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Congestive heart failure and CPAP.

Heart failure occurs when the ventricles pump out diminished amounts of blood. Ventricular action can be hindered: 1) if an excessive amount of blood is allowed to enter the ventricles (i.e., volume overload); 2) if heart tissue is damaged by infarction; or 3) if too little blood enters the ventricles. Mitral valve prolapse and atrial fibrillation are conditions which can result in heart failure. Mitral valve prolapse allows overfilling of the ventricle and atrial fibrillation reduces the amount of blood entering the ventricles.


Usually, heart failure involves the left ventricle but the right ventricle or even both ventricles can be involved. With the ventricles unable to expel blood efficiently, surplus blood remains in the heart. This surplus creates increased hydrostatic pressure in the heart vessels, pulmonary vessels, and other vessels throughout the body. Increased hydrostatic pressure causes fluid to flow out of the vessels into interstitial tissue. The result is a build up of fluid in the lungs (i.e., pulmonary congestion) or limbs (i.e., edema). Heart failure that involves pulmonary congestion and/or edema is, of course, congestive heart failure.

People with congestive heart failure have an increased incidence of sleep problems. A study by Erickson et al. in which CHF subjects completed a sleep survey, found that 56% of the subjects had sleeping difficulties; about 30% used sleeping medications; 51% had trouble sleeping flat; 44% had restless sleep; 40% had trouble going to sleep; and 39% awoke early. Polysomnographic studies of people with CHF find that sleep architecture is altered by sleep-disordered breathing (particularly the alternating pattern of waxing and waning breaths of Cheyne-Stokes respiration) and frequent non-respiratory related arousals.

Many of these sleep problems result from the fact that congestive heart failure induces activation of the sympathetic nervous system. With sympathetic activation increased, a person has difficulty initiating and maintaining sleep and has frequent arousals from sleep. A beneficial effect of sympathetic activation is that it initially counteracts congestive heart failure by increasing heart rate and strengthening heart contractions. But later, the chronic activation can result in the depletion and destruction of the sympathetic nerve terminals. This can worsen heart function by impairing the heart's ability to contract and relax rhythmically. Currently, vasodilators, diuretics, and inotropic drugs are used to treat CHF but a common treatment for sleep apnea may soon be added to the treatment regimen. Recent studies show that both continuous and bi-level positive airway pressure (CPAP, BiPAP) can improve heart function as well as sleep in people with CHF.

A study by Matthew Naughton et al. examined the effects of CPAP on sleep and heart function in CHF subjects. They had 9 CHF subjects use nasal CPAP in addition to standard drug treatment while 9 other CHF subjects remained on standard therapy alone. Both groups had a baseline study and then were reassessed one month later. When the subjects were reassessed, Naughton et al. found that: 1) total sleep decreased by 2% in the standard therapy group but increased by 3% in the CPAP group; 2) the amount of arousals decreased by 10% in the standard therapy group but decreased by 37% in the CPAP group; and 3) heart function as reflected by left ventricular ejection (percentage of blood ejected from the ventricles per contraction) decreased by 5% in the standard therapy group but increased by 38% in the CPAP group. These results show that CPAP improves heart function and improves sleep in people with CHF.

They also measured the all-night (i.e., 8-hour) urinary levels of the, catecholamines epinephrine and norepinephrine in the subjects. At the outset of the study, the epinephrine and norepinephrine levels were high in both groups. This suggested activation of the sympathetic nervous system since catecholamines rise with sympathetic activation. After 30 days, the epinephrine and norepinephrine levels fell dramatically in the CPAP group but remained close to their baseline levels in the standard treatment group. Naughton et al. believe that the nocturnal reduction in epinephrine and norepinephrine levels in the CPAP group reveals that CPAP induced an overall reduction in sympathetic activity.

Exactly how positive airway pressure reduces sympathetic nerve activity is unknown but scientists have been debating several ideas. One, CPAP may reduce sympathetic activation by causing a resetting of baroreceptor sensitivity. Baroreceptors (pressure-sensitive receptors found in major vessels such as the aorta) trigger sympathetic activation when blood pressure is decreased and triggers or sympathetic deactivation when blood pressure is increased. This reflex appears to be altered in people with CHF the sympathetic system remains activated even though a higher-than-normal pressure exists in the aorta in people with CHF. It may be that CPAP allows the baroreceptors to return to a more normal function. Two, CPAP may reduce sympathetic activation by increasing intrathoracic pressure. It is thought that increased intrathoracic pressure pushes against the ventricles thereby helping to reduce their work in expelling blood. Three, CPAP may reduce sympathetic activation by improving hemodynamics. Changes in blood gases (i.e., hypoxia, hypercapnia) resulting from Cheyne-Stokes respiration or other respiratory disturbances triggers sympathetic activation. CPAP, by counteracting sleep-disordered breathing, may help improve hemodynamics reducing sympathetic activation.

Recent studies have investigated the effect of BiPAP on heart failure. Christian Guilleminault et al., for example, found that BiPAP but not CPAP improved sleep in 5 CHF subjects. On the average, subjects had a total sleep time of 5.7 hours, 19 respiratory events/hour, sleep efficiency of 67% and 19 arousals/hour. When the subjects were given CPAP treatment, they continued to have respiratory events (hypopneas) and arousals. Guilleminault et al. then tried the patients on BiPAP. Total sleep time increased to 6.4 hours and subjects averaged 3 respiratory events/hour. Before treatment, cardiac arrhythmias averaged 2-10 events/minute. BiPAP treatment reduced arrhythmias to 44 events for the sleep period. Guilleminault et al. concluded that BiPAP may be more beneficial than CPAP in some people with CHF.

Andrea Bellone et al. compared the ability of BiPAP vs. CPAP to reduce CHF. They found that both versions of positive airway pressure had equal ability to improve heart function. For example, CPAP increased LVEF from 18.8% to 23.6% and BiPAP increased LVEF from 18.7% to 22.8%.

Drug therapy for CHF work by reducing the amount of blood entering the heart (vasodilators, diuretics) or by strengthening heart contractions (inotropic drugs). Unfortunately, each class of drugs has side effects which can make treatment or compliance with a treatment plan difficult. Vasodilators (e.g., captopril) can result in postural hypotension (sudden reduction of blood pressure on standing), a persistent dry cough, renal insufficiency, and high blood calcium. Loop diuretics (e.g., furosemide) can cause impaired hearing, increase blood levels of uric acid (thereby bringing on attacks of gout), deplete potassium, cause hypotension, and cause heart arrhythmias. Thiazide diuretics (e.g., hydrochlorothiazide) have the same adverse effects as the loop diuretics and additionally may increase blood sugar in diabetics and increase blood calcium levels. Inotropic drugs (e.g., digoxin) are toxic and can result in severe arrhythmias, nausea, vomiting, anorexia, and dizziness.

CPAP/BiPAP treatment can improve heart function without these adverse effects. Potentially, this means that CPAP/BiPAP may be another treatment option if a person is unable to tolerate certain drugs used to treat CHF. Research on the use of CPAP/BiPAP in people with CHF continues. Current results look promising but more studies are needed to reveal the extent that CPAP/BiPAP increases survival rate and improve the quality of life of people with CHF.

For notes and references, please feel free to contact the author, Regina Patrick, via e-mail at

by Regina Patrick RPSGT
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Title Annotation:SLLEP MEDICINE
Author:Patrick, Regina
Publication:FOCUS: Journal for Respiratory Care & Sleep Medicine
Date:Jun 22, 2004
Previous Article:Pleural effusion--a review.
Next Article:A study to evaluate the competency of ICU personnel in mechanical ventilation.

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