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Inotropic Agent (inotropic + agent)
Selected AbstractsHeart failure: a hemodynamic disorder complicated by maladaptive proliferative responsesJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 1 2003A. M. Katz Abstract Heart failure has traditionally been viewed as a hemodynamic syndrome characterized by fluid retention, high venous pressure, and low cardiac output. Over the past decade, however, it has become clear that because of deterioration and progressive dilatation (remodeling) of the diseased heart, this is also a rapidly fatal syndrome. The importance of prognosis came to be appreciated when clinical trials showed that therapy which initially improves such functional abnormalities, as high venous pressure and low cardiac output, often fail to improve survival, and that some drugs which improve hemodynamics worsen long-term prognosis. The latter is true for most vasodilators which, in spite of alleviating the adverse short-term consequences of high afterload, shorten survival. Notable exceptions are ACE inhibitors, whose vasodilator effects do not explain their ability to prolong survival; instead, these drugs slow both deterioration and remodeling of the failing heart. Inotropic agents, while providing immediate relief of symptoms, generally shorten long-term survival, whereas ,-blockers slow deterioration and remodeling, and reduce mortality. Aldosterone antagonists exert beneficial effects on prognosis that are not easily explained by their diuretic effects, but instead can be explained by their ability to inhibit signaling pathways that stimulate maladaptive hypertrophy, remodeling, apoptosis and other deleterious responses that cause deterioration of the failing heart. These and other findings demonstrate that heart failure is more than a hemodynamic disorder; these patients suffer from maladaptive proliferative responses that cause cardiac cell death and progressive dilatation that play a key role in determining the poor progressive in this syndrome. [source] Review article: Inotrope and vasopressor use in the emergency departmentEMERGENCY MEDICINE AUSTRALASIA, Issue 5 2009Ainslie Senz Abstract Shock is a common presentation to the ED, with the incidence of septic shock increasing in Australasia over the last decade. The choice of inotropic agent is likely dependent on previous experience and local practices of the emergency and other critical care departments. The relatively short duration of stay in the ED before transfer leaves little room for evaluating the appropriateness of and response to the agent chosen. Delays in transfer to inpatient facilities means that patients receive advanced critical care within the ED for longer, requiring initiation and titration of vasoactive agents in the ED. This article discusses the general concepts of shock and the indicators for inotrope and vasopressor use, revises the various agents available and reviews the current evidence for their use. [source] Growth hormone and insulin-like growth factor 1 levels and their relation to survival in children with bacterial sepsis and septic shockJOURNAL OF PAEDIATRICS AND CHILD HEALTH, Issue 4 2004N Önenli-Mungan Objectives: Despite improved supportive care, the mortality of sepsis and septic shock is still high. Multiple changes in the neuroendocrine systems, at least in part, are responsible for the high morbidity and mortality. A reduced circulating level of insulin-like growth factor and an elevated level of growth hormone are the reported characteristic findings early in the course of sepsis and septic shock in adults. The aim of this study was to evaluate the changes of growth hormone/insulin-like growth factor 1 axis in sepsis and septic shock and investigate the relationship between these hormones and survival. Methods: Fifty-one children with sepsis (S), 21 children with septic shock (SS) and 30 healthy, age- and sex-matched children (C) were enrolled in this study. Growth hormone, insulin-like growth factor 1 and cortisol levels of the sepsis and septic shock groups were obtained before administration of any inotropic agent. Results: Growth hormone levels were 32.3 ± 1.5 µIU/mL (range 4,56), 15.9 ± 0.6 µIU/mL (range 11,28) and 55.7 ± 2.7 µIU/mL (range 20,70) in S, C and SS groups, respectively. The difference between the growth hormone levels of the S and C groups, S and SS groups, and C and SS groups were significant (P < 0.001). Non-survivors (54.7 ± 1.6 µIU/mL) had significantly higher growth hormone levels than survivors (29.4 ± 1.5 µIU/mL) (P < 0.001). Insulin-like growth factor 1 levels were 38.1 ± 2.1 ng/mL (range 19,100), 122.9 ± 9.6 ng/mL (range 48,250) and 22.2 ± 1.9 ng/mL (range 10,46) in the S, C and SS groups, respectively, and the difference between the insulin-like growth factor 1 levels of the S and C, S and SS, and C and SS groups were significant (P < 0.001). Non-survivors (8.8 ± 1.1 µg/dL) had significantly lower cortisol levels than survivors (40.9 ± 2.1 µg/dL) (P < 0.001). We detected a significant difference between the levels of cortisol in non-survivors (19.7 ± 1.8 µg/dL) and survivors (33.9 ± 0.9 µg/dL) (P < 0.01). Conclusions: There were elevated levels of growth hormone with decreased levels of insulin-like growth factor 1 in children during sepsis and septic shock compared to healthy subjects. In addition, there were even higher levels of growth hormone and lower levels of insulin-like growth factor 1 in non-survivors than in survivors. We think that both growth hormone and insulin-like growth factor 1 may have potential prognostic value to serve as a marker in bacterial sepsis and septic shock in children. As there is insufficient data in the paediatric age group, more studies including large numbers of patients and additionally evaluating cytokines and insulin-like growth factor binding proteins are needed. [source] Critical management in patients with severe enterovirus 71 infectionPEDIATRICS INTERNATIONAL, Issue 3 2006JIEH-NENG WANG Abstract Objective: The aim of this study was to analyze clinical details occurring in children with severe enterovirus 71 (EV71) infection and synthesize the critical care experience for patients with severe EV71 infection. Methods: A retrospective clinical, laboratory, and hemodynamic study was performed in a pediatric intensive care unit in a university hospital. From March 1998 to April 2000, seven consecutive pediatric patients with severe EV71 infection were retrospectively analyzed as the comparison group. From May 2000 to March 2003, eight consecutive patients with severe EV71 infection who had received the protocol therapy were enrolled as the study group. Detailed information about clinical treatment and pharmacological therapy was collected for comparison. Results: The clinical presentations and laboratory findings between the comparison and the study groups were not significantly different. The amount of intravenous fluid in the first 24 h was significantly higher in the comparison group (9.2 ± 5.0 vs 4.9 ± 1.3 mL/kg per h). More patients in the study group received low doses of dopamine infusion, patients in the comparison group received more epinephrine, and none of them received milrinone. The acute-stage and long-term survival rates were higher in the study group (100% vs 43%, 87% vs 29%). Conclusion: Early cardiopulmonary support may prevent the vicious cycle of cardiopulmonary failure and improve the clinical outcome of severe EV71 infection. Milrinone may be the ideal inotropic agent for these patients. Echocardiography, a central line, and an arterial line could be an alternate method to replace direct intracardiac hemodynamic monitoring for guiding critical management. [source] Inotropes in the beta-blocker eraCLINICAL CARDIOLOGY, Issue S3 2000B. D. Lowes M.D. Abstract Beta-adrenergic blocking agents are now standard treatment for mild to moderate chronic heart failure (CHF). However, although many subjects improve on beta blockade, others do not, and some may even deteriorate. Even when subjects improve on beta blockade, they may subsequently decompensate and need acute treatment with a positive inotropic agent. In the presence of full beta blockade, a beta agonist such as dobutamine may have to be administered at very high (> 10 ,g/kg/min) doses to increase cardiac output, and these doses may increase afterload. In contrast, phosphodiesterase inhibitors (PDEIs) such as milrinone or enoximone retain their full hemodynamic effects in the face of beta blockade. This is because the site of PDEI action is beyond the beta-adrenergic receptor, and because beta blockade reverses receptor pathway desensitization changes, which are detrimental to PDEI response. Moreover, when the combination of a PDEI and a beta-blocking agent is administered long term in CHF, their respective efficacies are additive and their adverse effects subtractive. The PDEI is administered first to increase the tolerability of beta-blocker initiation by counteracting the myocardial depressant effect of adrenergic withdrawal. With this combination, the signature effects of beta blockade (a substantial decrease in heart rate and an increase in left ventricular ejection fraction) are observed, the hemodynamic support conferred by the PDEI appears to be sustained, and clinical results are promising. However, large-scale placebo-controlled studies with PDEIs and beta blockers are needed to confirm these results. [source] Clinical and Hemodynamic Effects of Nesiritide (B-Type Natriuretic Peptide) in Patients With Decompensated Heart Failure Receiving , BlockersCONGESTIVE HEART FAILURE, Issue 2 2005William T. Abraham MD The use of , blockers in congestive heart failure presents a therapeutic challenge for patients with acute episodes of decompensation. Such patients may be less responsive to positive inotropic agents, whereas the beneficial effects of nesiritide, which are not dependent on the ,-adrenergic receptor signal-transduction pathway, may be preserved. This analysis of the Vasodilation in the Management of Acute CHF trial evaluated the safety and efficacy of nesiritide in decompensated congestive heart failure patients receiving , blockers. The Vasodilation in the Management of Acute CHF trial was a multicenter, randomized, controlled evaluation of nesiritide in 489 hospitalized patients with decompensated congestive heart failure. One hundred twenty-three patients were on chronic ,-blocker therapy at enrollment (31 randomized to placebo, 50 to nesiritide, and 42 to nitroglycerin). Primary end points included pulmonary capillary wedge pressure and dyspnea evaluation at 3 hours. Patients receiving nesiritide, but not IV nitroglycerin, had significantly reduced pulmonary capillary wedge pressure vs. placebo at 3 hours regardless of ,-blocker use. The use of , blockers did not alter the beneficial effects of nesiritide on systemic blood pressure, heart rate, or dyspnea evaluation. In nesiritide-treated subjects, safety profiles were similar regardless of ,-blocker use. Thus, the clinical and hemodynamic benefits and safety of nesiritide are preserved in decompensated congestive heart failure patients receiving chronic , blockade. [source] Anti-ischemic effects of inotropic agents in experimental right ventricular infarctionACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 7 2009M. HEIN Background: Right ventricular (RV) function is an important determinant of survival after myocardial infarction. The efficacy of reperfusion therapy might be increased by the cardioprotective action of inotropic agents, which are used for symptomatic therapy in situations with compromised hemodynamics. Therefore, we used a porcine model of RV ischemia and reperfusion (IR) injury to study the influence of milrinone, levosimendan and dobutamine on the extent and degree of myocardial injury. Methods: IR injury was induced by temporary ligation of the distal right coronary artery for 90 min, followed by 120 min of reperfusion. Treatment was initiated 30 min after coronary artery occlusion. A bolus of milrinone (n=12; 50 ,g/kg) and levosimendan (n=10; 24 ,g/kg) was applied in different groups, followed by continuous infusion of the drugs at 0.5 and 0.2 ,g/kg/min, respectively. The effects on myocardial injury and inflammation were compared with a control (n=12) and a dobutamine group (n=10), where treatment was started with an infusion of 5 ,g/kg/min. Results: Milrinone and levosimendan reduced the resulting infarct size with respect to the area at risk (41.7±10.2%, 45.7±8.1%) when compared with the control group (58.3±6.1%). In contrast, dobutamine had no effect (55.8±7.7%). All drugs reduced the number of neutrophils infiltrating into the different myocardial regions and the circulating levels of interleukin-6. Increased levels of tumor necrosis factor , during reperfusion were only abated by milrinone and levosimendan. Conclusions: Cardioprotective properties of milrinone and levosimendan were demonstrated for the first time in a clinically relevant model of RV infarction. [source] Hospitalized patients with acute decompensated heart failure: Recognition, risk stratification, and treatment reviewJOURNAL OF HOSPITAL MEDICINE, Issue S6 2008Alpesh Amin MD Abstract Acute decompensated heart failure (ADHF) has emerged as a major healthcare problem. It causes approximately 3% of all hospitalizations in the United States, with the direct medical cost of these hospitalizations estimated at $18.8 billion per year. Early recognition, risk stratification, and evidence-based treatment are crucial in reducing the morbidity, mortality, and costs associated with this disorder. Classic signs and symptoms of ADHF, such as rales, dyspnea, and peripheral edema, may be absent at hospital presentation and, even when present, are not specific to this disorder. As a result, serum B,type natriuretic peptide level is now used to rapidly and accurately detect ADHF. Multivariate analyses have identified renal dysfunction, hypotension, advanced age, hyponatremia, and comorbidities as significant and independent mortality risk factors. Based on these factors, mortality risk can be stratified from very low to very high using published algorithms that have been validated in independent populations. Evidence-based guidelines for the treatment of ADHF are available from both the European Society of Cardiology and the Heart Failure Society of America. In general, an intravenous loop diuretic, either alone or in combination with a vasodilator, is recommended as initial therapy in patients with volume overload, depending on the patient's clinical status. Use of inotropic agents should be limited to the small subset of patients with low-output syndrome and significant hypotension. In any event, frequent monitoring of clinical response is essential, with subsequent therapy determined by this response. Finally, focused patient education during hospitalization may help reduce readmissions for ADHF. Journal of Hospital Medicine 2008;3(Suppl 6):S16,S24. © 2008 Society of Hospital Medicine. [source] | |||||||||||||||||||