Acute heart failure: a novel approach to its pathogenesis and treatment

Abstract

Acute heart failure (HF) is one of the most common syndromes in emergency medicine, however, its exact pathogenesis has remained largely unknown. Based on clinical and hemodynamic data we have sub-divided acute HF into four syndromes: cardiogenic shock, pulmonary edema, hypertensive crisis and exacerbated HF. Cardiogenic shock is caused by a severe reduction in cardiac power which is not met by an adequate increase in peripheral vascular resistance leading to significant decrease in blood pressure and end organ perfusion. Hence the treatment of cardiogenic shock should be directed at improving cardiac performance (by optimizing filling pressure, intra-aortic balloon pump and immediate revascularization) and administration of peripheral vasoconstrictors. The other acute HF syndromes (pulmonary edema, HTN crisis and exacerbated HF) are caused by a combination of progressive excessive vasoconstriction superimposed on reduced left ventricular functional reserve. The impaired cardiac power and extreme vasoconstriction induce a vicious cycle of afterload mismatch resulting in a dramatic reduction of CO and elevated left ventricular end diastolic pressure, which is transferred backwards to the pulmonary capillaries yielding pulmonary edema. Therefore, the immediate treatment of these acute HF syndromes should be based on the administration of strong, fastacting intravenous vasodilators such as nitrates or nitroprusside. After initial stabilization, therapy should be directed at reducing recurrent episodes of acute HF, by prevention of repeated episodes of excessive vasoconstriction along with efforts to optimize cardiac function. ᮊ

The Development of a Simple Risk Score to Predict Early Outcome in Severe Acute Acidotic Cardiogenic Pulmonary Edema

“…[12][13][14][15][16][17][18] Often, the development of acute cardiogenic pulmonary edema is dominated by a marked hypertensive response that is implicated in either its causation or the marked stress response to the clinical condition. 5,24 It is perhaps surprising that history of myocardial infarction, vascular disease, or previous cardiac failure did not independently predict outcome unlike previous findings. 17,18 This may reflect the inaccuracies of history ascertainment at the time of presentation or suggests that such features are poor predictors of early outcome that is dominated more by age and physical and hemodynamic reserve.…”

I Diretriz Latino-Americana para avaliação e conduta na insuficiência cardíaca descompensada

“…In this setting, there are evidences of volume overload or, if not, the shock is not reverted by volume restoration 121 .…”

Acute Heart Failure Syndromes: Emergency Department Presentation, Treatment, and Disposition: Current Approaches and Future Aims

“…Ce modèle physiopathologique est, en outre, jugé applicable à toutes les catégories de patients, les seules variations tenant à son degré de sévérité. [96][97][98] Cela a conduit à adopter des stratégies thérapeutiques à court terme telles que celle faisant appel à l'administration de diurétiques intraveineux dans le but de réduire rapidement la surcharge liquidienne, cela sans qu'aucun essai clinique n'ait été entrepris pour vérifier la tolérance et l'efficacité à long terme de ces traitements. Or, force est de constater que les données émanant de plusieurs registres de patients insuffisants cardiaques écornent notablement le classique modèle de bas débit cardiaque personnifié par le patient de sexe masculin atteint d'IC ischémique en montrant que le syndrome considéré sous-tend un ensemble beaucoup plus complexe d'entités physiopathologiques différentes.…”