Abstract
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.
Highlights
Most clinicians are familiar with patients that have heart failure with preserved ejection fraction (HFpEF) or reduced ejection fraction (HFrEF) with normal or low cardiac output accompanied by increased systemic vascular resistance [1]
With the growing rate of obesity in the U.S, clinicians are caring for an increased number of patients with high output heart failure associated with decreased systemic vascular resistance [2]
There are a variety of conditions and diseases such as obesity, anemia, cirrhosis, and hyperthyroidism resulting in high output heart failure [4, 5]
Summary
Most clinicians are familiar with patients that have heart failure with preserved ejection fraction (HFpEF) or reduced ejection fraction (HFrEF) with normal or low cardiac output accompanied by increased systemic vascular resistance [1]. Heart failure is common, with 500,000 new cases reported annually, the incidence and prevalence of high output failure are much lower [8] This has been attributed to conditions resulting in a high output state, including an increased metabolism with an associated demand for blood and a bypass of the arterioles and capillary bed, leading to increased oxygen consumption with a low systemic resistance [9, 10]. Factors that play a role in the development of high output heart failure include low systemic vascular resistance, reduced arterial-venous oxygen gradient, and an elevated cardiac output. The myocardium undergoes excessive vascular dilatation to increase oxygen consumption to maintain contractility Over time, this hypermetabolic state retains excessive blood resulting in extreme vasodilation. It has been reported that mitochondrial diseases contribute to the development of high output heart failure
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