Key result
High output heart failure is characterized by excessive vasodilation and is most frequently caused by obesity, liver dysfunction, and arteriovenous shunts.
This review summarizes the pathophysiology and common clinical causes of high output heart failure, emphasizing the role of reduced systemic vascular resistance.
May prompt evaluation for listed conditions in high-output HF; leaves open prospective validation of management.
In the U.S., each year, there are more than 500,000 new cases of all types of heart failure. With high output cardiac failure, there is an elevated cardiac output associated with several conditions and diseases, including obesity, chronic anemia, systemic arterio-venous fistula, hypercapnia, mitochondrial dysfunction, and hyperthyroidism. The underlying pathophysiologic mechanisms relate to a reduction in systemic vascular resistance from arterio-venous shunting or peripheral vasodilation. Often there is a decrease in systemic arterial blood pressure and neurohormonal activation leading to heart failure symptoms of dyspnea and fatigue. In a persistent high output state, patients may experience tachycardia, valvular abnormalities, and ventricular dilatation and/or hypertrophy. In this article, there is a review of high output heart failure, including the prevalence, pathophysiology, and common clinical causes of this disease.
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Shen et al. (2020) conducted a review in High output heart failure. High output heart failure is characterized by excessive vasodilation and is most frequently caused by obesity, liver dysfunction, and arteriovenous shunts.
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