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R Rutherford

Publications and source records attributed to R Rutherford.

At least 37 records · Page 2Linked to original sources
PubMed1991

Obstructive sleep apnoea in patients with dilated cardiomyopathy: effects of continuous positive airway pressure.

The combined effects of negative intrathoracic pressure swings during obstructive sleep apnoeas (OSAs) and increased sympathetic nervous system tone associated with hypoxia and sleep arousal may lead to pulmonary oedema or left-ventricular hypertrophy. Therefore, we have done a study of patients with congestive heart failure secondary to idiopathic dilated cardiomyopathy to see whether OSA could contribute to impaired left-ventricular function and to assess nasal continuous positive airway pressure (NCPAP) for treatment. Eight men (aged 29-69 years) took part in the study; all were obese. Left-ventricular ejection fraction (LVEF) was measured while on stable medication and then 4 weeks after the start of nocturnal NCPAP. NCPAP was associated with abolition of OSA (mean [SE] number of apnoeas and hypopnoeas per hour of sleep 54.1 [7.2] and 1.0 [0.4] for pretreatment and NCPAP nights, respectively, p less than 0.0001). Mean (SE) LVEF increased from 37 (4)% pretreatment to 49 (5)% after four weeks' NCPAP therapy (p less than 0.0001). Withdrawal of NCPAP for 1 week in four patients was associated with a reduction in LVEF from 53 (6)% to 45 (5)% (p less than 0.001). OSA may contribute to impaired left-ventricular function in some patients with dilated cardiomyopathy of otherwise unknown origin, and reversal of OSA by NCPAP can lead to significant improvement in LVEF.

Adult↗
PubMed1990

Sleep apnea in patients with left ventricular dysfunction: beneficial effects of nasal CPAP.

Five patients with congestive heart failure (CHF) and 1 with left ventricular dysfunction but without CHF were found to have sleep apnea. Central sleep apnea (CSA) related to Cheyne-Stokes respiration was seen in 4 cases while obstructive sleep apnea (OSA) was seen in 2. All patients had symptoms of sleep apnea. Nasal continuous positive airway pressure (NCPAP) was effective in reversing CSA and OSA in all patients with improvement in sleep structure and alleviation of symptoms of sleep apnea. In addition, all experienced a reduction in cardiac dyspnea. This was associated with a 5% or greater increase in left ventricular ejection fraction while on NCPAP, compared to baseline value off NCPAP in 5 patients and resolution of chronic pleural effusion and pulmonary edema in the sixth. We conclude that Cheyne-Stokes respiration during sleep may give rise to a CSA syndrome that is reversible by NCPAP. In addition, NCPAP therapy may lead to a reduction in cardiac dyspnea and improvement in left ventricular function in patients with left ventricular dysfunction and sleep apnea.

Arousal↗
PubMed1989

Effect of nasal continuous positive airway pressure on sleep apnea in congestive heart failure.

We studied five patients with chronic stable congestive heart failure (CHF), all of whom demonstrated recurrent apneas in association with Cheyne-Stokes respiration (CSR) during sleep. All five patients had symptoms consistent with a sleep apnea syndrome. Nasal continuous positive airway pressure (NCPAP) was administered at 8 to 12.5 cm H2O to all patients during sleep. The number of apneas fell from (mean +/- SE) 60 +/- 12/h of sleep on the control night to 9 +/- 7/h of sleep (p less than 0.01) on the NCPAP night, whereas mean nocturnal SaO2 rose from 88 +/- 2% on the control night to 92 +/- 2% (p less than 0.025) while on NCPAP. This was associated with resolution of symptoms of sleep apnea. In addition, resting left ventricular ejection fraction (LVEF) as measured by radionuclide angiography (RNA) rose from 31 +/- 8% while off NCPAP to 38 +/- 10% (p less than 0.05) while on NCPAP. Furthermore, all five patients experienced marked improvement in symptoms of heart failure from functional classes III and IV (New York Heart Association Classification) prior to NCPAP therapy to class II after NCPAP therapy was instituted. We conclude that, in certain patients, CSR during sleep associated with chronic CHF constitutes a sleep apnea syndrome, which can be alleviated by NCPAP. In addition, NCPAP therapy may lead to a reduction in cardiac dyspnea and improvement in left ventricular function.

Aged↗
PubMed1987

Reversal of sleep-induced hypoventilation and chronic respiratory failure by nocturnal negative pressure ventilation in patients with restrictive ventilatory impairment.

The efficacy of negative pressure ventilation (NPV) in alleviating sleep-induced reductions in alveolar ventilation and in producing long-term clinical benefits was studied in 5 patients (54 +/- 8 yr of age; mean +/- SD) with chronic respiratory failure secondary to restrictive ventilatory impairment (VC, 40 +/- 14% predicted; TLC, 72 +/- 18% predicted; FEV1/FVC, 89 +/- 15%). In control sleep studies, arterial O2 saturation decreased from 81 +/- 6% during wakefulness to 79 +/- 1% during non-REM sleep and to 67 +/- 3% during REM sleep, and transcutaneous PCO2 increased from 80 +/- 16 mm Hg during wakefulness and non-REM sleep to 87 +/- 16 mm Hg during REM sleep. Nocturnal NPV in a cuirass ventilator improved baseline ventilation during wakefulness and prevented deterioration of alveolar ventilation during sleep. Upper airway obstruction during sleep induced by NPV was successfully managed with either a tricyclic medication or nasal CPAP. After 8 wk of nocturnal NPV, all patients felt considerably better. Daytime resting arterial PCO2 decreased from 56 +/- 2 to 46 +/- 3 mm Hg (p less than 0.05) and PO2 increased from 51 +/- 9 to 70 +/- 10 mm Hg (NS). Four patients have continued NPV at home on a regular basis and have returned to full-time employment. We conclude that nocturnal NPV is an effective method of preventing sleep-induced reductions in alveolar ventilation and a practical method of long-term management of patients with nonobstructive chronic respiratory failure.

Carbon Dioxide↗
PubMed1986

Clinical and physiologic heterogeneity of the central sleep apnea syndrome.

We examined the clinical and respiratory physiologic characteristics of 18 patients in whom a diagnosis of central sleep apnea syndrome was established by overnight polysomnographic studies. The patients could be readily divided into 2 groups on the basis of physiologic and clinical criteria. Five patients had an awake arterial PCO2 (PaCO2) of 53 +/- 4 (SEM) mmHg in the absence of intrinsic bronchopulmonary disease, a ventilatory response to CO2 of 0.6 +/- 0.2 L/min/mmHg, and a hemoglobin concentration of 180 +/- 6 g/L. Their clinical course was dominated by recurrent episodes of respiratory failure. In contrast, the other 13 patients had an awake PaCO2 of 35 +/- 1 mmHg (p less than 0.001), a CO2 response of 2.9 +/- 0.4 L/min/mmHg (p less than 0.005), and a hemoglobin concentration of 150 +/- 5 g/L (p less than 0.005). Clinically, they presented with features typical of sleep apnea; none had a history of respiratory failure. Despite the clinical and physiologic differences between the 2 groups, there were no differences between them in the frequency or duration of nocturnal apneic events or in sleep architecture. The findings indicate that the central sleep apnea syndrome is not a homogeneous disease entity. Rather, it includes 2 groups of patients that are clinically and physiologically distinct, with 1 group chronically hypoventilating and the other group either chronically hyperventilating or ventilating normally.

Adult↗
PubMed1986

Role of diffuse airway obstruction in the hypercapnia of obstructive sleep apnea.

The mechanisms responsible for the development of chronic hypercapnia in patients with obstructive sleep apnea (OSA) are not well defined. Therefore, we tested the hypothesis that diffuse airway obstruction may be involved by studying 50 patients with a well-documented OSA syndrome. Seven patients had daytime hypercapnia with a mean PaCO2 of 51 +/- 2 (SEM) mm Hg, compared to a PaCO2 of 35 +/- 1 in the other 43 patients. There were no differences between the 2 groups in the number or duration of nocturnal obstructive events. In contrast, the hypercapnic patients were significantly heavier than the normocapnic patients (body weight, 189 +/- 11 versus 148 +/- 6% of ideal; p less than 0.005) and had evidence of diffuse airway obstruction, as indicated by an increased residual volume and a reduction in all expiratory flow rates. When the hypercapnic patients were compared with a weight-matched group of 9 normocapnic patients (body weight, 196 +/- 8% of ideal), there were still no differences in nocturnal obstructive events, but the differences in tests of airway mechanics persisted. Multiple regression analysis of PaCO2 against several anthropometric, respiratory physiologic, and polysomnographic variables revealed that only 2 variables (expiratory reserve volume and FEV1/FVC), both of which are influenced by airway mechanics, were significantly correlated with PaCO2 (multiple r = 0.78; p = 0.0001). The findings suggest that OSA alone does not produce daytime hypercapnia even in obese patients, and that the presence of diffuse airway obstruction is an important predisposing factor to the development of chronic CO2 retention in such patients.

Adult↗
PubMed1985

Physiological determinants of nocturnal arterial oxygenation in patients with obstructive sleep apnea.

Among patients with similar degrees of obstructive sleep apnea (OSA) there is considerable variability in the degree of associated nocturnal hypoxemia. The factors responsible for this variability have not been clearly defined. Therefore we studied 44 patients with OSA to identify the physiological determinants of nocturnal arterial O2 saturation (SaO2). All patients underwent pulmonary function testing, arterial blood gas analysis, and overnight polysomnography. Mean nocturnal SaO2 ranged from 96 to 66% and apnea-hypopnea index from 11 to 128 per hour of sleep. Several anthropometric, respiratory physiological, and polysomnographic variables that could be expected to influence nocturnal SaO2 were entered into a stepwise multiple linear regression analysis, with mean nocturnal SaO2 as the dependent variable. Three variables [awake supine arterial PO2 (PaO2), expiratory reserve volume, and percentage of sleep time spent in apnea] were found to correlate strongly with mean nocturnal SaO2 (multiple R, 0.854; P less than 0.0001) and accounted for 73% of its variability among patients. Body weight, other lung volumes, and airflow rates influenced awake PaO2 and expiratory reserve volume but had no independent influence on nocturnal SaO2. In a further group of 15 patients with OSA a high correlation was obtained between measured nocturnal SaO2 and that predicted by the model (r = 0.87; P less than 0.001). We conclude that derangements of pulmonary mechanics and awake PaO2 (generally attributable to obesity and diffuse airway obstruction) are of major importance in establishing the severity of nocturnal hypoxemia in patients with OSA.

Adult↗
PubMed1985

Role of daytime hypoxemia in the pathogenesis of right heart failure in the obstructive sleep apnea syndrome.

Although right heart failure is a recognized complication of obstructive sleep apnea, the incidence and pathogenesis of this complication have not been established. We therefore studied 50 consecutive patients with obstructive sleep apnea to determine the incidence of right heart failure and the factors involved in its development. Six patients (12%) were found to have right heart failure. There were no differences in the number of apneas between those with right heart failure (mean +/- SE, 30 +/- 10 per h sleep) and those without right heart failure (33 +/- 4 per h sleep). In contrast, mean nocturnal oxygen saturation was lower in patients with right heart failure (76 +/- 3%) than in those without right heart failure (90 +/- 1%; p less than 0.001). Furthermore, patients with right heart failure also had a substantially lower awake arterial PO2 (52 +/- 4 mmHg versus 75 +/- 2 mmHg; p less than 0.001) and a higher PCO2 (51 +/- 2 mmHg versus 36 +/- 1 mmHg; p less than 0.001) than those without right heart failure. Severe nocturnal hypoxemia in the absence of diurnal hypoxemia was not associated with right heart failure. Daytime hypoxemia in the patients with right heart failure was associated with a higher residual volume (p less than 0.001) and lower forced expiratory volume in one second (p less than 0.001) than in the patients without right heart failure. The findings suggest that sustained hypoxemia and/or hypercapnia over a 24-h period is a necessary prerequisite for the development of right heart failure in patients with obstructive sleep apnea, and that diffuse airway obstruction plays a major role in causing such hypoxemia.

Circadian Rhythm↗
PubMed1984

Chronic ventilatory failure caused by abnormal respiratory pattern generation during sleep.

A 67-yr-old man presented with a 4-yr history of chronic ventilatory failure in the absence of any restrictive or obstructive ventilatory defect. Detailed neurologic investigations were unremarkable, and the response of minute volume of ventilation to inhaled CO2 was normal. During sleep there was no evidence of upper airway obstruction, and minute volume of ventilation averaged 6.7 L/min, compared with 7.2 L/min during quiet wakefulness. However, sleep was associated with a rapid and shallow pattern of breathing, resulting in high dead space ventilation, inadequate alveolar ventilation, hypoxemia, and hypercapnia. Correction of the abnormal ventilatory pattern during sleep by diaphragmatic pacing abolished all features of chronic respiratory failure. The findings indicate that a disorder of respiratory pattern during sleep can produce chronic ventilatory failure, despite normal respiratory drive.

Aged↗
PubMed1983

Arteriovenous fistulas following central venous catheterization.

We report three patients in whom arteriovenous fistulas probably occurred following placement of central venous catheters. Two fistulas apparently followed internal jugular vein catheterization (or attempts), and one was demonstrated angiographically following subclavian vein cannulation. One fistula was repaired operatively, and in this case two separate fistulas in the same anatomical region were found. One patient refused surgery but remained asymptomatic after 6 months of follow-up. In the third patient the fistula probably spontaneously disappeared within one week of its appearance. We discuss two methods of central vein cannulation which should decrease the occurrence of complications following the procedure.

Adult↗
PubMed1982

Beneficial effect of oxygen in primary alveolar hypoventilation with central sleep apnea.

A 58-yr-old man with primary alveolar hypoventilation, central sleep apnea, and secondary polycythemia failed to improve when treated with respiratory stimulant medications, including oxtriphylline, acetazolamide, and medroxyprogesterone. In contrast, after institution of treatment with low-flow nocturnal oxygen, there was a marked decrease in the number and duration of sleep apneas, and an increase in the level of ventilation during sleep. These changes were sustained during 5 months of nocturnal oxygen therapy. The improvement produced by oxygen may have been due to the fact that the patient had no demonstrable ventilatory response to hypoxia during wakefulness, and therefore may have developed hypoxic brainstem depression during sleep. The findings suggest that oxygen therapy during sleep may be beneficial in patients with primary alveolar hypoventilation and central sleep apnea who demonstrate no ventilatory response to hypoxia during wakefulness.

Humans↗
PubMed1982

Obstructive apneas during sleep in patients with seasonal allergic rhinitis.

The possible role of high nasal airway resistance in the pathogenesis of obstructive sleep apnea has been examined in 7 patients with seasonal (ragweed) allergic rhinitis, a naturally occurring model of reversible nasal obstruction. Measurements of nasal resistance and overnight polysomnographic studies were performed during the ragweed season when the patients complained of nasal obstruction; and 6 to 8 wk later when the symptoms had subsided (control study). During the symptomatic phase, mean (+/- SE) nasal resistance was 4.9 +/- 0.8 cm H2O/L/s, and the patients experienced 1.7 +/- 0.3 obstructive apneas per hour of sleep. In contrast, at the time of the control study, nasal resistance had decreased to 2.5 +/- 0.3 cm H2O/L/s (p less than 0.01); and the rate of obstructive apneas had decreased to 0.7 +/- 0.4 per hour of sleep (p less than 0.005). The duration of these apneas had also decreased from 15.5 +/- 0.8 s to 6.1 +/- 2.9 s (p less than 0.01). Apneas were rarely associated with significant O2 desaturation and were fewer in number than typically seen in a clinically significant sleep apnea syndrome. In male patients there was a direct relationship (r = 0.9) between the change in nasal resistance from symptomatic to control studies and the corresponding change in frequency of obstructive sleep apneas. Coincident with these respiratory changes at the time of the control study was an increase in the amount of slow-wave sleep (p = 0.05) and a small reduction in the frequency of arousals during sleep (p = NS). We conclude that in patients with allergic rhinitis, obstructive sleep apneas are longer and more frequent during a period of symptomatic nasal obstruction than when symptoms are absent. The results support the concept that a high nasal resistance may be a contributing factor in the pathogenesis of obstructive sleep apneas in general.

Adult↗
PubMed1979

The influence of maternal somatostatin administration on fetal brain cell proliferation and its relationship to serum gorwth hormone and brain trophin activity.

The effect of maternal somatostatin administration from days 14 to 20 of gestation was examined. Fetal body growth was unchanged but brain cell DNA synthesis per gram of tissue decreased. Maternal serum levels of growth hormone and brain trophin were elevated following treatment conclusion. It was suggested that this was a rebound phenomenon and that short term blockade of pituitary growth hormone release during somatostatin treatment had impaired fetal brain cell DNA synthesis.

Animals↗
PubMed1977

Correlation between maternal weight gain during gestation and fetal and placental growth in rats.

In rats, maternal weight gain during the later third of pregnancy was correlated with fetal body weight, brain weight and DNA content as well as placental weight near term. Fetal body and placental growth was unrelated to maternal weight increases during pregnancy. A significant inverse correlation between fetal brain DNA content and maternal weight gain was found. This was related to litter size since the smaller the litter size, the less the maternal weight gain during pregnancy and the greater the DNA content of the fetal brain. These data emphasize the importance of controlling for litter number in growth studies.

Animals↗
PubMed1970

Surgic grand rounds.

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Adenocarcinoma, Bronchiolo-Alveolar↗