Elsevier

Progress in Cardiovascular Diseases

Volume 51, Issue 4, January–February 2009, Pages 339-349
Progress in Cardiovascular Diseases

Sleep in Heart Failure

https://doi.org/10.1016/j.pcad.2008.02.001Get rights and content

Sleep plays a large role in patients with heart failure. In normal subjects, sleep is usually in a supine position with reduced sympathetic drive, elevated vagal tone and as such a relatively lower cardiac output and minute ventilation, allowing for recouperation. Patients with heart failure may not experience the same degree of autonomic activity change and the supine position may place a large strain on the pulmonary system. More than half of all heart failure patients have one of two types of sleep apnea: either obstructive or central sleep apnea. Some patients have both types. Obstructive sleep apnea is likely to be a cause of heart failure due to large negative intrathoracic pressures, apnea related hypoxemia and hypercapnia, terminated by an arousal and surge in systemic blood pressure associated with endothelial damage and resultant premature atherosclerosis. Reversal of obstructive sleep apnea improves blood pressure, systolic contraction and autonomic dysfunction however mortality studies are lacking. Central sleep apnea with Cheyne Stokes pattern of respiration (CSA-CSR) occurs as a result of increased central controller (brainstem driving ventilation) and plant (ventilation driving CO2) gain in the setting of a delayed feed back (ie low cardiac output). It is thought this type of apnea is a result of moderately to severely impaired cardiac function and is possibly indicative of high mortality. Treatment of CSA-CSR is best undertaken by treating the underlying cardiac condition which may include with medications, pacemakers, transplantation or continuous positive airway pressure (CPAP). In such patients CPAP exerts unique effects to assist cardiac function and reduce pulmonary edema. Whether CPAP improves survival in this heart failure population remains to be determined.

Section snippets

Heart Failure: Prevalence, Incidence, and Pathogenesis

Heart failure is defined as the inability to maintain cardiac output for a given task. Symptoms include exertional dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. Four classes of HF have been identified: (a) high risk no symptoms, (b) structural heart disease but asymptomatic, (c) structural heart disease and previous or current symptoms, and (d) refractory symptoms requiring special intervention.1

The prevalence of HF in a westernized community aged more than 45 years is estimated to

Pathogenesis Linking OSA with HF

Strong epidemiological links exist between snoring, OSA, and HF. Children who have OSA have thicker ventricular walls compared with nonsnoring controls.16 More than 55% of patients with OSA have diastolic dysfunction.17 Large community studies have identified significant relationships between OSA and self-reported HF.18

There are 4 key pathophysiologic features of OSA that could adversely affect function of the left ventricle:(a) generation of exaggerated negative intrathoracic pressure, (b)

Pathogenesis Linking CSA-CSR with HF

The prevalence of sleep disordered breathing in patients with HF is strikingly high, and depending upon definitions, CSA-CSR ranges from 30% to 50% and OSA ranges from 20% to 40%.40, 41, 42

Patients with HF with OSA or CSA-CSR present with significantly higher sympathetic nerve activity while awake, as compared with HF patients and no sleep disordered breathing.43 The negative effects of sleep disordered breathing may cause a more dramatic effect in patients with HF. For instance, the

Treatment of OSA in HF

The precise treatment for OSA depends on its severity, duration, and cause in addition to the patient's age. Obstructive sleep apnea occurs in all age groups with differing contributing factors and thus treatment options. In children, anatomic factors predominate (tonsillar hypertrophy, retrognathia). In adults, weight gain, alcohol, and sleep deprivation predominate causation. In the elderly, complications of underlying medical conditions or their treatment and ageing-related hypotonia of

Treatment of CSA-CSR in HF

Cheyne-Stokes respiration is thought to be a consequence of the failing heart. In accordance to this view, CSA-CSR was abolished in most of the patients with HF after heart transplant.82 In addition, cardiac resynchronization in patients with CHF associated with conduction disturbances83 was able to significantly ameliorate CSA-CSR in conjunction with a significant improvement in heart function.

The effects of drug therapies targeting the failing heart on CSA-CSR are controversial. Solin et al41

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