High output heart failure is a poorly understood condition characterized by signs and symptoms of heart failure and a resting cardiac index above 4 l/min x m2. Classical heart failure treatment can be detrimental in this instance.
Patients with high output heart failure present with dyspnea, tachypnea, non-productive cough, fatigability, pulmonary rales, pleural effusion and peripheral edema, as a result of pulmonary and venous congestion due to neurohormonal activation and increased salt and water retention. Also, they are often tachycardic, with a heart rate between 85 and 105 beats per minute. A third heart sound and bilateral basal crackles are often heard in these patients [1]. Jugular and femoral venous hum may be sometimes observed. Peripheral vasodilatation leads to warm extremities.
High output heart failure is caused by a number of conditions each with their own signs and symptoms, that can sometimes also be found in affected individuals, such as chronic anemia, systemic arterio-venous fistulae, Paget's disease, hyperthyroidism, chronic hypercapnia, obesity, beriberi heart disease and sepsis.
Anemia causes cutaneous pallor and fatigability which overlaps with that induced by the heart failure, peripheral vasodilatation caused by vascular nitric oxide synthase [2] and low systemic vascular resistance [3].
Arteriovenous fistulae are associated with a specific hum on auscultation and may be congenital or acquired. They lead to a decrease in the systemic vascular resistance and thus high output heart failure [4]. Fistulae may be found in the context of certain congenital diseases, such as Osler-Weber-Rendu disease, Parkes-Weber or Klippel–Trénaunay syndrome. They can cause decreased pulse pressure distal to their location [1].
Paget's disease is associated with pain and warmth of the affected area, but a large amount of bone must be involved before heart failure occurs. A similar mechanism for the malfunction of the heart has been described in multiple myeloma, and Albright's disease [5].
Hypercapnia caused by chronic obstructive pulmonary disease may also cause high output heart failure [6]. The pulmonary pathology is recognized by auscultation and symptoms like dyspnea and fatigability.
Hyperthyroidism causes tachycardia-mediated cardiomyopathy and thus high output heart failure [7] and is often accompanied by atrial fibrillation [8].
Sepsis causes systemic vasodilatation, arterial hypotension and heart failure [9] and is recognized most often using laboratory workup, but also by fever, tachycardia, and tachypnea.
Beriberi is associated with chronic alcohol consumption or impaired nutrient absorption, that lead to weight loss and steatorrhea. Heart beriberi causes peripheral edema and fatigability and decreased systemic vascular resistance, leading to high output heart failure.
Obesity leads to systolic and diastolic malfunction of the heart and increased total blood volume, thus causing high output heart failure [10].
Blood workup shows elevated levels of atrial and brain natriuretic peptide in high output heart failure patients [11] [12]. Venous oxygen saturation, if high (above 75%), is an indirect indicator of a high output state. The oxygen content of arterial and mixed venous blood samples is expected to be decreased.
As in all heart failure individuals, a chest radiography is useful, as it might show cardiomegaly, pleural effusion or pulmonary congestion. A diagnosis of pneumonia in a septic patient with high output heart failure should lead the physician to suspect it as the underlying cause of the failure.
The diagnosis is ultimately confirmed with echocardiography showing an increased cardiac index. This investigation may show eccentric remodeling, chamber dilatation, and increased ventricular filling pressures, with a high ejection fraction. Pulmonary hypertension is another common finding in these patients.
Cardiac catheterization confirms increased cardiac filling pressures, high pulmonary artery pressure, stroke volume, ventricular preload, ejection fraction and decreased afterload as a result of low systemic vascular resistance [13].