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)

Sixteen cases of lactic acidosis are reported: 7 phenformin treated diabetes, 5 cardiovascular diseases (2 myocardial infractions, 2 pulmonary embolisms, 1 heart failure). In 2 patients no etiology was found. Concomittant renal failure or liver diseases were found in respectively 9 and 4 cases. Patients presented the usual criteria of lactic acidosis: clinical, polypnea, severe hypotension (9/16), peripheral symptoms of shock (12/16), hypothermia (9/16), abdominal pain (9/16): biologically, acidosis (pH = 6,99 +/- 0,01, HCO3- = 5,9 +/- 1,5 mmol), hyperlactatemia (14,1 +/- 3,6 mmol/l) with hig lactate/pyruvate ratio (105 +/- 73), and anion gap (24,3 +/- 4,2 mmol/l). Sodium bicarbonate infusion was performed in all cases (2,5 to 42 mmol/kg). Few cases required volhemic expansion or furosemid induced diuresis. One patient was treated with extrarenal dialysis. 13 patients were alkalinised with less than 185% of estimated deficit measured from alkalin reserve: 12 died. 3 patients received 185% more than this deficit, associated with furosemid (1,8 to 12,5 mg/kg): only one patient died ten days after by casual disease, with lactatemia of 3,2 mmol/l. In spite of the small number of patients, these findings suggest that an early and massive alkalinisation, with large doses of furosemid, can improve the severe lactic acidosis prognosis.
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PMID:[Lactic acidosis and intensive care. 16 cases (author's transl)]. 23 77

The present study was undertaken to examine the effects of changes in PaCO2 and pHa on myocardial blood flow and central hemodynamics during acute ischemic left ventricular failure. Six closed-chest dogs anesthetized with pentobarbital were hyperventilated, and CO2 was added to the inspiratory gas to induce: a) normocapnia, b) hypocapnia, c) hypercapnia, and d) hypercapnia with sodium carbonate given to correct pH. Embolization of the left coronary artery with 50-microns microspheres resulted in deterioration of left ventricular function, as indicated by increased left ventricular end-diastolic pressure and mean pulmonary arterial pressure, while cardiac output decreased. During hypocapnia with left ventricular failure, the central hemodynamics remained unchanged, while a minor but nonsignificant decrease in myocardial blood flow was observed. Hypercapnia aggravated the heart failure, as indicated by increased left ventricular end-diastolic pressure, mean right atrial pressure, and mean pulmonary arterial pressure; however, the pump function of the heart was unchanged, as demonstrated by the unaltered cardiac output, heart rate, and mean aortic blood pressure. The changes in the central hemodynamics were reversed when pH was normalized during hypercapnia. Thus, in the present study pH, and not PaCO2, was responsible for the hemodynamic deterioration observed during hypercapnia in the failing heart.
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PMID:Effects of carbon dioxide and pH on myocardial function in dogs with acute left ventricular failure. 311 92

An elderly patient with bipolar manic-depressive psychosis, stabilised satisfactorily on lithium carbonate, developed acute symptoms of lithium toxicity shortly after commencing mefenamic acid. Vulnerability factors for the interaction may have included age, history of cardiac failure, and impaired glomerular function. It is hypothesised that the interaction may have been mediated by inhibition of prostaglandin activity.
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PMID:Lithium toxicity and mefenamic acid. A possible interaction and the role of prostaglandin inhibition. 350 11

Over the last ten years the efficacy of lithium salts in cluster headache has been well demonstrated. Our patient, who had been suffering from cluster headache for approximately 30 years, had been in haemodialysis treatment for the last ten years for chronic renal failure. Moreover, he was affected by heart failure and peptic ulcer. The patient was currently under therapy with Digitalis, Isorbide dinitrate, and ranitidine and was dialyzed three times a week for a total of five hours each time. Neither prophylactic headache therapy nor high doses of analgesic drugs had proved effective. Although this patient was in haemodialysis, lithium treatment was indicated. The administration of lithium carbonate 300 mg during dialysis days and 150 mg during non-dialysis days improved the attacks. Complete recovery from the attacks was obtained when the serum levels of lithium reached the therapeutic range. No side effects were noted.
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PMID:Cluster headache: clinical efficacy of lithium salts in a haemodialysis treated patient. 401 22

Two cases of death associated with the use of lithium carbonate are described. The first one concerns a 39-year-old man who was found suddenly dead on his hospital bed. Toxicologic analysis revealed "therapeutic" levels of lithium, nitrazepam, flurazepam, and phenobarbital. The second case involves a 54-year-old woman initially treated for acute cardiac failure and hypertension, who was finally recognized as a case of lithium intoxication; she died of cardiac arrest without evident cardiac lesions and without lithium ions in serum and urine. The medicolegal aspects of both cases are discussed, with reference to the problems of diagnosis, clinical and toxicological correlations, and the medical responsibility.
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PMID:Two cases of death associated with the use of lithium carbonate. 679 20

In 18 patients with acute myocardial infarction admitted to the Cardiological Care Department within 6 hours after the onset of chest pain, before administration of drugs and then in the 2nd, 3rd, 5th and 7th day, the levels of glucose, pyruvate, lactate in venous blood, the lactate/pyruvate ratio (L/P) and pH, actual hydrocarbons, PCO2 and PO2 in capillary arterialized were determined. Depending on the clinical status at admission the patients were classified into 2 groups: I--without complications (I class according to Killip-Kimbal; n = 10), and II--with complications (II-IV class of cardiac failure according to Killip-Kimbal and/or complex ventricular arrhythmias e.i. III-V class according to Lown and heart block of Mobitz--type II and III degree; n = 8). None of the patients had diabetes, chronic respiratory tract diseases, renal failure and liver cirrhosis. The control group consisted of 11 healthy persons. On the first day of myocardial infarction, the significant increase of blood glucose, lactate, pyruvate, as well as significant decrease of blood pH, HCO3- and PO2, and non significant increase of L/P ratio were observed in both groups as compared to the control group. Also there were non significant difference of the glucose, lactate, pyruvate L/P ratio and pH, PCO2 and HCO3- values between the I and II group on the first day of the acute myocardial infarction, with exception of the PO2, which was significantly lower in the group II. In the following days an increase of PO2 was observed. Since this effect coincided with a decrease of lactate concentration (significant only in the group II) it could be concluded, that the observed decrease of the lactate concentration resulted from the higher supply of oxygen. The obtained results have shown, that increase of glycaemia values and decrease of PO2 values may be considered as biochemical markers for hemodynamic complications of acute myocardial infarction.
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PMID:[Lactate metabolism in acute myocardial infarction]. 780 May 82

It is shown that, in a multicompartmental homeostatic system, the extent of interaction between any two compartments can be assessed by determination of the difference in free energy change of one particular reaction, or a series of coupled reactions, operative in both of the compartments under consideration. Hydrogen ion concentration and carbon dioxide tension have been used to determine free energy change difference relationships between the venous and arterial compartments (-deltadeltaG(a-v)) of the circulatory system. Data from the literature (from two studies of congestive heart failure and one study of experimentally induced cardiac arrest) are used to calculate -deltadeltaG(a-v). It was found that in control subjects -deltadeltaG(a-v) is close to zero, whereas in congestive heart failure or cardiac arrest, the value rises to 150 cal mol(-1) or more, whereas in blood, the approach towards equilibrium between hydrogen and bicarbonate ions and dissolved carbon dioxide (aqueous CO2) is known to be only moderately rapid. It is concluded that, in the system under study, and with respect to the reaction H+ + HCO3- = CO2 + H2O, a high value for the free energy change difference between the two compartments (high -deltadeltaG(a-v)) must be due to an insufficient blood circulation rate. Accordingly, -deltadeltaG(a-v) is probably a quantitative measure of cardiac insufficiency.
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PMID:Thermodynamic considerations of arteriovenous gradients of hydrogen ion concentration and carbon dioxide tension. 1073 55

Doxorubicin, a broad-spectrum antitumor antibiotic, causes dose-dependent cardiomyopathy and heart failure. Although the exact molecular mechanisms of cardiotoxicity are not well established, oxidative mechanisms involving doxorubicin-induced superoxide anion production have been proposed. In this study, we show that bicarbonate, a physiologically relevant tissue component, greatly amplified doxorubicin-induced cardiomyocyte injury. Bicarbonate also enhanced inactivation of aconitase, a crucial tricarboxylic acid cycle enzyme, in cardiomyocytes exposed to doxorubicin. The cell-permeable superoxide dismutase mimetic, Mn(III)tetrakis (4-benzoic acid) porphyrin, reversed doxorubicin-induced cardiomyocyte injury. Bicarbonate enhanced the inactivation of purified mitochondrial aconitase in the xanthine/xanthine oxidase system, generating superoxide. The results suggest that bicarbonate amplifies the prooxidant effect of superoxide. Bicarbonate also caused an increased loading of cardiomyocytes with doxorubicin. We conclude that the bicarbonate-mediated increase in doxorubicin toxicity is due to increased intracellular loading of doxorubicin in cardiomyocytes and subsequent exacerbation of superoxide-mediated cardiomyocyte injury.
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PMID:Bicarbonate exacerbates oxidative injury induced by antitumor antibiotic doxorubicin in cardiomyocytes. 1104 80

In this prospective study 37 children (ranging 2 months-15 years) with acute pneumonia were evaluated by Doppler echocardiography for the presence of pulmonary hypertension (PH). The goal of this study was to determine the frequency of PH in children with acute pneumonia because the diagnosis of PH influenced the treatment of pneumonia in these patients. The patients who had more than 35 mmHg of systolic pulmonary arterial pressure were considered to have PH. In our study PH was found in 15 (40.5%) of 37 patients. We did not find any significant difference for the parameters including the age, weight, height, clinical symptoms and signs (fever, cough, dyspnea, tachycardia and tachypnea etc.), and laboratory findings such as hemoglobin, PCO2, HCO3 and PO2 between the patients with and without PH (p>0.05). However, there was a significant difference in cyanosis, cardiac failure, blood pH level and O2 saturation measured by pulse oximetry between the patients with and without PH (p<0.05).
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PMID:Doppler echocardiographic evaluation of pulmonary artery pressure in children with acute pneumonia. 1189 Feb 20

Though sudden cardiac death accounts for as much as 15% of all cause mortality in uremia, reports concerning advanced A-V block, requiring permanent cardiac pacing in end-stage renal disease (ESRD) hemodialysed (HD) patients are very few. This is the first long term prospective study reporting on systematic permanent pacemaker implantation, in a cohort of ESRD patients from a single HD unit. Between 01/06/1997 and 30/12/2001, 396 pacemakers were inserted for advanced, symptomatic A-V block in our institution, including 5 in ESRD, HD patients (M/F--4/1, age 47-73, M +/- SD--61 +/- 12 years) from a single dialysis center, treating 137 patients during the study period. Thus, the incidence and prevalence of A-V defects treated by permanent pacing in uremic patients was 0.81% and 3.65% respectively. Conversely, the incidence and prevalence of ESRD treated by hemodialysis, among patients with advanced A-V conduction disturbances, requiring permanent pacing were 0.28% and 1.26%. Mitral valve calcifications were present in all patients; 3 subjects also had extensive aortic valve calcifications. Left ventricular hypertrophy (echocardiographic Framingham criteria) was present in 4 patients, but the systolic function (ejection fraction and fractional shortening index) was normal in all cases, although a clinical picture of chronic heart failure was seen in 3 subjects preoperatively. A-V conduction defects were attributed to extensive metastatic calcifications, involving the cardiac squeleton, consecutive to severe hyperparathyroidism and inadvertent use of calcitriol and calcium carbonate as phosphate binders. No technical difficulties, short or long-term complications related to pacemaker implantation (4 VVI and 1 VVD devices) were encountered. Acute threshold and sensing values were similar with those of non-uremic patients. During follow-up, one patients died from a non cardiac death. If optimal hemodialysis is provided, benefits of permanent pacing are equal in uremic or non uremic patients and pacemaker implantation should be instituted as a prompt life-saving method in all dialysis patients with chronic symptomatic advanced A-V blocks.
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PMID:[Permanent cardiac pacing for chronic symptomatic atrioventricular block in uremic hemodialysed patients. A prospective study]. 1263 71


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