# Truths and Lies from the Polysomnography ECG Recording: An Electrophysiologist Perspective

Authors: Adrian Baranchuk; Christina Quinlan; Kevin Michael; Christopher S. Simpson; Damian P. Redfearn; Michael Fitzpatrick
Journal: Case Reports in Medicine
 (2009)

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## Abstract

Polysomnography remains the gold standard for diagnosis of Sleep Apnea (SA) and evaluation of the apnea/hypopnea index (AHI) which is used as the primary index of SA severity. The electrocardiogram (typically a single lead) obtained during the polysomnographic study is usually used to report the association between SA and cardiac rhythm disturbances. These findings help in guiding medical decisions but they could also represent a source for confusion. Electrophysiologists are frequently consulted to determine whether interventions need to be taken. We present 2 cases where the ECG during a polysomnography study required the intervention of an electrophysiologist to help with management.


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## Body

## 1. Introduction

Polysomnography remains the gold standard for diagnosis of Sleep Apnea
(SA) and evaluation of the AHI, the primary index of Sleep  Apnea severity [1].
It typically consists of simultaneous recording of electroencephalography,
electrooculography, electromyography, electrocardiogram (ECG), right and left
anterior tibialis EMG, oxygen saturation, as well as oronasal airflow; and thoracic and
abdominal movement and body position via infrared video monitoring. The ECG
(frequently a single lead) obtained during the study is usually used to report
the cardiac rate and rhythm and any association between SA and cardiac rhythm
disturbances. These findings help in guiding medical decisions but they could
also represent a source of confusion. Electrophysiologists are frequently
consulted to determine whether interventions need to be taken.Case 1.
A 67-year-old man with history of lightheadedness and hypertension was
referred to the Sleep Disorder Clinic. The patient was on no antiarrhythmic
drugs and was taking hydrochlorothiazide 50 mg/d, fosinopril 40 mg/d
and amlodipine 10 mg/d for blood pressure control.
The sleep study showed no evidence of SA but several pauses due to sinus
arrest were observed (Figure1, black arrow). The longest pause lasted for 7
seconds. The pauses were not preceded nor followed by apneic episodes. The
patient was referred to the Arrhythmia Service, and Holter monitoring was
performed. Several diurnal sinus node pauses longer than 5 seconds were
detected. A pacemaker was implanted which resulted in total resolution of the
symptoms at 18 months followup.Figure 1
25 seconds snap shot from
stage 2 non-REM study in patient number 1. Black arrow shows the onset of sinus
arrest lasting 4.5 seconds. After the pause, junctional rhythm is observed.  Upper channels (C4-A1)  (C3-A2)
(O2-A1): electroencephalogram; fourth and fifth channel (ROC-A1) (LOC-A2):
oculogram; sixth channel: chin electromyogram; seventh channel: oxygen
saturation; eigth channel: electrocardiogram; ninth channel: airflow; tenth
channel: chest movement; eleventh channel: abdomen movement.Case 2.
A 58-year-old train driver with excessive daily sleepiness, fatigue, and
frequent snoring was referred to the Sleep Disorder Clinic. The patient was on
no antiarrhythmic drugs and receiving ramipril 20 mg/d for blood pressure
control.
The study showed moderate obstructive SA with AHI of 17. The ECG of the
polysomnography was reported as second degree AV block Mobitz II (Figure2(a)). The patient was referred to the Arrhythmia Service for consideration
of pacemaker insertion.
A closer look to the ECG recording suggests the presence of ectopic beats
followed by a postextrasystolic pause rather than what were considered to be
nonconducted P-waves (Figure2(b), white arrows). A 12-lead ECG was
obtained showing right bundle branch block and frequent premature ventricular
contractions (PVC) with a possible  left ventricular outflow tract  origin
(Figure 2(c), white arrows). The PR interval and the QRS width in sinus
rhythm measured 178 ms and 176 ms, respectively.
An event monitor showed isolated PVCs with fixed coupling interval.
The patient was discharged from the Arrhythmia Service without specific
recommendations and was encouraged to initiate C-PAP for treating SA.(a) 25 seconds snap shot from sleep
study in patient number   2 during wakefulness. White arrows show the beats that were
initially reported as non-conducted P-waves.   Upper channels (C3-A1) (01-A1):
electroencephalogram; third and fourth channel (L-EOG-A1) (R-EOG-A1):
oculogram; fifth channel (EMG1) (EMG2): electromyogram; sixth channel (EKG1) (EKG2): electrocardiogram; seventh channel (SaO2): oxygen saturation;
eighth channel (LEG1) (LEG2): leg movement; ninth channel: airflow; tenth
channel: chest movement; eleventh channel: abdomen movement. (Panel (b)) Amplification of the area
under the highlighted rectangle in panel (a). White arrows show the PVCs followed
by a post-extrasystolic pause.  (Panel (c)) 12-lead ECG shows right bundle
branch block. White arrows show PVCs arising probably from the left outflow
tract.
(a)(b)(c)


## 2. Discussion

These 2 cases represent fairly typical and common consultation requests
for the cardiac electrophysiologist. Sometimes the single lead ECG recording
during polysomnography  may help uncover a conduction disorder that requires
specific cardiac  intervention, as   in case 1.  However, on other occasions, this
single lead recording may be difficult to interpret as in case  2.Several case reports have linked SA to bradyarrhythmias in the past [2].
However, the largest epidemiological study to date has failed to demonstrate a
significant association between these two conditions [3]. The main
hypothesis supporting  the association of SA and  bradyarrhythmias is based on
autonomic imbalance produced by the recurrent apnea and repetitive episodes of
hypoxemia [4, 5].Several consults arrive to the arrhythmia service to evaluate patients
with SA and suspected conduction disorders for possible cardiac pacing. It is
clear that some patients may require a pacemaker insertion to treat the
bradyarrhythmia that may or may not be associated with SA, and which does not
infer that the SA will improve with cardiac pacing.In the first case presented in this paper, the patient had no clear
indication of sleep apnea; however, the ECG recording during polysomnography
was the key finding that led to further appropriate investigation and treatment.
The Holter monitoring not only confirmed the presence of diurnal pauses but
also permitted symptom-rhythm correlation. After implant, complete resolution
of symptoms occurred, suggesting that bradycardia was the cause of symptoms.The second case was more challenging because a conduction disorder was
diagnosed at the sleep disorder clinic orienting this patient towards device
implantation. The initial analysis may be confusing with small waves suggesting
the  presence of non-conducted P-waves. A closer look and 12-lead ECG permitted
one to determine the presence of a premature
QRS followed by a compensatory
post-extrasystolic pause. This matches with the PVCs observed in the 12-lead
ECG. Given the absence of symptoms suggesting paroxysmal AV block and the finding
of isolated PVCs in a structurally normal heart, the decision was to recommend
SA treatment without further electrophysiologic investigations.


## 3. Conclusions

It is of the utmost importance for  electrophysiologists to become
familiar with ECG tracings during polysomnography study. In cases such as those
described herein, proper polysomnography ECG tracing interpretation may help in
the decision-making process regarding pacemaker implantation.



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*Source: 675078-2009-05-04.xml*