Ventilation Parameters under Adaptive Servo Ventilation: A Comparison on Behalf of CSA-Pattern, BNP/NT-pro-BNP, and Ejection Fraction.

BACKGROUND: The SERVE-HF study has raised questions concerning the higher mortality under adaptive servoventilation. The ventilatory mode was discussed as a possible aggravating factor. OBJECTIVES: We wondered if the data recorded by the adaptive servo-ventilation (ASV)-devices in heart failure patients with CSA-CSR ± OSA are different in terms of respiratory parameters and therapeutic pressures compared to patients with CPAP-resistant/emergent-CSA with normal BNP/NT-pro-BNP. METHODS: Patients were included, if ASV had normalized respiratory disturbance index in the first night of application and after at least 6 weeks. ASV-device data were analyzed in terms of respiratory rate (RR), min ventilation (MV), endexpiratory (EEP), peak inspiratory pressure (Ppeak) and median pressure. RESULTS: Compared to CPAP-resistant/emergent-CSA with normal BNP/NT-pro-BNP (n = 25), CSA-CSR- (n = 13) CSA-CSR+OSA-patients (n = 32) with elevated BNP/NT-pro-BNP had higher RR (p < 0.01) in the first night of ASV therapy and during follow-up (15.3 ± 1.3 vs. 17.3 ± 2.4/min) with similar MV (6.5 ± 1.3 vs. 6.6 ± 1.3 L), resulting in significantly lower tidal volumes. EEP (5.6 ± 1.1 vs. 5.5 ± 1.1 hPa), Pmedian and Ppeak (9.8 ± 1.5 vs. 9.7 ± 1.2 hPa) were comparable. Ventilatory parameters were not different between LVEF < 40, 40-49, and ≥50%, neither within the whole group nor the group of CSA-CSR ± OSA and heart failure. CONCLUSION: Patients with heart failure and CSA-CSR ± OSA have higher RRs but similar MV under ASV-therapy than patients with CSA and normal BNP. This indicates higher dead space ventilation. EF was not found to have an influence on the ventilatory parameters.

Acetazolamide attenuates Hunter-Cheyne-Stokes breathing but augments the hypercapnic ventilatory response in patients with heart failure.

RATIONALE: Acetazolamide has been used to attenuate Hunter-Cheyne-Stokes breathing with central sleep apnea (CSA) associated with heart failure. However, the mechanisms underlying this improvement remain to be fully elucidated. OBJECTIVES: We hypothesized that acetazolamide stabilizes CSA by attenuating the ventilatory sensitivity to CO2, which is increased in patients with heart failure and is thought to be the major mechanism mediating CSA. METHODS: Six consecutive male patients with stable systolic heart failure and CSA (apnea-hypopnea index [AHI] ≥ 15 episodes/h) were randomized to a double-blind crossover protocol with acetazolamide or placebo received 1 hour before bedtime for six nights with 2 weeks of wash-out. Under both conditions, we measured the hypercapnic ventilatory response (HCVR), arterial blood Pco2, steady-state metabolic CO2 production, overnight attended polysomnography, and also assessed cardiac and pulmonary function. MEASUREMENTS AND MAIN RESULTS: Compared with placebo, acetazolamide significantly decreased the AHI (65 ± 32 vs. 31 ± 19 events/h, mean ± SD). Acetazolamide increased the HCVR slope by 55% (3.3 ± 1.7 vs. 5.1 ± 2.4 L/min/mm Hg; P = 0.03), an increase that far exceeded the 12% fall in arterial Pco2 (P = 0.02). The acetazolamide-induced change in the balance of these effects (ΔHCVR × Pco2) was inversely associated with the reduction in AHI (r = 0.8; P = 0.045). CONCLUSIONS: This placebo-controlled study indicates that acetazolamide improves CSA in patients with heart failure despite an increase in the slope of the HCVR. However, because the degree of HCVR elevation inhibits the improvement in unstable breathing, an increased CO2 chemosensitivity may be a key mechanism underlying an incomplete resolution of CSA with acetazolamide.

C-reactive protein is elevated in heart failure patients with central sleep apnea and Cheyne-Stokes respiration.

BACKGROUND: Manifestation of central sleep apnea (CSA) with Cheyne-Stokes respiration is of major prognostic impact in chronic heart failure (CHF). Inflammatory processes have been linked to a progression of cardiovascular diseases, including heart failure. While an association of C-reactive protein (CRP) levels to obstructive sleep apnea has been documented before, there is a lack of information regarding variation of CRP levels in patients with CSA. OBJECTIVES: The objective of this study was to investigate a potential association of CRP levels to CSA severity in CHF patients. METHODS: High sensitivity CRP levels were analyzed in 966 patients with CHF (BMI 26.3 ± 4.6, New York Heart Association class 2.6 ± 0.5, left ventricular ejection fraction 29.4 ± 7.9%, N-terminal pro-brain natriuretic peptide, NT-proBNP, level 2,209 ± 3,315 pg/ml) without sleep-disordered breathing (SDB; Apnea-Hypopnea Index, AHI, <5/h) or various degrees of CSA, documented by in-hospital cardiorespiratory polygraphy or polysomnography. RESULTS: The CRP concentration in CHF patients was 0.550 ± 0.794 mg/dl in patients without SDB (AHI 0-4/h, n = 403) versus 0.488 ± 0.708 mg/dl in patients with mild CSA (AHI 5-14/h, n = 123, p = n.s.) and 0.660 ± 0.963 mg/dl in patients with moderate CSA (AHI 15-29/h, n = 160, p = n.s.). In patients with severe CSA (AHI ≥ 30/h, n = 280), significantly higher CRP concentrations were documented (0.893 ± 1.384 mg/dl, p < 0.05). Stepwise regression analysis revealed AHI, NT-proBNP and heart rate to be independently associated with elevated CRP levels. CONCLUSION: Severe CSA in CHF patients is associated with elevated levels of CRP, a systemic marker of inflammation and cardiovascular risk. This might explain in part the negative prognostic impact of CSA in these patients.

[Influence of adaptive servoventilation on B-type natriuretic petide in patients with Cheyne-Stokes respiration and mild to moderate systolic and diastolic heart failure]. / Einfluss der Adaptiven Servoventilation auf das BNP bei Patienten mit Cheyne-Stokes-Atmung und leicht- bis mittelgradiger systolischer und diastolischer Herzinsuffizienz.

BACKGROUND: CPAP therapy has a variable effect on central sleep apnea with Cheyne-Stokes respiration (CSA-CSR). Adaptive servoventilation (ASV) is more effective in normalising breathing in patients with heart failure. We hypothesised that, by normalising AHI, ASV reduces elevated BNP levels in patients with mild systolic and diastolic heart failure. METHODS: From April 2004 to October 2006, patients with CSA-CSR with and without concomitant obstructive sleep apnea (OSA), clinical evidence of heart failure, regardless EF, and elevated BNP levels (> 100 pg/mL) were selected for treatment with ASV, unless CPAP therapy had reduced AHI to < 15 per hour of sleep. Follow-up polysomnographies and BNP analyses were performed after 6 weeks. RESULTS: 15-male patients (AHI 48.3 +/- 14.6/h) fulfilled all inclusion criteria; 7 patients had CSA-CSR + OSA, 8 had CSA-CSR. After 6 weeks of ASV, BNP decreased from 415 +/- 196 pg/mL to 264 +/- 146 pg/mL (p = 0.0009). There was only a significant BNP reduction in the CSA-CSR+OSA subgroup (p = 0.0002). CONCLUSION: ASV can normalise AHI in patients with mild systolic and diastolic heart failure and CSA-CSR +/- OSA, thus leading to a significant reduction of BNP levels. These findings suggest that effective suppression of sleep apnoea in such heart failure patients improves cardiac function.

[Acute effects of adaptive servo-ventilation therapy on neurohormones and Cheyne-Stokes respiration in the patients with heart failure]. / Kalp yetersizligi olan hastalarda adaptif servo-ventilasyon tedavisinin nörohormonlar ve Cheyne-Stokes solunumu üzerine akut etkisinin degerlendirilmesi.

OBJECTIVE: Cheyne Stokes respiration (CSR) is frequently seen in the patients with heart failure (HF) and it increases mortality. In the present study, we aimed to evaluate acute effects of adaptive servo ventilation (ASV) on CSR and neurohormones in the patients with HF. METHODS: Nineteen males and 1 female patients with HF in the functional capacity of NYHA II-III were included into the study prospectively. One night polysomnography (PSG) was performed to all patients. In addition to medical treatment, 10 patients having CSR were applied ASV in another night together with PSG.. Arterial blood gases, plasma epinephrine and norepinephrine, serum N-terminal -pro-B type brain natriuretic peptide (NT-pro-BNP) were studied in the first night and after ASV treatment. A Wilcoxon test was used for comparison of parameters before and after treatment;and Mann-Whitney-U test was used for comparison of parameters between the patients with CSR and without CSR. RESULTS: Mean age of 10 patients with CSR was 62.2+/-11.1 years. Their etiologies were ischemic in 9 patients and idiopathic dilated cardiomyopathy in 1 patient. While there were no significant differences in the levels of PaCO2, HCO3, PH, before and after treatment; PaO2 (75.3 mmHg) and SatO2 (94.7%) significantly increased after the therapy (84.7 mmHg, 96.5% and p=0.007 and p=0.008 respectively). While NT-proBNP (3029.6+/-1450.5 pg/ml), norepinephrine (625.4+/-304.7 pg/ml) and epinephrine (65.4+/-24.1 pg/ml) were higher than normal before ASV treatment, all of them showed significant reductions after treatment (1694.0+/-925.9 pg/ml, 333.9+/-165.4 pg/ml and 45.0+/-20.5 pg/ml; p=0.005, p=0.005 and p=0.02, respectively). CONCLUSION: One night ASV treatment improves CSR, partial pressure of oxygen in arterial blood, and oxygen saturation and provides significant reductions in plasma catecholamines and NT-proBNP levels in the patients with HF and CSR. Prospective studies are needed to evaluate long-term effects of ASV treatment on morbidity and mortality in the patients with HF.

Clinical significance of chemosensitivity in chronic heart failure: influence on neurohormonal derangement, Cheyne-Stokes respiration and arrhythmias.

Increased chemosensitivity has been observed in HF (heart failure) and, in order to clarify its pathophysiological and clinical relevance, the aim of the present study was to investigate its impact on neurohormonal balance, breathing pattern, response to exercise and arrhythmic profile. A total of 60 patients with chronic HF [age, 66+/-1 years; LVEF (left ventricular ejection fraction), 31+/-1%; values are means+/-S.E.M.] underwent assessment of HVR (hypoxic ventilatory response) and HCVR (hypercapnic ventilatory response), neurohormonal evaluation, cardiopulmonary test, 24-h ECG monitoring, and assessment of CSR (Cheyne-Stokes respiration) by diurnal and nocturnal polygraphy. A total of 60% of patients had enhanced chemosensitivity. Those with enhanced chemosensitivity to both hypoxia and hypercapnia (i.e. HVR and HCVR), compared with those with normal chemosensitivity, had significantly (all P<0.01) higher noradrenaline (norepinephrine) and BNP (B-type natriuretic peptide) levels, higher prevalence of daytime and night-time CSR, worse NYHA (New York Heart Association) class and ventilatory efficiency [higher VE (minute ventilation)/VCO(2) (carbon dioxide output) slope], and a higher incidence of chronic atrial fibrillation and paroxysmal non-sustained ventricular tachycardia, but no difference in left ventricular volumes or LVEF. A direct correlation was found between HVR or HCVR and noradrenaline (R=0.40 and R=0.37 respectively; P<0.01), BNP (R=0.40, P<0.01), N-terminal pro-BNP (R=0.37 and R=0.41 respectively, P<0.01), apnoea/hypopnoea index (R=0.57 and R=0.59 respectively, P<0.001) and VE/VCO(2) slope (R=0.42 and R=0.50 respectively, P<0.001). Finally, by multivariate analysis, HCVR was shown to be an independent predictor of both daytime and night-time CSR. In conclusion, increased chemosensitivity to hypoxia and hypercapnia, particularly when combined, is associated with neurohormonal impairment, worse ventilatory efficiency, CSR and a higher incidence of arrhythmias, and probably plays a central pathophysiological role in patients with HF.

Brain natriuretic peptide for prediction of Cheyne-Stokes respiration in heart failure patients.

Cheyne-Stokes respiration (CSR) is indicative of adverse outcome in patients with chronic heart failure (CHF). We evaluated the use of brain natriuretic peptide (BNP) plasma levels to predict CSR in CHF patients. In this cross-sectional study, overnight polygraphy and cardiac work-up were performed and neurohumoral activation was determined in 102 consecutive CHF patients (25-82 years). Demographic characteristics did not significantly differ among patients with (n=38) or without CSR (n=64); BNP (median: 377 vs. 142 pg/ml, p<0.001) and norepinephrine levels (459+/-283 vs. 346+/-204 pg/ml, p=0.02) were significantly increased in patients with CSR. BNP concentrations were significantly associated with the central apnoea/hypopnoea index (y=253+/-5.3x; r=0.26, p=0.01). The area under the ROC curve that used BNP to predict CSR was 0.780 (95% CI: 0.688 to 0.873). Using established cut-off limits of BNP plasma levels, heart failure patients with BNP levels >500 pg/ml displayed a 13 fold increased risk of CSR (95% CI: 2.34-73.50; p=0.03) compared to patients with BNP levels <100 pg/ml. In multiple logistic regression analysis p(a)CO2 (point estimate 0.84, 95% CI: 0.72 to 0.98; p=0.02) and higher BNP class (point estimate 3.14, 95% CI: 1.38-7.144; p=0.006) emerged as parameters independently predicting the presence of CSR in our cohort of CHF patients. In conclusion, CSR is associated with neurohumoral activation in CHF patients. Specifically, BNP levels are associated with the severity of cardiac and sleep-related disease, and may be helpful in the diagnosis of CSR and more appropriate use of polysomnography in CHF patients.

Efficacy of nasal bi-level positive airway pressure in congestive heart failure patients with cheyne-stokes respiration and central sleep apnea.

BACKGROUND: Cheyne - Stokes respiration with central sleep apnea (CSR-CSA) contributes to the poor prognosis in patients with congestive heart failure (CHF). Bi-level positive airway pressure (bi-level PAP) may be an effective alternative for treating CSR-CSA and CHF. METHODS AND RESULTS: Fourteen patients with CSR-CSA were divided into 2 groups, a control group that included 7 patients who decided to receive only conventional medications and a group of 7 patients that received bi-level PAP. Left ventricular ejection fraction (LVEF), mitral regurgitation (MR) area, plasma brain natriuretic peptide (BNP) concentration and the New York Heart Association (NYHA) functional class were evaluated initially (baseline) and 3 months later. In the control group, there were no significant changes in cardiac function during the study period. In contrast, in the group that received bi-level PAP, there were significant improvements in LVEF (from 36.3+/-2.9% to 46.0+/-4.0%, p = 0.02), MR area (from 30.4+/-7.6% to 20.0+/-5.1%, p = 0.02), BNP (from 993.6+/-332.0 pg/ml to 474.0+/-257.6 pg/ml, p = 0.02) and NYHA functional class (from 3.1+/-0.1 to 2.1+/-0.1, p = 0.03). CONCLUSION: Treatment with bi-level PAP improved cardiac functions in CHF patients with CSR-CSA.

Brain natriuretic peptide in patients with congestive heart failure and central sleep apnea.

STUDY OBJECTIVE: To assess the possible relationship between Cheyne-Stokes respiration (CSR) associated with central sleep apnea (CSA) syndrome and brain natriuretic peptide (BNP) in an outpatient population presenting with stable congestive heart failure (CHF). MEASUREMENTS AND RESULTS: Ninety patients with CHF due to systolic dysfunction (left ventricular ejection fraction

Ventricular arrhythmia, Cheyne-Stokes respiration, and death: observations from patients with defibrillators.

OBJECTIVE: To determine whether ventricular arrhythmia related to nocturnal hypoxaemia during Cheyne-Stokes respiration (CSR) explains the observation that CSR is an independent marker of death in heart failure. DESIGN: Prospective, observational study. PATIENTS: 101 patients at high risk of clinical serious ventricular arrhythmia fitted with an implantable cardioverter-defibrillator (ICD). MEASUREMENTS: Patients were studied at baseline for CSR during sleep. Arrhythmia requiring device discharge was used as a surrogate marker for possible sudden cardiac death. RESULTS: 101 patients (42 with CSR) were followed up for a total of 620 months. Twenty six patients experienced 432 ICD discharge episodes. Twenty four (6%), 210 (49%), 125 (29%), and 73 (17%) episodes occurred across the time quartiles 0000-0559, 0600-1159, 1200-1759, and 1800-2359, respectively. Kaplan-Meier analysis showed a relative risk of 1 (95% confidence interval 0.5 to 2.2, p = 1) for device discharge in the CSR group. The average (SED) numbers of nocturnal ICD discharges per patient per month of follow up were 0.01 (0.01) and 0.04 (0.02) for patients with and without CSR, respectively (p = 0.6). CONCLUSION: These findings refute the proposition that CSR is related to heart failure death through nocturnal serious ventricular arrhythmia.

Oxygen desaturation and heart rate variability due to Cheyne-Stokes respiration in congestive heart failure patients.

Cheyne-Stokes respiration is common in congestive heart failure patients and causes cyclical fluctuation of the RR interval. We studied the characteristics of apnea-related heart rate variability (apnea HRV) and the relation between apnea HRV and oxygen desaturation was examined. Ambulatory electrocardiograms and data on respiration (oronasal flow, tracheal sounds, abdominal wall movement and oxygen saturation) were simultaneously recorded by a multi-channel digital recorder for 16 congestive heart failure patients (10 men and 6 women; mean age, 68 +/- 13 years). HRV occurred as a result of cyclical apnea attacks between 0.005 and 0.03 Hz (apnea band). Apnea HRV was obtained as the power ratio of apnea HRV normalized by the very low frequency band (0.003-0.04 Hz). Apnea HRV increased with the number of apnea episodes and the oxygen desaturation index, but no relation between apnea HRV and either mean oxygen density or oxygen desaturation time was observed. We concluded that apnea HRV is a predictor of the number of apnea attacks or oxygen desaturation, but does not reflect the degree of oxygen desaturation in Cheyne-Stokes respiration.

Characterisation of breathing and associated central autonomic dysfunction in the Rett disorder.

AIM: To investigate breathing rhythm and brain stem autonomic control in patients with Rett disorder. SETTING: Two university teaching hospitals in the United Kingdom and the Rett Centre, Sweden. PATIENTS: 56 female patients with Rett disorder, aged 2-35 years; 11 controls aged 5-28 years. DESIGN: One hour recordings of breathing movement, blood pressure, ECG R-R interval, heart rate, transcutaneous blood gases, cardiac vagal tone, and cardiac sensitivity to baroreflex measured on-line with synchronous EEG and video. Breathing rhythms were analysed in 47 cases. RESULTS: Respiratory rhythm was normal during sleep and abnormal in the waking state. Forced and apneustic breathing were prominent among 5-10 year olds, and Valsalva breathing in the over 18 year olds, who were also most likely to breathe normally. Inadequate breathing peaked among 10-18 year olds. Inadequate and exaggerated breathing was associated with vacant spells. Resting cardiac vagal tone and cardiac sensitivity to baroreflex were reduced. CONCLUSIONS: Labile respiratory rhythms and poor integrative inhibition in Rett disorder suggest brain immaturity. Linking this to an early monoaminergic defect suggests possible targets for the MECP2 gene in clinical intervention. Exaggerated and inadequate autonomic responses may contribute to sudden death.

Effects of inhaled carbon dioxide and oxygen on cheyne-stokes respiration in patients with heart failure.

We hypothesized that in patients with congestive heart failure (CHF), reductions in PaCO2 sensed at the peripheral chemoreceptors trigger central apneas during Cheyne-Stokes respiration (CSR-CSA), and that raising PaCO2 by inhalation of a CO2 would eliminate these events. The effects of CO2 inhalation on the frequency of apneas and hypopneas during stage 2 (S2) sleep were studied in 10 CHF patients with CSR-CSA. The time from the breath with the minimal end tidal fraction of CO2 (FETCO2) during hyperpnea until the onset of apnea correlated strongly with the lung to ear circulation time (LECT) (r2 = 0.90, p < 0.0001), a measure of lung to carotid body circulatory delay. Among the six patients who also inhaled O2, CO2 inhalation increased transcutaneous PCO2 (PtcCO2) (36.4 +/- 4.6 mm Hg versus 38 +/- 4.4 mm Hg, p < 0.002), abolished central apneas and hypopneas (43.0 +/- 8.4 per hour on air versus 1.6 +/- 2.6 per hour on CO2, p < 0.0001), and increased SaO2. In contrast, O2 inhalation causing a similar rise in SaO2 had no significant impact on either PtcCO2 or the frequency of central events. We conclude that central apneas in patients with CHF are triggered by a low PaCO2 most likely sensed at the peripheral chemoreceptors, and that inhalation of CO2 reverses central apneas by raising PaCO2.

Left ventricular volume in patients with heart failure and Cheyne-Stokes respiration during sleep.

In patients with congestive heart failure (CHF), elevated, left ventricular (LV) volume might lead to pulmonary congestion and hypocapnia, which would create a predisposition to the development of Cheyne-Stokes respiration with central sleep apnea (CSR-CSA). In addition, because LV volume affects cardiac output, it should influence the lengths of hyperpneas. We therefore evaluated LV volumes and transcutaneous PCO2 (PtcCO2) during wakefulness and stage 2 sleep in 16 patients with CHF due to nonischemic dilated cardiomyopathy (NIDC). Data were then compared between those with (n = 7) and those without CSR-CSA (n = 9). LV end-diastolic volume (LVEDV) was significantly higher in patients with than those without CSR-CSA (585 +/- 118 versus 312 +/- 41 ml, p < 0.05). Compared with patients without CSR-CSA, those with CSR-CSA had lower mean stage 2 sleep PtcCO2 (36.3 +/- 2.2 versus 41.2 +/- 1.2 mm Hg, p < 0.05) and a lesser change in PtcCO2 from wakefulness to stage 2 sleep (-0.4 +/- 0.3 versus 2.0 +/- 0.4 mm Hg, p < 0.001). Among patients with CSR-CSA, hyperpnea length was inversely related to LVEDV (R = 0.769, p = 0.043) owing to the direct relationship of cardiac output to LVEDV (R = 0.791, p = 0.034). We conclude that CSR-CSA in patients with CHF due to NIDC is associated with increased LV volumes possibly through the direct or indirect influence of LV volume on PaCO2 and cardiac output.

Role of hyperventilation in the pathogenesis of central sleep apneas in patients with congestive heart failure.

Periodic breathing with central apneas during sleep is typically triggered by hypocapnia resulting from hyperventilation. We therefore hypothesized that hypocapnia would be an important determinant of Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) in patients with congestive heart failure (CHF). To test this hypothesis, 24 male patients with CHF underwent overnight polysomnography during which transcutaneous PCO2 (PtcCO2) was measured. Lung to ear circulation time (LECT), derived from an ear oximeter as an estimate of circulatory delay, and CSR-CSA cycle length were determined. Patients were divided into a CSR-CSA group (n = 12, mean +/- SEM of 49.2 +/- 6.3 central apneas and hypopneas per h sleep) and a control group without CSR-CSA (n = 12, 4.9 +/- 0.8 central apneas and hypopneas per h sleep). There were no significant differences in left ventricular ejection fraction, awake PaO2, mean nocturnal SaO2, or LECT between the two groups. In contrast, the awake PaCO2 and mean sleep PtcCO2 were significantly lower in the CSR-CSA group than in the control group (33.0 +/- 1.2 versus 37.5 +/- 1.0 mm Hg, p < 0.01, and 33.2 +/- 1.2 versus 42.5 +/- 1.2 mm Hg, p < 0.0001, respectively). Neither group had significant awake or sleep-related hypoxemia. In addition, CSR-CSA cycle length correlated with LECT (r = 0.939, p < 0.001). We conclude that (1) hypocapnia is an important determinant of CSR-CSA in CHF and (2) circulatory delay plays an important role in determining CSR-CSA cycle length.

The effect of short-term nasal CPAP on Cheyne-Stokes respiration in congestive heart failure.

We studied male patients (BMI = 27.6 +/- 3.4, mean +/- SD), mean age 54.1 +/- 8.9 years, with stable NYHA class 3-4 congestive heart failure (CHF) (LVEF = 24.3 +/- 11.5 percent) and normal daytime arterial blood gas values. These patients underwent three consecutive nights of full polysomnography; adaptation, control, and treatment with nasal CPAP. Each night's study was followed during the day by cognitive testing and multiple sleep latency tests (MSLT). The purpose of the study was to document the effect of nasal CPAP on these variables. The main findings of the study showed no significant differences between control and treatment nights with respect to the amount of Cheyne-Stokes respiration (CSR) observed, the nocturnal oxygenation, or sleep quality. Both subjective and objective measures of sleep quality showed no change from night to night. In addition, the degree of cognitive functioning and daytime sleepiness (as measured by MSLT) showed no significant differences between control and treatment nights. We conclude that short-term treatment with nasal CPAP in patients with CHF does not improve either CSR, nocturnal oxygenation, or sleep quality. Furthermore, most of our patients did not tolerate nasal CPAP therapy.

Cyclic haemodynamic and arterial blood gas changes during Cheyne-Stokes breathing.

A 74-year-old patient presented with congestive heart failure and continuous periodic breathing. Left ventricular ejection fraction was 20% and the lung-to-brain circulation time was prolonged to 35 s. We report on the phasic changes of the patient's arterial blood gas tensions and on the periodic fluctuations of pulmonary artery pressures and cardiac output that we observed during Swan-Ganz catheterisation.