Relationship between congestive heart failure and sleep apnea

How sleep apnea affects the heart - Harvard Health

relationship between congestive heart failure and sleep apnea

Congestive heart failure (CHF) is a disorder associated with an increasing prevalence and a volume are factors which contribute to LV afterload by virtue of the Laplace relationship. Sleep apnoea is commonly found in patients with CHF. Complex sleep apnoea (complexSA) is defined as the emergence of central sleep .. Developed in collaboration with the Heart Failure Association of the ESC. Sleep apnea in congestive heart failure. Naughton MT(1), Bradley TD. Author information: (1)Sleep Research Laboratory, Rehabilitation Institute of Toronto.

Thirty-seven percent of the treatment group patients reported non-serious therapy-related discomfort that was resolved with simple system reprogramming in all but one patient. All prespecified hierarchically tested secondary sleep and quality of life measure endpoints were improved in the treatment group compared to control. In the HF group, tolerability and safety were similar to those of the overall population.

The therapy was well tolerated, with only two patients who were unable to adjust to therapy, and first implant success was high. Procedural complications, including lead dislodgements, were comparable with other implantable devices using transvenous lead technology. However, it might not be appropriate or valid to assume that the effects of ASV on the outcomes of patients with advanced HF also apply to the effects of neurostimulation in a different population.

Exploratory post-hoc analyses of the pivotal trial suggested that indeed the effects of neurostimulation in the subgroup of patients with HF were consistent with the findings in the overall trial population. Specifically, while ASV delivers positive airway pressure, the diaphragmatic contraction triggered by neurostimulation generates negative intrathoracic pressure.

The relationship between congestive heart failure, sleep apnea, and mortality in older men.

In fact, unilateral transvenous stimulation has been the only therapy to show a reduction in sleep-related arousals, which are a manifestation of acute neurohormonal activation. Neurostimulation was associated with an improvement in quality of life measures, whereas ASV was not, suggesting clinical benefits beyond just that of improved sleep variables.

Additional investigation will be warranted to study the hemodynamic effects of negative intrathoracic pressure in patients with HF, as well as trials focusing on cardiovascular outcomes to provide further supportive data. Open ppt Supplemental Oxygen Observational studies in patients with HFrEF have shown that nocturnal nasal oxygen improves CSA, with data suggesting improvement in exercise capacity; decreases in nocturnal urinary norepinephrine excretion; improvement in ventricular arrhythmias, and quality of life.

It can be used along with positive airway pressure therapy, or may also be considered for patients who do not tolerate or fail positive airway pressure therapy. However, oxygen therapy remains contraindicated in patients without hypoxemia, as there can be theoretical detrimental effects to this treatment strategy, such as lengthening apnea duration and accelerating CO2 retention.

relationship between congestive heart failure and sleep apnea

Further randomised controlled trials are needed to determine the role of oxygen in treating sleep apnea in HFrEF. Pharmacologic Therapies Patients who do not tolerate positive airway pressure therapy during sleep may consider treatment with a respiratory stimulant, such as acetazolamide or theophylline.

Acetazolamide is a carbonic anhydrase inhibitor and a weak diuretic. It causes mild metabolic acidosis, which stimulates respiration and is shown to decrease the frequency of central apnea episodes. Knowledge Gaps Randomised control trials are needed to provide further assessment of the role of any sleep apnea intervention on cardiovascular associated morbidity and mortality. Low adherence to CPAP therapy has been a major limitation in clinical trials, and continues to be a dilemma with clinical application of mask-based therapies.

Treatment of CSA with ASV could be harmful, and further trials are needed to determine whether newer generation devices may be of benefit. Unilateral transvenous neurostimulation shows promise for the treatment of CSA, but will need further validation for long-term cardiovascular outcome benefit. Conclusion Our understanding of the causes and subsequent pathological consequences of SDB in HF has been greatly expanded over the past few decades. SDB is now recognised as an important, independent risk factor for the development of incident HF, worsening HF status, and reduced survival in patients with HF.

Unfortunately, SDB is often under-recognised, and not tested for routinely; and yet, we know that treatment can improve outcomes in these patients. Vigilance in diagnosis, testing, and treatment is paramount in this population.

Therapies for CSA remain more complex. Because the pathological consequences of CSA are known to worsen HF, treatment strategies remain vital to management. Optimising medical therapy as first approach remains of utmost importance, as research has shown that often when HF is clinically improved, CSA often improves as well. However, limitations of this study with utilisation of older generation devices and limited treatment algorithms still pose several questions.

Future randomised control trials with unilateral transvenous neurostimulation for HF should be powered to determine cardiovascular outcomes. Mechanisms and clinical consequences of untreated central sleep apnea in heart failure. J Am Coll Cardiol ; Changes in the venous return and transmural cardiac pressure, however, may still occur. One cannot discount the impact of this vigorous respiratory effort in a patient with systolic heart failure.

In one study, improvement in respiratory muscle workload in patients with heart failure and CSA was associated with improvement in left ventricular ejection fraction. Several small studies have demonstrated a link between CSA and poor outcome in patients with heart failure, including an effect on mortality.

In these patients, the low cardiac output state would have persisted despite optimal management of the underlying heart failure. These are precisely the patients who have poor prognosis but who are also likely to derive symptomatic benefit from identification and treatment of the concomitant CSA. The impact of treatment of CSA on survival will require large, randomized controlled trials.

Prevalence and Presentation of Central Sleep Apnea in Patients with Heart Failure Studies of the prevalence and distribution of SDB in heart failure yielded widely varying estimates depending on the population studied. Earlier studies evaluated only65 or predominantly49 elderly males with severe systolic dysfunction. It is likely that patients with heart failure and CSA will report sleepiness. Fatigue, sleepiness, reduced physical activity level, and impaired cognitive function may be due to either CSA or heart failure.

The symptoms therefore do not aid in determining which patients to screen for SDB. As such, it is imperative to maintain a very high index of suspicion for this diagnosis. In patients with heart failure, risk factors for CSA include lower left ventricular ejection fraction, more dilated myocardium, and male age.

The severity of CSA is correlated with severity of the underlying systolic dysfunction. When a heart failure patient is diagnosed with CSA, it is likely that the patient will already be on optimal treatment and will require additional treatment targeted to CSA. Improvement in CSA was reported with atrial overdrive pacing,77 likely due to the associated increase in cardiac output.

relationship between congestive heart failure and sleep apnea

Similarly, improvement in CSA occurs with cardiac resynchronization,78,79 probably due to improved underlying cardiac output. They confirm that optimal treatment, whether pharmacological or electromechanical, of underling heart failure will improve the associated CSA.

CPAP and other forms of positive airway pressure exert additional effects on cardiovascular function in patients with heart failure, including decreased respiratory and cardiac muscle workload,39 improved myocardiac contractile efficiency,81 and increased left ventricular ejection fraction. Earlier underpowered trials suggested that CPAP was beneficial in this setting. The results of this trial, however, were negative and there was no survival benefit for treatment with CPAP in patients with systolic dysfunction and CSA.

Adaptive Pressure Support Servo Ventilation This is a new modality of ventilatory support that delivers baseline-positive airway pressure along with machine-generated breaths during central apneas. These devices are equipped with sensitive sensors that can detect central apneas. Therefore, the mechanism of effect of this modality is by preventing the increase in PaCO2 during the apnea and subsequently preventing the hyperventilation that follows the apnea, in effect breaking the periodic breathing cycle.

Several small trials have demonstrated significant benefit of adaptive pressure support servo ventilation ASV in eliminating central events, increasing left ventricular ejection fraction, and improving quality of life.

Bilevel-positive airway pressure has also been used effectively in small trials to treat CSA. Oxygen Therapy Given that the primary lesion in CSA responsible for the cardiovascular consequences is intermittent hypoxia, it is logical to expect that nocturnal oxygen may be an effective treatment in preventing sympathetic activation.

Moreover, supplemental oxygen will improve the oxygen store in patients with heart failure, subsequently dampening the ventilatory response to the increase in PaCO2 during apnea.

Another possible mechanism of action would be a direct effect on the peripheral chemoreceptors, decreasing their background chemosensitivity to PaCO2and dampening the ventilatory overshoot following apnea-induced hypercapnea.

Subsequently, oxygen therapy is not the standard of care for these patients. The effectiveness of these modalities was demonstrated in small human trials, but safety and efficacy have not yet been evaluated in randomized controlled trials. These approaches, therefore, are not all part of current clinical practice.

Sleep-Disordered Breathing Congestive Heart Failure

Respiratory Stimulants Respiratory stimulants such as theophylline have been suggested for the treatment of CSA in heart failure. Proposed mechanisms include increased ventilatory responsiveness below eupnea, resulting in increased proximity between eupneic PaCO2 and the apnea threshold. Other potential mechanisms include a stimulatory effect on cardiac function, which is a concern. This has limited the use of theophylline in clinical practice. Only one double-blinded crossover study has examined the short-term effects of theophylline on CSA in 15 patients with stable heart failure.

Compared with placebo, theophylline decreased the central events and the severity of oxygen desaturation, but without improvement in left ventricular ejection fraction. Acetazolamide induces metabolic acidosis and has a stimulatory effect on ventilation, increasing the proximity between the eupneic PaCO2 and the apnea threshold. The potential for urinary potassium wasting leading to hypokalemia and increased arrhythmia risk with acetazolamide remains a serious concern.

The role of acetazolamide in the long-term treatment of CSA has yet to be determined. Administration of small doses of exogenous CO2 directly or indirectly by increased dead space is another intriguing treatment modality for CSA.

CO2 is a respiratory stimulator that can stabilize the breathing pattern. Again, long-term adequately powered trials are lacking and preclude consideration of this modality. Furthermore, the practicalities of delivery and safety remain cardinal concerns with this treatment option.

The mechanism of action was presumed to be a decrease in arousal-related ventilatory overshoot. Early pilot reports showed a decrease in the number of nocturnal arousals, but no change in the severity of respiratory events or nocturnal oxygen desaturation was found.