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

Recent advances in technology have not substantially changed the high mortality rate associated with acute renal failure (ARF). To obtain a simple, valid prognostic index, we retrospectively evaluated the relative importance of demographic data, causes (acute insults) of renal failure, and comorbid clinical conditions for the outcome in 102 ARF patients who received renal replacement therapy with an overall mortality rate of 65% (66 of 102). There were no significant differences between survivors and nonsurvivors in age and gender. Mortality according to acute insults was similar to that of the whole population studied. Of the 10 clinical conditions at the time of the first renal replacement therapy, mechanical ventilation (p = 0.0002), cardiac failure (p = 0.0006), hepatic failure (p = 0.003), central nervous system dysfunction (p = 0.005), and oliguria (p = 0.04) were found to be significantly related to mortality by univariate analysis. Furthermore, multivariate analysis demonstrated that only mechanical ventilation, cardiac failure, and hepatic failure were significant risk factors. Survival was directly related to the number of significant variables in univariate analysis: zero, 89% (8 of 9); one, 62% (21 of 34); two, 19% (5 of 27); three, 10% (2 of 20); four, 0% (0 of 8); five, 0% (0 of 4). This simple and early prognostic index, derived from the assessment of clinical conditions which were easily determined at the patient's bedside, could be useful for outcome prediction in ARF patients requiring renal replacement therapy.
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PMID:A simple and early prognostic index for acute renal failure patients requiring renal replacement therapy. 955 58

Signs of exsiccation are to be found in almost every fourth acutely ill patient admitted to the geriatric department. The major clinical signs are those associated with reduced general condition, together with somnolence, possibly agitation, oliguria, dry skin, orthostatic hypotension, and a tendency to be bedridden. In such cases, subcutaneous infusion is a simple-to-apply and for the patient stress-free, largely pain-free possibility for fluid replacement. Properly applied and with account being taken of the contraindications--in particular emergency situations, decompensated cardiac insufficiency and severe coagulation disturbances--the risks of s.c. infusion are negligible.
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PMID:[Dehydration in geriatric patients. Fluid substitution--also subcutaneous!]. 1110 4

A case of acute poisoning with amlodipine with deep hypotension, transient oliguria and clinical signs of acute heart failure was described. A woman of 23 years swallowed intentionally 60 tablets of amlodipine (600 mg). After eleven hours of ingestion she was admitted to Warsaw Poison Control Centre. She was in severe clinical condition; tachycardia and deep hypotension were the prominent signs of poisoning. There was not CNS depression. Intensive treatment with i.v. catecholamines (dopamine, norepinephrine), crystalloids (with continuous control of central venous pressure), and i.v. calcium salts (with control of plasma calcium concentration) was started immediately. The patient did not improve but got worse. Acute heart failure developed, especially of left ventricle, so i.v. crystalloids were stopped and dubutamin, morphine, nitroglycerin and glucagon were introduced. Because of oliguria and insufficient effect of high doses of furosemide four-hours hemodiafiltration was set in. The patient's condition slowly improve after third and forth day of hospitalization. The systolic blood pressure rose, heart work was really better and on sixth day--the stabilization of diastolic blood pressure was definitely achieved. The patient was discharge in good condition with heart ejection fraction of 65% measured echocardiographically.
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PMID:[Deep hypotension with transient oliguria and severe heart failure in course of acute intentional poisoning with amlodipine]. 1186 80

Epidemic dropsy results from the consumption of edible oils adulterated with Argemone mexicana oil by unscrupulous traders. Twenty consecutive 'in-door' patients of dropsy were intensively studied during the recent Delhi epidemic. Samples of edible oil used by them, their urine and their serum samples tested positive for sanguinarine on thin layer chromatography. The illness starts as a gastro-enteric illness followed by oliguria and pedal oedema. The following are often observed: cutaneous erythema with blanching and tenderness on pressure; violacious pigmentation of the skin; shortness of breath with orthopnoea; right-sided heart failure with normal left ventricle (LV) functions; as well as severe anaemia and hypoalbuminaemia. Renal function tests showed: bland urinary sediments; decreased glomerular filtration rate (GFR); mild to moderate azotaemia; acute tubular necrosis; patchy pneumonitis; moderate hypoxia with respiratory alkalosis; and restrictive ventilatory defects on blood gas analysis; and spirometry suggestive of interstitial pulmonary oedema of non-cardiogenic origin. 99mTc colloid sulphur liver scans showed colloid shift. There was marked dilatation and proliferation of dermal capillaries in the absence of significant inflammation in the biopsy specimens. Toxic alkaloids of Argemone mexicana oil induce widespread capillary dilatation and permeability causing leakage of protein rich plasma into the interstitial tissues of various organs. A hypovolaemic state is thus induced producing renal hypoperfusion which may progress to acute tubular necrosis. Interstitial fluid in alveoli causes restrictive ventilatory dysfunction with hypertension and right-sided failure with well-preserved LV function. The hepatic venous congestion induces Kupffer's cell dysfunction, which results in colloid shift on a radionuclide liver scan.
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PMID:Epidemic dropsy: observations on pathophysiology and clinical features during the Delhi epidemic of 1998. 1193 Dec 4

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

Beriberi (BB), thiamine deficiency, has been described in the Asian literature in the 17th century and is characterized by peripheral neuropathy and muscle weakness, also called "dry" beriberi (BB) to differentiate it from "wet" BB, with essentially cardiovascular manifestations. Wet can be either "classic" wet BB in which signs and symptoms of right-sided heart failure with normal or high cardiac output are the presenting features or the "shoshin" BB variant with severe biventricular failure and metabolic acidosis, which must be treated early to prevent the rapid development of low cardiac output failure and sudden death. In this case, we report a 58 year old alcoholic woman who developed dyspnea, oliguria, edema, cardiac failure with high output, metabolic acidosis, renal tubular dysfunction and serum lactate level of 5.6 mEq/L. Neurological examination revealed peripheral neuropathy in the lower legs and cognitive alteration. She was treated with a loading dose of 100 mg of intravenous thyamine and responded with a marked increase in urine output, correction of acidosis, reduction in pulmonary-capillary wedge pressure and a change of the hemodynamic pattern. We conclude that shoshin-BB is uncommonly encountered but not widely recognized. In lactic acidosis and/or hyperdynamic circulation without any other apparent etiology in patients with possible vitamin B1 deficiency, the diagnosis of BB must be considered and thiamine should be administered.
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PMID:[Acute cardiovascular beriberi (shoshin-beriberi)]. 1232 90

Septic shock may be defined as hypotension caused by bacteremia and accompanied by decreased peripheral blood flow, evidenced by oliguria. Clinically, a shaking chill is the warning signal. The immediate cause of hypotension is pooling of blood in the periphery, leading to decreased venous return: later, peripheral resistance falls and cardiac failure may occur. Irreversible shock is comparable to massive reactive hyperemia. Reticuloendothelial failure, histamine release, and toxic hypersensitivity may be factors in the pathogenesis of septic shock. Adrenal failure does not usually occur, but large doses of corticosteroid are employed therapeutically to counteract the effect of histamine release or hypersensitivity to endotoxin. The keys to successful therapy are time, antibiotics, vasopressors, cortisone and correction of acidosis.
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PMID:SEPTIC SHOCK. 1406 36

Cardiac transplantation is the definitive treatment for eligible patients with end-stage cardiac failure. Techniques have evolved to reduce surgical mortality to under 5%. Immediate and subsequent long-term survival is more dependent on acute and chronic rejection and the complications of immunosuppressive therapy. Ten-year survival is greater than 50%.The success of transplantation over the last 20 years has been largely due to the advances in immunosuppression. The most notable and dramatic milestone was the introduction of cyclosporine in the early 1980s, which resulted in a significant improvement in allograft and patient survival. Cyclosporine is a peptide that inhibits the immune system by suppressing T-helper cell activation via inhibition of calcineurin, a critical intracellular enzyme. Tacrolimus has a similar (but not identical) mechanism of action, and was introduced in the 1990s. Drugs such as cyclosporine and tacrolimus, generically referred to as calcineurin inhibitors, have become the cornerstones of immunosuppressive protocols. As a group, calcineurin inhibitors have adverse effects, including neurotoxicity, hypertension, and nephrotoxicity, which complicate their use. Early renal insufficiency manifests as postoperative oliguria (<50 mL/h urine output) or rising serum creatinine levels. There are a variety of postulated causes for calcineurin inhibitor-associated early renal insufficiency including direct calcineurin inhibitor-mediated renal arteriolar vasoconstriction, increased levels of endothelin-1 (a potent vasoconstrictor), as well as decreased nitric oxide production and alterations in the kidney's ability to adjust to changes in serum tonicity. Once early renal insufficiency occurs, no single treatment has been shown to be effective. Approaches discussed in this paper include reduction in calcineurin inhibitor dosages, as well as various drugs to promote increased renal perfusion such as misoprostol and dopamine. In addition, the paper emphasizes the importance of ruling out other causes of renal insufficiency in the early postoperative period, including volume depletion, depressed cardiac output, and mechanical obstruction to urine flow. Given that there is no highly efficacious treatment for this syndrome, ways to avoid its occurrence are desirable. One paper is referenced that suggests that avoidance of rapid changes in tacrolimus level during the first three days of therapy is associated with a low occurrence of early renal insufficiency.
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PMID:Calcineurin inhibitor-associated early renal insufficiency in cardiac transplant recipients: risk factors and strategies for prevention and treatment. 1496 63

Although previous reports have attributed acute renal failure (ARF) following cardiovascular surgery to acute tubular necrosis (ATN), little emphasis has been placed on renal failure due to congestive heart failure (CARF). Of 100 cases of ARF studied prospectively over an 18-month period, 36 occurred after open-heart surgery. Nineteen of these cases were associated with heart failure. The remaining 17 had ATN as manifested by high urinary sodium, low urine/plasma creatinine, and abnormal urinary sediment. At the onset of CARF, intravascular volume expansion was universally present, and oliguria with pulmonary edema was common. Urinary chemistries were (mean +/- SD): sodium (mEq/L) 8 +/- 7, U/P creatinine 72 +/- 45, and FENa (%) 0.1 +/- 0.1. Therapy consisted of digoxin, furosemide (F), vasopressors (V), and, when indicated, intraaortic balloon counterpulsation. Survivors of CARF responded more frequently to F and required less V. Ultimately, survival depended upon improvement in cardiac performance. All oliguric ATN patients failed to respond to F. Mortality for the CARF group was 52%. In contrast, 82% of the oliguric ATN group expired, whereas overall ATN mortality was 60%. Cardiogenic acute renal failure is a frequent cause of ARF after open-heart surgery in our institution. It is characterized by prerenal urinary chemistries, has a high mortality, and may be reversible.
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PMID:CARDIOGENIC ACUTE RENAL FAILURE (CARF) FOLLOWING OPEN-HEART SURGERY. 1521 6

Recombinant human brain natriuretic peptide, nesiritide, has recently been used in limited studies to enhance postoperative diuresis. A retrospective chart review was conducted at a university hospital to assess the efficacy of nesiritide in cardiac surgery patients with fluid overload refractory to diuretics and dopamine. Nine out of 137 patients who underwent coronary artery bypass grafting at the institution from May 2003 to July 2004 exhibited fluid overload despite diuretics and dopamine. Those who did not respond to the therapy, as manifested by oliguria and heart failure, were started on nesiritide. Urine output, weight change, central venous pressure (CVP), pulmonary artery wedge pressure (PAWP), and serum creatinine were the main outcome measures. Within 6 hours after initiation of nesiritide, the average urine output increased from 28 to 130 mL/h. Serum creatinine levels were not significantly different after 24 hours. The mean CVP decreased from 14 to 10 within 12 hours while the PAWP decreased from 24 to 17 mm Hg. Systemic pressures did not change. One patient had to eventually undergo hemodialysis for complications of renal failure. Our experience demonstrates that infusion of nesiritide in patients with heart failure and fluid overload improves diuresis and hemodynamics without major side effects.
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PMID:Administration of nesiritide in patients after coronary artery bypass surgery induces brisk diuresis. 1646 21


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