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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies on the incidence and pathophysiology of hypotension in fulminant hepatic failure showed that 82 out of 94 patients developed arterial hypotension with a systolic blood pressure of less than 80 mmHg. Such episodes accounted for 16% of the total time spent in grade IV coma. Factors such as haemorrhage, cardiac or respiratory abnormalities, extracorporeal perfusion, or hypotension which occurred during the terminal stages of the illness, could be implicated for only 40% of this time, leaving 60% as unexplained. Further investigation of these unexplained factors showed that peripheral vasodilatation rather than primary heart failure was responsible, and in all but three patients construction of ventricular function curves showed a normal ventricular response to volume expansion with a corresponding increase in blood pressure. A small, but significant, slowing of the heart rate occurred during these periods of unexplained hypotension. This, together with the association that was found between the occurrence of hypotension and cerebral oedema with coning, suggests that central vasomotor depression may be important in its pathogenesis.
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PMID:Pathophysiology of hypotension in patients with fulminant hepatic failure. 60 28

A case of chlorpropamide-induced, symptomatic hyponatremia in a diabetic patient is reported. The hyponatremia was associated with loss of appetite, nausea, and vomiting. These symptoms caused reduced food intake which provoked severe hypoglycemia with disturbed consciousness. The hyponatremia developed when the chlorpropamide doses were increased from 400 to 600 mg/day. Withdrawal of chlorpropamide was followed by remission of hyponatremia. Chlorpropamide-induced hyponatremia is a rare complication and is due to an antidiuretic effect of chlorpropamide caused by increased secretion of adiuretin and potentiation of the effect of chlorpropamide caused by increased secretion of adiuretin and potentiation of the effect of adiuretin in the tubuli of the kidney. This case report and the analysis of 18 published cases in the literature show the following characteristics for chlorpropamide-induced hyponatremia: (1) Hyponatremia is a rare complication in the treatment of diabetics with chlorpropamide. The patients typically are female and over sixty. The dosage of chlorpropamide usually was 500 mg daily or even more. (2) Hyponatremia is often unrecognized for a long time because the symptoms are not specific. The characteristic symptoms include loss of appetite, nausea, vomiting, abdominal pain, confusional state and, rarely, convulsions and coma. Recovery occurs spontaneously after withdrawal of the drug. (3) The incidence of this type of hyponatremia is increased in cases of preexisting tendency to water retention such as heart failure and renal failure, and in cases of diuretic therapy. In the light of these findings, the authors believe that chlorpropamide is no longer a drug of choice in the treatment of diabetic women, especially in cases of preexisting tendency to water retention and in diuretic therapy. In such cases, a sulfonylurea without antidiuretic effect is to be preferred.
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PMID:[Hyponatremia and hypoglycemia after treatment with chlorpropamide. Case histories with review of the literature on 18 cases of chlorpropamide induced hyponatremia]. 66 98

Little information is available on the toxicity of monochloroacetic acid. We report the case of a 38 year-old man who was splashed with an 80% monochloroacetic acid solution on 25-30% of his body surface. In addition to epidermal and superficial dermal burns, features of systemic poisoning occurred within a few hours including disorientation, agitation, cardiac failure and coma. He later developed severe metabolic acidosis, rhabdomyolysis, renal insufficiency and cerebral edema, and died due to uncal herniation on d 8. The 4 h post exposure plasma monochloroacetic acid concentration was 33 mg/L confirming skin absorption. In addition to its corrosive action, monochloroacetic acid probably blocks the tricarboxylic acid cycle (Kreb's cycle) and may also react with sulfhydryl groups in enzymes, causing severe tissue damage in energy-rich organs.
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PMID:Fatal systemic poisoning after skin exposure to monochloroacetic acid. 143 33

In the period from Jan. 1988 to Jan. 1991 operations for the formation of an aortocoronary shunt were carried out in 437 patients at the Department of Combined Affections of the Coronary and Peripheral Arteries, Bakulev Research Institute. In some cases the operation was combined with resection of a postinfarction aneurysm of the left ventricle. Cerebral complications developed in the postoperative period in 28 (6.4%) patients. Their analysis showed the prevalence of severe forms of consciousness disturbances: coma and comatose states were encountered in 85.7% of cases. The main causes of the complications were acute heart failure (64.3%) and arterial embolism (14.3%). In only one case concomitant affection of the branches of the aortic arch was found to be the main cause of the development of a transitory ischemic attack. It is concluded that the development of acute heart failure in the patients may sharply increase the incidence of neurologic complications.
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PMID:[The causes of cerebral complications in patients with ischemic heart disease following myocardial revascularization operations]. 148 86

We report the case of a 59-year-old woman suffering from profound accidental hypothermia promoted by intoxication with codeine, sedatives, and a beta-blocking agent ingested in a suicidal attempt. Treatment was further complicated by ventricular fibrillation and asystole that was refractory to therapeutic interventions. The comatose patient (Glasgow score 3) was found outdoors in rainy weather--environmental temperature approximately 10 degrees C (50 degrees F)--by children. The skin was rosy when the emergency team arrived. The respiratory rate was low and the ECG showed sinus rhythm with a heart rate of 28/min. No arterial pulsations were detectable, even at the carotid and femoral sites. Because catecholamine therapy failed to increase the heart rate, the patient was suspected to be profoundly hypothermic. After confirming core hypothermia with a rectal temperature of 25 degrees C (77 degrees F) at the initial receiving hospital, transfer to an institution with cardiac surgery facilities was initiated. During this transport and after arrival, ventricular fibrillation occurred at decreasing intervals followed by asystole, which was refractory to large doses of epinephrine. The patient was transferred to the operating room under continuous resuscitation maneuvers and cardiopulmonary bypass was instituted via the femoral vessels. After 110 min of extracorporeal circulation (ECC, flow 4.5 l/min) normothermia was achieved and the asystole reverted spontaneously to sinus rhythm. The patient's course was subsequently complicated by worsening pulmonary gas exchange with signs of pulmonary edema on X-ray films and cardiac failure, which was treated successfully with epinephrine and dopamine. No neurological deficits were detectable after consciousness had returned.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Successful therapy of a cardiac arrest during accidental hypothermia using extracorporeal circulation]. 156 99

The clinical spectrum of toxic effects and serum concentrations after ingestion of carbamazepine were studied in 82 pediatric patients. Serum carbamazepine level was related to the depth of coma (p less than 0.001), convulsions (p = 0.002), hypotension (p less than 0.001), and the requirement for mechanical ventilation (p less than 0.001). In 10 patients in deep coma with a Glasgow Coma Scale (GCS) of 3-4, the mean serum level was 213 mumol/L (range 143 to 343); seizures, ventilatory failure, or hypotension caused by myocardial failure and conduction defects were observed. In four of these, large doses of inotropic agents were required, one patient was treated with plasmapheresis, and two died--one of cardiac failure and one of aspiration pneumonitis. In 27 patients with moderate coma (GCS 5-8), the mean serum level of carbamazepine was 112 mumol/L (range 63 to 176); convulsions were observed in two patients in this group. In 45 patients whose conscious state was mildly depressed or normal (GCS 9-15), the mean serum level was 73 mumol/L (range 37 to 128); additional effects were drowsiness (80%), ataxia (53%), nystagmus (38%), vomiting (17%), and dystonia (7%). I conclude that patients with serum carbamazepine levels of approximately 100 mumol/L require close observation, whereas those with levels greater than 150 mumol/L may require intensive life support.
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PMID:Acute toxic reaction to carbamazepine: clinical effects and serum concentrations. 164 Mar 2

Scabies was first found in a 71-year-old female who had been diagnosed as having leukemic transformation of primary myelofibrosis and had undergone treatment for the disease. She was admitted to the hospital in December 1986, because of abdominal fullness and a generalized subcutaneous tumor that proved to be myeloblastoma. For treatment of the underlying disease, the regimen of the combination of vindesine, cyclophosphamide, 6-mercaptopurine, and prednisolone was selected. She developed cardiac failure and fell into a coma one month after starting the anticancer therapy. She was put on artificial respiration and on additional steroid therapy as well. Dexamethasone was administrated at 16 mg/day. Since the myeloblastomas found on admission regressed, the steroid therapy was continued. She was in coma for a few days before her skin lesions turned red and formed a grayish crust in the lower abdominal region. Several days later, the doctor responsible for the treatment of this patient developed pruritus and exanthema on both arms, and soon many nurses in the same hospital-ward developed similar symptoms. At approximately the same time, the patient with myelofibrosis was diagnosed as having Norwegian scabies: the crusted skin lesions revealing many Sarcoptes scabiei mites. Two doctors (2/18), 17 nurses (17/19) and 3 other patients (3/51) were found to have contracted scabies, and we recognized the hospital spread of the infection. The first patient was isolated in a private room, and we avoided direct contact with her. The persons with scabies were treated with crotamiton liniment. The first scabies patient died of cardiac failure 1 month after falling into a coma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hospital spread of scabies from an immunocompromised patient with Norwegian scabies]. 176 99

Since January 1988 till June 1990 145 patients with combined coronary and vascular pathology have been operated on. Concomitant damage of aortic arch branches was observed in 54 patients (37.2%), and aortocoronary bypass surgery was performed in 40 patients without correction of the carotid vascular bed pathology. These patients comprised the basic group, which was divided into two subgroups depending on the clinical pattern of the disease: subgroup I--18 asymptomatic patients (45.0%), subgroup II--22 patients (55.0%) with clinical signs of the disease. The basic group comprised 257 patients with CHD alone and no damages of the aortic arch branches. In the postoperative period 10 out of 40 patients of the basic group developed neurological complications: brain hypoxia, delirious syndrome (3 patients); brain hypoxia, pre-comatose condition (3 patients); brain hypoxia, comatose condition (2 patients); transitory ischemic attack (2 patients). No significant differences in the development of complications have been observed in patients of both subgroups. In the control group neurological complications developed in 9 out of 257 patients (3.5%). The comparison of reasons responsible for the onset of complications in both groups has shown that acute heart failure was significantly predominant (10%) in the basic group, as compared to control group (1.9%). It has been concluded that after aortocoronary bypass surgery the risk of neurological complications was higher in patients with the accompanying damage of the aortic arch branches than in patients with CHD alone; the onset of acute heart failure in the early postoperative period increases the risk of neurological complications in such patients.
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PMID:[The risk of neurological complications following aortocoronary bypass in patients with multifocal atherosclerosis]. 178 76

Thirty out of 287 patients (10.4%) admitted to hospital for infective endocarditis between December 1970 and January 1990 had neurological complications. Twenty-three patients had native valve infectious endocarditis and 7 had prosthetic valve endocarditis. The clinical features were characterized by the frequency of aortic valve involvement (23 out of 30) and other complications, especially cardiac failure (16 cases) and peripheral vascular manifestations (7 cases). The commonest organism was the staphylococcus (53% of identified organisms) but the number of negative blood cultures was high (50% of cases). The neurological complication was often the presenting symptom of the endocarditis (19 cases) but it occurred after bacteriological cure in 4 cases. The complications observed were cerebral ischemia (16 cases), cerebral haemorrhage (11 cases), coma (2 cases), and one peripheral neuropathy causing a Claude Bernard Horner syndrome. These complications presented with hemiplegia in 17 cases, a meningeal syndrome in 8 cases, a convulsion in 1 case, a Von Wallenberg syndrome in 1 case, and a Claude Bernard Horner syndrome in 1 case. Twelve patients had a transient or permanent neurological coma. Cerebral CT scan showed ischemic lesions in 7 cases and haemorrhagic lesions in 10 cases. Carotid angiography demonstrated mycotic aneurysms in 6 patients. Twelve patients died: the cause of death was neurological coma (7 cases), low cardiac output (4 cases) and haemorrhagic shock (1 case). Four patients underwent neurosurgery: 3 for clipping a mycotic aneurysm and 1 for drainage of an intracerebral haematoma. Poor prognostic factors were: coma, cardiac failure, cardiac valve prosthesis and, above all, the extent and multiplicity of the neurological lesions. The authors propose the following measures to improve the prognosis: early surgery in cases of large and/or mobile vegetations especially when the infecting organism is a staphylococcus and when a systemic embolism has occurred; routine CT scanning and/or digitised cerebral angiography in all patients with infective endocarditis to detect surgically accessible mycotic aneurysms.
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PMID:[Neurologic manifestations of infectious endocarditis]. 201 89

The causes, clinical indications and diagnosis and differential diagnosis of cardiac disorders which may lead to cerebral symptoms are illustrated on the basis of a review of the present day level of scientific research. Principally involved are cerebral ischaemias arising from cerebral embolisms or from reduction of cardiac output in cardiovalvular and myocardial disorders. The incidence of all embolisms of cardiac origin makes up 10% of all ischaemic cerebral infarcts, with auricular fibrillation, irrespective of its origin, mitral stenosis, myocardial infarct, mitral insufficiency and combined mitral valve defects, and, in younger patients, mitral valve prolapse, being, in this order of frequency, of primary clinical significance. The other cardiovalvular and myocardial disorders have, in comparison, a relatively low incidence of cerebral embolisms. Haemodynamically induced cerebral ischaemias frequently occur in the form of complications following acute cardiac arrest, in myocarditis and in case of primary cardiomyopathies resulting from cardiac insufficiency or complicating bradyarrhythmia. They are clinically apparent in the form of syncope, and other impairments of consciousness of various levels of seriousness with and without indications of cerebral origin, extending up to coma. In view of the high incidence of 25% of acute cerebral ischaemias in cases of cardiac disease, not only neurological but also detailed cardiological investigation is vital in all cases for a correct diagnosis and for the selection of a suitable course of treatment. Cerebral complications in bradyarrhythmia and endocarditis are discussed in the context of a review of the relevant literature together with consideration of their epidemiology, aetiology, pathophysiology and clinical profile. Pathological sinus-bradycardia, bradyarrhythmia absoluta, sinu-atrial and atrio-ventricular blockages, carotid-sinus and sick-sinus node syndrome, paroxysmal atrial tachycardia, AV-node tachycardias, and auricular fibrillation and flutter, taken as a whole, lead to cerebral complications affected patients in 5 to 10% of afflictions of the central nervous system occur in 50% of patients suffering from complete AV blockage and, at a not precisely definable frequency, in patients suffering from other bradyarrhythmias. In addition to transitory, uncharacteristic symptoms such as dizziness, vertigo, impairment of vision and balance, presyncope, syncope and Adams-Stokes syndrome dominate the clinical profile. Endocarditis, with an incidence of 0.01 to 0.05% in the overall population, results in central nervous system complications in 12 to 25% of cases on average.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Heart diseases as a cause of cerebral symptoms and syndromes]. 222 59


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