| Abstrakt: |
Introduction: The knowledge on High-Output Cardiac Failure (HOCF) has greatly improvedin the last two decades. One of the advances was the identification of a new phenotype ofHOCF, characterized by the absence of ventricular dilation, already associated with liver disease,Arteriovenous Fistulas (AVF), lung disease, myelodysplastic syndromes, and obesity. However, ithas been noted that any aetiology can present with one of the two phenotypes, depending on theevolution. Objective: The study aims to describe, through an integrative review, the physiopathology and aetiologiesof HOCF and to discuss phenotypes associated with this condition. Methods: Revisions, guidelines, case-controls, cohort studies and clinical studies were searched inMEDLINE and LILACS, using the connectives in the “cardiac output, high” database (MeSHTerms) OR “high cardiac output” (All Fields). Discussion: Two distinct phenotypes are currently described in the HOCF, regardless of the aetiology:1) one with enlarged cardiac chambers; and 2) with normal heart chambers. The mechanisms relatedto HOCF are vasodilation, arteriovenous shunts that cause increased microvascular density,Reduced Systemic Vascular Resistance (RSVR), and high metabolism. These mechanisms lead toactivation of the renin-angiotensin-aldosterone system, sodium and water retention, activation ofneprilysin, of the sodium-glucose-2 transporter, which promote interstitial fibrosis, ventricular remodelingand a consequent increase in cardiac output >8L/min. Conclusion: Many aetiologies of HOCF have been described, and some of them are potentially curable.Prompt recognition of this condition and proper treatment may lead to better outcomes. |
