-慢性心衰中的中枢性睡眠呼吸暂停（- central sleep apnea in chronic heart failure）

1、11-慢性心衰中的中枢性睡眠呼吸暂停（11- central sleep apnea in chronic heart failure）Central sleep apnea in chronic heart failureLi Wei, (90405130), Li Mingjia (90405134), Huang Xiantao (904-5133), Wang Kang (904-5135), Zhang heavy (90405138)Disease physiology experiment 04 groups, 04 basic classesKeywords CHF, CSA,

2、 BNPChronic heart failure (Chronic, heart, failure, CHF) is a heart failure caused by cardiovascular or other multisystem disorders. Heart failure is still a cardiovascular disease with a high morbidity and mortality, and is the leading cause of hospitalization in people over the age of 65. Central

3、sleep apnea (Central sleep, apnea, CSA) is sleep disordered breathing (Sleep disordered, breathing, SDB) a loss generated during the suction process due to the failure of the short central respiratory rhythm, obstructive sleep disorder and expiratory pause (OSA) on the contrary. CSA and OSA are comm

4、on in patients with severe chronic heart failure, and studies have shown that CSA is associated with a significant prognosis for heart failure, whereas OSA is not. CSA and CHF are reciprocal causation, a vicious cycle, which seriously affects the prognosis of patients.This review summarizes the mech

5、anisms of action of CSA and CHF, the clinical symptomatic treatment of CSA, and the new guiding role of BNP in the diagnosis of CHF associated with CSA.Mechanisms of action of 1.CSA and CHF:It includes two aspects: CHF produces and aggravates CSA; CSA aggravates CHF and affects prognosis.Pathogenesi

6、s of 1.1.CSA:The control of respiratory rhythm in 1.1.1. normal body includes two points: the control of the autonomic nervous metabolism system, the control of respiratory rhythm, and the control of the respiratory rhythm by the waking state.The autonomic nervous metabolic system controls respirato

7、ry rhythms, i.e., chemical signals such as changes in CO2 and H+ concentrations that regulate respiration, which is the most sensitive and rapid regulation of respiratory movements.The control of respiratory rhythm in waking state. The human body in the awake state, awakening system located in the b

8、rainstem reticular system by stimulating signal transduction, activation of neurons to activate the upper pons discharge, the respiratory center also located in the brainstem, thereby maintaining the normal respiratory rhythm.In the sleep after the start, reduce the neurotransmitter activity in the

9、respiratory arousal system, thus inhibited the respiratory rate and pulmonary ventilation volume decreased, when the blood Pco2 decreased to a certain value (apnea threshold) below, will stop breathing. Under normal circumstances, the body will be through the negative feedback regulation of autonomi

10、c nervous system metabolism, blood Pco2 increased, thus maintaining normal breathing; and in pathological conditions, sleep at the beginning of the Pco2 in the blood did not increase, more easily reduced to below the threshold, resulting in CSA.1.1.2.CHF acts on the autonomic nervous metabolism syst

11、em and leads to the CSA mechanism:CHF affects many systems and organs, and their combined effect is to cause hyperventilation and reduce Pco2 in the blood and cause CSA.First of all, the compensatory body in patients with CHF due to the increased sympathetic activity, increase catecholamine release,

12、 and catecholamine hormone levels will improve the peripheral chemoreceptor sensitivity increased, leading to ventilation gain respiratory center to increase CO2, lead to excessive ventilation. Hyperventilation results in lower levels of Pco2. When sleep begins, it is easier to fall below the apnea

13、threshold and trigger CSA.Second, CHF leads to decreased cardiac output, blood circulation slows, blood Pco2 changes caused by negative feedback regulation becomes delay, declining respiratory center can not be timely aware Pco2, respiratory control system over the role of hyperventilation, apnea th

14、reshold level of Pco2 dropped to below, causing CSA.Third, CHF with pulmonary edema leading to lung tissue distraction, J receptor and C activation of vagus nerve fiber sensors; at the same time, lung congestion and oxygen diffusion dysfunction, which will increase the ventilation on respiratory ref

15、lect, causing excessive ventilation, the Pco2 below the apnea threshold caused by CSA.The effect of 1.1.3. micro arousal on apnea:Sleep is segmented, such as sleep, sleep in four stages (especially REM sleep), as well as the awakening of central and central segments between each dominant breathing d

16、ifferent sensitivity to chemical stimuli. The apnea and arousal threshold threshold in Pco2 is similar to that of lower end low ventilation caused extreme decline of oxygen saturation will cause arousal, reaction of respiratory center of CO2 increased, triggering hyperventilation, and Pco2 overexpre

17、ssion decreased, triggering another apnea, so as to produce periodic breathing cycle.1.2. CSA worsens CHF:Repeatedly occurs during sleep CSA causes the body to cause hypoxemia, aggravate tissue hypoxia, aggravate myocardial damage, promote heart failure; sleep during repeated arousals can lead to in

18、creased catecholamine release, increase in sympathetic activity, causing heart muscle hypertrophy, necrosis, myocardial contractile performance decreased, aggravate the severity of CHF CSA; intrathoracic negative pressure, right atrial pressure drops, venous return volume increased, increased right

19、ventricular preload, and hypoxia can lead to pulmonary vasoconstriction caused by pulmonary hypertension, increased right ventricular afterload, which promote the development of right heart failure, right heart failure leads to systemic congestion, increased left ventricular afterload and trigger or

20、 aggravation of left heart failure.2.CSA clinical treatmentCSA and CHF promote each other, easy to form a vicious circle. CSA is not only a common clinical symptom of CHF, but also aggravates the condition of CHF and leads to poor prognosis. Therefore, targeted treatment and reduction of CSA can imp

21、rove the prognosis of CHF.Because of the degree of heart failure, location, age, heredity and other factors, the individual difference of CSA treatment is obvious. Different individuals may have different effects on the same treatment. At present, there are many clinical treatment methods, which are

22、 divided into two parts according to the role of the heart and respiratory regulation.2.1. optimize cardiac function:Since CSA is mainly caused by heart failure, optimizing cardiac function plays an important role in the treatment of CSA. (1) diuretics, angiotensin converting enzyme inhibitor use AC

23、EI to a certain extent, improve heart function, so as to relieve the symptoms of CSA patients; (2) recent studies show that the use of cardiac pacemaker also had a positive effect on patients with CSA of stroke patients who install slow atrioventricular synchronization pacemakers, apnea phenomenon h

24、ad moderate relief. The possible mechanism is the pacemaker can cause cardiac output, increased alveolar capillary pressure and ventricular pressure drop, thereby reducing the left ventricular ejection fraction; (3) for serious heart failure patients, heart transplantation for treatment of heart dys

25、function or CSA are good measures. After the body gets a healthy heart, CSA will be completely cured. Of course, because after heart transplantation to individual body fat, and easily lead to obstructive pulmonary hypertension and quality of life related to the suspension of OSA, so the transplant p

26、atients need to pay attention to diet and lifestyle after surgery.2.2. improves respiratory regulation:(1) increase the oxygen breathing at night: a systematic study of causes of chronic heart failure in patients with CSA showed that the increase of oxygen supply to the body at night can effectively

27、 improve the patients with left ventricular ejection fraction, improve the secretion of neuropeptide, or apnea symptoms, the possible mechanism for the act by oxygen free radicals, but the measures can reduce the mortality of patients with heart failure is still unknown; (2) beta blockers: chronic h

28、eart failure caused by central apnea is forming part of the body to CO2 central and peripheral chemoreceptor sensitivity. Beta blockers can remember the sympathetic nervous system, thereby reducing the bodys chemical sensitivity to CO2 and contributing to the treatment of CSA. However, because beta

29、blockers block the formation of N- acetyl -5- by the adrenergic system at the same time, the latter play an important role in maintaining sleep. Thus, beta blockers have adverse effects on sleep, and attention should be given to the use of doses in the treatment of CSA;3 (3): acetazolamide and theop

30、hylline as a respiratory stimulant, which can effectively stimulate respiration, thereby alleviating CSA. The mechanism may be related to the competitive binding of theophylline adenosine receptors, thereby inhibiting the respiratory sedative effect, but not as a conventional drug CSA, because it is

31、 easy to cause the patients with arrhythmia and sudden death; the possible mechanism of acetazolamide for metabolic acidosis leads to the body, thereby reducing the partial pressure of CO2 apnea threshold.2.3. continuous positive airway pressure (Continuous, Positive, Airway, Pressure, CPAP):CPAP is

32、 a non-invasive ventilation treatment. A case study shows that is not consistent with the efficacy of CPAP in patients with CSA in patients with severe reaction, obtained better than CSA in patients with mild symptoms, the treatment measures for chronic heart failure caused by the CSA of patients wi

33、th severe symptoms. The mechanism is not yet clearly understood and may be related to the potentially increased lung O2 capacity. Study on multiple institutions showed no CPAP treatment CSA and reduce the mortality rate of patients, but there is a phenomenon of increased CPAP induced mortality, so n

34、ow for the treatment of CSA still needs further study. Four3., BNP plays a guiding role in the diagnosis of CHF associated with CSABNP (Brain, natriuretic, peptide), brain natriuretic peptide, also called B-type natriuretic peptide (B), is a neuroendocrine substance secreted by ventricular myocytes

35、in the condition of heart failure, atrioventricular dilation and pressure overload. Plasma BNP levels are a highly sensitive indicator of heart failure exacerbations. Peter A. McCullough reported in a 2002 article, will join the plasma BNP in diagnosis of heart failure diagnosis standard, the succes

36、s rate can be increased from 74% to 81%; the plasma level of BNP is higher than 100pg/ml to identify cases of uncertainty, the failure phenomenon is not obvious, the success rate of 74%. OnePlasma BNP levels have important implications for clinical diagnosis of CHF, and Carmen Carmona-Bernal studies

37、 show a specific association between BNP and CHF associated with CSA. Compared with patients with pure heart failure, the plasma levels of BNP in patients with heart failure complicated with central respiratory depression increased significantly, almost three times that of the former. The results re

38、mained significant after controlling for age, sex, and other factors. Plasma BNP concentration has a high specificity and negative correlation with the stability of central respiratory depression complicated by heart failure. 2, therefore, the use of BNP diagnosis can predict the probability of CHF

39、in patients with CSA, and can also be used to distinguish between central respiratory depression caused by heart failure and other causes of central respiratory depression.There is no immediate study of the relationship between BNP levels and central respiratory depression. The causes of BNP elevati

40、on may be: CSA promotes the release of epinephrine, increases heart rate, increases arterial blood pressure, and increases left ventricular afterload. Studies have shown that hypoxia also increases BNP levels in CSA. In addition, BNP has been reported to treat decompensated heart failure, which reduces systemic vascular resistance, pulmonary capillary, central venous pressure, and increases cardiac output. Therefore, BNP is not a simple CHF index, but the specific mechanism is not clear.Although the CSA and BNP related mechanisms are still under study, they may not be directly re