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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new clinical index of dyspnea and fatigue has been applied to rate the condition of patients with congestive heart failure. The index has 3 components, each rated on a scale from 0 to 4, for the magnitude of the task that evokes dyspnea or fatigue, the magnitude of the pace (or effort) with which the task is performed and the associated functional impairment in general activities. The ratings for each component are added to form an aggregated score, which can range from 0, for the worst condition, to 12, for the best. Because dyspnea and fatigue are prime symptoms and sources of clinical distress, the index helps reflect the quality of life in patients with congestive heart failure. In double-blind trials of therapy, changes in the index showed good correlations with patients' self-selected ratings of improvement. The posttherapeutic changes in the index ratings were significantly higher with a new active agent (lisinopril) than with placebo or another active agent (captopril).
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PMID:Changes in dyspnea-fatigue ratings as indicators of quality of life in the treatment of congestive heart failure. 254 92

The safety and tolerability of lisinopril (1.25-160 mg daily) were assessed in 3,270 patients (2,688 hypertensives and 582 patients with congestive heart failure (CHF] and 280 healthy subjects. The duration of therapy ranged from a single dose to 43 months; 438 patients received lisinopril for at least 12 months (mean 20 months). In the hypertensive population, the most frequent adverse events reported were headache, dizziness, cough, nausea, diarrhoea and fatigue, although not all of these events were thought to be related to lisinopril; 6.1% discontinued lisinopril due to adverse clinical events, most commonly cough and nausea. Twelve hypertensive patients died (0.45%), but most of these were not receiving lisinopril at the time of death and none was considered to be drug-related. In CHF patients, the most frequently reported adverse events were dizziness, dyspnoea, diarrhoea, hypotension and fatigue. Again, not all of these reports were considered to be drug-related. Therapy was withdrawn in 9.6% of patients--hypotension, dizziness, diarrhoea and rash being the most frequent reasons. Fifty-three CHF patients died (9.1%) and in three cases death was considered to be related to lisinopril therapy. Hypotension, orthostatic effects or dizziness following the initial dose of lisinopril occurred infrequently (in 1.3% of the hypertensive group, including those receiving hydrochlorothiazide, and in 4.8% of CHF patients). Changes in laboratory parameters were generally minor and seldom resulted in discontinuation of therapy. Long-term treatment of hypertension and CHF with lisinopril for at least 3 years confirms that the drug is well tolerated. Overall, the side-effect profile is very similar to that of other ACE inhibitors with regard to class-specific effects. However, taste disturbance was rarely observed.
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PMID:Clinical experience with lisinopril. Observations on safety and tolerability. 255 Jun 41

19 cases of pacemaker syndrome were observed in 121 patients implanted with VVI pacemakers. The main manifestations of pacemaker syndrome were dizziness, lightheadedness, fatigue, hypotension and congestive cardiac failure after permanent ventricular pacing. The incidence of pacemaker syndrome was 20% in patients with sick sinus syndrome and 13.2% with A-V block. Pacemaker ECG showed retrograde ventriculoatrial conduction in 25 of 121 cases. Among these patients, 14 (56%) had pacemaker syndrome, while only 5 of 96 cases without ventriculoatrial conduction had this syndrome, so the incidence of the two groups were quite different, P less than 0.0001. The frequency of ventriculoatrial conduction in patients with sick sinus syndrome was higher than in patients with A-V block (16/45 vs 9/76, P less than 0.05). The electrophysiologic study were performed in 17 cases before PM implantation. 3 cases had 170-190 ms ventriculoatrial 1:1 conduction. Retrograde ventriculoatrial conduction in pacemaker ECG were present during ventricular pacing in all of them.
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PMID:[Pacemaker syndrome and retrograde ventriculoatrial conduction]. 262 75

The records of 5 patients with congenital coronary arteriovenous fistula, diagnosed by echocardiogram, cardiac catheterization, angiocardiography and confirmed by cardiac surgery between 1982 and 1988, were studied. Their ages ranged from 3 months to 13 years. Among them, 3 were asymptomatic; one developed congestive heart failure shortly after birth, and was treated with digoxin and furosemide. Another patient had exertional dyspnea and fatigue. A grade 3-4/6 continuous murmur was heard over the right or left lower sternal border in four patients; only a pansystolic murmur was heard over the left lower sternal border in the remaining one patient. All the five patients had right coronary arteriovenous fistula terminating into the right ventricle. All received cardiac surgery. Direct epicardial ligation of the fistula was performed in one patient. The rest four cases required cardiopulmonary bypass and suture closure through the right ventricle by direct suture of the orifice in one patient, and Dacron patch closure in other three patients. No postoperative complications occurred in all patients. In conclusion, since the operation was quite safe, if patient had significant shunts and/or clinical symptoms, surgical correction should be considered.
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PMID:[Congenital coronary arteriovenous fistula: analysis of five cases]. 263 92

The renin-angiotensin-aldosterone system plays an important role in the development of congestive heart failure (CHF). In patients with chronic heart failure, angiotensin-converting enzyme (ACE) inhibitors, such as captopril, enalapril, and quinapril, have been shown to improve hemodynamics, reduce symptoms of fatigue and dyspnea, increase exercise capacity, correct hyponatremia, reduce diuretic requirements and ventricular arrhythmias, and conserve potassium and magnesium. ACE inhibitors reduce circulating levels of angiotensin II and aldosterone and may reduce plasma norepinephrine and vasopressin levels. They are equally effective in patients with mild to moderate heart failure and in patients with severe cardiac impairment. ACE inhibitors are at least as beneficial as digitalis in patients with mild heart failure, and they may even be considered as first-line therapy. Promising results have also been obtained in patients with myocardial infarction, in whom long-term therapy with ACE inhibitors has prevented an increase in heart size. ACE inhibitors improve prognosis in patients with severe heart failure and in patients with hyponatremia; the question of effect on survival in mild to moderate heart failure has yet to be answered.
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PMID:ACE inhibitors in congestive heart failure. 267 Feb 20

In 12 patients with severe congestive heart failure (CHF), captopril in doses of 25 to 150 mg, every 8 hours, was given for a period of 2 months, in addition to cardiac glycoside and diuretic drugs. After this treatment left ventricular end-diastolic diameter (EDD) decreased from 6.4 +/- 0.5 to 6.2 +/- 0.6 cm (p less than 0.05), left-ventricular end-systolic diameter (ESD) decreased from 5.7 +/- 0.5 to 5.4 +/- 0.6 cm (p less than 0.001), the ejection fraction increased from 30.8 +/- 7.0 to 36.2 +/- 6.9% (p less than 0.005) and mean velocity of circumferential fiber shortening (Vcf) increased from 0.51 +/- 0.12 to 0.62 +/- 0.13 circ/sec (p less than 0.001). Captopril markedly relieved dyspnea and fatigue. Three patients improved from class IV to class III, 4 patients from class IV to class II and 3 patients from class III to class II. These data suggest that captopril may be effective in the treatment of severe chronic CHF.
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PMID:The effects of captopril in severe congestive heart failure. An echocardiographic study. 268 8

Exercise tolerance in patients with normal cardiac function can improve with an exercise program. Controversy exists whether this is also true for patients with congestive heart failure (CHF). The limiting symptoms in patients with CHF are shortness of breath and fatigue. Hemodynamic parameters do not correlate well with exercise capacity in patients with CHF. These symptoms may be more related to factors that cause fatigue during exercise than to hemodynamic parameters or even to changes in pulmonary capillary pressure. The factors that cause symptoms include an increased lactate production and metabolic and blood flow abnormalities in the skeletal muscle. Exercise training can improve vasodilation and oxidation capacity, thereby reducing lactate production. Exercise programs may improve exercise capacity in the majority of patients with CHF due to coronary artery disease or idiopathic cardiomyopathy. However, certain patients with ischemia and with anterior infarctions may experience a detrimental effect on their cardiac function. Further studies are needed to better enable recognition of these patients but until this is possible, good clinical judgement must suffice.
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PMID:Cardiac rehabilitation for heart failure patients. 268 76

The most common congenital cardiac defect is VSD. This malady accounts for 20 to 30 per cent of all congenital cardiac defects and is representative of a cardiac lesion that increases pulmonary blood flow. Although lesions, which increase pulmonary blood flow, may vary in incidence, they frequently have common symptomatology. Over time, congestive heart failure becomes a problem. Poor respiratory status leads to weight loss, poor feeding, and failure to thrive. If unrepaired, the child often presents with cyanosis and tachypnea. The history may include frequent respiratory infections, exercise intolerance, generalized malaise, or fatigue. In spite of poor weight gain, the child may be edematous and have a large liver. Definitive diagnosis of each lesion may be made by echocardiogram, cardiac catheterization, or both. With these data and a detailed history, treatment and management decisions are determined. In most cases, as the child gets older, symptoms become more evident. This is the result of high pulmonary pressure. High pressure over time causes a thickening of the alveolar tissue, which decreases the permeability of the alveolar membranes for gas exchange. Lung changes can become irreversible, but it is unusual for irreversible changes to occur before 1 year of age. All the lesions described in this article are amendable to primary repair before 1 year of age, affording the best functional results. Postoperative nursing care includes management of persisting CHF and PVR while maintaining adequate cardiac output. Many factors, including electrolyte balance, nutritional status, conduction disturbances, stress, and parental anxiety, influence the management of these infants. The outcome depends greatly on the assessment skill of a highly competent cardiac intensive care nurse and an environment conducive to collaborative practice.
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PMID:Caring for patients with lesions increasing pulmonary blood flow. 281 77

Congestive heart failure is the most arrhythmogenic disorder in cardiovascular medicine. As left ventricular performance deteriorates and symptoms of dyspnea and fatigue become progressively more severe, nearly all patients with heart failure experience frequent and complex ventricular tachyarrhythmias and nearly half die suddenly during long-term follow-up. This imminent risk of sudden death appears to be present for all patients with congestive heart failure; ambulatory electrocardiographic monitoring and programmed electrical stimulation are not useful in distinguishing patient subsets that are particularly predisposed to fatal arrhythmic events. Although conventional antiarrhythmic agents are widely prescribed as a nonspecific approach to prevent sudden death in these patients, there is little evidence to indicate that these drugs possess clinically important antiarrhythmic activity in patients with congestive heart failure, and these agents frequently serve to exacerbate the heart failure state and the underlying ventricular tachyarrhythmia. A useful approach to the prevention of sudden death in patients with congestive heart failure addresses the reversible causes of lethal ventricular arrhythmias in these individuals. Both experimental and clinical evidence indicates that circulating neurohormones and electrolyte deficits (particularly of potassium and magnesium) interact to provoke malignant ventricular ectopic rhythms and that the prevention of electrolyte depletion and the use of neurohormonal antagonists may exert clinically important antiarrhythmic actions. This physiologic approach may prove to be a more effective means of ameliorating the problem of sudden death than the empiric administration of conventional antiarrhythmic drugs.
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PMID:Hormone-electrolyte interactions in the pathogenesis of lethal cardiac arrhythmias in patients with congestive heart failure. Basis of a new physiologic approach to control of arrhythmia. 287 53

The value of beta blockade after myocardial infarction is extremely well documented. Close to 50 randomized trials have been performed, involving about 40,000 patients with short- or long-term follow-up. Over 20,000 patients have been included in more than 20 placebo-controlled trials with a follow-up period of 3 months or more. In long-term follow-up studies, about 1 to 2 weeks to 1 year after myocardial infarction, mortality was reduced by 21% and reinfarction by 24% (about 20,000 patients in 24 trials). The trial medication was withdrawn in about 20% in both placebo and beta-blocker groups in the major trials. In addition to reduction of mortality and reinfarction rate, benefits have clearly been demonstrated on severity of chest pain, arrhythmias, and other thromboatherosclerotic complications, as well as on readmissions. Significantly more patients experienced congestive heart failure, hypotension, bradycardia, and cold hands with beta-blocker treatment, whereas no clear-cut difference was found for atrioventricular block, bronchial constriction, and intermittent claudication. Some studies have reported more tiredness, depression, and gastrointestinal disturbances. In the Stockholm metoprolol trial, analyses on quality of life have been performed. In this trial, 3 years of metoprolol treatment after myocardial infarction resulted in a prolongation of both survival and time spent completely asymptomatic, as well as in an optimal functional state. Furthermore, less time was spent disabled after serious atherosclerotic complications. Long-term beta blockade after myocardial infarction reduces mortality and morbidity but causes adverse reactions in some patients. With proper selection of patients and type and dosage of beta blocker, survival without atherosclerotic complications and side effects can be prolonged.
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PMID:Use of beta blockers in postinfarct prophylaxis: aspects on quality of life. 288 38


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