The increasing incidence of both diabetes and sleep apnea coincides with the epidemic of obesity. An increasing body of evidence suggests that the connections between diabetes and obstructive sleep apnea-hypopnea syndrome (OSAH) are not simply due to the common risk factor of obesity. Physiologic derangements that result from OSAH appear to lead to impaired glucose metabolism, increasing the likelihood of diabetes and impairing the efficacy of its treatment.
OSAH is characterized by abnormal breathing patterns during sleep. These abnormal patterns include obstructive apneas, obstructive hypopneas, and respiratory effort related arousals (RERAs). Patients who have sleep apnea typically experience symptoms including excessive daytime sleepiness, fatigue, and neurocognitive dysfunction. Considerable interest has been focused on the recognized associations between OSAH and organ system dysfunction like systemic hypertension, pulmonary artery hypertension,myocardial infarction,cerebrovascular disease, and cardiac arrhythmias. Although considerable literature supports a true cause-effect relationship between OSAH and these diseases, the exact mechanisms remain controversial. This chapter will focus on a brief overview of OSAH and the current literature regarding associations between OSAH and diabetes mellitus (see Fig. 37.1).
Obstructive Sleep Apnea–Hypopnea Syndrome
“Sleep disorders medicine is a clinical specialty which deals with the diagnosis and treatment of patients who complain about disturbed nocturnal sleep, excessive daytime sleepiness, or some other sleep-related problem.” Investigations at Stanford University in the 1970s pioneered research in sleep medicine and used respiratory and cardiac sensors combined with electroencephalography, electro-oculography and electromyography in all-night, polygraphic recordings. Holland and colleagues in 1974 named this continuous all-night array of data gathering polysmonography (see Fig. 37.2).
Sleep disordered breathing patterns (apnea, hypopnea, and RERA) are defined based on polysomnographic criteria.
Apnea – A decrease in the airflow to less than 20% of the baseline, lasting at least 10 s, in adults. Obstructive apnea – Absence of airflow but persistence of ventilatory effort defines obstructive apnea and is caused by the complete or near complete closure of the upper airway (see Fig. 37.2b). Central apnea – Absence of both airflow and ventilatory effort defines central sleep apnea (see Fig. 37.2a).
Mixed apnea – A combination of both obstructive and central apnea defines a mixed apnea. Hypopnea – Hypopnea is defined as a decrease in the airflow (to less than 70% of baseline airflow), but not to the extent that is seen with apnea (less than 20% of the baseline), lasting for at least 10 s, and associated with at least a 3% oxyhemoglobin desaturation.
Respiratory effort related arousals (RERAs) – RERAs are defined as a sequence of breaths lasting at least 10 s and characterized by increasing respiratory effort or flattening of the nasal pressure waveform (indicating increased upper airway resistance), leading to arousal from sleep but not meeting the criteria for apnea or hypopnea.
Apnea-hypopnea index (AHI) – the total number of apneas and hypopneas per hour of sleep constitutes the AHI.
Respiratory disturbance index (RDI) – the total number of apneas, hypopneas, and RERAs per hour of sleep constitutes the RDI.
Obstructive sleep apnea-hypopnea syndrome (OSAH) – OSAH is defined as the presence of an AHI or a RDI >5 events/h in a symptomatic patient or an AHI or a RDI >15 events/h in an asymptomatic patient. The severity of OSAH is defined based on the AHI or the RDI (mild OSAH 5–15 events/h; moderate OSAH 15–40 events/h; severe OSAH > 40 events/h).
Fig. 37.1 Proven and putative interactions between obstructive sleep apnea–hypopnea syndrome (OSAH) and diabetes (DM). FRC = functional residual capacity, VC = vital capacity, IL6 = interleukin-6, TNFα = tumor necrosis factor alpha, GH = growth hormone
Fig. 37.2a (a) Central Sleep Apnea. The figure shows a 2-min segment (four 30-s epochs) of an overnight polysomnogram in a patient with central sleep apnea. The epoch reveals absence of airflow during period of apnea (light gray wide arrows) associated with absence of any thoracic or abdominal movement (dark gray wide arrows). This combination of absent airflow and absent ventilatory effort (manifested by lack of abdominal/thoracic movement) defines central sleep apnea. The periods of apnea can be seen to alternate with periods of respiration (narrow dark gray arrows) and each period of apnea is followed by a microarousal (C4, C3, O2, O1: EEG leads; ROC, LOC: Eye leads; NAF: Nasal air flow; THO: Thorax). The authors acknowledge Mangala Narasimhan, DO, for providing this clinical example. (b) Obstructive sleep apnea. The figure shows a 30-s epoch from an overnight polysomnogram of a patient with obstructive sleep apnea. The epoch reveals absence of airflow (light gray arrows) with persistence of abdominal and thoracic movements (dark gray arrows). This combination of absent airflow with persistent ventilatory effort is characteristic of obstructive sleep apnea. Also noticeable is the oxygen desaturation that is associated with the apnea boxed area in the oxygen saturation channel (SaO2) (F4, F3, C4, C3, O2, O1: EEG leads; ROC, LOC: Eye leads; NAF: Nasal air flow; THO: Thorax). The authors acknowledge Mangala Narasimhan, DO, for providing this clinical example
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