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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The starting point of cardiogenic shock is an extensive myocardial infarction. Through a backward and forward failure of the left ventricle a shock-specific disturbance of the microcirculation occurs with a reduction of the circulation in the periphery of the body and development of a tissue acidosis (metabolic acidosis). Fall in blood pressure and cardiac volume, congestion of blood in the region of the pulmonary vessels and signs of reduced circulation in the body periphery (severe physical weakness, apathy, cold and clammy skin, oliguria) determine the clinical picture of cardiogenic shock. Therapeutically, intra-aortal balloon counter-pulsation, possibly combined with a cardiosurgical intervention, has reduced the mortality of cardiogenic shock after acute myocardial infarction from 90--100% to 60--70%.
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PMID:[Cardiogenic shock following acute myocardial infarction. Pathophysiology and clinical aspects (author's transl)]. 10 80

To characterize the relation between clinical and hemodynamic state in acute myocardial infarction, 200 patients with acute infarction were evaluated with clinical and hemodynamic criteria. Patients were classified clinically on the basis of peripheral hypoperfusion (hypotension, tachycardia, confusion, cyanosis, oliguria) and pulmonary congestion (rales, abnormal chest roentgenogram). Four clinical subsets were defined that correlated with cardiac index (Cl, liters/min per m2) and pulmonary capillary pressure (PCP, mm Hg): (see article). Parallel hemodynamic subsets were developed independently on the basis of depressed cardiac index (2.2 liters/min per m2 or less) and elevated pulmonary capillary pressure (greater than 18 mm Hg). The rate of accuracy of clinical examination in predicting hemodynamic abnormalities was 83 percent. Mortality rates were similar in the clinical and hemodynamic subset calssifications, averaging 2.2 percent in subset I, 10.1 percent in subset II, 22.4 percent in subset III and 55.5 percent in subset IV. Drug interventions in the course of hospitalization resulted in a 38 percent increase in depressed cardiac index and 34 percent decrease in elevated pulmonary capillary pressure. Resolution of clinical abnormalities paralleled this hemodynamic improvement in 70 percent of patients. These data suggest that clinical performance and both clinical and hemodynamic subsets are directly relevant to establishing prognosis and the selection of therapy in patients with acute myocardial infarction.
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PMID:Correlative classification of clinical and hemodynamic function after acute myocardial infarction. 83 73

We report a patient presenting rapid deterioration of renal function due to primary cholesterol atheroembolism. The patient was 75-year-old hypertensive male and was admitted to a hospital because of rt. hemiplegia which developed 2 weeks earlier. On admission, his blood pressure was 200/100 mmHg and serum creatinine level was 2.9 mg/dl with urinalysis 1+ both for protein and hematuria. 2 weeks later, an angiotensin converting enzyme inhibitor (ACE inhibitor, delapril 15 mg/day) was given to control high blood pressure. Immediately after this medication, his renal failure rapidly progressed with a fall in blood pressure (110/60 mmHg) and oliguria (100 ml/day). Although he was transferred to our hospital and was treated with hemodialysis, he died of an attack of acute myocardial infarction in a week. At post-mortem examination, microscopic findings of the kidney disclosed numerous occlusions of medium-sized artery by cholesterol emboli. These emboli were also observed in other organs, but not so prominent as in the kidney. The coronary arteries exhibited severe sclerosis. In this presented case, acute deterioration of renal function was caused by ACE-inhibitor, although which was administered in a volume depleted condition. Therefore, further study would be necessary whether or not ACE-inhibitors predispose the patients with this disease to acute renal failure.
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PMID:[A case of renal failure due to primary cholesterol atheroembolism]. 187 61

The definition and classification of the various forms of circulatory shock are outlined, together with the causes and management of cardiogenic shock. The pharmacotherapeutic possibilities in patients with shock following myocardial infarction are discussed: over the last 15 years several alpha and beta adrenergic stimulants, as well as alpha-blocking agents, have been included in the treatment of this severe circulatory failure; today the most commonly used drugs in cardiogenic shock are dopamine and dobutamine, sometimes in combination with vasodilators. Dopamine appears to be indicated when low cardiac output, arterial hypotension and oliguria are present; dobutamine, a positive inotropic acting drug, should be used when arterial hypotension is only moderate but combined with elevated filling pressures. Despite the various therapeutic approaches the mortality of cardiogenic shock, which reaches 10-15% of patients with acute myocardial infarction, is still high (70-90%); an improvement may be expected with newer forms of therapy (fibrinolysis, dilatation). Finally, a concept for the management of cardiogenic shock following myocardial infarction is presented.
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PMID:[Pharmacotherapy of cardiogenic shock]. 289 69

Seventeen patients who developed cardiogenic shock after acute myocardial infarction were treated with intravenously infused dopamine. In eight of these patients a stable blood pressure was attained, but oliguria or anuria persisted, and oral treatment with prazosin was instituted. Diuresis occurred in seven of these patients, but was followed by transient hypotension associated with a rapid rise in plasma prazosin levels in three. Four patients left hospital, and there were two long-term survivors. Prazosin may be a useful adjunct to dopamine in the treatment of cardiogenic shock.
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PMID:Use of dopamine and prazosin combined in the treatment of cardiogenic shock. 742 22

To explore the natural history of critically ill patients with acute renal failure due to acute tubular necrosis, we evaluated 256 patients enrolled in the placebo arm of a randomized clinical trial. Death and the composite outcome, death or the provision of dialysis, were determined with follow-up to 60 d. The relative risks (RR) and 95% confidence intervals (95% CI) associated with routinely available demographic, clinical, and laboratory variables were estimated using proportional hazards regression. Ninety-three (36%) deaths were documented; an additional 52 (20%) patients who survived received dialysis. Predictors of mortality included male gender (RR, 2.01; 95% CI, 1.21 to 3.36), oliguria (RR, 2.25; 95% CI, 1.43 to 3.55), mechanical ventilation (RR, 1.86; 95% CI, 1.18 to 2.93), acute myocardial infarction (RR, 3.14; 95% CI, 1.85 to 5.31), acute stroke or seizure (RR, 3.08; 95% CI, 1.56 to 6.06), chronic immunosuppression (RR, 2.37; 95% CI, 1.16 to 4.88), hyperbilirubinemia (RR, 1.06; 95% CI, 1.03 to 1.08 per 1 mg/dl increase in total bilirubin) and metabolic acidosis (RR, 0.95; 95% CI, 0.90 to 0.99 per 1 mEq/L increase in serum bicarbonate concentration). Predictors of death or the provision of dialysis were oliguria (RR, 5.95; 95% CI, 3.96 to 8.95), mechanical ventilation (RR, 1.53; 95% CI, 1.07 to 2.21), acute myocardial infarction (RR, 1.95; 95% CI, 1.24 to 3.07), arrhythmia (RR, 1.51; 95% CI, 1.04 to 2.19), and hypoalbuminemia (RR, 0.56; 95% CI, 0.42 to 0.74 per 1 g/dl increase in serum albumin concentration). Neither mortality nor the provision of dialysis was related to patient age. These observations can be used to estimate risk early in the course of acute tubular necrosis. Furthermore, these and related models may be used to adjust for case-mix variation in quality improvement efforts, and to objectively stratify patients in future intervention trials aimed at favorably altering the course of hospital-acquired acute renal failure.
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PMID:Predictors of mortality and the provision of dialysis in patients with acute tubular necrosis. The Auriculin Anaritide Acute Renal Failure Study Group. 955 72

Adrenomedullin (AM) has vasodilatory, diuretic and natriuretic actions. Two molecular forms of AM circulate in human plasma: an active, mature form of AM (AM-m) and an intermediate, inactive, glycine-extended form of AM (AM-Gly). In the present study we investigated the pathophysiological significance of the two molecular forms of AM in plasma and urine in patients with acute myocardial infarction. We serially measured venous and arterial plasma levels and urinary excretion of AM-m, AM-Gly and total AM (Am-T; =AM-m+AM-Gly) over 2 weeks using our recently developed immunoradiometric assay in 26 consecutive patients with acute myocardial infarction and in age-matched normal controls, and studied the relationships between AM levels and clinical parameters. Plasma AM-m, AM-Gly and AM-T levels were increased on admission in patients with acute myocardial infarction compared with age-matched normal controls. Levels of AM-m, AM-Gly and AM-T in plasma reached a peak 24 h after the onset of symptoms. Plasma AM-m, AM-Gly and AM-T levels were significantly correlated with plasma levels of brain natriuretic peptide and pulmonary arterial pressure. Plasma AM-Gly levels in the vein were similar to those in the artery, whereas plasma AM-m levels were significantly lower in the artery than in the vein. Urinary excretion of AM-m, AM-Gly and AM-T was also increased on admission, and reached a peak at 12 h after the onset of symptoms. Urinary excretion of AM-m and AM-Gly was significantly correlated with urinary sodium excretion. The AM-m/AM-T ratio was significantly higher in the urine than in the vein or artery. AM-m levels were significantly correlated with AM-Gly levels in both the urine and plasma; however, there were no significant correlations between plasma and urinary AM levels. The results suggest that levels of both molecular forms of AM are increased in the urine as well as in the plasma in the acute phase of myocardial infarction. Since AM exerts potent cardiovascular and renal effects, increased concentrations of AM in plasma and urine in the acute phase of myocardial infarction may be involved in the defence mechanism against further elevations of peripheral and pulmonary vascular resistance and oliguria in acute myocardial infarction.
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PMID:Elevation of two molecular forms of adrenomedullin in plasma and urine in patients with acute myocardial infarction treated with early coronary angioplasty. 1111 26

Heart failure during the immediate period of an acute myocardial infarction constitutes a major insult to this pathology; since, once installed, it is associate to ventricular dysfunction and expansion of the left ventricle. It can appear either early or delayed. Subsequent to the acute insult, the myocardium is subjected to diverse changes in its anatomical conformation and to diastolic and systolic alterations, which will affect the hemodynamic constants of the patient. Changes in the parietal ventricular architecture as well as at the neurohumoral level will also occur. The clinical signs of heart failure are: dyspnea, pallor, tachycardia, diaphoresis, cold skin, oliguria, somnolence, and gallop, which can be observed at the very beginning of the coronary occlusion. Its clinical identification, through in-hospital studies supported by adequate hemodynamic monitoring, is of utter relevance since it will lead to appropriate and fast treatment. The groups of patients with acute myocardial infarction with high risk for the development of cardiac failure are: patients with extensive Q wave infarction, diabetic, patients over 65 years of age, and those with a history of previous myocardial infarction(s). The cornerstone of treatment must be focused on reducing the myocardial ischemia, which can be achieved through the use of modern therapeutics and, given the case, pharmacological agents, coronary intervention procedures, or cardiac surgery must be taken into account. At present it is known that angiotensin converting enzyme inhibitors, betablockers, inotropics, are useful to improve ventricular function in patients with acute myocardial infarction.
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PMID:[Heart failure in acute myocardial infarction]. 1200 71

Atheroembolic disease is a rarely recognized clinical entity. The growing use of antiplatelet and thrombolytic therapy and of invasive cardiovascular procedures in acute coronary syndromes has nevertheless transformed this feared iatrogenic complication into an increasingly frequent diagnosis. The authors review this entity through the case of a 71-year-old man who, fifteen days after undergoing thrombolysis for acute myocardial infarction with ST-segment elevation, followed by elective percutaneous coronary revascularization under triple antiplatelet therapy, came to the emergency department with a clinical setting of mental confusion, gastrointestinal bleeding, oliguria and cutaneous eruptions on the lower limbs; laboratory tests revealed severe azotemia and hyperkalemia. With a diagnostic hypothesis of systemic atheroembolization, a cutaneous lesion biopsy was performed, which confirmed the diagnosis. Supportive treatment led to neurological and cutaneous recovery, but the patient developed chronic renal failure. The pathophysiology, forms of presentation, treatment and prognosis of atheroembolic disease are discussed, highlighting the importance of a high degree of clinical suspicion for diagnosis.
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PMID:Post-percutaneous coronary angioplasty atheroembolization--a feared iatrogenic complication. 1807 26

A 69-year-old man was referred to our hospital due to acute myocardial infarction. Systolic heart murmur was first noted on the 23rd day after the onset, but no cardiac shunt flow was detected by echocardiography at that time. Six days later, cardiac function deteriorated rapidly, followed by oliguria and shock. Re-do echocardiography showed ventricular septal perforation. Emergency operation was performed, and septal perforation was seen on the anterior portion of the septum. In addition to infarct-exclusion-technique (Komeda-David method) with the equine pericardial patch, direct closure of the septal defect was performed (double closure technique). Fibrin glue was applied between the ventricular septum and the patch. After surgery, he suffered from Candida mediastinitis and received omentum plombage. Furthermore tracheotomy was performed for pneumonia. He recovered gradually, and was discharged about 3 months after surgery. Echocardiography showed no residual shunt.
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PMID:[Candida mediastinitis after double closure technique for repairing ventricular septal perforation]. 1928 Sep 53


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