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)

A 14-year-old boy who ingested 8000 mg of propranolol developed sudden onset of arrhythmias, cardiac failure and convulsions. He responded to ventilator support, transvenous pacing, and massive dosage of isoprenaline. The clinical features and management of propranolol overdosage are outlined.
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PMID:Self-poisoning with propranolol. 723 Dec 57

22 patients with severe preeclampsia-eclampsia were treated in our Intensive Care Unit from 1972 to 1978. Control of convulsions was achieved by diazepam, diphenylhydantoin and phenobarbital. In 11 comatose patients brain monitoring was carried out by frequent neurological examination and use of computerized x-ray tomography; aspiration of gastric contents was prevented by nasotracheal intubation. Brain oedema therapy included controlled hyperventilation, steroids and mannitol (7 patients). 10 patients with respiratory failure (due to pulmonary oedema, "shock lung" or aspiration pneumonitis) were treated by mechanical ventilation. Diastolic blood pressure above 100 mm Hg was reduced by hydralazine. Diuresis was induced by normalization of hypovolaemia with albumin and plasma expanders. Six patients died (27%); main causes of death included intracerebral haemorrhage, brain oedema, heart failure, acute pulmonary thromboembolism and bleeding from DIC.
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PMID:[Intensive care of severe preeclampsia-eclampsia. A report on 22 cases (author's transl)]. 742 60

The objectives of exercise testing in congestive heart failure (CHF) may be summarized as follows: (a) detect impaired cardiac performance, (b) grade severity of cardiac failure and classify functional capability, and (c) assess effects of interventions. Several different methods are available to make these assessments, and we have to ask ourselves how well exercise testing achieves these objectives. It has to be kept in mind that the power generated by the exercising muscles is dependent on the oxygen delivery to the skeletal muscles. Oxygen uptake is the result of an integrated performance of the lungs, heart, and peripheral circulation. In patients, as well as in normal subjects, oxygen uptake is related to hemodynamic indices such as cardiac output, stroke volume, or exercise duration when a stepwise regulated maximal exercise protocol is used. However, there are major differences in the concept of a true maximum in normal subjects versus heart failure patients. Fit-normal subjects will achieve a real maximal oxygen uptake, whereas patients may stop testing before a maximum is reached because of symptoms such as dyspnea or leg fatigue. Therefore, it is better if the actual oxygen uptake can be measured. "Peak" rather than true maximal oxygen uptake has been suggested for the classification of the severity of heart failure. Peripheral factors modify the cardiac output through such factors as vascular resistance, organ function, and hormonal release. Maximal exercise will stress the cardiovascular system to a point where the weakest chain will impose a limiting effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of exercise testing in heart failure. 751 35

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

We report a 46-year-old man with bacterial endocarditis and cardiac failure, who developed status epileptics. The patient was apparently well until July of 1991 when there was a gradual onset of fever and general fatigue. He was hospitalized to the cardiology service of our hospital where diagnosis of bacterial endocarditis and aortic insufficiency was made. On October 9, 1991, he suddenly developed cardiogenic shock, and emergency replacement of the aortic valve was made; at the operation, the main trunk of the left coronary artery showed embolic occlusion, and the myocardial movement was markedly diminished; serum creatine kinase was 3.150 IU/l. His cardiac failure did not resolve, and renal failure developed in December 1991, for which peritoneal dialysis was necessary. On February 2, 1992, he suddenly developed a clonic seizure which started from his face with a transient post-ictal left hemiparesis; a cranial CT scan was unremarkable. He was treated with phenytoin and glycerol, however, he developed status epileptics on February 3; he developed cardiac arrest after the injection of phenytoin 750 mg. He was resuscitated, however, his status did not resolve. Neurological consultation was asked on February 4. On physical examination, his blood pressure was 80/40 mmHg heart rate 77/min and regular, and body temperature 39.1 degrees C. The palpebral conjunctiva were slightly anemic, however, the bulbar conjunctiva were not icteric. No cervical adenopathy was noted. Glade II systolic murmur was heard in the apex; the lungs were clear. The abdomen was flat and soft without organomegaly. No edema was present in the legs. On neurologic examination, he was comatose without response to painful stimuli. He repeatedly had convulsion lasting for 30 seconds every 2 to 3 minutes; his convulsions started with the conjugate deviation of the eyes to the left followed by turning of the head toward left, and then clonic convulsions started in this left upper limb extending to other extremities. The optic fundi were unable to visualize because of corneal clouding; light reflex was sluggish on the right side; no oculocephalic response was elicited; corneal reflex was also lost bilaterally. Extremities were hypotonic, and no automatic movement was seen. The triceps brachii reflex was diminished, but all the other deep reflexes were lost; no plantar response was elicited. Meningeal sign was absent. He was treated with intravenous diazepam; the interval of convulsions prolonged, however, blood pressure dropped to 40 to 40 mmHg. On February 4, intravenous thiopental anesthesia was instituted, and assisted respiration was started.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 46-year-old man with cardiac failure and statues epileptics]. 794 26

Graves' disease, which is an organ-specific autoimmune disorder, is the most frequent cause of thyrotoxicosis. Females are more often affected than males. The clinical pattern varies, however, and nearly every organ system may be involved. This case study describes a formerly healthy young woman with Graves' disease who was admitted to the hospital with cardiac failure, convulsions and generalized lymphoid hyperplasia. A reversible thyrotoxic cardiomyopathia combined with hyperdynamic circulation may result in cardiac failure even in younger patients, and the cardiac function normalizes in the euthyroid state. Seizures may occur in association with hyperthyroidism. High doses of propranolol may precipitate the condition by lowering the threshold for seizures.
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PMID:[Heart failure and convulsions in thyrotoxicosis. A young woman with Graves' disease]. 797 5

Acute alcohol ingestion can affect life expectancy and is directly responsible for 3,500 deaths per year. Acute lung diseases are mainly caused by pneumococci, Gram negative bacilli and anaerobic germs, and are often due to multiple microbes. In this case, evolution toward abscess can be feared. Septicaemia and enterobacterial peritonitis are frequently observed in cirrhotic patients. Ethanol, hypokaliemia and hypophosphoraemia also lead to rhabdomyolysis. Rhabdomyolysis can be complicated with acute renal failure and hyperkaliaemia. Alcoholic ketoacidosis and the hypoglycaemia favored by prolonged inadequate nutrition, are corrected by infusion of glucose solutions. Hyponatraemia can be complicated by convulsions and central pontine myelinolysis. Minor forms of alcoholic hepatitis remiss after stopping alcohol intoxication. The major forms can evolve toward fatal encephalopathy; treatment with corticosteroids improves the prognosis in severe hepatitis. The cardiac failure with lactic acidosis in shoshin beriberi rapidly evolves to collapsus; treatment is based on emergency administration of vitamin B1. Management of patients in acute alcohol episodes requires great vigilance. Careful clinical examination and biological tests should eliminate severe somatic complications before concluding to simple alcoholic intoxication.
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PMID:[Severe somatic complications of acute alcoholic intoxication]. 813 83

The presentation, pattern of acute illness, and incidence of learning difficulties are described in 63 (33 boys, 30 girls) children with salt wasting 21-hydroxylase deficiency, drawn from a cohort study of congenital adrenal hyperplasia in the South West Region of England between 1968 and 1988. Thirty boys presented with a salt losing crisis from birth whereas the other three boys presented between 2 and 14 months of age with failure to thrive and hyponatraemia. Diagnostic uncertainty led to 13 (43%) of 30 girls developing a salt losing crisis. Five girls were misassigned as boys at birth. There were four deaths in the group, two due to salt losing crisis, one to complications of prematurity possibly compounded by 21-hydroxylase deficiency, and one from heart failure probably related to an excess of steroids. Acute admissions were common, especially during the first year of life, with convulsions in 7% of admissions. The 9% incidence of hypoglycaemia was considered to be an underestimate as blood glucose was measured in only 56 (22%) of 254 admissions. No convulsions occurred in the 38 (15%) admissions where the parents had given intramuscular hydrocortisone before bringing the child to hospital. A high incidence of learning difficulties was found among the 59 surviving children (9/30 (30%) boys and 6/29 (21%) girls), and in only two children could any factor other than 21-hydroxylase deficiency be invoked. Analysis of the subgroup with learning difficulties indicated that they were more ill at presentation with a significantly higher incidence of hypoglycaemia, and that growth in the first year was significantly worse. It is concluded that congenital adrenal hyperplasia remains a formidable disorder with an appreciable mortality and morbidity. The high incidence of learning difficulties seen in salt wasting 21-hydroxylase deficiency needs further attention. A prospective study is indicated to examine the effect of neonatal screening on morbidity from congenital adrenal hyperplasia, particularly the intellectual impairment seen in this study.
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PMID:Presentation, acute illness, and learning difficulties in salt wasting 21-hydroxylase deficiency. 813 66

Topical congenital pulmonary vein stenosis is a uncommon defect, both isolated or associated to other cardiac abnormalities. Only the localization of the lesions seems to affect the survival, because 60% of survival cases has unilateral stenosis; the severity of associated cardiac lesions become the prognosis poor. We describe two cases: 1st case, a 43 days old boy presented with heart failure and convulsion and had a diagnosis of pulmonary hypertension, atrial septal defect and tricuspid regurgitation, without pulmonary abnormalities. He had recurrent pulmonary infections and a cerebral ischemia in the following months, and died at 15 months of age for sepsis. Autopsy revealed stenosis and atresia in all pulmonary veins, with venous and arterial hypertension. There was also aortic hypoplasia and aortic and tricuspid valves indifferentiation; 2nd case, a 7 days old girl had a diagnosis of aortic coarctation and atrial and ventricular septal defects. Surgical corrections, at 38 and 46 days old, firstly of the aortic coarctation and after for the septal defects, disclosed and relief a supra-valvar mitral stenosis, but she remained on heavy respiratory insufficiency. At 6 months old, she returned to the hospital with dyspnea and cianosis, heart failure and hemoptisis; a sepsis developed and she died. At autopsy, there were severe pulmonary vein stenosis on the left and in the superior right veins, with pulmonary hypertension and hemorrhage.
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PMID:[Pulmonary vein stenosis. Report of 2 cases and review of the literature]. 854 96

Hearts fail because myocardial power fails. Assist, support, or replacement devices fail, at least in part, because their blood-contacting surfaces fail. Mechanical repowering of a failing heart might circumvent these difficulties by preserving a largely healthy endocardium while correcting the basic deficit, power. Any serious consideration of doing this though must confront some difficult requirements. Effective indefinite support must be coupled with preservation or restoration of valve competence, coronary flow, rapid low-impedance refilling and independent left and right pressures; the avoidance of wall coaptation; hardware that fits in the available space; and unless muscle powered, adaptability to a deliverable form of power. Despite earlier intense interest in acute mechanical devices and later empiric study of muscle wraps, little systematic methodical work has been done on elucidating and meeting these practical requirements. Concerted efforts toward developing research tools and techniques for their study and then finding mechanisms to meet them could well yield one or more effective modalities that circumvent a major obstacle to the indefinite mechanical treatment of heart failure.
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PMID:Long-term ventricular wall actuation: can and should it be systematically explored? 864 33


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