Grant N. Willson

Prognosis and sleep disordered breathing in heart failure

Abnormal breathing in heart failure as originally described by Cheyne1 and subsequently by Stokes2 was observed in apparently awake patients as an agonal breathing pattern. “. . . The only peculiarity in the last period of his illness was in the state of the respiration. For several days his breathing was irregular, then it would become perceptible, though very low, then by degrees it became heaving and quick, and then it would cease again: this revolution in the state of his breathing occupied about a minute, during which there were about 30 acts of respiration (Cheyne, 1818) . . .” The patient described in this report was an obese, elderly, alcoholic who had suffered a substantial, and ultimately, fatal stroke. He probably had obstructive sleep apnoea prior to the stroke and developed central apnoea subsequently. In the literature subsequent to these reports periodic respiration associated with central apnoeas was believed to be a terminal consequence of end stage heart failure.3-5 More recently it has been recognised that central apnoeas occur commonly in heart failure, especially during sleep, being reported in 40–50% of patients, predominantly men, with stable, medically treated congestive heart failure.6 This sleep breathing abnormality leads to sleep fragmentation, alterations in sleep architecture—with relative increases in stage 1 and 2 sleep and reduction in REM sleep—and a clinical sleep disorder with symptoms of tiredness and sleepiness in some patients.7 The sleep disorder in central sleep apnoea is a consequence of the development of congestive heart failure. Although the pathophysiology is not completely understood, hyperventilation,8 increased chemoreceptor drive,9 and increased circulation time4 10 11 are all believed to be important factors promoting this sleep disorder. Identification of obstructive sleep apnoea (OSA) in patients with primarily left ventricular (LV) dysfunction and clinical heart …

Noninvasive pressure preset ventilation for the treatment of Cheyne-Stokes respiration during sleep

Cheyne-Stokes respiration (CSR) during sleep is common in patients with congestive heart failure (CHF). This pattern of breathing fragments sleep, leading to daytime symptoms of sleepiness and fatigue. It was hypothesized that by controlling CSR with noninvasive pressure preset ventilation (NPPV), there would be a decrease in sleep fragmentation and an improvement in sleep quality. Nine patients (eight males, one female; mean +/- SD 65 +/- 11 yrs) with symptomatic CSR diagnosed on overnight polysomnography (apnoea/hypopnoea index (AHI) 49 +/- 10 x h(-1), minimum arterial oxygen saturation (Sa,O2, 77 +/- 7%) and CHF (left ventricular ejection fraction 25 +/- 8%) were studied. After a period of acclimatization to NPPV (variable positive airway pressure (VPAP) II ST, Sydney, NSW, Australia and bilevel positive airway pressure (BiPAP), Murraysville, PA, USA), sleep studies were repeated on therapy. NPPV almost completely abolished CSR in all patients with a reduction in AHI from 49 +/- 10 to 6 +/- 5 x h(-1) (p<0.001). Residual respiratory events were primarily due to upper airway obstruction at sleep on-set. Arousal index was markedly decreased from 42 +/- 6 to 17 +/- 7 x h(-1) (p <0.001). Sleep architecture showed a trend toward improvement with a reduction in stage 1 and 2 (79 +/- 7% during the diagnostic night versus 72 +/- 10% during NPPV, (p=0.057)), whilst sleep efficiency, slow-wave sleep (SWS), and rapid eye movement (REM) were not altered. Controlling Cheyne-Stokes respiration with noninvasive pressure preset ventilation resulted in reduced arousal and improved sleep quality in the patients with congestive heart failure. Noninvasive pressure preset ventilation should be considered a potential therapy for Cheyne-Stokes respiration in congestive heart failure in those patients who do not respond or fail to tolerate nasal continuous positive airway pressure therapy.

Nasal versus full face mask for noninvasive ventilation in chronic respiratory failure

This study was undertaken to determine the efficacy of nasal mask (NM) versus full face mask (FFM) for the delivery of noninvasive ventilation (NIV) in subjects with nocturnal hypoventilation. A total of 16 patients (11 males) were enrolled, all with nocturnal hypoventilation currently treated at home with NIV via pressure preset devices. Subjects underwent full polysomnography on three occasions; on the first night current therapy on NM was reviewed, followed by two experimental studies in randomised order using either NM or FFM. NIV settings and oxygen flow rate were the same under both conditions. Notably, 14 of the 16 subjects required the use of a chinstrap to minimise oral leak. Apnoea-hypopnoea indices were within normal limits under both conditions (1.7±3.4 NM versus 1.6±2.4 h FFM). The type of interface did not significantly affect gas exchange during sleep (minimum average arterial oxyhaemoglobin saturation total sleep time 93.4±2.1 NM versus 92.8±2.5% FFM, Delta transcutaneous carbon dioxide nonrapid eye movement sleep to rapid eye movement sleep (0.58±0.36 NM versus 0.50±0.40 kPa FFM). Sleep efficiency was significantly reduced on the FFM (78±9 NM versus 70±14% FFM), although arousal indices were comparable under both conditions (15.6±9.8 NM versus 15.8±8.8 h FFM). Full face masks appear to be as effective as nasal masks in the delivery of noninvasive ventilation to patients with nocturnal hypoventilation. However, a chinstrap was required to reduce oral leak in the majority of subjects using the nasal mask.

Moderate concentrations of supplemental oxygen worsen hypercapnia in obesity hypoventilation syndrome: a randomised crossover study

Introduction In people with obesity hypoventilation syndrome (OHS), breathing 100% oxygen increases carbon dioxide (PCO2), but its effect on pH is unknown. This study investigated the effects of moderate concentrations of supplemental oxygen on PCO2, pH, minute ventilation (VE) and physiological dead space to tidal volume ratio (VD/VT) among people with stable untreated OHS, with comparison to healthy controls. Methods In a double-blind randomised crossover study, participants breathed oxygen concentrations (FiO2) 0.28 and 0.50, each for 20 min, separated by a 45 min washout period. Arterialised-venous PCO2 (PavCO2) and pH, VE and VD/VT were measured at baseline, then every 5 min. Data were analysed using general linear model analysis. Results 28 participants were recruited (14 OHS, 14 controls). Among OHS participants (mean±SD arterial PCO2 6.7±0.5 kPa; arterial oxygen 8.9±1.4 kPa) FiO2 0.28 and 0.50 maintained oxygen saturation 98–100%. After 20 min of FiO2 0.28, PavCO2 change (ΔPavCO2) was 0.3±0.2 kPa (p=0.013), with minimal change in VE and rises in VD/VT of 1±5% (p=0.012). FiO2 0.50 increased PavCO2 by 0.5±0.4 kPa (p=0.012), induced acidaemia and increased VD/VT by 3±3% (p=0.012). VE fell by 1.2±2.1 L/min within 5 min then recovered individually to varying degrees. A negative correlation between ΔVE and ΔPavCO2 (r=−0.60, p=0.024) suggested that ventilatory responses were the key determinant of PavCO2 rises. Among controls, FiO2 0.28 and 0.50 did not change PavCO2 or pH, but FiO2 0.50 significantly increased VE and VD/VT. Conclusion Commonly used oxygen concentrations caused hypoventilation, PavCO2 rises and acidaemia among people with stable OHS. This highlights the potential dangers of this common intervention in this group.

Night-to-night variability in sleep in cystic fibrosis

OBJECTIVES The impact of night-to-night variability (NNV) on polysomnography (PSG) has been reported mainly in normal subjects, the elderly and patients with obstructive sleep apnea with focus on changes in the apnea/hypopnea index, rather than measures of nocturnal oxygenation. There is very limited data on NNV in patients with cystic fibrosis (CF). The goal of this study was to assess for first-night effect and reliability of PSG measurements on nocturnal oxygenation and respiratory disturbance in CF. METHODS A prospective observational study was performed in patients with CF who consented to PSG on two consecutive nights. Paired t-tests and intra-class correlation coefficients (ICCs) were calculated for repeated measures of sleep stage time, sleep efficiency, arousal indices, measures of nocturnal oxygenation, and respiratory events in all sleep stages. RESULTS Thirty-one patients with CF were studied, aged 27+/-8 (mean+/-1 SD) years and forced expiratory volume in 1 s (FEV(1)) of 37+/-11% of predicted. Relative to the first-night PSG, on the second PSG, we observed the following: shorter latency to rapid eye movement (REM) sleep (P<0.001), increased sleep efficiency (P<0.01), decreased wake after sleep onset (WASO) time (P<0.01), decreased percentage of non-REM time with oxyhemoglobin saturation by pulse oximetry (SpO(2))< or =90% (P<0.05), decreased number of central apneas per hour (P<0.05) and reduced respiratory rate in stage 2 sleep on night 2 (P<0.05). Despite these changes, the ICCs between night 1 and night 2 showed good repeatability/reliability for measures of nocturnal oxygenation and indices of respiratory disturbance, including the percentage of total sleep time with SpO(2)< or =90% (ICC=0.85) and apnea-hypopnea index (ICC=0.75). Likewise, the ICCs were extremely high for respiratory rate in stage 2 (ICC=0.94), slow wave sleep (ICC=0.97), and REM sleep (ICC=0.96). CONCLUSION Although a first-night effect is seen with sleep efficiency, REM latency, and WASO, a single-night PSG in patients with CF yields reliable information on nocturnal oxygenation and respiratory disturbance.

Treatment of central sleep apnoea in congestive heart failure with nasal ventilation

Cheyne-Stokes respiration (CSR) is common in patients with congestive heart failure (CHF).1 This characteristic crescendo-decrescendo pattern of breathing is often seen during sleep in patients with CHF and is a form of central sleep apnoea.2 Disordered nocturnal breathing leads to oxygen desaturation, poor sleep quality, and altered sleep architecture.3 These features may lead to complaints of daytime somnolence, fatigue, insomnia, and many of the symptoms typical of sleep disordered breathing. It has been proposed that CSR during sleep in patients with heart failure is an indicator of a poor prognosis.4 5 The likely adverse effects of CSR on daytime performance and myocardial function have resulted in the introduction and evaluation of a range of treatments aimed at reducing CSR. These include low flow oxygen,6 theophylline,7 and nasal continuous positive airways pressure (nCPAP).8 In one controlled study nCPAP was shown to improve both sleep quality and daytime myocardial function.8 Other groups have found nCPAP to be ineffective in controlling CSR.9-11 Nocturnal nasal intermittent positive pressure ventilation (nIPPV) is the accepted treatment for patients with chronic respiratory failure due to hypoventilation during sleep.12 13 We hypothesised that nIPPV may also effectively treat central sleep apnoea in heart failure by controlling ventilation and carbon dioxide in patients whose disordered breathing has been linked to fluctuating carbon dioxide levels, relative hyperventilation, and hypocapnia.14 15Nasal IPPV was administered in an attempt to mechanically ventilate the patient through the apnoeic portion of the Cheyne-Stokes cycle, thereby preventing fluctuations in carbon dioxide levels and consequently abolishing CSR. This study describes the use of nocturnal nIPPV in a group of patients with heart failure and Cheyne-Stokes respiration during sleep. The effects of this therapy on respiratory disturbance and sleep quality following an in-hospital acclimatisation period are …

Nocturnal nasal ventilatory support in the management of daytime hypercapnic respiratory failure

Nasal ventilation is becoming increasingly recognised as an effective therapeutic strategy to minimise or correct hypercapnia in patients with respiratory failure. Intervention may be required on a short or long term basis. In the majority of patients, respiratory failure develops initially during sleep. Assessing patients at risk of nocturnal hypoventilation, and instituting appropriate therapy, is becoming an increasingly important aspect of respiratory care. This review outlines methods and practices involved in commencing nasal ventilation therapy. Twenty-nine patients presenting with hypercapnic respiratory failure were managed with nocturnal nasal ventilation over a 12 month period. With the use of this therapy PaCO2 fell from 64(2) to 50(1)mmHg (Mean(SE)) (p<0.001), while PaO2 improved from 55(2) to 68(2)mmHg (p<0.001) during a mean ventilation time of 10(0.8) days. Those factors which must be addressed for a successful program outcome are discussed.

Validation of respiratory inductive plethysmography (LifeShirt) in obesity hypoventilation syndrome.

Validation of respiratory inductive plethysmography (LifeShirt system) (RIPLS) for tidal volume (VT), minute ventilation (V˙E), and respiratory frequency (fB) was performed among people with untreated obesity hypoventilation syndrome (OHS) and controls. Measures were obtained simultaneously from RIPLS and a spirometer during two tests, and compared using Bland Altman analysis. Among 13 OHS participants (162 paired measures), RIPLS-spirometer agreement was unacceptable for VT: mean difference (MD) 3 mL (1%); limits of agreement (LOA) -216 to 220 mL (±36%); V˙E MD 0.1 L min(-1) (2%); LOA -4.1 to 4.3 L min(-1) (±36%); and fB: MD 0.2 br min(-1) (2%); LOA -4.6 to 5.0 br min(-1) (±27%). Among 13 controls (197 paired measures), RIPLS-spirometer agreement was acceptable for fB: MD -0.1 br min(-1) (-1%); LOA -1.2 to 1.1 br min(-1) (±12%), but unacceptable for VT: MD 5 mL (1%); LOA -160 to 169 mL (±20%) and V˙E: MD 0.1 L min(-1) (1%); LOA -1.4 to 1.5 L min(-1) (±20%). RIPLS produces valid measures of fB among controls but not OHS patients, and is not valid for quantifying respiratory volumes among either group.

Validity of arterialised-venous PCO2, pH and bicarbonate in obesity hypoventilation syndrome

This prospective study investigated the validity of arterialised-venous blood gases (AVBG) for estimating arterial carbon dioxide P CO2, pH and bicarbonate (HCO3(-)) in people with obesity hypoventilation syndrome (OHS). AVBGs were obtained from an upper limb vein, after heating the skin at 42-46°C. Arterial blood gas (ABG) and AVBG samples were taken simultaneously and compared using Bland Altman analysis. Between-group differences were assessed with independent t-tests or Mann-Whitney U tests. Forty-two viable paired samples were analysed, including 27 paired samples from 15 OHS participants, and 15 paired samples from 16 controls. AVBG-ABG agreement was not different between groups, or between dorsal hand, forearm and antecubital AVBG sampling sites, and was clinically acceptable for P Co2: mean difference (MD) 0.4 mmHg (0.9%), limits of agreement (LOA) -2.7-3.6 mmHg (± 6.6%); pH: MD -0.008 (-0.1%), LOA -0.023-0.008 (± 0.2%); and HCO3(-): MD -0.3 mmol L(-1) (-1.0%), LOA -1.8-1.2 mmol L(-1) (± 5.3%). AVBG provides valid measures of [Formula: see text] , pH, and HCO3(-) in OHS.

Electroencephalographic arousals during sleep do not alter the pressor response to Cheyne–Stokes respiration in subjects with chronic heart failure

This study examined the influence of electroencephalographic (EEG) arousal on the magnitude and morphology of the pressor response to Cheyne–Stokes respiration (CSR) in subjects with congestive heart failure (CHF). Thirteen subjects with stable CHF (left ventricular ejection fraction, 26 ± 7%) and CSR (apnea–hypopnea index 52 ± 15 h−1) underwent overnight polysomnography with beat‐to‐beat measurement of systemic arterial blood pressure (BP). CSR events were divided into those with or without an EEG arousal defined according to the criteria of the American Sleep Disorders Association. The pressor response was quantified in terms of the delta BP change (difference between the minimum BP during apnea and maximum BP during hyperpnea). Changes in the morphology of the pressor response were assessed by subdividing individual respiratory events into six periods (three during apnea: A1, A2, A3; and three during hyperpnea: H1, H2, H3). Considerable fluctuations in BP and heart rate (HR) were observed across the CSR cycle (delta mean BP 20.2 ± 6.5 mmHg). The presence of an EEG arousal did not alter the amplitude of fluctuations in BP. Mean blood pressure (MBP) increased 21.0 ± 7.5 mmHg with arousal versus 19.3 ± 5.8 mmHg without arousal (NS). A repeated measures ANOVA showed no significant interaction between the presence of arousal and the proportional change in mean BP across the six periods, indicating that an EEG arousal had no effect on the morphology of MBP change during CSR [F(5,60) = 1.44, P = 0.22]. This study showed that EEG‐defined arousal does not amplify the pressor response to CSR in CHF.