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

Transthoracic and whole-body bioimpedance monitoring has been commercially available for years; however, attention to its use as a diagnostic and event-monitoring modality has not been routinely applied in patients with heart failure (HF). In 2005, intrathoracic bioimpedance monitoring via an implantable cardioverter defibrillator brought new awareness of bioimpedance technology. In addition, new knowledge about congestion in HF, including length of time a patient is congested before seeking emergency care, lack of sensitivity of common signs and symptoms used to monitor congestion and diagnose HF exacerbation, and poor clinical outcomes when hypervolemia is present, heightened the need for more aggressive assessment and management. Bioimpedance device monitoring provides data needed to make treatment decisions that promote euvolemia and optimal cardiac performance. This review summarizes three options for measurement of bioimpedance hemodynamic data, discusses its use in preventing HF hospitalization, and describes issues that need to be overcome before bioimpedance monitoring can be routinely used in HF management.
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PMID:Bioimpedance to prevent heart failure hospitalization. 1691 6

A 53-yr-old previously healthy man was admitted to our hospital for thyrotoxicosis without ophthalmopathy. Initial therapy with propylthiouracil caused an acute elevation of liver enzymes. Then, he received a first course of 131I therapy (20 mCi). At the end of 6-mo follow-up after 131I, he was still thyrotoxic and developed moderately severe ophthalmopathy. The patient refused thyroid surgery and decided to undergo second course of 131I therapy (30 mCi). Concomitantly with the 131I, we opted to give high-dose pulse glucocorticoid therapy (PGT) to prevent further deterioration of GO. The patient was started on intravenous methylprednisolone pulse therapy 1 g daily in a cycle (one cycle every 2 wk, each cycle comprising two infusions on alternate days). After the end of the second day of PGT administration, he suddenly developed onset of acute pulmonary edema and hypertension. There was no previous history of cardiac disorder or conditions predisposing to cardiac failure other than thyrotoxicosis. A presumptive diagnosis of fluid overload and/or hypertension- induced acute heart failure was made. After prompt investigations excluding cardiogenic causes, we thought that this condition was triggered by PGT that was superimposed on thyrotoxicosis-related hemodynamic instability. Graves' patients with uncontrolled thyrotoxicosis should be under careful surveillance when PGT is planned. To our knowledge, this is the first reported case of life-threatening acute pulmonary edema caused by PGT in GO.
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PMID:New-onset acute heart failure after intravenous glucocorticoid pulse therapy in a patient with Graves' ophthalmopathy. 1694 91

In the United States, 90% of one million annual hospitalizations for heart failure are due to symptoms of volume overload. Hypervolemia contributes to heart failure progression and mortality. Treatment guidelines recommend that therapy for patients with heart failure be aimed at achieving euvolemia. Intravenous loop diuretics induce a rapid diuresis that reduces lung congestion and dyspnea. However, loop diuretics' effectiveness declines with repeated exposure. Unresolved congestion may contribute to high re-hospitalization rates. Furthermore, loop diuretics may be associated with increased morbidity and mortality due to deleterious effects on neurohormonal activation, electrolyte balance, and cardiac and renal function. Ultrafiltration is an alternative method of sodium and water removal, which safely improves hemodynamics in patients with heart failure. Application of this technology has been limited by the need for high flow rates, large extracorporeal blood volumes, and large-bore central venous catheters. A modified ultrafiltration device has overcome these limitations. Ultrafiltration may be a safe and effective alternative to intravenous diuretics in the treatment of decompensated heart failure.
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PMID:The role of ultrafiltration in the management of heart failure. 1703 70

Patients with congestive heart failure (CHF) resistant to conventional treatment have a poor prognosis. Extracorporeal ultrafiltration (UF) appears to be the therapy of choice for short-term management of such patients with severe fluid overload, whereas peritoneal dialysis (PD) may be the therapy of choice for the long-term treatment. Fluid removal results in reduction of plasma volume, improvement of hyponatremia, reduction in pulmonary capillary wedge pressure, improvement of New York Heart Association functional heart failure class, improvement of functional rehabilitation and quality of life, reduction of hospitalizations and readmissions, as well as improvement in diuretic responsiveness. Whether extracorporeal UF and/or PD modifies the survival rate of patients with refractory CHF needs to be determined in prospective randomized controlled trials.
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PMID:The role of peritoneal dialysis in the management of treatment-resistant congestive heart failure: A European perspective. 1708 Jan 15

Despite being as common as an acute myocardial infarction in the emergency department, the diagnostic criteria and the therapeutic guidelines for heart failure treatment are much less well defined. Thanks to the recently published guidelines of the European Society of Cardiology (ESC) the diagnosis of acute heart failure syndromes (AHFS) is now better standardized. The ESC distinguishes between six AHFS: (I) acute decompensated chronic heart failure, (II) acute heart failure with hypertension/hypertensive crisis, (III) acute heart failure with pulmonary edema, (IV) cardiogenic shock, (V) high-output failure, and (VI) right-sided acute heart failure. To distinguish between these entities in a clinical setting, a well-structured clinical examination is of paramount importance. Signs of peripheral hypoperfusion and congestion/fluid overload need to be recognized rapidly. These two clinical parameters permit the assessment of the patient based on the Clinical Severity Classification. Further diagnostic work-up should include chest X-ray, echocardiography, clinical chemistry, and blood gas analysis. The invasive coronary angiography is only beneficial in the context of an acute ST elevation myocardial infarction or NSTEMIs with persistent symptoms of angina. In all other cases cardiac catheterization should be deferred until the patient is recompensated. Diagnostic algorithms help to maintain a high standard in clinical diagnosis and improve the safety and efficacy of subsequent therapeutic interventions.
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PMID:[Acute heart failure: rational diagnostics in clinical practice and the emergency department]. 1714 75

Arginine vasopressin (AVP) is a neuropeptide hormone that plays an important role in circulatory and sodium homeostasis, and regulating serum osmolality. Several clinical conditions have been associated with inappropriately elevated levels of AVP including heart failure, cirrhosis of the liver and the syndrome of inappropriate secretion of antidiuretic hormone. Three receptor subtypes that mediate the actions of AVP have been identified (V(1A), V(2) and V(1B)). Activation of V(1A) receptors located in vascular smooth muscle cells and the myocardium results in vasoconstriction and increased afterload and hypertrophy. The V(2) receptors located primarily in the collecting tubules mediate free water absorption. The V(1B) receptors are located in the anterior pituitary and mediate adrenocorticotropin hormone release. The cardiovascular and renal effects of AVP are mediated primarily by V(1A) and V(2) receptors. Antagonism of V(1A) receptors results in vasodilatation and antagonism of V(2) receptors resulting in aquaresis, an electrolyte-sparing water excretion. Several non-peptide AVP antagonists (vasopressin receptor antagonists [VRAs]) also termed 'vaptans' have been developed and are vigorously being studied primarily for treating conditions characterised by hyponatraemia and fluid overload. Conivaptan is a combined V(1A)/V(2)-receptor antagonist that induces diuresis as well as haemodynamic improvement. It has been shown in clinical trials to correct euvolaemic and hypervolaemic hyponatraemia, and has been approved by the US FDA for the treatment of euvolaemic hyponatraemia as an intravenous infusion. Tolvaptan, a selective V(2)-receptor antagonist, has undergone extensive clinical studies in the treatment of hyponatraemia and heart failure. It has been shown to effectively decrease fluid in volume overloaded patients with heart failure and to correct hyponatraemia. A large outcome study (n = 4133 patients) will define its role in the management of heart failure. Lixivaptan and satavaptan (SR-121463) are other selective V(2)-receptor antagonists being evaluated for the treatment of hyponatraemia. In addition, a potential role for the vaptans in attenuating polyuria in nephrogenic diabetes insipidus and cyst development in polycystic kidney disease is being explored. Ongoing clinical trials should further define the scope of the potential therapeutic role of VRAs.
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PMID:Therapeutic potential of vasopressin receptor antagonists. 1742 3

As a consequence of the expanded use of long-term hemodialysis and extended life spans, complications of chronic renal failure are encountered with an increased frequency among uremic patients. Such patients may develop many thoracic and extrathoracic problems--most frequently uremic pleuritis and pericarditis, uremic pneumonia, infection, and metastatic pulmonary calcification. We retrospectively analyzed the medical records of 257 patients who had received long-term hemodialysis between 1990 and 2006 to better understand the incidence, causes, and clinical features of pleural effusions in this population. The incidence of pleural effusion in hospitalized patients receiving long-term hemodialysis was 20.2% (n=52; mean age, 55.83 +/- 16.56 years; male-to-female ratio, approximately 3:2). Pleural effusion resulted from hypervolemia in 61.5% and was bilateral in 68.8% of patients. Unilateral effusion was present in 25 of 52 (48%) patients. The most frequent causes of unilateral effusion were hypervolemia (n=9) and parapneumonic effusion (n=5). Thoracenteses were performed in 14 of the 52 patients in the study group. Of thoracenteses performed, 64.3% of the patients had transudative pleural effusion and 35.7% had exudative effusion. Transudative pleural effusion resulted from hypervolemia in 66.7% and heart failure in 22.2%. Of the patients with transudative effusion, 85.7% were bilateral. The most frequent cause of exudative pleural effusion was uremic pleuritis, which occurred in 40% of the patients. The most common symptom was dyspnea, which occurred in 53.8% of patients. In conclusion, pleural effusions are common in patients receiving chronic hemodialysis. Thoracentesis may be performed in patients with unilateral pleural effusion. Since hypervolemia was the most common cause of pleural effusion, this complication should not be considered an obstacle in renal transplant recipients.
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PMID:Pleural effusion in long-term hemodialysis patients. 1752 41

We observed acute, postoperative renal failure requiring dialysis in 33 patients from the entire group of adult patients who received cardiac surgery in 2004 in The Silesian Center for Heart Diseases in Zabrze. Over 50% of these were qualified for emergency operation. During the early postoperative period all of the examined patients had cardiac failure and circulatory insufficiency requiring high doses of catecholamine and intraaortic balloon pump support. In the analyzed group of patients the frequency of multi-organ failure was high (neurologic dysfunction, the need for prolonged mechanical ventilation, mesenteric ischemia). Hemodiafiltration was used as a renal replacement therapy with the dialisate volume not exceeding 11/h. The volume of ultrafiltrate was regulated on the basis of fluid overload and directed to optimize intravascular filling. The average start of hemofiltration was the 3rd postoperative day and was continued for 5 days. The mortality rate in the analyzed group was 81.8%. The renal function substitution based on hemodiafiltration performed in the way described above is easy to start, easy to manage, generates low costs, nevertheless its efficacy is low.
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PMID:[Acute renal failure as a complication of cardiac surgery]. 1760 62

Currently, the use of diuretics in heart failure (HF) remains more of an art than a science. Diuretics are the principle means for relieving congestion in patients with decompensated HF. Unfortunately, they persist as the only major therapy in HF that has not been subjected to a large randomized clinical trial, precisely because no comparable therapy exists that can so easily, efficiently, and inexpensively treat fluid overload. Nonetheless, diuretics have many potential drawbacks, including electrolyte abnormalities, neurohormonal activation, hypovolemia, renal dysfunction, and direct myocardial effects. Until definitive answers about mortality are settled, the lowest dose of a diuretic that can produce euvolemia should be employed and these agents should be discontinued when possible. Many outpatients with HF can be managed quite well without diuretics once adequate neurohormonal blockade with angiotensin-converting enzyme inhibitors and beta blockers has been achieved.
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PMID:Optimal use of diuretics in patients with heart failure. 1776 Nov 18

Over the past few years, acute worsening of renal function has emerged as a powerful and independent predictor of adverse cardiac outcomes among patients hospitalized with acute heart failure exacerbation. This phenomenon has been recently termed acute cardio-renal syndrome. Acute cardio-renal syndrome is not uncommon, affecting roughly one third of acute decompensated heart failure patients. The mechanism of acute cardio-renal syndrome is poorly understood and difficult to elucidate in light of the complex and multifactorial comorbidities associated with acute heart failure syndrome. Acute cardio-renal syndrome is commonly explained by hypoperfusion of the kidney with intravascular volume depletion, hypotension and low flow state ("pre-renal syndrome"). This perception, however, is challenged by the actual hemodynamics present during acute cardio-renal syndrome characterized by hypervolemia, normal cardiac output, and elevated filling pressures of the systemic and venous circulation. This review discusses the long-standing and unnoticed evidence in support of the notion that right-sided failure with raised filling pressure of the renal vein by itself can indeed lead to acute worsening renal function with oliguria, azotemia, and reduced glomerular filtration rate.
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PMID:Acute cardio-renal syndrome: progression from congestive heart failure to congestive kidney failure. 1788 88


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