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a case of sleep disordered breathing after coronary artery bypass graft surgery

Reviewed By Sleep and Respiratory Neurobiology Assembly

Submitted by

Dries Testelmans, MD, PhD

Fellow

Department of Pulmonology

University Hospitals Leuven

Leuven, Belgium

Natalia Siyanko, MD

Fellow

Sleep Laboratory and EFCR, Department of Rehabilitation and Physiology

UniversityHospital Grenoble

Grenoble, France

Renaud Tamisier MD, PhD

Associate Professor of Physiology

Sleep Laboratory and EFCR, Department of Rehabilitation and Physiology

UniversityHospital Grenoble

Grenoble, France

Submit your comments to the author(s).

History

A 56-year old man with a history of ischemic chronic heart failure was referred to our clinic in order to be screened for associated pulmonary conditions. Four weeks prior, he had undergone a double coronary artery bypass following an acute myocardial ischemia episode. The patient had no history of cerebrovascular or metabolic disease and stopped smoking since his surgery. Two weeks after surgery, he started a cardiac rehabilitation program. According to the cardiologist, the patient was clinically stable, asymptomatic and no new medication was planned to be introduced. The left ventricular ejection fraction (LVEF) was 34%.

The patient had NYHA class II dyspnea, but did not complain about dyspnea during sleep. He did not report snoring, or daytime sleepiness; he had an Epworth Sleepiness Score of 6.

Physical Exam

Physical Examination

The patient had a height of 173 cm and weighed 49 kg; his BMI was 16.4 kg/m2. Respiratory and cardiovascular examinations were normal and no signs of pulmonary edema were found. His blood pressure was 130/70 mmHg, with a heart rate of 62 beats/min.

Pulmonary function test

FEV1: 2.68 L (80% predicted) - FVC: 4.04 L (97% predicted) - FEV1/FVC 0.66 -TLC: 7.96 L (118% predicted)

Arterial blood gases: PaO2: 97.2 mmHg - PaCO2: 32.3 mmHg - pH: 7.39 – HCO3-: 19.2 mmol.l-1 – SaO2: 98%

Figure 1 and 2:

figure1

Figure 1: Representative trace of recorded sleep study showing typical central respiratory events followed by hyperventilation. Note the absence of respiratory effort on thoracic and abdominal belts (see arrows). Most of apneic events are responsible for significant desaturations, with changes in heart rate despite the patient being on beta-blockers and severe peripheral vasoconstriction as assessed by the decrease in finger pulse wave oximetry amplitude.

figure 2

Figure 2: Representative trace of a 10-minute recorded ventilation during the sleep study showing typical Cheyne-Stokes Respiration (CSR). CSR is defined by 3 consecutive cycles of cyclical crescendo and decrescendo change in breathing amplitude (Figure 2) and at least 1 of the following: 1) Five or more central apneas or hypopneas per hour of sleep and/or 2) The cyclic crescendo and decrescendo change in breathing amplitude has a duration of at least 10 consecutive minutes.

Diagnostic Respiratory Polygraphy: The total apnea/hypopnea index (AHI) was 34.5 per hour with an obstructive AI of 0.1 and a central AI of 19.9 per hour. During the night, there was no pronounced drop in oxygen saturation (SpO2), with the lowest SpO2 of 95% and a mean SpO2 of 98%.

Question 1

What is likely to be your diagnosis?


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