A 49-year-old Caucasian man with heart failure (HF) is referred to the sleep disorders center for evaluation of sleep apnea. He denies any sleep complaints and questions why he was referred for a sleep study. He typically goes to bed at 11 p.m. and falls asleep within a few minutes. He wakes up five to seven times per night for no apparent reason other than an occasional abrupt arousal feeling short of breath. His usual wake up time is 7 a.m., and he generally feels refreshed in the morning. He estimates a total sleep time of 8 hours. He is a habitual supine sleeper and his wife rarely notes light snoring which resolves when he rolls onto his side. He and his wife deny gasping, choking, or breathing pauses in sleep as well as daytime sleepiness (his Epworth Sleepiness Scale score is 6). However, he reports fatigue since a myocardial infarction one year prior that has affected his ability to participate in activities he enjoys, including golf and gardening. He typically drinks three 8-oz cups of coffee per day and denies using alcohol and recreational drugs.
His medical history is significant for Type II DM, MI complicated by HF, and recurrent AF status post placement of an implantable cardioverter defibrillator. Current medications include aspirin, clopidogrel, atorvastatin, lisinopril, carvedilol, spironolactone, furosemide, and digoxin. He has a 20-pack year tobacco history but quit one year prior to presentation. A trans-thoracic echocardiogram shows normal left ventricular size, ejection fraction of 15%, severe hypokinesis of the mid inferior and anterior left ventricular segments with Stage 3 diastolic function, and normal right ventricle size and systolic function. Laboratory results include BNP of 105 pg/ml (normal: 0-99) and normal hemoglobin, thyroid stimulating hormone, and electrolytes.
Physical examination reveals a blood pressure of 122/88 mm Hg, pulse of 88 beats per minute, respiratory rate of 18 breaths per minute, weight of 140 kg, height of 186 cm (BMI 41 kg/m2), and neck circumference of 46 cm. The oropharnyx is crowded with a Grade III Friedman tongue position. Heart exam is significant for an irregularly irregular rhythm without murmur. Lungs are clear. There is no jugular venous distention. Mild edema to the distal calves is present.
A five minute representative epoch from the overnight polysomnogram shows the following:
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Figure 1
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Figure legend: Recurrent respiratory events are observed in the nasal pressure, airflow, and effort channels that are associated with microarousals on the EEG, oxygen desaturations, and fluctuations in CO2. Channels are as follows: electro-oculogram (left: E1-M2, right: E2-M1), chin electromyogram (Chin), electroencephalogram (left frontal [F3], central [C3], and occipital [O1] electrodes to right mastoid [M2] reference), EKG, snore microphone, leg EMG (right and left tibialis anterior placements), nasal pressure transducer, nasal-oral airflow, respiratory effort (thoracic, abdominal) and oxygen saturation (SaO2), and end-tidal CO2 (ETCO2).
The correct answer is: C. The polysomnogram confirms the diagnosis of CSA due to Cheyne Stokes Breathing (CSB) in the setting of HF. Treatment with PAP therapy is indicated.
Sleep related breathing disorders (SRBD) represent an important, often unrecognized co-morbidity in patients with HF, affecting up to 50% of cases. CSA due to CSB and OSA often co-exist. CSA is characterized by recurrent episodes of cessation of respiration lasting 10 seconds or longer due to temporary loss of ventilatory drive. CSB is a specific form of periodic breathing characterized by a crescendo-decrescendo pattern of respiration between central respiratory events. The 2012 revised International Classification of Sleep Disorders redefined CSB as episodes of at least three consecutive central respiratory events separated by a crescendo-decrescendo change in breathing amplitude with a cycle length of at least 40 seconds (typically 45 to 90 seconds) and five or more central respiratory events per hour associated with the crescendo-decrescendo breathing pattern recorded over at least two hours.
SRBD produce a state of increased sympathetic activity due to recurrent oxygen desaturation and arousal, thereby contributing to HF progression. The presence and amount of CSB has prognostic significance in HF patients with a higher central apnea-hypopnea index and longer CSB duration associated with higher BNP, longer hospital stay, and increased risk of heart transplantation and mortality. In addition, SRBD contribute to poor quality of life in the HF population.
In contrast to patients with OSA who typically present with snoring, daytime sleepiness, and obesity, those with CSA due to CSB tend to experience fatigue, paroxysmal nocturnal dyspnea, and recurrent arousals and awakenings, symptoms common in the HF population. Risk factors for CSA due to CSB in HF patients include male gender, older age (> 60 years), presence of AF, and hypocapnia (wake PaCO2 ≤ 38 mm Hg). The case illustrates the importance of maintaining a high clinical suspicion for SRBD in HF patients.
The polysomnogram shows repeated central respiratory events with a crescendo-decrescendo pattern, excluding OSA as the primary diagnosis. Primary CSA is not a consideration in this case as the patient has HF. The diagnosis of CSA due to drugs or substance abuse is made in the setting of opioid use for at least two months or a history of substance abuse, neither of which were present in this case. Unlike CSB, the respiratory phase (between central respiratory events) in primary CSA or narcotic induced central apnea doesn't usually have a crescendo-decrescendo pattern and the duration of the respiratory phase is typically shorter than 40 seconds. The sleep history is typical of CSA and the lack of daytime sleepiness, snoring, and observed apneas should not delay diagnostic polysomnography or treatment.
The patient underwent a PAP titration study. Adaptive servo-ventilation (ASV) therapy abolished respiratory events, periodic breathing, cyclical arousals, and desaturations. Treatment with ASV significantly reduced his fatigue, resulting in an increase in daytime activity and weight loss. An echocardiogram six months later showed an improved ejection fraction of 30%.
References
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- Berry RB, Budhiraja R, Gottlieb DJ et al. Rules for scoring respiratory events in sleep: update of the 2007 AASM Manual for the Scoring of Sleep and Associated Events. J Clin Sleep Med 2012;8:597-619.
- Garcia-Touchard A, Somers VK, Olson LJ, Caples SM. Central sleep apnea: Implications for congestive heart failure. Chest 2008;133:1495–1504.
- Hanly PJ, Zuberi-Khokhar NS. Increased mortality associated with Cheyne-Stokes respiration in patients with congestive heart failure. Am J Respir Crit Care Med 1996;153:272-276.
- Hastings PC, Vazir A, Meadows GE, et al. Adaptive servo-ventilation in heart failure patients with sleep apnea: A real world study. Int J Cardiol 2010;139:17-24
- Lanfranchi PA, Braghiroli A, Bosimini E, et al. Prognostic value of nocturnal Cheyne-Stokes respiration in chronic heart failure. Circulation 1999;99:1435-40.
- Pepin JL, Couri-Pontarollo N, Tamisier R, Levy P. Cheyne-Stokes respiration with central sleep apnoea in chronic heart failure: Proposals for a diagnostic and therapeutic strategy. Sleep Medicine 2006; 33–47.
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