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

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

Thirteen neonates presented with central cyanosis due to right-to-left shunting across the foramen ovale or the ductus arteriosus or both. In three infants shunting occurred secondary to pulmonary vascular obstruction, presumably related to pulmonary vasospasm (persistence of the fetal or transitional circulation). In ten neonates right-to-left shunting was associated with heart failure; seven of these neonates had systemic hypotension.
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PMID:Disturbances of the transitional circulation: spectrum of pulmonary hypertension and myocardial dysfunction. 95 9

Pulmonary hypertension results from many causes: left cardiac failure, increased pulmonary blood flow, proximal vascular obstruction, decrease of the distal vascular bed (by loss of vessels, narrowing of their luminal diameter, or endoluminal obstruction). A part from passive hemodynamic responses, active processes contribute to pulmonary hypertension by vasomotricity and remodeling of the vascular wall. The biopathology of vasomotor mediators, as well as of endothelial and smooth muscle cell interactions just begins to be understood.
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PMID:[Etiology and physiopathology of pulmonary artery hypertensions (PAHT)]. 185 21

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

This article reviews the types, mechanisms of action and therapeutic applications of currently used vasodilators. Vasodilators have little value if there is vascular obstruction but are effective in the treatment of systemic hypertension and of myocardial ischemia and heart failure. Since the various groups of vasodilators have widely different actions on the coronary arteries, the peripheral arterial circulation and venous tone, an understanding of the specific modes of action and of the systemic effects of these drugs is essential if they are to be used appropriately and their side effects minimized.
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PMID:Vasodilators. 634 63

The pathophysiology and the treatment of heart failure in patients with chronic cor pulmonale is described. The patients with chronic cor pulmonale were divided into two categories in terms of the cause of the disease, that is, due to chronic respiratory failure and due to chronic pulmonary vascular obstruction. The treatment for the patients in the first category is, mainly to control respiration and to continue chronic oxygen therapy, and in the second category is, to utilize vasodilator and anticoagulant therapy. The results of these treatments are rather poor, though in terms of improvement in the quality of life and the survival. In the patients with chronic respiratory disease, the prevention of chronic cor pulmonale and heart failure is essential.
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PMID:[Chronic cor pulmonale and heart failure]. 833 4

Pulmonary embolism is nearly always a complication of deep venous thrombosis. The evaluation of risk factors for venous thromboembolism not only aids diagnosis but also guides decisions about the intensity of prophylactic measures. As both the extent and chronicity of pulmonary vascular obstruction vary widely, pulmonary embolism can produce widely differing clinical pictures. From the clinical, pathophysiological and therapeutical point of view, it is convenient to classify pulmonary embolism into four types: acute minor embolism (dyspnoea with or without pleuritic pain or haemoptysis), acute massive embolism (hemodynamic instability), subacute massive embolism (mimicking heart failure or indolent pneumonia), and chronic thromboembolic pulmonary hypertension (slowly progressing dyspnoea). This classification is of importance not only for the rational diagnosis and differential diagnosis, but also for the institution of adequate therapy. Because the disease has many nonspecific manifestations but no pathognomonic symptoms or signs, it is impossible to prove the diagnosis of pulmonary embolism alone on the basis of clinical presentation.
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PMID:[Clinical characteristics of pulmonary embolism]. 1121 69

We report an autopsy case of acute pancreatitis with a high serum IgG4 concentration complicated by systemic amyloid A amyloidosis and rheumatoid arthritis (RA). The patient was a 42-year-old Japanese female with a 22-year history of rheumatoid arthritis. She was diagnosed with myasthenia gravis when she was 31-year old. At the onset of pancreatitis, the patient was anti-nuclear antibody-positive, and had high serum gamma globulin and IgG4 levels. Dexamethasone and conventional therapy induced clinical remission and significantly decreased the serum IgG4 and gamma globulin. However, despite the decreased disease parameters, the patient developed a bleeding pseudocyst and died of cardiac failure. In the autopsy examination, it was determined that pancreatitis was probably caused by ischemia due to vascular obstruction caused by amyloid deposition in the pancreas. Even though acute pancreatitis is a rare complication in RA patients, we speculate that an autoimmune pancreatitis-related mechanism and ischemia due to vascular obstruction by amyloid deposition might be attributable to a single source that leads to acute pancreatitis in our particular case.
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PMID:An autopsy case of acute pancreatitis with a high serum IgG4 complicated by amyloidosis and rheumatoid arthritis. 1580 Oct 1

An acute cardiac tamponade from any cause may result in rapid deterioration of hepatic function in a previously healthy patient. We describe a case of an acute ascending aortic dissection that presented as acute hepatic failure, due to an acute cardiac tamponade and severe right heart failure. The differential diagnosis of the aetiology of acute liver failure is extensive and includes poisonings, vascular obstruction and sepsis, particularly on the background of decompensated liver disease. Many of these conditions are associated with hypotension. The acute presentation in our patient, combined with the lack of a characteristic history delayed the diagnosis of a proximal (type A) dissection with tamponade and subsequent hepatic failure. Severe right-sided heart failure as a result of conditions such as cardiac tamponade should be excluded in patients presenting with acute hepatic failure of unknown aetiology.
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PMID:Acute hepatic failure caused by an acute aortic dissection with cardiac tamponade: a case report. 1656 89

Erythropoietin (EPO) mobilises endothelial progenitor cells and promotes neovascularisation in heart failure. The present authors studied the effects of EPO on pulmonary vascular and cardiac remodelling in a model for flow-associated pulmonary arterial hypertension (PAH). PAH was induced in adult male Wistar rats by the injection of monocrotaline combined with an abdominal aortocaval shunt 1 week later (PAH or experimental group). Immediately afterwards, rats were randomised into those who received treatment with EPO (PAH+EPO group) and controls. Pulmonary and systemic haemodynamics, and right ventricular and pulmonary vascular remodelling were evaluated 3 weeks later. Vascular occlusion of the intra-acinar pulmonary vessels (13.4+/-0.7 versus 16.7+/-1.3% in PAH+EPO and PAH, respectively) and medial wall thickness of the pre-acinar arteries (wall-to-lumen ratio 0.13+/-0.01 versus 0.17+/-0.01 in PAH+EPO and PAH, respectively) decreased after treatment with EPO. Moreover, right ventricular capillary density was increased by therapy (2,322+/-61 versus 2,100+/-63 capillaries x mm(-2) in PAH+EPO and PAH, respectively). Increased mean pulmonary arterial pressure and decreased right ventricular contractility in the model were not altered by EPO treatment. In this rat model of flow-associated pulmonary arterial hypertension, erythropoietin treatment beneficially affected pulmonary vascular and cardiac remodelling. These histopathological effects were not accompanied by significantly improved haemodynamics.
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PMID:Effects of erythropoietin on advanced pulmonary vascular remodelling. 1789 19


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