Understanding Your Sleep Study Results: RDI, Desaturation, and Sleep Architecture

It is surprising how little patients know about the critical results of a sleep study test. Hardly ever does the patient even possess a copy of the study report.

Obtaining a Sleep Study Report Copy

The best time to get a copy is when you see your sleep doctor to discuss the results. If that occasion has already passed, however, don't wait for the next appointment. Send a letter to the doctor requesting a copy. Mention that your letter represents a consent for release of this information to yourself. You should not only sign and date this, but get a witness to sign and date it as well, and keep a copy for yourself.

If you have access to a fax machine, this is a quicker and more compelling way to transmit the request to your doctor.

Understanding the Report: AHI and RDI

One of the most important numbers on the whole report is the Apnea Hypopnea Index (AHI), or Respiratory Distress Index (RDI). The reason for its importance is the the AHI or RDI usually plays a key role in diagnosing or ruling out sleep apnea, and also plays an important role in gauging its severity.

RDI (or AHI) is calculated, by dividing the total sleep time (in hours) into the sum of the total number of apneas plus hypopenas.

RDI is usually a number between 0 and 120, which represents the frequency, per hour of sleep, of "respiratory events" such as apneas (cessation of breathing for 10 seconds or longer) or hypopneas (decrease of breathing for the same duration).

Although different clinicians use different criteria to define normal through severe apnea, you need only get a sense of how this number relates to diagnosis and severity. Some would label sleep apnea syndrome to any RDI over 5; others would use 10 or 15 as a cut-off.

RDI (or AHI) is calculated, by dividing the total sleep time (in hours) into the sum of the total number of apneas plus hypopenas.

Oxygenation Desaturation

Oxygenation desaturation, or reduced blood oxygen, is one effect of prolonged apneas. Desaturation is often summarized with reference to the lowest level of oxygen saturation reached during the night.

Normally, oxygen saturation should not dip below the lower 90's; however, in severe apnea, it has been known to go as low as 40%. This degree of oxygen desaturation is dangerously capable of damaging various organs of the body, and deserves special attention.

However, a person might have quite frequent apneas, or especially hypopneas, without much desaturation, especially if none of these respiratory events are prolonged. These briefer events still disrupt the continuity of sleep, causing daytime sleepiness, and can trigger physiological changes like rises in blood pressure, which is one mechanism by which sleep apnea contributes to hypertension.

How to Interpret Sleep Architecture

The interpretation of sleep architecture--the proportionate amounts and timing of the different sleep stages (I, II, III, IV, and REM) throughout the night--presents much more complexity than that of respiratory events. However, you can start by realizing that a normal person has a certain proportion of each stage during the course of a night's sleep, whereas a person with a sleep disorder may have very little or none of one or another stage, especially Rapid Eye Movement (REM), or dreaming sleep, and the deeper stages (III and IV) of non-REM, so-called "slow wave" sleep. These are among the most common abnormalities seen in cases of sleep apnea.

Normally, a person enters sleep through stage 1, enters the first episode of REM 90 minutes later, and throughout the night alternates REM and NREM sleep at intervals of 90 minutes. However, as the night wears on, REM episodes grow progressively longer, so that slow wave sleep predominates in the first third of the night and REM in the last third.

What untreated sleep disorders often do to sleep architecture is to greatly reduce REM and slow wave sleep, leaving predominantly the lighter stages of sleep (1 and 2), as well as reducing total sleep time and sleep efficiency. However, other causes exist for deficits in sleep stages. One of the most common is medication of many sorts, especially antidepressants, which tend to suppress REM sleep.

Another abnormality to look for if you are suspected of having narcolepsy is the occurrence of the first REM sleep much sooner after falling asleep than the usual 90-minute delay. Some shortening of REM delay or "latency" can represent a sign of depression, but this does not usually cause the same degree of shortening as narcolepsy.