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Central Sleep Apnea: clinical presentation
Clinical and Physiologic Heterogeneity of the Central Sleep Apnea Syndrome.
Bradley TD, McNicholas WT, Rutherford R, Popkin J, Zamel N, Phillipson EA.
American Review of Respiratory Disease 1986; 134:217-221.
This is the first study to classify central sleep apnea (CSA) into two distinct types based on clinical and physiological features. This study included 18 patients referred for a variety of sleep complaints to a sleep clinic, and who were then found to have central sleep apnea (CSA) on a sleep study defined as having at least 5 central apneas or 10 central apneas and hypopneas per hour of sleep.
The authors found that patients could be classified into either of two distinct groups based on their daytime arterial blood carbon dioxide (CO2) levels: a hypercapnic group whose level of CO2 in a sample of arterial blood was elevated, and a non-hypercapnic group whose CO2 level was either normal or low. Five people were found to have hypercapnic CSA, and 13 to have non-hypercapnic CSA.
In the hypercapnic CSA group, the average age was 44 years, and 40% were men. All had a history of respiratory failure characterized by high CO2 and low oxygen (O2) levels in arterial blood. In 3 of the 5 hypercapnic patients, respiratory failure was due to weakness of the respiratory muscles (that is, the diaphragm and rib cage muscles) so that they did not have enough strength to take in and breathe out an adequate amount of air. In the other 2 it was due to a lack of sensitivity of the respiratory centres in the brain to CO2 and O2. Normally, an elevated level of CO2 or a reduced level of O2 stimulates the brain to send out signals to the respiratory muscles to breathe more deeply in order to blow off excess CO2 (the harmful byproduct of digesting or burning food), and to take in enough O2 (the essential fuel needed to sustain life). When the brain fails to respond to high CO2 or low O2, breathing stays too shallow to get rid of excess CO2 or to take in enough O2. As a result, CO2 increases to dangerously high and O2 decreases to dangerously low levels. The tendency to under-breathe is worsened during sleep because the respiratory muscles relax and the brain becomes even less sensitive to high CO2 and low O2 levels, and as a result outright stoppages of breathing (apneas) can occur repeatedly. Breathing only resumes when a sense of suffocation arises that causes the patients to wake up briefly, which allows them to breathe more deeply until they fall back asleep again. The recurrent awakenings at night caused restless sleep and morning headaches in 40%, as well as daytime sleepiness in 80% of the patients. Snoring was present in 40%, but none complained of choking during the night or of nasal congestion. High blood pressure was present in only 20%. Because lack of O2 puts stress on the right side of the heart, 60% of patients experienced a build up of fluid in the veins of the legs causing them to swell; a condition known as edema. Hypercapnic CSA is therefore a serious, sometimes life-threatening condition.
In the 13 patients with non-hypercapnic CSA, who had normal to low blood CO2 and normal O2 levels, patients presented with features similar to someone with obstructive sleep apnea. For example, 92% were men, 92% snored, 46% complained of restless sleep, 31% complained of choking or shortness of breath during sleep, 62% had high blood pressure, 77% complained of daytime sleepiness, 62% complained of nasal congestion and most were overweight. None had a history of respiratory failure, and only 8% had leg edema. They had normal brain sensitivity to CO2 and O2 and none had weakness of their respiratory muscles. Because the cause of central apneas in this group of patients was not determined, they were said to have “idiopathic” CSA, which means CSA of unknown cause.
On the overnight sleep studies, both groups had frequent awakenings causing fragmentation of sleep. In the hypercapnic group, the central apneas were more frequent and longer during rapid-eye movement, and were accompanied by severe degrees of hypoxia (O2 deprivation). In contrast, in the non-hypercapnic group, central apneas were most frequent in the lighter stages of non-rapid eye movement sleep and were not accompanied by a significant degree of hypoxia. In addition, unlike the hypercapnic group, central apneas were most pronounced when the patient slept on his/her back. Because of the lack of respiratory failure these patients with non-hypercapnic CSA, it was concluded that they had a less serious, non-life threatening condition compared to the patients with hypercapnic CSA.
This study was very important because it was the first to show that people with CSA fall into two distinct groups with different causes, symptoms and medical problems that would probably require different treatments. Prior to this, it was generally thought that all CSA was the hypercapnic kind and, therefore was potentially life-threatening and required aggressive treatment. However, this study showed that most patients with CSA have the less severe, non-life-threatening non-hypercapnic from, and may require different and less aggressive treatment than those with hypercapnic CSA. As a consequence, it expanded the understanding of this group of disorders and helped to change the way in which people with CSA are evaluated and treated.
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