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AASMMembershipSectionsNewsletter
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Issue #5
Discussion
Limitinghypopnea scoring toonly those eventswith4%desatu-
rationor greater,without aquantificationof sleepdisruption arising
from sleep apnea, fails to identify the appropriatediagnosis and
treatment in this case,Obstructive SleepApnea andCPAP, respec-
tively. Figure 1 shows conspicuous flow changes on the semi-quanti-
tativenasal pressure signal, clearlyprecipitating arousal and exces-
sivemovements thatwouldbequantified asmerelyperiodic limb
movements if hypopnea scoringwas byRuleBonly. The secondary
reflexive limbmovements from this patient’sOSAHShad a very
robust improvement onCPAP (Figure 2). Limitinghypopnea scor-
ing to a less sensitivemethod (AASMHypopneaRuleB) leavesno
way toquantify that this patient’s obvious symptoms of sleep apnea
(snoring,witnessed apnea, hypertension, and excessivedaytime
sleepiness) shouldbe attributed tohis sleep apnea. In this scenario,
summarydatawouldmislead and imply aprimaryperiodic limb
movement disorder. Our labutilizes the recommendsAASM ruleA
for scoring. We also score ruleBhypopnea simultaneouslyusing a
slightlydifferent label,which adds little tono extra technologist time
andpermits calculationof aCMS-4%-AHI (RuleB) in addition to
AASM-AHI (RuleA) inorder to counsel patientswith access to care
basedonCenter forMedicare Services guidelines.
BothhigherAHIs andhigher rates ofObstructive SleepApnea
havebeen reportedwithAASMhypopnea ruleA compared to the
CMS-4%hypopnea rule consistentwithAASM ruleB (Berry2012,
Guilleminault 2009,Ward2013,Warren2009). For over 30years it
has beenbelieved that upper airway collapse inObstructive Sleep
ApneaHypopneaSyndromehas two immediate consequences of
fragmented sleep and impairedbreathing, thoughwe still have an
incompleteunderstandingof how these immediate consequences
translate intodownstream effects onhealth, qualityof life, andneu-
ro-cognition.Oxygendesaturations, time spentwithdesaturation,
sleepdisruption, autonomicdysregulation, inflammatory responses,
platelet activation, and intra-thoracicnegativepressure fromOSAHS
appear tomediate the connections betweenOSAHS and itsnumer-
ous associated co-morbidities. We lack a clear understandingof
how eachof thesemediators contribute, though it is likely that some
pertain to certain co-morbiditiesmore thanothers (i.e. time spent
indesaturationmaybemore relevant toheart failure,whiledisor-
ganizationof sleepmaybemore relevant to certainneurocognitive
complaints). Increases innegative intra-thoracicpressure and auto-
nomicperturbation canbe causedby events bothwith andwithout
desaturation. Though inclusionof assessment of autonomic instabil-
ity and intra-thoracicpressurewouldbe ideal, this underscores the
need to analyzepolysomnographicdataquantifying events resulting
in either arousal or desaturation.
References
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Paper speeddisplayed is too fast permit adequate inspectionof
