Today is World Sleep Day. Although central sleep apnea (CSA) is less common than obstructive sleep apnea (OSA), it is a frequently encountered problem in sleep medicine, accounting for about 5% to 10% of clinical patients. It is characterized by intermittent repetitive stops and/or decreased breathing without force. Let's learn about the diagnosis and treatment of CSA today.
Compiled and sorted out by Yimaitong, please do not reprint without authorization
classify
➤ CSA can be primary (idiopathic) or secondary and is associated with conditions such as Cheyne-Stokes respiration (CSR), drug-induced, chronic renal failure, or high-altitude periodic respiration.
➤ Another way to classify CSA is to classify it as hyperventilatory or hypoventilatory related.
Risk factors
Risk factors for CSA include age, sex, heart failure (HF), previous stroke, opioid use, and other less common conditions, including neuromuscular disease.
➤ Age: Older adults may be more susceptible to conditions commonly associated with the development of CSA, such as heart failure and stroke. Age itself may not be a true risk factor for CSA.
➤ Gender: The incidence is higher in males than in females. This difference is currently considered to be due to the effect of hormones on the apnea threshold (AT).
➤ Heart failure (HF): HF is probably the most well-known CSA-related condition, more specifically, related to CSR patterns (Figure 1). CSR is a distinct subgroup of cyclic breathing. Risk factors for CSA-CSR in patients with heart failure include male sex, older age, atrial fibrillation, and awake hypocapnia. Central events most often occur during the milder phases of non-rapid eye movement (NREM) sleep, especially after altered wakefulness and sleep stages. It is hypothesized that male sex is a risk factor for CSA due to the often unstable sleep structure. Interestingly, although an association between OSA and atrial fibrillation is well known, atrial fibrillation has been shown to be a risk factor for CSA, but not for OSA. In older people, atrial fibrillation leads to an increase in left ventricular filling pressure, in addition to decreasing ventricular compliance and increasing the incidence of pulmonary venous congestion. The additive effect of these cardiovascular changes over time may explain why advanced age has been listed as a risk factor for CSA-CSR in patients with heart failure.
Figure 1 shows an example of a PSG for the CSA-CSR pattern. (Courtesy of Margarita Oks, MD, New York.)
➤ Stroke: Stroke is considered a risk factor for the development of CSA. Early prospective cohort studies showed that 70% of patients developed CSA within the first 72 hours after stroke. However, CSA was detected in only 7% of patients after 3 months, which may indicate that stroke-related CSA is self-limited.
➤ Some other common diseases have also been linked to the development of CSA. One of them is chronic kidney disease (CKD).
Clinical presentation and evaluation
Older patients with these risk factors and associated clinical manifestations should be evaluated for CSA. Patients often present with typical sleep disruption symptoms such as excessive daytime sleepiness, poor subjective sleep quality, and difficulty concentrating. Symptoms due to repeated nocturnal oxygen desaturation may also be reported, including paroxysmal nocturnal dyspnea, morning headache, and nocturnal angina. Alternatively, CSA may be suspected first when oxygen desaturation is detected in hospitalized patients with apnea or arrhythmias.
There was no specific physical examination or specific serologic abnormalities for CSA. Therefore, cautious assessment of previously described symptoms is the most reliable screening tool. These symptoms may go unnoticed due to insidious onset, and in passive monotonous situations (eg, driving or watching TV), careful evaluation to detect drowsiness or fatigue is essential. Patients with CSA with consistent symptoms and risk factors should undergo monitored laboratory polysomnography (PSG).
Diagnostic criteria
Home sleep apnea testing has not been proven for the diagnosis of CSA, and PSG remains the gold standard. PSG can also help elucidate other sleep disorders that may contribute to the patient's symptoms. A variety of conditions must be considered, including OSA, periodic limb movement disorder, and narcolepsy.
In standard PSG, various physiological variables are recorded during sleep and wakefulness. Sleep stages are assessed by EEG, electrooculogram, and submental electromyography. Breathing is measured by muscle activity, airflow, and oxygen saturation. Heart rate and rhythm can also be measured with a continuous ECG. Based on the information obtained, apnea and hypopnea episodes were identified.
Apnea is when the airflow comes to a complete or near-complete stop. Recording apnea on PSG requires a reduction in airflow of 90% or more (via a nasal sensor or oronasal thermistor) for at least 10 seconds. Central apnea meets this criterion. Hypopnea is also airflow arrest, but to a lesser extent (30% decrease from baseline), with a 3% oxygen desaturation or electroencephalogram (EEG) arousal.
As you can imagine, it is difficult to distinguish between obstructive and central hypoventilation due to the persistent nature of thoracic and abdominal movements. Currently, the American Academy of Sleep Medicine (AASM) recommends that hypopnea be classified as obstructive when upper airway narrowings (such as snoring or flat inhalation) are also found. In the absence of these symptoms, hypopnea is classified as a central event.
The remaining diagnostic criteria vary according to the type of CSA and are shown in Tables 1-4. Some of these include the absence of hypoventilation. Although hypoxaemia on PSG can indicate hypoventilation, objective measurement of carbon dioxide is required to determine. Hypoventilation is defined as a carbon dioxide level greater than 55 mm Hg or 10 mm Hg above daytime baseline for at least 10 minutes during sleep. Carbon dioxide levels can be assessed by transcutaneous or end-tidal monitoring.
Table 1 Primary central sleep apnea
Table 2 Central sleep apnea-Cheyne-Stokes breathing
Table 3 Central sleep apnea caused by periodic breathing at high altitude
Table 4 Central sleep apnea caused by drugs or substances
treat
CSA treatment is aimed at normalizing breathing disorders and preventing sleep-related oxygen saturation. The need for treatment for CSA is controversial. The urgency of treatment may depend on the severity of the patient's symptoms, with mild cases requiring treatment of the underlying associated condition and severe cases requiring PAP therapy. Optimization of chronic diseases, such as HF, CKD, opioid use, and central nervous system pathology, may lead to improvement in CSA.
Persistent PAP (CPAP) is the initial treatment of choice. ASV and BPAP ST are second-line options for patients with left ventricular ejection fraction greater than 45%.
医脉通编译自：Ishikawa O, Oks M. Central Sleep Apnea. Clin Geriatr Med. 2021 Aug; 37(3):469-481. doi: 10.1016/j.cger.2021.04.009. Epub 2021 Jun 4. PMID: 34210451.