Chronic systolic heart failure (CHF) is a complex clinical syndrome with shortness of breath, fatigue, and decreased cardiac function as the main manifestations. Sleep disordered breathing is also a more common disorder, which can also be complicated by CHF at a later stage. It is not uncommon for CHF to be combined with sleep disordered breathing, but because some symptoms of CHF mask some symptoms of sleep disordered breathing, only the diagnosis of CHF is recognized clinically, and the combined sleep disordered breathing is often missed, and breakthroughs have been made in the research of CHF combined with sleep disordered breathing in the past 10 years or so. This paper is intended to review the progress of research in this field to improve clinical understanding and benefit the majority of patients. Epidemiological studies The prevalence of CHF in the general population is 0.3%-2%, and up to 3%-13% in people aged 65. The prevalence of sleep breathing disorders, especially obstructive sleep apnea hypoventilation syndrome (OSAHS), is also common, with a prevalence of 1% to 5% in the population. 40% to 60% of patients with CHF have a combination of sleep breathing disorders, mainly central sleep apnea (CSA), including Chen-Schiff’s respiration (CSR), and a few have a combination of obstructive (OSA) or mixed (MA) sleep apnea. S Javaheri et al. observed 81 patients with stable CHF with left ventricular ejection fraction (LVEF) <45%, 40% with combined CSA and 11% with combined OSA, while Joseph Chan et al. observed 20 patients with diastolic CHF, 11 of whom (55%) had combined sleep apnea (SDB). The patients were more obese with a body mass index (BMI) of (28±3.2) kg/m2 and still had predominant CSA (7 cases, 63.6%). Hooker et al. applied polysomnography (PSG) to monitor 42 elderly patients with stable CHF, and the mean apnea hypoventilation index (AHI) was (48.6±16.3) breaths/h, including 11 cases (36.1%) with OSAHS and AHI (10.7±9) breaths/h, and 19 cases (45.2%) with CSA and AHI (37.9±10.5) breaths/h. The same abnormal respiratory pattern was described again by Stokes in 1854. CSR is typically characterized by a gradual increase in the volume of breath (tidal volume), followed by a decrease, and finally by apnea or hypoventilation, which occurs continuously, also known as periodic breathing. CSR mostly occurs in non-rapid eye movement sleep stages I and II and can last 15-130 seconds, while apnea lasts more than 5-60 seconds, and awakening often occurs when the amplitude of inspiration reaches its maximum. Patients with acute heart failure (ACF) may even experience CSR during the daytime waking state, but studies have found that it is not an indicator of the severity of the condition. Some CSA can occur suddenly without the typical CSR, which is most often seen in patients with severe chronic systolic heart failure, but also in acute heart failure, cerebrovascular disease, neonates, and normal individuals who are new to the plateau. The mechanism of combined CSR or CSA in patients with CHF is still not well understood and may be related to the level of stored oxygen (O2) and carbon dioxide (CO2) in the body, but the two have different affinities for tissues, with larger stores of CO2 and relatively smaller stores of O2. The larger stores of CO2 provide a greater buffer, resulting in more stable arterial blood gas values when transient changes in ventilation occur. However, patients with CHF have reduced functional residual gas volume due to pulmonary vascular congestion, which results in a reduction in both the body's O2 and CO2 stores, making the respiratory system more unstable, with larger changes in arterial partial pressure of oxygen (PaO2) and partial pressure of carbon dioxide (PaCO2) when transient changes in ventilation occur. The individual's ventilatory response to hypercapnia leads to overcompensation of respiration and the development of secondary hypocapnia. Thus, hyperventilation-mediated hypocapnia is an important determinant of combined periodic breathing in patients with CHF. CSR is typically initiated by a single arousal accompanied by a deep, large breath, resulting in an increase in tidal volume and a sudden, large drop in PaCO2, and arousal-mediated hyperventilation may also be an initiating factor for idiopathic CSA. As cardiac output decreases, pulmonary congestion increases, prolonging the conduction time between the lungs and chemoreceptors that occurs between the endothelium of the alveolar capillaries exchanging gas and the peripheral chemoreceptors (carotid bodies), which delays the feedback of information from the peripheral chemoreceptors to the medulla oblongata, thus leading to instability of the gas self balance and the occurrence of periodic breathing. In addition, temporally related cyclic alterations in brain, respiratory and cardiovascular function resulting from changes in the nature of central nervous activity may also play a role in the pathogenesis of CSR. On the one hand, CSR aggravates the degree of hypoxia and myocardial damage; on the other hand, prolonged circulation time, increased extravascular fluid and decreased tissue perfusion trigger abnormal respiratory responses, which form a vicious circle with each other. Clinical manifestations Patients with CHF are often combined with sleep apnea, often with frequent awakening at night, paroxysmal dyspnea, decreased sleep quality, decreased total sleep time and decreased sleep efficiency despite increased bedtime. Due to the psychological fear caused by nighttime sleep fragmentation and frequent awakening of hypoxemia, many patients complain of insomnia, difficulty in falling asleep, and a series of symptoms such as fatigue, snoozing and drowsiness during the day. Snoring is mostly seen in obese patients with combined OSA, while it is rare in patients with CSA-CSR. The sleep of healthy elderly people without sleep disorders compared with young people, that is, suggests the characteristics of difficulty in falling asleep and maintaining sleep, rapid eye movement sleep, slow wave sleep, reduced total sleep time, and increased nocturnal awakenings, while the above sleep changes are more obvious in elderly CHF patients. Treatment Pharmacological treatment: oxygen, theophylline and angiotensin inhibitors (ACEI) such as captopril can reduce further myocardial injury, increase left ventricular ejection fraction and cardiac output, reduce left ventricular volume and pulmonary capillary wedge pressure, reduce sympathetic hyperexcitation, shorten pulmonary circulation time, reduce pleural effusion and pleural exudation, increase functional residual air, reduce or eliminate hyperventilation, and make ventilation during sleep Stability is improved. Wash et al. studied eight patients with mild to moderate heart failure, and the mean AHI decreased from 35 to 25 times/h after using captopril. Non-pharmacological treatment: In recent years, the clinical application of transnasal non-invasive positive pressure ventilation (NPPV) in the treatment of CHF has made a breakthrough, which not only improved the patients' It not only improves patients' symptoms, improves the quality of survival, but also improves the prognosis and reduces the morbidity and mortality rate. Sin DD et al. observed that in 14 patients with CHF combined with CSR or CSA treated with continuous positive pressure ventilation (CPAP) for 3 months, the left ventricular ejection fraction increased from 20.6% to 23.1%, and the 5-year combined death and heart transplantation rate was 29% (49% in the control group). Several investigators have also suggested that AHI is strongly correlated with the prognosis of clinically stable CHF, that patients with AHI >30 beats/h have a high risk of subsequent cardiac death, and that CHF with CSR has a higher morbidity and mortality rate than patients without CSR during sleep. ◆ Conclusion CHF has a higher prevalence of CSR or/and CSA. Patients with CHF with CSR or CSA have more pronounced hypoxemia or hypocapnia, which further aggravates the damage to the heart and central nervous system and increases mortality in CHF, and appropriate pharmacological treatment can improve the symptoms. Transnasal NPPV treatment not only improves patients’ symptoms and quality of survival, but also improves the long-term prognosis and reduces the morbidity and mortality rate of CHF patients.