Editorial Sleep apnea: what does that really mean? A commentary on Baranchuk: “Sleep apnea, cardiac arrhythmias, and conduction disorders” Dr Adrian Baranchuk has provided readers of this journal with an excellent brief tour of the overlap of abnormal cardiac electrophysiology and sleep-disordered breathing in his article “Sleep apnea, cardiac arrhythmias, and conduc- tion disorders.” 1 The intimate relationship between these clinical conditions is increasingly being appreciated, and a more nuanced understanding of the terminology used in sleep research may be helpful to interested clinicians. A factor that should be kept in mind is that sleep-disordered breathing is a potentially manageable condition and that management, through lifestyle changes and/or various respiratory support devices, has potential benefits on cardiovascular physiology. This complex topic is beyond the scope of the current commentary. A term that requires clearer definition is “having sleep apnea.” As quoted by the Baranchuk review, “Obstructive SA (OSA) is defined by repetitive upper airway collapse that occurs during sleep, producing an interruption of ventilation that results in subsequent hypoxia, hypercapnia, sleep arousals, shifts in intrathoracic pressure, and heightened sympathetic activity.” This precise-sounding definition is actually somewhat vague, just as describing a patient as “having ventricular arrhythmias” by describing ventricular premature beats and their sequelae would be. Sleep apnea is identified by categorizing a measurement called the Apnea Hypopnea Index (AHI in events per hour of sleep). Obstructive events (apneas) are not separated from partially obstructive events (hypopneas) in this index. Thus, the term obstructive sleep apnea hypopnea syndrome (OSAHS) is often used and is interchangeable with OSA. Because it is this AHI that defines if a patient “has OSA,” the necessarily quick review by Baranchuk illustrates the importance of asking “OSA by what criteria?” Cut points in different studies for clinically significant OSA vary from AHI greater than 5 per hour to AHI greater than 20 or even 30 per hour, and in children, an AHI greater than 3 per hour may be seen as being clinically important. Polysomnograms (PSGs), the criterion standard for detecting OSAHS, are scored in 30-second (or sometimes 20 seconds) epochs, usually by sleep technicians, and the patient must be asleep by electroencephalogram (EEG)– based criteria for more than 1/2 of an epoch for an event to be counted as occurring during sleep. Obstructive apnea events are relatively straightforward to count, except that they must last at least 10 seconds (not 9.5) and occur during an epoch scored as sleep (although uncounted events may occur during wake if the waking up is a result of the OSA). Actually, even in the case of obstructive events, there is a continuum of possibilities, pure obstruction (in most cases) where the patient is clearly trying to breathe against a collapsed airway, to a failure to try to breathe (central apnea), and everything in between (mixed events), with varying degrees of oxygen desaturation (including none), and the apnea component of the AHI may count all of them together. Furthermore, in the older studies, cessation of airflow was determined using a thermocouple positioned close to the nostrils (and prone to moving and underreporting airflow), but more recent studies use a nasal cannula to measure airflow pressure. The AHI, then, also includes hypopneas, that is, partial cessations of airflow, and most patients have both types of events. Hypopneas are considered to be clinically significant as well, supporting the use of the AHI as an index of severity. So the term OSA patient does not generally mean a patient having only obstructive events. However, to make this a little more complicated, the criteria for scoring an event as a hypopnea have changed over time. The original criteria, published in 1999 (the Chicago criteria), defined a hypopnea as lasting at least 10 seconds and being associated with at least a 50% reduction in airflow compared with the prior 2 minutes of stable breathing (measured by nasal pressure), or else, if the breathing is not stable, the average of the largest 3 breaths in the past 2 minutes. 2 An additional possibility for a hypopnea, at the time, was a clear reduction in breathing associated with an O 2 desaturation of 3% or more or an EEG arousal. As can be readily appreciated by the reader, this definition, like the visual estimation of % stenosis on catheterization laboratory films, has tremendous room for subjectivity. In addition, scored events that were relatively severe (ie, large O 2 desaturations, longer apnea durations) were counted in the same AHI with events that were much milder. This is not necessarily specified in study results. Furthermore, older studies were based on hand scoring of reams of paper that recorded the different PSG signals for airflow, respiration, EEG, electrocardiogram (ECG), muscle movements, and O 2 saturations, whereas more modern studies, like more modern ECG machines, use electronically recorded and scored signals that are overread. As mentioned, scoring criteria for hypopneas changed over time (most recently in 2009) when a new Scoring Manual was published. 3 There are now 2 recommended Available online at www.sciencedirect.com Journal of Electrocardiology 45 (2012) 513 – 514 www.jecgonline.com 0022-0736/$ – see front matter © 2012 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2012.06.013