Describe The Differences In The Pattern Of Breathing And Resultant Minute Ventilation Between Quiet Wake, Nrem And Rem Sleep

Patterns of breathing differ between times of being awake and times of sleep. When awake, breathing is more often than not irregular, as a result of actions undertaken, such as: speaking, emotions, activities, and location and position amongst others. In general, when sleeping the partial pressure of carbon dioxide (pCO2) is at a high and ventilation is at a low, resulting in lower minute ventilation. In the perceived 'normal' person (subject), at the moments prior to NREM entrance oscillation occurs at sometime between the progressions from arousal stage into stage I and stage II sleep. When subjects begin to fall asleep, respiration decreases, and this leads to a higher pCO2 than when at initial wakefulness. Such a situation can cause hypoventilation or at worse sleep apnea. Furthermore, during sleep human respiration is controlled by the brainstem.

Non-REM (NREM) Sleep
Ventilation: At the NREM stage of sleep breathing is notably very regular, both in its amplitude and frequency, especially when measured against other stages of sleep. When sleeping, breathing variability is found to be at its lowest during steady NREM. It is widely recorded that during stage II sleep and slow wave sleep (or NREM Stage III) that minute ventilation lowers by 13% and 15%, respectively. At the same time, average inspiratory flow decreases, yet the respiratory duration cycle remains the same as initial set point, and this leads to a decrease in tidal volume.
Respiratory Muscle Contribution: The rib cage muscles (or intercostal muscles) play a major role during REM sleep, at which stage they are activated and induce movement of the chest wall which is primarily lateral. In addition, diaphragm activity is increased very little or remains constant during REM, and abdominal muscle activity only increases slightly.
Upper Airway Resistance: During NREM airway resistance usually increases by circa 230%. However, elastic capacity and flow resistance of the lung do not relate to the different sleep stages. The primary mechanism which causes an increase in upper airway resistance during NREM comes from the retroepiglottic region. During such sleep, activities with the pharyngeal dilator muscles of the upper airway fall, leading to increased resistance. As a result, additional ventilatory muscles attempt to account for such increased resistance, and thus the overall amounts of airflow decrease at lower rates than the level of resistance increases.
Blood Gases Result: The partial pressure of carbon dioxide increases by circa 3-7mmHg, and the partial pressure of oxygen falls by circa 3-9mmHg, at which time oxygen saturation is reduced by circa 2%. However, a reduction in oxygen consumption of circa 10-20% leads to a metabolic rate decrease, and so a blood gas result still occurs. This would conclude why hypoventilation can also occur, when such metabolism rates decrease.
Pulmonary Arterial Pressure: Pulmonary arterial pressure experiences various pressure changes at random intervals and at different times during sleep. During NREM, an increase of between 4 and 5 mmHg is observed, in both the pulmonary arterial systolic and diastolic pressures.
Effect of Arousal: NREM sleep induces 'transient arousal', during which many events take place, for example: 1) electromyogram (EMG) observations indicate that diaphragm activity increases by somewhere between 130-160%, upper airway muscle dilation activity increases by up to circa 250%, 3) there is an approximate increase measured at 160% concerning airflow and tidal volume, and 4) upper airway resistance normally decreases.

REM sleep
Ventilation: During REM sleep respiration is irregular, and sleep apneas with durations of between 10 to 30 seconds have been recorded. Such apneas intermittently lead to changes in respiratory amplitude and frequency. Such interruptions are a result of physiological changes, and thus are not the same as other abnormal sleep changes to breathing. Many researchers have found that these irregularities in breathing are not random, but are associated to eye movements. In addition, such breathing abnormalities are not regulated by the chemoreceptors but are known to result from the instinctual respiratory control system having been affected by rapid eye movement. Airflow measurement can also be quite varied at the REM stage, and sometimes is exhibited as increased, decreased or constant, when compared against levels of the 'awake' stage. Tidal volume has also exhibited a similar trend, in that it may increase, decrease or also remain at a constant.
Respiratory Muscle Contribution: As previously mentioned, during REM there is an observed decrease in respiration levels, and this leads to reactions by the rib cage which, in turn, lead to reduced intercostal muscle activities. This is due to suppression of the alpha motoneuron drive during REM, pertaining particularly to the supraspinal area. During REM, and in contrast to NREM, diaphragm activity is increased in opposition to intercostal muscle activity. Such reduced intercostal muscle activity is a major reason that hypoventilation in a subject with obtuse pulmonary functions would occur.
Upper Airway Resistance: Upper airway resistance is normally at its peak during REM, and this leads to some degree of airway collapse, plus reduced activity in the pharyngeal dilator muscles. Although some research in REM displays stable airway resistance during this stage of sleep, the same cannot be said for NREM, at which stage it always increases.
Blood Gases Result: Hypoventilation during REM sleep causes subjects to be effected by an hypoxemic state, but wide ranging studies in blood gases during REM have not been widely completed.
Pulmonary Arterial Pressure: During REM sleep, pulmonary arterial pressures constantly vary, dependent upon varying respiration rates, although they do tend to rise.
Effect of Arousal: Stimulation of the dilator muscle activities are virtually the same between REM and being 'awake', and thus both states (awake and REM) exhibit similar airway resistance and airflow measurements.
5. Outline the evidence that genetic determinants of craniofacial morphology explain some of the variation in OSA incidence across different populations. (12 marks)
Ans. Numerous previous studies have shown that obstructive sleep apnea occurrence is largely genetic. A study by Strohl described a family in which multiple male relatives were presenting with symptoms of excessive daytime tiredness and night-time restlessness; with three patients suffering from apnea during sleep. Familial predisposition can be explained in that most risk factors are related to the prevalence of obstructive sleep apnea syndrome, which is genetically determined.
The prevalence of obstructive sleep apnea syndrome is observed to be generally greater amongst ethnic groups, i.e. African-Americans, in which it tends to present at a younger age and may be more severe than European-Americans. Additionally, one experiment conducted a case-control family study which explained the occurrence of sleep-disordered breathing (SDB) in African-Americans and Caucasians. The results concluded that African-Americans with SDB (37.2 +/- 19.5) were younger than Caucasians, with a SDB (45.6 +/- 18.7, p < 0.01). Such variations may be related to obesity, a cause which is more frequent in African-Americans than European-Americans. Anatomical characteristics specific to each race, such as larger upper airway soft tissues in African-Americans, seem to play a major role. Important influences for obstructive sleep apnea include being over-weight, respiratory reflex control abnormalities and craniofacial morphology. To ensure that genetics plays an essential part in the predisposition of obstructive sleep apnea, two current methods are used for detection: 1) a systematic genome scan in multiplex families, and 2) a study of candidate gene markers using case-control designs.
Genetic Determinants of Craniofacial Morphology: numerous researches have presented the association between many facial morphological factors and obstructive sleep apnea syndrome. Concerning maxillo-mandibular abnormalities, it has been found that SNA and SNB values have obviously been reduced in patients with obstructive sleep apnea syndrome, especially pertaining to the relationships between micrognathia, retrognathia and such spectrum of disease. In addition, there are other factors to be considered, such as: an increase in soft palate size leads to a decrease in the diameter of the upper airway, and can aggravate the risks of obstructive sleep apnea syndrome. A study by Riha illustrated that lower positioning of the hyoid bone (the bone to which the lingual muscles are attached), when compared to the mandibular plane, significantly involves the occurrence of obstructive sleep apnea syndrome. When the setting of the hyoid bone is lower, it causes a narrowing of the upper pharyngeal airway, due to the fact that the tongue is pulled down. The association between genetics and OSA is explained by familial incidences of disease. Moreover, this genetic relationship can be explained in studies of twins.
Guilleminault's research presented that a higher percentage of obstructive sleep apnea patients have at least mild craniofacial disproportions. After that, he launched an article which mentioned that infants who suffered from life-threatening sleep apnea always have family members with obstructive sleep apneas and small upper airways, diagnosed using cephalometric roentgenograms and volume CT scans. Mathur's study also showed that cases which present with narrower pharyngeal and glottic cross-sectional areas (the structures representing retro-positioned maxillae and mandibles) and longer soft palates, when compared with control subjects, have a greater opportunity of developing OSAS. All of these studies strongly conclude that craniofacial familial characteristics can be an important risk factor in the development of obstructive sleep apnea syndrome.
There are several genetic diseases which can also lead to craniofacial dysmorphisms, and this could imply a link between genes and obstructive sleep apnea syndrome. For instance, OSAS in Down's syndrome is very common, and Marfan syndrome, controlled by FBN1 gene, may cause craniofacial morphology and laxity of the upper airway connective tissues, leading to obstructive sleep apnea. In conclusion, craniofacial morphology is an essential intermediate phenotype leading to obstructive sleep apnea, and therefore is an important component for studying the genetic issues relating to obstructive sleep apnea.

6. Most people who travel to high altitude develop SDB. Briefly describe the pattern of breathing they develop and explain the physiological mechanisms responsible for it. (8 marks)
Ans. Most people who visit high altitude areas generally suffer with difficulty when sleeping at night. Such a sleep problem can result from many aspects or from a combination of some of them, such as the cold weather or the hypoxic environments of such high altitudes. Periodic breathing during sleep is an important condition which can further lead to severe sleep fragmentation problems, as follows: A major interruption of high-altitude sleep arises from more frequent arousal, and sometimes awakening. These serve to significantly impair daytime performance, especially if periodic breathing (sometimes with central sleep apneas) and arousal occur more frequently. One study found that higher altitude levels stimulate short 3 to 5 second arousals from the sleep stage, which are greater than the average at sea level, at circa 8 times per hour at 7620m (282mmHg). The number of arousals varied from 1 time/minute, in the fewest of cases, to 3-4 times/minute in more severe cases. When more frequent arousals take place, these cause more severe sleep fragmentations which can impair daytime performance, i.e. judgment and capability, as a result.
Periodic breathing is a common breathing problem during the sleep stage at high altitudes. One particular study explained this characteristic of periodic breathing pattern as consisting of a series of 3-5 breaths followed by a short respiratory pause, or apnea. Almost all people who visit high altitudes present with such a breathing pattern.
As a result, this breathing pattern is accompanied by 3-5 breaths, followed by a cease in breathing for several seconds. The chemoreceptor responds with a hypoxic state command to the brain, to increase breathing, which then causes the lungs to expire CO2. In contrast, the carbon dioxide chemoreceptor senses amounts of gas in the body and commands the brain to stop breathing as carbon dioxide is getting low. Hence, apnea can take place for approximately 12 seconds, until the oxygen sensors take over again. The result is an irregular pattern of breathing, with 4 or so large breaths followed by no breaths. Periodic breathing responses can happen in all sleep stages: but it rapid eye movement (REM sleep) at higher altitudes, a lower amount of time is spent in slow wave sleep. The period and number of periodic breaths at high altitude is associated with a person's ventilatory drive, in that those with the highest sensitivity to hypoxic ventilatory responses have a higher number of episodes of periodic breathing.
The peripheral chemoreceptor function is one of the main factors which leads to a destabilisation of the respiratory control system, which relates to periodic breathing occurring at high altitudes. The mechanism of periodic breathing comes from an increase in chemoreceptor responses (such as the condition in those with a strong hypoxic ventilatory response), and this leads to destabilisation of the respiratory system and to periodic breathing. Furthermore, that study found that the cycle length, i.e. time from one apnea to the next, decreases when the altitude is higher. This can imply that the frequency of apnea increases as altitude increases. Transient arousals from sleep are commonly considered as auto-responses happening when the onset of the hypercapneic phase of periodic breathing is detected.
When we consider arterial oxygen saturation, night-time oxygen saturation is regularly lower than daytime values at higher altitude. Many researchers believe that the lower night-time arterial oxygen saturation may result from periodic breathing, yet some other studies suggest that periodic breathing actually improves arterial oxygen saturation during sleep at high altitude. Periodic breathing can be realised as a risk factor to some high altitude illnesses, and some medications, such as carbonic anhydrase inhibitors (e.g. acetazolamide) decrease nocturnal periodic breathing, but do improve arterial oxygen saturation as consequence.

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