Elsevier

Sleep Medicine

Volume 11, Issue 2, February 2010, Pages 143-148
Sleep Medicine

Original Article
Impact of sleeping position on central sleep apnea/Cheyne–Stokes respiration in patients with heart failure

https://doi.org/10.1016/j.sleep.2009.05.014Get rights and content

Abstract

Background

The present study determines the influence of sleeping position on central sleep apnea (CSA) in patients with heart failure (HF).

Methods

The apnea/hypopnea index (AHI) during different body positions while asleep was examined by cardiorespiratory polygraphy in 71 patients with HF (ejection fraction <45%).

Results

Twenty-five of the patients having predominantly CSA (central apnea index ⩾10/h) with a lower obstructive apnea index (<5/h) were assigned to groups with positional (lateral to supine ratio of AHI <50%, n = 12) or non-positional (ratio ⩾50%, n = 13) CSA. In the non-positional group the BNP level was higher, the ejection fraction was lower and the trans-tricuspid pressure gradient was higher than in the positional group. Multiple regression analysis revealed more advanced age (p = 0.006), log10 BNP (p = 0.017) and lung-to-finger circulation time (p = 0.020) as independent factors of the degree of positional CSA. Intensive treatment for HF changed CSA from non-positional to positional in all eight patients tested. Single night of positional therapy reduced CSA (p < 0.05) and BNP level (p = 0.07) in seven positional patients.

Conclusion

As cardiac dysfunction progresses, severity of CSA also increases and positional CSA becomes position-independent. Positional therapy could decrease CSA, thereby having a valuable effect on HF.

Introduction

Up to 50% of patients with heart failure (HF) have sleep-related breathing disorders; 40% exhibit central sleep apnea (CSA) or Cheyne–Stokes respiration, and 10% have obstructive sleep apnea (OSA) [1], [2].

The level of respiratory distress during sleep among patients with OSA varies according to position. For instance, patients have 40–50% lower apnea–hypopnea index (AHI) when sleeping on their side than in the supine position [3]. Cartwright defined “positional sleep apnea” as a 50% decrease in AHI in the lateral position compared with the supine position [4]. In fact, the severity of OSA in these patients is mostly related to the amount of time asleep in the supine position [5]. In contrast, patients in whom AHI in the lateral position does not decrease by ⩾50% relative to the supine position are defined as having “non-positional sleep apnea” [6]. Those with non-positional OSA have lower mean oxygen saturation, higher AHI and worse sleep quality than those with positional OSA [6].

Similarly to OSA, the effect of body position on Cheyne–Stokes respiration was first described in patients with stroke [7]. Several reports also indicate that CSA is improved in patients with various diseases when sleeping in the lateral position compared with the supine position [8], [9]. Interestingly, the AHI does not decrease in some patients when sleeping in the lateral position. Additionally, sleeping position could affect the severity of CSA in patients with HF, but the impact of sleeping position on CSA with Cheyne–Stokes respiration in patients with HF is not as well understood. Moreover, the prevalence and characteristics of positional and non-positional types of CSA have never been investigated thoroughly in such patients. Therefore, the present study examined the influence of sleeping position on CSA with Cheyne–Stokes respiration in patients with HF.

Section snippets

Patients

The study cohort comprised 71 consecutive patients with stable HF (51 men and 20 women) who underwent cardiopulmonary polygraphy and whose left ventricular ejection fraction was <0.45, determined by radionuclide or contrast ventriculography. The etiologies of HF were ischemic in 24 and non-ischemic in 47 patients. The amount of physical activity was measured using a specific activity scale in questionnaires regarding ordinary physical activities [10]. Patients with stroke, respiratory failure,

Results

The AHIs were <5.0, 5.0–14.9 and ⩾15.0/h in 15, 18 and 38 of the 71 patients, respectively. Five patients were excluded as they slept for <20 min in either the lateral or the supine position, while one patient was excluded because the body position sensor was lost during polygraphy. Of the 34 patients with AHI ⩾15.0/h, OSA dominated in 6 and CSA dominated in 28, and 25 with CAI ⩾10/h with less OAI (<5/h) (mean AHI, 28 ± 8/h and CAI, 21 ± 10/h) constituted the study group.

Discussion

Although positional sleep apnea in OSA is established, it has not been thoroughly investigated in patients with HF and CSA. The major findings of the present study are as follows: (1) hemodynamic features were more deteriorated in patients with non-positional CSA; (2) age, log10 BNP and LFCT were independent factors of the severity of positional CSA; (3) intensive treatment for HF changed non-positional to positional CSA in all eight patients tested; and (4) single night of positional therapy

Limitations

The present study has several limitations. First, our patients did not undergo polysomnography. A previous study [8] found greater central AHI during sleep stages 1 and 2 (43 and 37/h) and lower central AHI during slow-wave and rapid eye movement sleep (28 and 23/h). Moreover, the L/S ratio was also higher during sleep stages 1 and 2 (0.74 and 0.82) and lower during slow-wave and rapid eye movement sleep (0.25 and 0.52). Because sleep quality tended to be lower in patients with severe HF, we

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