SRBDs refer to an abnormal respiratory pattern or an abnormal reduction in gas exchange during sleep. An apnea in adults is scored when there is a drop in the peak signal excursion by ≥90 % of pre-event baseline for ≥10 s. Hypopnea in adults is scored when the peak signal excursions drop by ≥30 % of pre-event baseline for ≥10 s in association with either ≥3 % arterial oxygen desaturation or an arousal [3]. Apneas plus hypopneas per hour of sleep define the apnea hypopnea index (AHI). Roughly, SRBDs are divided into three groups: obstructive sleep apnea (OSA), central sleep apnea (CSA), and sleep-related hypoventilation/hypoxemia syndromes.

OSA is clinically defined by the occurrence of daytime sleepiness, loud snoring, witnessed breathing interruptions, or awakenings caused by gasping or choking in the presence of at least five obstructive respiratory events per hour of sleep. The presence of 15 or more obstructive respiratory events per hour of sleep in the absence of sleep-related symptoms is also sufficient for the diagnosis of OSA because of the greater association of this severity of obstruction with important consequences such as increased cardiovascular risk [4].

The CSA syndromes are characterized by sleep-disordered breathing associated with diminished or absent respiratory effort, coupled with the presence of symptoms including excessive daytime sleepiness, frequent nocturnal awakenings, or both. CSA may be related to Cheyne-Stokes respiration (CSR), which is characterized by an absence of air flow and respiratory effort followed by hyperventilation in a crescendo-decrescendo pattern [4]. CSR most often occurs in patients with congestive heart failure but can also occur in patients with stroke or renal failure. CSA may also be related to high altitude or to medications such as opioids.

Sleep-related hypoventilation/hypoxemia syndromes are characterized by reduced alveolar ventilation. In addition to rare idiopathic or congenital forms, hypoventilation syndromes occur in lung diseases, neuromuscular diseases, or obesity. For adults, sleep hypoventilation is scored when the arterial pCO₂ (or surrogate) is >55 mmHg for ≥10 min or there is an increase in the arterial pCO₂ (or surrogate) ≥10 mmHg (in comparison to an awake supine value) to a value exceeding 50 mmHg for ≥10 min [3].

Most evidence concerning indications for ventilation therapy and outcome exists for patients with OSA. Patients with an AHI ≥15/h or symptomatic patients with an AHI ≥5/h should be considered for treatment of OSA [4]. OSA should be approached as a chronic disease requiring long-term multidisciplinary management [4]. PAP is the treatment of choice for mild, moderate, and severe OSA and should be offered as an option to all patients. Continuous PAP (CPAP) is the first choice of treatment and is recommended as standard for patients with moderate to severe disease and as an option for patients with mild disease [4, 5]. Other modalities such as bi-level PAP (BPAP), autotitrating PAP, or pressure relief may be considered in patients with CPAP failure [4].

For nonobstructive sleep apnea, the evidence of treatment and outcome is rather limited. In patients with CSA, CPAP therapy targeted to normalize AHI is indicated for the initial treatment of CSA related to congestive heart failure. If suppression of AHI is not sufficient by CPAP, adaptive servo-ventilation (ASV) or BPAP therapy in a spontaneous timed mode may be applied [6]. In case of hypoventilation/hypoxemia syndrome with proven hypercapnia, BPAP therapy as noninvasive positive pressure ventilation with true ventilatory support should be considered.

In a strict sense, CPAP is not a form of ventilation but an application of a constant pressure during spontaneous breathing. At first sight, effectiveness is quite simple: PAP acts as a “pneumatic splint” and, therefore, prevents partial or full occlusion of the upper airway during sleep in OSA syndrome. Thus, the pathophysiologic cascade, which includes hypoxemia, intrathoracic pressure swings, repetitive arousals, and adrenergic stimulation, is avoided. However, there are other, mostly positive hemodynamic effects, especially in heart failure patients, and an unloading of the respiratory system. Because end expiratory lung volume rises, there are beneficial effects on gas exchange. Beyond these acute effects, it should be kept in mind that CPAP is known to reduce cardiovascular risk [1] and has positive effects on clinical course of coronary artery disease [7], restenosis after coronary stent implantation [8], and ventricular remodeling after myocardial infarction [9].

Auto CPAP (APAP) is a particular form of CPAP. Specific algorithms were evolved to detect variations of airway obstruction and adjust pressure level. In clinical practice, areas of application developed: APAP could be used to titrate CPAP pressure to save costs. Moreover, it could be used in patients with sleep apnea only during rapid eye movement sleep or respiratory events related to position [10]. Because APAP allows adaption of pressure to current requirement, median nocturnal pressure is lower compared with conventional CPAP [11]. This might contribute to better acceptance and, therefore, higher adherence to therapy. If exhalation against positive pressure is associated with patient discomfort, some devices allow an expiratory pressure contour modification [12]. APAP should not be used in patients with severe comorbidities such as heart failure, chronic obstructive pulmonary disease (COPD), or hypoventilation syndromes [12].

Although OSA can be treated effectively by CPAP in most patients, problems can occur under some conditions. In this context, it should be considered that sleep apnea is associated generally with increased work of breathing, especially in hypercapnic patients [13]. There are three main reasons to step up CPAP to noninvasive ventilation (NIV) in patients with SRBDs: