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

Acute heart failure has recently become a very common syndrome. Therefore, even if you are not a cardiologist, you should know how to diagnose and treat it. A basic technique is here summarized. Diagnosis of heart failure can be performed from a simple criteria including coarse crackles, an extra-sound (S3), a distention of the cervical vein, cardiomegaly, pulmonary edema, and serum levels of B-type natriuretic peptide (100 pg/ml<). After diagnosis, the severity should be assessed by the degrees of both pulmonary edema and cardiac output. For these evaluations, a Swan-Ganz catheter might not be needed, since we can evaluate them clinically, i.e., physical examinations and auscultation. We can then treat the patient with heart failure with a vasodilator and/or diuretics. If the blood pressure is low, we can administer a low dose of an inotropic agent. But an inotropic agent should be withdrawn as early as possible, because they can occasionally have deleterious effects. Finally, please bear in mind that the elimination of several triggers, e.g., infection, transient cessation of medication, and physical or metal stress, and also the detection of early symptoms of heart failure, e.g., shortness of breath on exertion, fatigue, increase in body weight, and appetite loss, are very important for the prevention of acute heart failure.
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PMID:[Diagnostic and therapeutic technique for acute heart failure]. 1567 66

Acute heart failure syndromes (AHFS) are related to several diseases affecting not only the heart but also the kidneys and blood vessels. Emerging evidence indicates that myocardial injury may also play a role in the pathophysiology of AHFS, as suggested by increased levels of markers of injury, such as cardiac troponin (cTn). Although cTn is a known prognostic marker, the release of cTn during hospitalization has not been evaluated prospectively with serial measures. We prospectively evaluated patterns of cTn release by conducting serial measures of cTnI and cTnT in patients hospitalized for AHFS. This study enrolled 51 patients with AHFS who were admitted with worsening heart failure (HF) and a history of coronary artery disease (CAD) in whom an acute coronary event was not suspected. Levels of cTnI and cTnT were measured at 8, 32, 56, and 80 hours after study entry. At baseline, 73.9% of patients had detectable cTnI, and 43.5% had detectable cTnT levels. The median concentrations of cTnI and cTnT were unchanged from 0 to 32 hours, increased from 32 to 56 hours, then either plateaued (cTnT) or decreased to baseline (cTnI). Of the 26 patients who had no detectable cTn levels at baseline, 2 (7.7%) developed detectable cTnT and 5 (41.7%) developed detectable cTnI release during hospitalization. Detectable levels of cTn at baseline were related to short-term clinical events. In this study of patients with CAD in whom an acute coronary event was not suspected, most had detectable levels of cTn present at admission, and some patients developed cTn release during hospitalization. Because cTn release may be a marker for myocardial injury, this study raises the possibility that injury occurred in most patients admitted with AHFS. Therefore, the goal of therapy for AHFS should be not only to improve symptoms and hemodynamics but also to salvage myocardium. Accordingly, therapies for AHFS that are aimed at improving hemodynamics may affect long-term prognosis by either injuring or salvaging myocardium.
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PMID:The Pilot Randomized Study of Nesiritide Versus Dobutamine in Heart Failure (PRESERVD-HF). 1618 19

Acute heart failure syndromes (AHFS) are among the most frequent causes of hospitalizations in the United States and Europe. Despite current therapies, patients with AHFS have high readmission and mortality rates. The randomized, controlled clinical trial is the standard by which contemporary therapies are evaluated, yet this tool of clinical science only recently has been rigorously applied to the development of novel therapies for patients with AHFS. This review briefly discusses some of the challenges presented in designing a clinical trial of therapies for AHFS and to describe some of the recent trials with respect to these issues in established drugs (such as milrinone, dobutamine, nitroglycerin, nitroprusside, and nesiritide) that have been approved by the US Food and Drug Administration (FDA). Recent trials of current investigational agents, such as levosimendan (the Randomized Multicenter Evaluation of Intravenous Levosimendan Efficacy Versus Placebo in the Short-Term Treatment of Decompensated Heart Failure [REVIVE], the Calcium Sensitizer or Inotrope or None in Low-Output Heart Failure [CASINO] study, and the Survival of Patients with Acute Heart Failure in Need of Intravenous Inotropic Support [SURVIVE] trial), tezosentan (the Randomized Intravenous Tezosentan [RITZ] study and the Value of Endothelin Receptor Inhibition with Tezosentan in Acute Heart Failure Studies [VERITAS]), and tolvaptan (the Acute and Chronic Therapeutic Impact of a Vasopressin Antagonist in Congestive Heart Failure [ACTIV-CHF] study), are also discussed.
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PMID:Overview of randomized clinical trials in acute heart failure syndromes. 1618 24

Acute heart failure and cardiogenic pulmonary edema is a common cause of respiratory distress among patients presenting to the emergency department. The emergency department is frequently the primary entry point into the health care system for these patients and is the site of initial stabilization, evaluation, and management of the patient.Emergency physicians, alongside cardiologists, play a critical role as these patients are treated in the emergency department and transferred to the cardiac ICU. The approach to the critically ill patient who has heart failure should be multidisciplinary and involve the emergency physician and the cardiologist who will care for the patient.
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PMID:Acute congestive heart failure in the emergency department. 1632 61

Acute heart failure syndromes (AHFS) is a broad spectrum of heterogeneous conditions including pulmonary oedema, hypertensive crisis, worsening exacerbated CHF and cardiogenic shock. HF hospitalizations have steadily risen with more than one million in 2004 in the United States and a similar number has been reported in Europe. Each year heart failure accounts for 6.5 million days spent in hospital in the USA and 1.4 million days in France. Mortality data are derived from registries or clinical trials. Registry data in patients admitted to general or cardiology wards such as in Euroheart Failure Survey and ADHERE provide a far more optimistic picture compared with data from consecutive unselected patients in the most acute situation. such as in EFICA. Four-week mortality was higher than 25% in this case. A great pathophysiologic understanding of the different features of the various AHFS is needed in order to identify targets for therapy and research. This includes hemodynamics, the role of myocardial injury, neurohormonal and cytokine abnormalities and the cardiorenal syndromes. So far, very little progress has been made in developing new, effective therapies and implementing management guidelines in this patient population. Future clinical trial endpoints should be better designed and tailored to the various pathophysiological conditions of this complex syndrome. The goal of AHFS therapy is not only to prevent disease progression but also to have a beneficial effect on an acute event that exacerbates disease progression. A combined endpoint assessing survival and rehospitalisation rates is becoming increasingly popular for acute therapies. Specific trials may also need to be designed according to the time of access to the patient.
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PMID:The challenge of acute decompensated heart failure. 1693 32

Acute heart failure (AHF) is defined as the rapid onset of symptoms and signs secondary to abnormal heart function which may occur with or without previous cardiac disease. Diagnosis and classification of severity are primarily based on clinical findings. The conditions leading to and reasons for acute heart failure which require specific therapeutic interventions should always be taken into consideration. Immediate goals in the guideline-oriented treatment of AHF are to improve the patient's symptoms and stabilize the hemodynamic condition. Medical therapy - besides oxygen supply - consists of the application of vasodilators, diuretics, and inotropes (especially dobutamine) depending both on the patient's clinical state and hemodynamic parameters. In the presence of ongoing signs of hypoxia, non-invasive ventilation has to be considered early. Bradycardia in AHF patients should initially be treated with atropine; a temporal pacemaker has to be inserted if no response is achieved by medical therapy. Ventricular fibrillation and tachycardia require immediate cardioversion.
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PMID:[Emergency therapy for acute heart failure]. 1761 27

Acute heart failure in young people may have other etiologies than myocarditis. We report about a twenty-year-old female developing acute heart failure following an anaphylactic reaction after a Prick test. Initially her left ventricular ejection fraction was severely compromised on echocardiography but normalized quickly. We postulated an anaphylactic shock-associated cardiomyopathy due to the close temporal association to an anaphylactic reaction, the presence of hypereosinophilia, and the absence of specific serologic, microbiologic, and immunologic abnormalities. Anaphylactic-associated cardiomyopathy very likely represents a common cause of acute heart failure and should be thought of in young people with known atopy.
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PMID:Anaphylactic shock-associated cardiomyopathy. 1765 28

Systolic heart failure is characterized by ventricular dilation and reduced ejection fraction, and this syndrome may be either chronic or acute. Left ventricular remodeling is the principal cause of progression of systolic heart failure. Acute heart failure resulting from cardiomyopathy has similar functional and morphologic abnormalities. This review discusses remodeling, initial therapy based on neurohormonal modulation, and treatment of decompensated and refractory heart failure. Diagnosis, prognosis, and management of acute myocarditis are also discussed.
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PMID:Systolic heart failure: chronic and acute syndromes. 1815 77

Acute heart failure poses a major healthcare problem. Recent guidelines for heart failure address management of outpatient chronic heart failure but do not address inpatient management. We present a unique, simple, yet comprehensive pathway that focuses on the differential diagnosis of new-onset heart failure and acute decompensation of chronic heart failure. An algorithm is presented for the optimal management of the patient with chronic heart failure who presents to the emergency room with acute symptomatic decompensation. The treatment algorithm provides recommendations for daily management and adjustments of therapy, which is primarily focused on a safe and rapid diuresis to the point of discharge from the acute care setting.
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PMID:Pathway for the management of acute heart failure. 1834 Jan 83

Acute heart failure is life threatening in adults and in the pediatric population. It represents the final pathway of complex physiological mechanisms that vary with age and underlying diseases. Strategies for treatment of heart failure should integrate to an concept of stepwise approach to heart failure. Evolving therapies, that are changing standard of care, are discussed. This paper gives an overview on principles for treatment of congestive heart failure, like diuretics, ss-beta-blockade, and angiotensin-converting enzyme blockers and discusses the approach to acute heart failure, including new and well known inotropic agents. Mechanical circulatory support and finally heart transplantation are focused as options in the last line.
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PMID:Strategies for the treatment of acute heart failure in children. 1850 93


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