral chemoreceptors in maintaining normalblood gases. Central and peripheral chempreceptors can respond quickly and sensitively to changes in arterialPCO2 are the key constituent of the negative feedback loop that coordinates that respiratoryactivity 8. The production of the H+ ions from the carbonic acid causes a pH reduction in theblood which is ultimately due to an increase in the CO2 concentration8. In response to this lowblood pH, the respiratory center located in the medulla send nerve impulses to the diaphragm andthe intercoastal muscles and the lung volume and the breathing rate increases during theinhalation8. Alkalosis is caused due to the hyperventilation .Alkalosis causes the feedbackresponse of reduced ventilation. , while acidosis can be caused by the hypoventilation, whichcauses a feedback response of the reduced ventilation, while acidosis can be caused byhypoventilation, which causes a feedback response of an increased ventilation8. The presence ofhypoxia will cause a feedback response that increases the ventilation ton increase the oxygenintake 9. Example, diarrhea causes acidosis and vomiting causes alkalosis, which will cause anappropriate respiratory feedback response 9. Central chemoreception is responsible for the maintenance of a constant, normal arterial PCO2as a negative feedback control loop, and the maintenance of a constant ph by using ventilator

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