Congestive heart failure (CHF) is a common problem, often presenting
with shortness of breath or fatigue as its primary symptoms. It
increases in frequency with age. There are 40,000 deaths and close
to one million hospitalizations annually in the United States from
heart failure. Smoking is a shared risk factor for both ischemic
heart disease, which leads to heart failure, and COPD. It may be
difficult to distinguish which of these disorders is causing problems
with sleep when the diseases coexist. Many patients with advanced
CHF describe fatigue, lack of energy, tiredness, or weakness with
exercise. A smaller number complain of sleepiness and drowsiness.
Cheyne–Stokes respiration, a type of central sleep apnea
characterized by an absent ventilatory effort with a waxing and
waning breathing pattern, is associated with excess mortality in
CHF. As many as 40–45% of people with heart failure
from systolic dysfunction may have the Cheyne–Stokes form of
central sleep apnea. Management of central sleep apnea in these
patients is an important component of their heart failure therapy,
and improves outcome.
Central apneas are defined as cessation of breathing without
any respiratory muscle effort. They appear to result from loss of
ventilatory drive. Carbon dioxide retention is rare. Hyperventilation leads
to hypocapnia and subsequent hypopnea or apnea until the arterial
carbon dioxide pressure (Paco2)
rises. Arousals from sleep are common during the hyperventilation
phase after a central apnea. These arousals lead to fragmented sleep
and subsequent daytime sleepiness. A hyperadrenergic state, common
in heart failure and sleep apnea, appears to worsen heart failure
itself. When lying in the supine position edema fluid that has pooled
in the legs during the day returns to the circulation and predisposes
patients with heart failure to pulmonary edema at night.
General symptoms of heart failure include shortness of breath
with exertion, fatigue, and often daytime sleepiness. Dyspnea may
worsen at night either as orthopnea or paroxysmal nocturnal dyspnea
(PND). Symptoms that awaken patients with heart failure exacerbation
are often nonspecific and may be difficult to distinguish from a
COPD exacerbation, a primary sleep disorder such as sleep apnea,
or a response to medications that interrupt sleep. A common presentation
of Cheyne–Stokes breathing in CHF is trouble staying asleep,
termed sleep maintenance insomnia. This is often characterized as
gasping, grunting, or choking during sleep, accompanied by frequent
body movements. After a sleepless night, daytime sleepiness ensues.
Frequent Cheyne–Stokes respirations are noted in up to
45% of patients with a low ejection fraction. Obstructive sleep
apnea is also seen in patients with heart failure.
Physical findings associated with a diagnosis of heart failure
include tachycardia, a diffuse point of maximal impact on cardiac
palpation, an S3 gallop, distant heart sounds, crackles in the lung bases,
jugular venous distention, hepatojugular reflux, tricuspid regurgitation,
ascites, and dependent edema. Although hypoxemia is often present
during sleep, many patients with severe central sleep apnea and
Cheyne–Stokes respiration do not desaturate below 90% oxygenation.
Techniques that quantify cardiac ejection fraction can confirm
left ventricular heart failure but are nonspecific with regard to
whether Cheyne–Stokes breathing is the cause of sleepiness.
These techniques include echocardiogram, nuclear medicine-gated
blood pool scan, and cardiac catheterization.
Oximetry at night is frequently used to identify oxyhemoglobin
desaturation. However, even with severe central apneas, oxygen saturation
may be preserved. This technique will not detect many patients with
central sleep apnea, and therefore is not recommended as a screening
tool for this condition. Polysomnography, an 18-channel sleep study,
is the recommended procedure if central sleep apnea is suspected.
Both central and obstructive sleep apnea can be diagnosed in patients with
heart failure with these studies. Other sleep study findings in
heart failure include light sleep and frequent arousals.
Diagnostic considerations for sleep problems in people with CHF
include obstructive sleep apnea, asthma, or COPD exacerbations.
Nocturnal ischemia can be difficult to distinguish from heart failure.
Additionally, medications used to treat CHF, hypertension, or hyperlipidemia
occasionally lead to insomnia. These include β-blockers
and statin medications used to treat hyperlipidemia. Cheyne–Stokes
respiration/central sleep apnea may be from causes other
than a low ejection fraction including cerebral disorders, uremia,
and dwelling at high altitude.
Treatment of heart failure with medications including β-blockers,
angiotensin-converting enzyme inhibitors, or angiotensin receptor
blockers may lessen the central apneic episodes and improve sleep
complaints. Some patients with CHF require diuretics such as furosemide.
Treatment of nocturnal ischemia, if present, with nitrates or calcium
channel blockers is also beneficial.
Oxygen therapy or continuous positive airway pressure (CPAP)
is a therapeutic option specific for central apnea once treatment
of heart failure has been optimized. Oxygen has been a mainstay
of treatment but is not universally successful. CPAP can be difficult
to implement but is often recommended as the treatment of choice,
improving the prognosis of CHF with central apnea. Clinical trials
are currently underway to further assess its efficacy. Bilevel mask
therapy (BiPAP, VPAP, and others) differs from CPAP in that there
is both a set inspiratory and expiratory pressure. It is sometimes
advocated in patients with CHF, but clinical trials of efficacy
are lacking. Another treatment option is theophylline. Alternatively,
benzodiazepines or other short acting hypnotic drugs such as zolpidem
have been tried to diminish the degree of hypocapnia and rebound
hypercapnia, prevent arousals, and promote sleep, but good clinical
data for this approach are lacking. If obstructive apnea coexists
with heart failure, assessment and treatment of this with weight
loss and CPAP therapy can lessen nocturnal hypoxemia.
The overall prognosis of CHF has improved with the use of after-load-reducing
(hydralazine/nitrates, angiotensin-converting enzyme inhibitors,
angiotensin receptor blockers) and β-blocking drugs.
Preservation of cardiac function and survival are both improved
with these treatments. Persons with Cheyne–Stokes breathing
and heart failure have a higher mortality than patients with heart
failure without central sleep apnea, however, this poor prognosis
can be improved with CPAP treatment. Specific improvements include
a lower mortality and decreased need for transplantation in patients
with Class III and IV heart failure and Cheyne–Stokes respiration.
Javaheri S: Treatment of central sleep apnea in
heart failure. Sleep 2000;23(Suppl 4):S224.
(The authors report a more detailed discussion of central sleep
apnea in heart failure and include methods of treatment.)
Sin DD et al: Effects of continuous positive airway pressure
on cardiovascular outcomes in heart failure patients with and without
Cheyne-Stokes respiration. Circulation 2000;102:61.
(This article indicates improved cardiac function and a trend to
improved mortality and transplantation rates for patients with heart
failure treated with continuous positive airway pressure.)
Yamashiro Y, Kryger MH: Review: sleep in heart failure. Sleep
of sleep and heart failure are discussed.)