title: Management and monitoring of haemodynamic complications in acute heart failure.
abstract: The pathophysiology of acute heart failure syndromes (AHFS), defined as a change or worsening in heart failure symptoms and signs, is complex. The variety of adverse neurohormonal adaptations includes increased levels of plasma renin, aldosterone and angiotensin II, all responsible for cardio-renal dysfunction. In fact, such alterations result in an array of clinical changes that include abnormal haemodynamics, altered ventricular filling pressures, pathological neurohormonal responses, leading to fluid overload, congestion and ultimately heart failure symptoms. Clinical pictures can be various: in spite of a usual improvement in dyspnoea, little weight change and significant morbidity are generally observed during hospitalization. Short-term outcomes are characterized by a high 60-day re-hospitalization and high mortality rates; apparently, both can be predicted from pre-discharge characteristics. The most frequently used treatments for AHF care include diuretics, inotropic agents, and vasodilator/vasoactive agents; however, the final therapeutic strategy is often individualized. Diuretics are currently the most used agents, but resistance to diuretic therapy is common. In addition, several studies have demonstrated that aggressive diuresis can contribute to reduced renal function, and high doses of diuretics have been associated with increased morbidity and mortality. Many patients with AHFS also suffer from acute or from chronic renal dysfunction (cardio-renal syndromes type 1 and 2, respectively), which further complicate the outcomes and treatment strategies. A personalized patient evaluation of the combined heart and kidney functions is advised to implement the best possible multidisciplinary diagnostic and therapeutic approach.
authors.affiliation: Department of Cardiology, San Filippo Neri Hospital, Rome, Italy. naspromonte@yahoo.it
authors.forename: Nadia
authors.initials: N
authors.lastname: Aspromonte
authors.forename: Dinna N
authors.initials: DN
authors.lastname: Cruz
authors.forename: Roberto
authors.initials: R
authors.lastname: Valle
authors.forename: Claudio
authors.initials: C
authors.lastname: Ronco
mesh_terms: D002316:Cardiotonic Agents / Q000008:administration & dosage / Q000009:adverse effects; D002319:Cardiovascular System / Q000294:innervation / Q000378:metabolism / Q000503:physiopathology; D019468:Disease Management; D004232:Diuretics / Q000008:administration & dosage / Q000009:adverse effects; D006333:Heart Failure / Q000150:complications* / Q000175:diagnosis / Q000188:drug therapy* / Q000378:metabolism / Q000401:mortality / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D007668:Kidney / Q000378:metabolism / Q000503:physiopathology; D008991:Monitoring, Physiologic; D011379:Prognosis; D051437:Renal Insufficiency / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D012084:Renin-Angiotensin System / Q000187:drug effects; D014665:Vasodilator Agents / Q000008:administration & dosage / Q000009:adverse effects; D014666:Vasomotor System / Q000187:drug effects / Q000503:physiopathology
chemical_list: D002316:Cardiotonic Agents; D004232:Diuretics; D014665:Vasodilator Agents