Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have evaluated the reliability of the transcutaneous (t.c.) method of measurement of arterial PO2 and PCO2 in adult man. In 33 simultaneous measurements of 9 normals and 12 patients with a wide range of hypoxemia, we found: t.c. PCO2 = 3.62 + 1.29 PaCO2 +/- 7.3 (r = 0.96) and t.c. PO2 = 11.14 + 0.86 PaO2 +/- 9.89 (r = 0.92). Recalculating t.c. PCO2 to 37 degrees C we can obtain: t.c. PCO2 = 2.7 + 0.97 X PaCO2, stating that there is no significant difference between t.c. PCO2 and PaCO2. The t.c. apparatus detects 10 and 90% O2 pressure changes with a delay of time of about 15 s and 1 min, respectively; the t.c. method is therefore not suitable for detecting changes in PaO2 caused by sleep apnea of short duration. On the contrary the t.c. method provided a useful monitoring of arterial PO2 and PCO2 changes during the night in chronic obstructive pulmonary disease (COPD) and non-COPD patients. A nocturnal monitoring of t.c. PO2 and PCO2 seems: (a) absolutely necessary in non-COPD hypoxemics, especially if total lung capacity (TLC) and/or residual volume (RV) are significantly reduced; (b) not absolutely necessary in COPD hypoxemics, provided they have an enlarged TLC and/or a very expanded RV; (c) advisable in intermediate situations, e.g., in COPD hypoxemics with an associated restrictive disorder caused by heart failure, congestion of pulmonary bed, parenchymal or rib cage disease, in order to establish the optimal concentration of oxygen for each patient and to avoid severe nocturnal hypoxemia without producing a dangerous rise in PaCO2.
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PMID:Value of nocturnal monitoring of transcutaneous O2 and CO2 pressures in adults with respiratory failure. 392 61

Neurologists are becoming increasingly aware of the frequency and clinical importance of sleep-related respiratory impairment. Sleep-induced narrowing of the upper airways underlies the widespread and supposedly trivial complaint of snoring, which may not only constitute a risk factor for the cardiocirculatory system, but in predisposed individuals, may lead to a sleep apnea syndrome, with its array of serious disturbances, including hypersomnia, systemic and pulmonary hypertension and ultimately heart failure. Idiopathic chronic alveolar hypoventilation, or Ondine's curse, is a fairly stereotyped clinical syndrome: sleep-related respiratory insufficiency in the absence of airways stenosis. Finally, sleep, and REM sleep in particular, significantly aggravates hypoventilation in patients with chronic obstructive pulmonary disease (COPD), kyphoscoliosis or chest musculoskeletal disorders.
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PMID:Sleep-related respiratory disorders. 408 59

Four infants with Down syndrome developed cor pulmonale and heart failure in association with chronic upper airway obstruction. Features of the sleep apnea syndrome were conspicuous; namely, noisy breathing with retraction, cyanosis and frequent apnea during sleep, and daytime lethargy and somnolence. The clinical picture masqueraded as cyanotic congenital heart disease. Arterial blood gas analyses revealed alveolar hypoventilation, especially during sleep. The nature of the obstructive element was variable. Adenoidectomy provided partial relief in one patient, and tonsillectomy and adenoidectomy resulted in temporary improvement in two others. Three patients were markedly benefitted by tracheostomy. Functional inspiratory pharyngeal closure was demonstrated fluorographically in one patient. Infants with Down syndrome may be predisposed to upper airway obstruction by virtue of hypoplasia of facial and oropharyngeal structures and generalized hypotonia. Additional obstructive elements may be contributed by hypertrophied lymphoid tissue, excessive secretions, and glossoptosis. Removal of the obstructive element is helpful, but functional obstruction may only be relieved by tracheostomy.
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PMID:Alveolar hypoventilation and cor pulmonale associated with chronic airway obstruction in infants with Down syndrome. 645 3

The prevalence of reported sleep disturbances in a general population is high. Many of the complaints are the result of sleep-related breathing disorders, due mainly to the occurrence of obstructive and central apnoeas. Obstructive sleep apnoea is a fully described and well-recognized entity. Central sleep apnoea (CSA) however, has been poorly studied. There is accumulating evidence that central sleep apnoea should be considered as the end of a spectrum. Instability in the breathing pattern is the main underlying mechanism and is due to the interaction of many factors. Breathing during sleep is dependent on metabolic control and the activity of the respiratory muscles. Decreased chemical drive and/or failing respiratory muscle function are associated with CSA and usually also with ongoing hypoventilation during wakefulness, characterized by chronic daytime hypercapnia. Central respiratory drive can also be inhibited by upper airway reflexes. Mostly, however, CSA occurs as the hallmark of unstable breathing during sleep brought about by an overall increase in loop gain (especially in light sleep stages) and the unmasking of a CO2 threshold. Arousal following central apnoeas acts as an amplification of the instability. Micro electroencephographic (EEG) arousals are often observed as a consequence of CSA. They are responsible for sleep fragmentation and hypersomnolence during the day. The daytime hypersomnolence and complaints of awakenings during sleep in patients with CSA can be striking. CSA can occur in specific pathologies, such as chronic heart failure and (post-traumatic) brain lesions, that are associated with irregular breathing. Treatment strategies are remarkably few in number. Use of nasal ventilation and the inhalation of CO2 are mainly of theoretical interest, since patients do not often tolerate these more invasive therapies. Drug treatment, especially with acetazolamide, is easier to perform. Stimulation of upper airway reflexes, by less invasive methods, seems to be promising for the near future.
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PMID:Central sleep apnoea, pathogenesis and treatment: an overview and perspective. 748 5

Obstructive sleep apnea in children may result in hypoxia, right-sided heart failure, and sudden death. Children with craniofacial deformities and/or cerebral palsy are at high risk for the development of obstructive sleep apnea. Prompted by the excellent results obtained in adults when sleep apnea was managed by an aggressive surgical approach, we undertook a similar treatment philosophy in children. Twenty-eight patients representing four diagnostic groups were evaluated and operated on for severe upper airway obstruction: Down syndrome (n = 5), cerebral palsy (n = 12), Goldenhar syndrome (n = 4), and a mixed apnea group (n = 7). Tracheostomy was avoided in 25 of 28 patients (89 percent), with a marked decrease in apnea (median 90 percent) and hypopnea (median 87 percent) episodes. Tongue hyoid suspension and skeletal expansion procedures, which were the mainstay of treatment, were applied for the first time in children and adolescents with obstructive sleep apnea.
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PMID:Surgical therapy for severe refractory sleep apnea in infants and children: application of the airway zone concept. 760 28

Patients with mitochondrial disease may present to the Intensive Care Unit (ICU) with a variety of neurological and general medical disorders. Eleven patients were admitted to a neurological ICU between 1970 and 1992 because of respiratory insufficiency, status epilepticus and/or metabolic encephalopathy associated with mitochondrial disease. Respiratory impairment occurred in eight patients and was associated with nocturnal hypoventilation due to respiratory muscle weakness, aspiration due to bulbar weakness and abnormalities of central control leading to a reduced CO2 drive, irregular respiratory patterns and sleep apnoea. Seven patients received continuous respiratory support during the acute illness; three were subsequently weaned to domiciliary ventilation, and four died. Five patients had stroke-like episodes, which in two were recurrent. Four patients developed tonic-clonic grand mal epilepsy associated with myoclonic fits (2 patients), absences (2), focal fits (1) and status epilepticus (2). Encephalopathy was associated with recurrent lactic acidosis (2 patients), cardiac failure (2), hyponatraemia (2), renal abnormalities (3) and complete heart block (1). Although rare, mitochondrial disease should be considered in any patient with unexplained respiratory failure, intractable epilepsy, lactic acidosis or recurrent stroke.
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PMID:Management of mitochondrial disease on an intensive care unit. 776 70

A previous uncontrolled study suggested that nasal continuous positive airway positive airway pressure (NCPAP) may improve left ventricular ejection fraction (LVEF) in patients with congestive heart failure (CHF) and Cheyne-Stokes respiration with central sleep apnea (CSR-CSA). In order to more critically evaluate the effects of NCPAP on cardiac function, we undertook a randomized, controlled trial of NCPAP in 29 patients with heart failure and CSR-CSA over a 3-mo period, with LVEF as the primary outcome measure. Patients with CHF and associated CSR-CSA who were receiving optimal medical therapy were randomly assigned to a control group (n = 15) or a group receiving nightly NCPAP (n = 14). Twelve patients in each group completed the study. There was a greater improvement of LVEF in the NCPAP group than in the control group during the study (mean +/- SEM = 7.7 +/- 2.5 versus - 0.5 +/- 1.5%, p = 0.019). In addition, there was a significantly greater reduction in the number of apneas and hypopneas (-28.5 +/- 3.9 versus -6.1 +/- 7.0 per hour of sleep, p = 0.012) in the NCPAP group than in the control group. Significantly greater improvements in symptoms of fatigue (5.6 +/- 1.2 versus 0.8 +/- 0.7, p = 0.005) and disease mastery (3.6 +/- 1.1 versus -0.7 +/- 0.7, p = 0.031) were also observed in the NCPAP group. We conclude that in patients with chronic heart failure and CSR-CSA, nightly administration of NCPAP can attenuate CSR-CSA, improve cardiac function, and alleviate symptoms of heart failure.
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PMID:Treatment of congestive heart failure and Cheyne-Stokes respiration during sleep by continuous positive airway pressure. 781 79

This study was designed to determine the impact of central sleep apnea with or without Cheyne-Stokes respiration (CSR) on morbidity and mortality. Central sleep apnea was found in 77 male general medical ward in-patients. Cheyne-Stokes respiration was found in 49 of the 77 men; in 15 men, CSR was severe, ie, > or = 25 percent of the night spent in CSR, in 34 men CSR was mild (1 to 25 percent CSR). Twenty-eight men had central sleep apnea but no CSR. An additional 31 patients had no sleep apnea and no CSR. The patients with severe CSR had more central apneas, more, but shorter desaturations, more awakenings and more wake time during the night, but spent more time in bed than those with no CSR or no apnea. Radiographic evidence was consistent with an association of CSR and heart failure. In addition, patients with severe CSR were at almost twice the risk of dying compared with those with no apnea and had a shorter survival time. Nevertheless, we could not confirm that CSR was an independent predictor of elevated mortality risk, implying that some other factors specific to severe CSR predispose these patients to shorter survival time.
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PMID:Comparison of patients with central sleep apnea. With and without Cheyne-Stokes respiration. 808 59

The histopathology, ultrastructure, and clinicopathologic correlations in six patients with cardiac failure and iron encrustation of lung elastic tissue were examined at autopsy. Transmission electron microscopy (TEM) and energy dispersive x-ray analysis were applied to two cases. Of the group, five patients had cardiac failure due to systemic hypertension (4 patients), valvular disease (4 patients), or coronary atherosclerosis (4 patients). Biventricular failure in one patient was associated with sleep apnea. Both iron and calcium, identified by histochemical stains, impregnated degenerated alveolar and vascular elastic fibers and were associated with a foreign body reaction and focal interstitial fibrosis. Energy dispersive x-ray analysis and TEM demonstrated iron and calcium on the microfibrillar portion of elastin. Morphometry indicated vascular changes of pulmonary venous hypertension. The authors concluded that mineral deposition probably represents nonspecific precipitation of metallic ions on altered elastic fibers in patients with cardiac failure. "Mineralizing elastosis" potentially contributes to lung restriction and, occasionally, can be a source of diagnostic confusion.
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PMID:Mineralizing pulmonary elastosis in chronic cardiac failure. "Endogenous pneumoconiosis" revisited. 827 51

Nasal continuous positive airway pressure (NCPAP) has been reported to improve daytime symptoms in patients with sleep disordered breathing due to heart failure. To examine this in a controlled manner, eight men with stable chronic heart failure (mean left ventricular ejection fraction 18% and mean frusemide dose 160 mg) were entered into a controlled trial of domiciliary nocturnal NCPAP. At polysomnography (with sleep apnea quantified as the number of > 4% dips in arterial saturation per hour), seven had nocturnal Cheyne-Stokes respiration (SaO2 dip rate 3 to 27/hr), and one both central and obstructive apneas (SaO2 dip rate 8/hr). After 2 wk nocturnal domiciliary NCPAP at < 1.5 cm H2O (placebo) and 7.5 cm H2O (active) in random order, bicycle exercise tolerance and heart failure symptoms (modified Likert questionnaire) were assessed by an observer unaware of the patients' NCPAP status. Pulse oximetry (all subjects) and radionuclide estimated left ventricular ejection fraction (three subjects) were also measured at the end of each period. Two subjects withdrew from the study because of worsening heart failure during active NCPAP (7.5 cm H2O), and one of these subjects died. In the remaining six subjects exercise tolerance, symptom scores, and the severity of sleep apnea were similar on active NCPAP compared with placebo. When it was measured, resting left ventricular ejection fraction was lower on active therapy than on placebo. These data exclude a 25% improvement in exercise tolerance with 95% confidence and suggest that a study of 160 subjects would be needed to exclude a 10% change in symptom score.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nasal continuous positive airway pressure in chronic heart failure with sleep-disordered breathing. 844 98


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