Respiration and Abnormal Sleep in Patients with Congestive Heart Failure

doi:10.1378/chest.96.3.480

Chest

Volume 96, Issue 3, September 1989, Pages 480-488

https://doi.org/10.1378/chest.96.3.480 Get rights and content

We investigated the interaction between respiration and sleep in ten male outpatients with severe, stable, maximally treated congestive heart failure (CHF). Cheyne-Stokes respiration (CSR), defined as periodic breathing with apnea or hypopnea, was found in all patients with a mean duration of 120±87 minutes [50.2±34.4 percent total sleep time (TST)]. The CSR was found predominantly during stage 1 (20.6±6.7 percent TST) and stage 2 (25.8±6 percent TST) NREM sleep and occurred rarely during slow wave sleep (SWS) (1.6±1 percent TST) and REM sleep (1.6±0.5 percent TST). All apneas and hypopneas were central. Despite normal awake arterial oxygenation (SaO₂) (96.1±1.6 percent), significant, severe hypoxemia was found during sleep in seven patients with SaO₂ less than 90 percent for 9 to 59 percent TST (mean ± SD, 23 ± 23 percent TST), and this was significantly related to the duration of CSR (r = 0.66, p<0.05). The mean minimum SaO₂ for sleep stage was lowest during stage 1 (82.1 percent ±2.6 percent) and stage 2 (78.9 percent ±2.8 percent) NREM sleep, intermediate during REM sleep (84.5 percent ±1.8 percent) and highest during SWS (87.6 percent ±2.7 percent). Sleep was disrupted to a variable extent in all patients with a short mean TST (287±106 minutes), a high proportion of stage 1 sleep (26±19 percent TST), virtual absence of SWS (5±7 percent TST) which was found in only four patients, and a high number of sleep stage changes (30±27/hour) and arousals (28±25/hour). Arousals occurred predominantly during stage 1 (17±20/hour) and stage 2 (10±7/hour) NREM sleep and the majority immediately followed the hyperpneic phase of CSR. The amount of CSR (percent TST) was inversely related to the length of TST (r = –0.73, p<0.05), and directly related to the number of sleep stage changes (r = 0.79, p<0.01) and the number of arousals (r = 0.66, p<0.05). We conclude that in severe, stable CHF, CSR occurs predominantly during light sleep, that despite normal awake arterial oxygen saturation, significant hypoxemia may develop during sleep due to CSR, and that sleep is unstable and disrupted due to frequent arousals caused by the hyperpneic phase of CSR. These sequelae of CSR may be important determinants of the clinical status and outcome of patients with severe CHF.

Section snippets

METHODS

Ten male patients were investigated from March 1987 to April 1988. All patients were referred by the cardiology service which had been informed of our study protocol. Inclusion criteria for participation in the study were as follow: (1) male patients less than 70 years old with a clinical diagnosis of significant, stable congestive heart failure (New York Heart Association class 3 or 4); (2) left ventricular ejection fraction <35 percent; (3) no evidence of neurologic disease, significant

RESULTS

Ten patients aged 40 to 66 years were studied (Table 1). None was morbidly obese. All had congestive heart failure which was due to ischemic cardiomyopathy in nine patients and alcoholic cardiomyopathy in one. Two patients had chronic atrial fibrillation and two had a permanent pacemaker in situ. Although their congestive cardiac failure was clinically stable (all were ambulatory outpatients), it was nevertheless severe as evidenced by New York Heart Association classification 3 to 4 and the

DISCUSSION

We found that sleep structure was grossly abnormal in heart failure. This study describes the role of sleep and arousal state in congestive heart failure with particular regard to the distribution of CSR during sleep and the interaction between CSR, arterial oxygen saturation and sleep architecture. Cheyne-Stokes respiration was found in all patients and occurred predominantly during stage 1 and 2 NREM sleep. Arterial oxygenation was normal during wakefulness, although awake breathing pattern

ACKNOWLEDGMENTS:

We are grateful to Ms Zoe Pouliot for typing the manuscript.

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Cheyne-Stokes respiration (CSA-CSR) is a form of central sleep apnea characterized by alternating periods of hyperventilation and central apneas or hypopneas. CSA-CSR develops following a cardiac insult resulting in a compensatory increase in sympathetic activity, which in susceptible patients causes hyperventilation and destabilizes respiratory control. The physiological changes that occur in CSA-CSR include hyperventilation, a reduced blood gas buffering capacity, and circulatory delay. In adults, 25% to 50% of patients with heart failure are reported to have CSA-CSR. The development of CSA-CSR in this group of patients is considered a poor prognostic sign. The prevalence, progression, and treatment outcomes of CSA-CSR in children remain unclear with only 11 children being described in the literature. The lack of data is possibly not due to the paucity of children with severe heart failure and CSA-CSR but because they may be under-recognized, compounded by the absence of routine polysomnographic assessment of children with moderate to severe heart failure. Building on much broader experience in the diagnosis and management of CSA-CSR in adult sleep medicine and our limited experience in a pediatric quaternary center, this paper will discuss the prevalence of CSA-CSR, its’ treatment options, outcomes in children, and the potential future direction for research in this understudied area of pediatric sleep medicine.
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Citation Excerpt :
The patient Hunter described had chronic irregularities of heart rhythm, presumably atrial fibrillation, a major predictor of CSA in subjects with heart failure (Javaheri, 2006). Within the last three decades, many studies (Hanly et al., 1989; Javaheri et al., 1995; Javaheri et al., 1998; Lanfranchi et al., 1999; Sin et al., 1999 and Javaheri, 2022a) have reported a high prevalence of both CSA and OSA in subjects with heart failure, both in HFrEF and HFpEF. Notably, a high prevalence has been reported even in asymptomatic subjects with reduced ejection fraction (for review, see Javaheri, 2022a).
Sleep disorders are prevalent in heart failure and include insomnia, poor sleep architecture, periodic limb movements and periodic breathing, and encompass both obstructive (OSA) and central sleep apnea (CSA). Polysomnographic studies show excess light sleep and poor sleep efficiency particularly in those with heart failure. Multiple studies of consecutive patients with heart failure show that about 50% of patients suffer from either OSA or CSA. While asleep, acute pathological consequences of apneas and hypopneas include altered blood gases, sleep fragmentation, and large negative swings in intrathoracic pressure. These pathological consequences are qualitatively similar in both types of sleep apnea, though worse in OSA than CSA. Sleep apnea results in oxidative stress, inflammation, and endothelial dysfunction, best documented in OSA. Multiple studies show that both OSA and CSA are associated with excess hospital readmissions and premature mortality. However, no randomized controlled trial (RCT) has been reported for OSA, but sensitivity analysis of two randomized controlled trials has concluded that use of positive airway pressure devices is associated with excess mortality in patients with heart failure and CSA. Phrenic nerve stimulation has shown improvement in sleep apnea events and daytime sleepiness; however, no randomized controlled trials have demonstrated improvement in survival in patients with heart failure. The correct identification and treatment of heart failure patients with sleep and breathing disorders could affect the long-term outcomes of these patients.
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The most apparent source of disability in patients with multiple sclerosis (MS) is the physical and mental impact. The pathophysiological mechanisms of cognitive dysfunction are multifactorial although hypoventilation secondary to respiratory dysfunction may contribute to cognitive decline.
This study was conducted on 146 MS patients with baseline clinical assessments including the Epworth sleepiness scale (ESS) and physical disability was assessed using the Expanded Disability Status Scale (EDSS). Cognitive testing was performed utilizing the Brief International Cognitive Assessment for Multiple Sclerosis (BICAMS) and the Perceived Deficits Questionnaire (PDQ). Respiratory functions were assessed by spirometry and the respiratory muscle functional assessment was done by maximal mouth pressure measurement.
The respiratory muscle function test had a significant negative correlation with the score of ESS and PDQ scale and a significant positive correlation with the BICAMS scale score (p < 0.001). The ESS and PDQ scores were significantly negatively correlated with forced expiratory volume in the first second (FEV1)/ forced vital capacity (FVC) (p = 0.03, 0.02), FVC supine (p = 0.03, 0.01), FVC upright- FVC supine (ΔFVC) (p < 0.001, <0.001) FEV1 (p < 0.001) and FVC (L) (p < 0.001), respectively. While the BICAMS showed a significant positive correlation with spirometry results except FVC upright. ESS scores were significantly correlated with the BICAMS and PDQ scale score (p < 0.001).
Among MS patients, impaired respiratory functions are significantly associated with sleep disturbance and cognitive impairment. Thus the spirometry and respiratory muscle strength assessment are necessary from the early phase of MS.
Temporal relationship between arousals and Cheyne-Stokes respiration with central sleep apnea in heart failure patients
2018, Clinical Neurophysiology
Citation Excerpt :
It is therefore possible that, since projections from chemoreceptors, and PaCO2 directly, may stimulate arousal centers (Ayas et al., 2000), some arousals may occur just before the resumption of ventilation. Second, some previous investigators had reported the presence of arousals “immediately preceding the hyperpneic phase” or “occurring within 3 s before or after termination of central apneas” (Hanly et al., 1989; Trinder et al., 2000). Third, in patients with idiopathic CSA, arousals occur just before or simultaneous with or shortly after the resumption of ventilation following apnea (Xie et al., 1994).
The interplay between arousals and respiratory events during Cheyne-Stokes respiration (CSR) with central sleep apnea (CSA) in heart failure (HF) patients is still not fully understood. We investigated the temporal relationship between arousals and CSR-CSA.
Episodes of CSR-CSA during sleep stages N1-N2 were analyzed in 22 HF patients with an apnea-hypopnea index ≥15/h, dominant CSA and central apnea index ≥5/h. For each CSR-CSA cycle (apnea + hyperpnea), we determined the onset (AR_onset, relative to hyperpnea onset) and duration of detected arousals.
Arousals (N = 2348) mostly occurred within the first half of the hyperpneic phase (42.6%, AR_onset = 10.6 ± 2.1 s; duration = 10.6 ± 5.2 s) or close to hyperpnea onset (21.5%, AR_onset = −0.1 ± 0.6 s; duration = 13.9 ± 5.4 s). Within-apnea arousals were less frequent (12.4%, AR_onset = −16.0 ± 4.7 s; duration = 3.8 ± 1.4 s). The proportion of CSR-CSA cycles without any hyperpnea-related arousal was 27.5 ± 18.2%. Hyperpnea-related arousability (total number of hyperpneic arousals/total duration of hyperpneas) and apnea-related arousability were 63.4 ± 21.0/h and 23.8 ± 16.9/h, respectively (p < 0.0001).
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View all citing articles on Scopus

Supported by Canadian Heart Association and St. Boniface General Hospital Research Foundation.

Manuscript received December 2; revision accepted February 1.

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Chest

Clinical InvestigationsRespiration and Abnormal Sleep in Patients with Congestive Heart Failure

Section snippets

METHODS

RESULTS

DISCUSSION

ACKNOWLEDGMENTS:

Lancet

Chest

Chest

Chest

Am J Med

Am J Med

Clin Chest Med

Clin Chest Med

Clin Chest Med

Electroencephal Clin Neurophysiol

Am J Med

A case of apoplexy in which the fleshy part of the heart was converted into fat

Dublin Hospital Rep

Cheyne-Stokes respiration: a review of clinical manifestations and critique of physiological mechanisms

Arch Intern Med

Cheyne-Stokes breathing: an instability in physiologic control

N Engl J Med

Cheyne-Stokes respiration revisited: controversies and implications

Crit Care Med

Congestive heart failure: Cheyne-Stokes respiration as the cause of paroxysmal dyspnea at the onset of sleep

Arch Intern Med

Disordered breathing and hypoxia during sleep in coronary artery disease

Chest

Clinical Investigations
Respiration and Abnormal Sleep in Patients with Congestive Heart Failure