Cheyne–Stokes respiration during sleep: mechanisms and potential interventions

Wang, Yan; Cao, Jie; Feng, Jing; Chen, Bao-yuan

doi:10.12968/hmed.2015.76.7.390

Cited by 5 publications

(1 citation statement)

References 41 publications

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“…3,4 In general, hypoxemia in patients with CSR is mild (oxygen saturation is usually above 80-85%). Some articles report that the presence of CSR is a poor prognostic factor for CHF, 5,6 but conflicting data exists that would indicate otherwise.…”

Section: Case Reportmentioning

confidence: 99%

Cheyne-Stokes Respiration Revisited: Clinical Clue to the Diagnosis for Acute Exacerbation of Congestive Heart Failure

Saraya¹,

Minami²,

Mikura³

et al. 2017

Pulm Res Respir Med Open J

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A 72-year-old man was admitted to the hospital to initiate chemotherapy for pleomorphic lung carcinoma (T4N0M1a, stage 4 cancer). He had a history of chronic systolic heart failure with severe mitral regurgitation diagnosed five years prior to this admission who had been receiving cardiac resynchronization therapy (CRT). He had complained of nocturnal dyspnea, especially when lying flat, as well as of dyspnea on exertion. A few weeks prior to his admission, his dyspnea worsened to the point that he could not even walk a few steps, demonstrating a rapid deterioration of performance status (PS).On examination, he was in mild distress, with a performance status of 3 out of a possible score of 5, defined as capable of only limited self care; confined to bed or chair more than 50 percent of waking hours.1 His vital signs were normal, except for his sinus tachycardia, with an elevated rate of 108 beats per minute. His oxygen saturation while breathing ambient air was above 90%. However, he was later noted to experience nocturnal desaturation as his oxygen saturation dropped to 80-85% at night while he was sleeping. His liver function tests (LFTs) were significant for aspartate aminotransferase (AST) 51 international units per litre (IU/L), alanine aminotransferase (ALT) 359 IU/L, alkaline phosphatase (ALP) 360 IU/L, and γ-glutamyl transpeptidase (γ-GTP) 125 IU/L.On the third day of the admission, he complained of increased shortness of breath at night. On examination, he was in respiratory distress and tachypnic. The body temperature was 37.3 °C, blood pressure of 94/70 mm Hg, pulse of 118 beats per minute, respiratory rate of 28 breaths per minute, and an oxygen saturation of 85% while he was breathing ambient air. He had cyclic crescendo-decrescendo breathing, which was accompanied by apnea and desaturation, and his apnea lasted for about 10 seconds per cycle, consistent with Cheyne-Stokes respiration (CSR) (Video 1). Although no apparent adventitious cardiac sounds were noted, his jugular venous pressure was slightly elevated to 10 cm H 2 O with cold extremities, as well as marked elevation of serum brain natriuretic peptide (BNP) level (1274 pg/mL). He was thus diagnosed with acute congestive heart failure (CHF) with a congestive liver and was treated with oral furosemide (20 mg per day). His dyspnea, nocturnal hypoxemia, and CSR, as well as abnormal LFTs, improved over the following few days, and he was transferred to the sub-acute care facility where he continued to receive further therapy.CSR has been recognized in 30-50% of patients with chronic CHF 2 and the prevalence is much higher when CHF is more severe.3,4 In general, hypoxemia in patients with CSR is

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Section: Case Reportmentioning

confidence: 99%

Cheyne-Stokes Respiration Revisited: Clinical Clue to the Diagnosis for Acute Exacerbation of Congestive Heart Failure

Saraya¹,

Minami²,

Mikura³

et al. 2017

Pulm Res Respir Med Open J

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Patients with Cheyne–Stokes respiration and heart failure: patient tolerance after three-month discontinuation of treatment with adaptive servo-ventilation

et al. 2017

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The recent SERVE HF study concluded that patients with chronic heart failure (CHF) and Cheyne-Stokes respiration (CSR) have increased mortality when treated with adaptive servo-ventilation (ASV). We, therefore, wanted to explore if these patients tolerated discontinuation of ASV treatment. The study was a prospective post-ASV treatment observational design with a 3-month follow-up period. 14 patients from our outpatient clinic, all male, were originally diagnosed with CHF and Cheyne-Stokes respiration, which is a clinical form of central sleep apnea. Left ventricular ejection fraction (LVEF) was ≤45% when ASV treatment was initiated. Median machine use was 68 (42-78) months when the patients were instructed to terminate ASV treatment. The patients were then followed during conventional CHF treatment for 3 months. Study baseline was set the last ASV treatment day. Sleep data were collected from the machine the last day of use. Apnea-hypopnea index (AHI), LVEF, 6-min walk test and 24-h ambulatory electrocardiogram recordings were performed at baseline and at study end. Life quality data were obtained using The Minnesota Living with Heart Failure Questionaire (MLHFQ). New York Heart Association Functional Classification (NYHA) was registered. An ambulatory sleep screening was performed at study end. AHI increased significantly after 3 months without ASV treatment [from 1.6 (0.8-3.2) to 39.2 (24.3-44.1, p = 0.001)]. Quality of life (QOL) decreased significantly: 30 (13-54) at discontinuation of ASV vs. 46 (24-67) (MLHFQ) at study end, p = 0.04. Though there was no significant change in NYHA functional class, patients especially reported increased shortness of breath, reduced concentration and reduced memory after discontinuation of ASV treatment. There were no significant differences in LVEF, heart rhythm data and physical capacity. Left ventricular function was preserved indicating that discontinuation of ASV in heart failure patients does not affect cardiac capacity. There was a significant decrement in QOL that must be considered in further treatment of these patients.

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