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

A systematic search for cases of lactic acidosis among diabetics on biguanides revealed ten during an eight-month period, while in the preceding ten years not a single case had been definitely diagnosed. This represents a prevelance of 1 in 2000 patients admitted to hospital. All ten were over 60 years old and had previously been treated for heart failure. Most of them had suffered from renal insufficiency for some time. There was no case of biguanide overdosage. Criteria for the diagnosis of lactic acidosis are lactic concentration in blood averaging 18.4 mmol/l and a low pH, averaging 6.9. Serum-biguanide concentration (measured by radioimmuno-assay) was markedly increased. Most of the patients were in circulatory shock on admission or soon after and all of them had a history of gastro-intestinal complaints. Despite intensive treatment with insulin and glucose and careful correction of the acidosis with bicarbonate four of the ten patients died.
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PMID:[Lactic acidosis in diabetics on biguanides (author's transl)]. 1 84

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

Detailed hemodynamic and metabolic studies were performed during the course of phenformin related lactic acidosis in two patients. Arterial blood lactate was increased to 11.5 and 26.1 mM/L and arterial blood pH was reduced to 7.05 and 6.80 units, respectively. A marked reduction in cardiac indices (0.94 and 1.15 L/min/m2), stroke volume, and stroke work were observed, with either normal or increased arterial resistance. Mild increases in pulmonary artery systolic pressure (50/11), 45/25 mmHg) were observed, but necropsy in both cases disclosed no evidence of pulmonary vascular obstruction. In the absence of increases in central venous and pulmonary artery wedge pressure, a cardiac failure was excluded as primary cause of the low output state. Hypovolemia was excluded on the basis of radioisotope dilution measurements of plasma volume and red cell mass and no increase in cardiac output followed volume expansion. Oxygen extraction from blood was not grossly impaired. These observations indicate that phenformin-related lactic acidosis may evolve as a circulatory defect characteristic of shock in which oxygen delivery rather than oxygen utilization is impaired. The hemodynamic defect is best explained by a defect in the intravascular distribution of blood volume.
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PMID:Circulatory defects during phenformin lactic acidosis. 50 Sep 42

After the acute onset of heart failure and in the absence of acute myocardial infarction, plasma volume may occasionally be depleted to the extent that the patient presents with clinical signs of circulatory shock. In five patients, the acute onset of clinical and radiographic signs of cardiogenic pulmonary edema were associated with reduction in arterial blood pressure and cardiac output. The pulmonary arterial wedge pressure was within normal limits but a reduction in plasma volume was demonstrated, which is best explained by the rapid translocation of plasma water that represented pulmonary (and most likely also peripheral) edema fluid. The infusion of 5 percent albumin solution significantly increased cardiac output, mean arterial pressure and cardiac work, reversed lactic acidosis, enhanced furosemide-induced diuresis and was followed by a decrease in both clinical and radiographic signs of pulmonary edema. These observations confirm that volume expansion may constitute appropriate treatment for some patients with cardiogenic pulmonary edema who may present with hypotension and who are unresponsive to conventional therapy.
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PMID:Hypovolemia and hypotension complicating management of acute cardiogenic pulmonary edema. 50 39

Disturbance in acid-base balance is commonly observed in patients with heart failure. The most common disturbance is metabolic alkalosis combined with hypokalemia, as a result of the excessive use of loop diuretics. Occasionary, hypoxia due to pulmonary edema stimulates ventilation, resulting in respiratory alkalosis. When pulmonary edema develops, carbon dioxide retention occurs, resulting in respiratory acidosis. Decreased tissue oxygen delivery may also produce lethal lactic acidosis. Compensatory mechanisms, coexistence of independent acid-base disorders and changes in electrolytes complicate acid-base balance in the individual patients. As acid-base disturbances have harmful effects on the cardiovascular system, precise diagnosis and proper treatment are highly important.
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PMID:[Acid-base disturbances in heart failure]. 143 8

An 83-day-old male infant had convulsions, hypertrophic cardiomyopathy, and lactic acidosis. Cranial computed tomography revealed low-density areas in both parieto-occipital lobes and in the left temporal lobe. Muscle biopsy did not reveal ragged-red fibers, but abnormal mitochondria were found in the capillary endothelial cells as well as in the muscle fibers. At 5 months of age, the patient developed purpura on the soles and palms. Skin biopsy showed degeneration of the endothelial cells with abnormal mitochondria in the arterioles and capillaries. Myelinated nerves in the skin had vacuolated axons with swollen mitochondria, and their myelin sheaths showed vacuolation. At 9 months of age, he died of heart failure, and autopsy revealed abnormal mitochondria in the myocardium but not in the coronary vessels. Our findings indicate that the symptoms of the mitochondrial encephalopathy, myopathy, lactic acidosis, and strokelike episodes (MELAS) syndrome cannot be fully explained by the mitochondrial angiopathy alone.
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PMID:MELAS of infantile onset: mitochondrial angiopathy or cytopathy? 186 30

Recent studies in patients with long-term heart failure have suggested that intrinsic abnormalities in skeletal muscle can contribute to the development of early lactic acidosis and fatigue during exercise. The present study provides an analysis of substrate and enzyme content, fiber typing, and capillarization in skeletal muscle biopsy samples obtained at rest from the vastus lateralis in 11 patients with long-term heart failure (left ventricular ejection fraction, 21 +/- 8%) and nine normal subjects. Patients demonstrated a reduced peak exercise oxygen consumption (13.0 +/- 3.3 ml/kg/min) when compared with normals (30.2 +/- 8.6 ml/kg/min, p less than 0.001) and had an accelerated rise in blood lactate levels during exercise. In mixed fiber skeletal muscle, total phosphorylase and glycolytic enzyme activities were not different in the two groups, whereas mitochondrial enzymes involved in terminal oxidation were decreased in patients as compared with normal subjects as indicated by reductions in succinate dehydrogenase (51 +/- 15 vs. 81 +/- 17 microM/g protein/min, p less than 0.001) and citrate synthetase (26 +/- 7 vs. 43 +/- 20 microM/g protein/min, p less than 0.05). 3-Hydroxyacyl-CoA-dehydrogenase, an important enzyme mediating beta-oxidation of fatty acids, was also reduced in patients as compared with normals (18 +/- 7 vs. 27 +/- 10 microM/g protein/min, p less than 0.05). There was no difference in high-energy phosphagens or lactate concentration of mixed muscle in the two groups, whereas glycogen content was decreased in patients (262 +/- 29 vs. 298 +/- 35 microM glucosyl units/kg dry wt, p = 0.01). Patients demonstrated a reduced percentage of slow twitch type I fibers (36 +/- 7% vs. 52 +/- 22%, p less than 0.05) and had a higher percentage of type IIb fast twitch fibers (24 +/- 9% vs. 11 +/- 12%, p = 0.02), which were smaller than the type IIb fibers seen in normal subjects (p less than 0.05). In patients, the number of capillaries per fiber was decreased for type I and type IIa fibers (both, p less than 0.03), but the ratio of capillaries to cross-sectional fiber area was not different for the two groups. These data demonstrate major alterations in skeletal muscle histology and biochemistry in patients with long-term heart failure, including fiber atrophy, a decrease in percentage of composition of type I fibers, and an increase in type IIb fibers accompanied by a decrease in oxidative enzyme capacity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Skeletal muscle biochemistry and histology in ambulatory patients with long-term heart failure. 229 59

The primary defect that characterizes circulatory shock is acute perfusion failure, in which oxygen metabolism is critically impaired by decreased delivery of oxygen to tissues. Four categories of hemodynamic deficits are described as the basic mechanisms of circulatory shock: hypovolemia, cardiac failure, distributive deficits, and vascular obstruction. Perfusion failure can be identified by the development of lactic acidosis, because anaerobic metabolism is the consequence of the oxygen deficit during circulatory failure. Lactic acidosis at present represents the best single objective measure of the severity of shock.
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PMID:Physiology of blood flow and oxygen utilization by peripheral tissue in circulatory shock. 238 64

After 4 weeks of total parenteral nutrition (TPN), a 12-yr-old girl exhibited an acute heart failure with high cardiac output, anuria, and severe lactic acidosis. The clinical, hemodynamic, and biological data suggested the diagnosis of shoshin beriberi which was proved by the low erythrocyte transketolase activity with elevated "TPP effect" and by the dramatic improvement of the patient after thiamin administration. Thiamin deficiency and severe neurological disorders have been described during long-term parenteral nutrition. To our knowledge, this is the first report of the cardiovascular complication of this vitamin deprivation in long-term TPN.
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PMID:Shoshin beriberi: an unusual complication of prolonged parenteral nutrition. 308 Jun 18

The reduced maximal exercise capacity of patients with heart failure has been attributed to skeletal muscle underperfusion with resultant intramuscular lactic acidosis and muscular fatigue. To investigate this hypothesis, the effect of dichloroacetate, a drug that decreases lactate formation by increasing pyruvate oxidation, on the maximal exercise performance of 18 patients with heart failure and reduced ejection fraction (25 +/- 9%) was examined. Exercise tests after parenteral dextrose (control) and dichloroacetate were performed 1 week apart. The sequence of interventions was randomized in a double-blind manner. Dichloroacetate decreased blood lactate at rest (control 8.0 +/- 2.5 versus dichloroacetate 5.6 +/- 2.9 mg/dl), throughout exercise and at peak exercise (control 26.0 +/- 14.3 versus dichloroacetate 19.4 +/- 10.8) (all p less than 0.05). In contrast, dichloroacetate had no effect on exercise time (control 15.2 +/- 6.0 versus dichloroacetate 15.9 +/- 6.2 min) or peak exercise oxygen consumption (control 1,280 +/- 498 ml/min versus dichloroacetate 1,312 +/- 530 ml/min) (both p = NS). In six subjects, dichloroacetate also had no effect at peak exercise on leg blood flow (control 2.8 +/- 1.1 versus dichloroacetate 3.0 +/- 0.6 liters/min) or femoral oxygen vein saturation (control 12.7 +/- 4.1% versus dichloroacetate 12.5 +/- 5.7%). These data suggest that intramuscular lactate accumulation is not responsible for muscular fatigue during exercise in patients with heart failure.
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PMID:Effect of dichloroacetate on the exercise performance of patients with heart failure. 319 43


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