High-output heart failure

Article written and reviewed by Dr Luca Moretti

High-output heart failure is a syndrome of congestion and/or relative inadequate perfusion in which cardiac output is elevated above normal values but insufficient to meet excessive metabolic demand or compensate for pathologically low systemic vascular resistance. Hemodynamically, cardiac output above 8 L/min or a cardiac index above 3.9 L/min/m² is often found; these values must be interpreted in relation to body size, anemia, fever, and the measurement method. It differs from an asymptomatic high-output state. Diagnosis of heart failure requires symptoms or signs, elevated filling pressures or organ damage, and a causative condition; tachycardia and a bounding pulse are insufficient. A preserved or increased ejection fraction does not exclude the syndrome because the critical variable is the relationship among flow, demand, and resistance. The most frequent contemporary causes are severe obesity, chronic liver disease, arteriovenous fistulas, and lung diseases; anemia, thyrotoxicosis, beriberi, sepsis, pregnancy, Paget disease, and myeloproliferative neoplasms complete the picture. Multiple mechanisms may coexist.

Chronically elevated cardiac output expands plasma volume, increases venous return and cardiac work, produces dilation, and raises pressures. The body continues to retain sodium because vasodilation reduces effective arterial blood volume, creating hyperdynamic congestion that may be mistaken for common HFpEF or dilated cardiomyopathy. Treatment does not consist of indiscriminately increasing already elevated inotropy or using diuretics alone. The source of increased flow or vasodilation must be identified and removed while maintaining oxygenation, euvolemia, and perfusion in the meantime; prognosis depends on the cause and reversibility. Correctable fistulas, anemia, or thiamine deficiency may allow marked recovery; advanced cirrhosis, severe obesity, or pulmonary disease maintain the load and increase recurrence.

Etiology, pathogenesis, and pathophysiology

Severe obesity increases metabolic mass, plasma volume, renal blood flow, and oxygen consumption; adipokines, sleep apnea, and tissue vasodilation reduce relative resistance; stroke volume increases and the ventricle dilates, while hypertension and stiffness may add diastolic dysfunction. The phenotype is therefore a mixture of high output and high pressures, not simply excess weight; fat mass requires less flow per kilogram than muscle, but its overall extent and associated lean tissue increase circulating volume. Indexing to body surface area may conceal a very high absolute cardiac output in large individuals. Obstructive sleep apnea and hypoventilation cause hypoxia and pulmonary hypertension, promoting right heart failure. The profile may thus become biventricular while systemic output remains high.

In cirrhosis, splanchnic vasodilation mediated by nitric oxide and other signals reduces resistance and activates the sympathetic nervous system, the renin-angiotensin system, and vasopressin. Retention, shunting, and collateral circulation increase cardiac output; with progression, cirrhotic cardiomyopathy may develop with insufficient contractile and chronotropic reserve; resting output may be high, but the response becomes inadequate during stress. Ascites and low albumin aggravate edema; infections, hemorrhage, or TIPS may unmask heart failure; TIPS reduces portal pressure by rapidly transferring blood to the heart and may precipitate congestion. Before the procedure, history, peptides, and echocardiography are needed, with further hemodynamic investigation in at-risk profiles.

An arteriovenous fistula creates a low-resistance circuit that increases venous return, heart rate, and stroke volume; the load depends on access flow, location, size, body mass, anemia, and cardiac reserve; proximal accesses often have higher flows. In hemodialysis, a flow above approximately 2 L/min or a high access flow/cardiac output ratio signals risk, but no diagnostic threshold is absolute. Temporary compression with a reduction in cardiac output and pressures supports causality if performed and interpreted correctly. Traumatic fistulas, malformations, hepatic vascular dysplasias, and iatrogenic shunts produce the same physiology. Hereditary hemorrhagic telangiectasia may combine hepatic shunts and anemia.

Anemia reduces arterial oxygen content; vasodilation, tachycardia, and increased stroke volume maintain delivery. When anemia is severe or chronic, the required cardiac output exceeds reserve and causes dilation, ischemia, and retention; risk depends on the rate of onset and preexisting heart disease. Thyrotoxicosis increases metabolism, beta-adrenergic sensitivity, heart rate, contractility, and volume while reducing resistance. Atrial fibrillation and tachycardia-induced cardiomyopathy may transform the hyperdynamic phase into a subsequent reduced ejection fraction. Fever, sepsis, and physiological pregnancy increase cardiac output through different mechanisms; heart failure appears when intensity, duration, or the substrate exceeds reserve; in sepsis, function may simultaneously become depressed.

Thiamine is a cofactor in oxidative metabolism. Severe deficiency causes vasodilation, elevated lactate, and high cardiac output, the cardiovascular form of beriberi; in the fulminant, or shoshin, variant, shock and acidosis may occur. Malnutrition, alcohol, bariatric surgery, hyperemesis, and diuretics increase risk; extensive Paget disease of bone creates high-flow vascular networks; heart failure is now rare and suggests a large disease burden. Myeloproliferative neoplasms may increase flow through metabolism, anemia, and intramedullary shunts. Vascular tumors, liver metastases, myeloma, and angiosarcoma may produce shunts. Localized murmurs and imaging help identify the site.

Reduced resistance causes effective arterial pressure to fall. Baroreflexes increase sympathetic and RAAS activity, retaining sodium and expanding volume; the heart works at a high heart rate and stroke volume. Over time, eccentric hypertrophy, atrial dilation, and functional valvular regurgitation appear; filling pressures increase because of volume, diastole shortened by tachycardia, preexisting stiffness, and interdependence. Pulmonary pressure may rise because of high flow even without primary arteriopathy; oxygen delivery is the product of cardiac output and oxygen content. In anemia, sepsis, or beriberi, numerically high output may not prevent tissue hypoxia; lactate and venous oxygen saturation require interpretation according to the cause.

Clinical manifestations

Dyspnea, orthopnea, fatigability, edema, and weight gain resemble those of other phenotypes. Hyperdynamic features include warm extremities, a bounding or collapsing pulse, tachycardia, an active precordium, and flow murmurs; these findings may diminish when shock develops. A wide pulse pressure reflects high stroke volume and low resistance, but anemia, aortic regurgitation, and stiff arteries are alternatives; mean pressure may be normal, low, or elevated if hypertension coexists. Crackles, jugular venous distention, a third heart sound, hepatomegaly, and ascites quantify congestion; a third heart sound in a hyperdynamic state does not necessarily imply reduced ejection fraction.

Signs of the cause are crucial. Pallor, bleeding, or pica suggests anemia; tremor, weight loss, heat intolerance, goiter, and ophthalmopathy point toward thyrotoxicosis. Neuropathy, malnutrition, and acidosis raise suspicion of thiamine deficiency. Stigmata of liver disease, ascites, and splenomegaly indicate cirrhosis; a continuous murmur over an access or a very extensive thrill suggests high flow. Mucocutaneous vascular lesions and recurrent epistaxis point toward hereditary telangiectasia. Bone pain and deformities may accompany Paget disease. Fever, vasodilation, and altered mental status require investigation for sepsis.

With a dialysis fistula, dyspnea and exercise tolerance may worsen after creation or increased flow; an aneurysmal or proximal access, or one with a strong thrill, warrants flow measurement; distal ischemia and cardiac overload may coexist. The occlusion test may increase blood pressure and reduce heart rate, the Nicoladoni-Branham sign, but the clinical maneuver does not replace flow measurements and invasive assessment when needed. After TIPS, worsening may arise days or months later. Persistent ascites does not prove failure to control portal hypertension if heart failure coexists.

Palpitations are frequent because of sinus tachycardia or fibrillation. An excessive heart rate shortens diastole and increases demand; however, rate control must not eliminate compensation before the cause of low resistance is corrected. Angina may result from high demand even without stenoses, particularly with anemia or thyrotoxicosis. Elevated troponin signals injury, but the distinction between infarction and supply-demand mismatch requires universal criteria and context. Syncope and hypotension indicate inability to maintain blood pressure, an arrhythmia, or another lesion. They are not reassuring features of a simple hyperdynamic state.

In advanced stages, a warm profile may become cold when contractility and vasoconstriction fail; a “normal” cardiac output may represent a relative decline from previously very high values; the hemodynamic trajectory is more informative than an isolated threshold. Right heart failure may predominate with edema, ascites, and hepatic involvement; high pulmonary flow, sleep apnea, liver disease, or vascular access may increase pulmonary pressure and right ventricular load. Muscle loss may be hidden by edema or obesity. Nutritional assessment distinguishes intentional weight loss, malnutrition, and congestion.

Investigations and diagnosis

Diagnosis begins with demonstration of heart failure and identification of a hyperdynamic context. ECG documents heart rate, fibrillation, hypertrophy, and ischemia; radiography and lung ultrasound detect congestion. BNP or NT-proBNP may be elevated, but obesity lowers them and kidney disease and the atrium increase them. A complete blood count with indices, reticulocytes, ferritin, and transferrin saturation defines anemia; TSH and thyroid hormones identify thyrotoxicosis. Liver tests, INR, albumin, kidney function, urine testing, CRP, cultures, and lactate are selected according to the suspected etiology. Plasma thiamine testing has limitations, and empirical treatment is appropriate when suspicion is high because it is safe and delay in the fulminant form is dangerous.

Echocardiography may show dilated chambers, high stroke volume, preserved or hyperdynamic ejection fraction, impaired diastolic function, and elevated pulmonary pressure. Doppler cardiac output is calculated from outflow tract area and the velocity-time integral; small errors in diameter are squared; calculation must be consistent with the method and body size. In aortic or mitral regurgitation, flow through a valve includes regurgitant volume and may overestimate effective systemic flow; right heart function, the pericardium, and valves help identify cofactors. A small, hyperdynamic ventricle with shock may suggest sepsis or hypovolemia, not necessarily chronic high-output heart failure.

Right heart catheterization confirms elevated cardiac output, low resistance, and filling pressures. The direct Fick method is accurate if oxygen consumption is measured; using estimated values may generate substantial errors in obesity, sepsis, and metabolic states. Thermodilution may be affected by tricuspid regurgitation, shunts, and extreme flows; physiological concordance among methods, oxygen saturations, and the clinical picture is necessary before labeling the patient. High venous oxygen saturation suggests reduced extraction or shunting; a step-up localizes communications. Wedge and atrial pressures quantify the congestive component.

Fistula flow is measured by ultrasound dilution during dialysis or Doppler. Its ratio to cardiac output expresses the proportion diverted; compression during catheterization or echocardiography may demonstrate a fall in output and pressures, supporting a causal relationship. CT, MRI, or angiography localizes deep shunts and malformations. In hereditary telangiectasia, hepatic and pulmonary imaging follows protocols and family history. Before reducing an access, dialysis alternatives, patency, and future need must be assessed; the decision is shared among the nephrologist, cardiologist, and vascular surgeon.

When cirrhosis is suspected, the severity of liver disease, portal involvement, ascites, and the indication for transplantation are defined. Stress echocardiography may detect reduced reserve, but no single test excludes cirrhotic cardiomyopathy; RHC is useful before TIPS or transplantation in selected patients. Paget disease is evaluated with alkaline phosphatase and bone imaging; scintigraphy defines its extent; neoplasms require a complete blood count, blood smear, protein studies, and a hematological workup. The differential diagnosis includes aortic regurgitation, sepsis without heart failure, physiological pregnancy, adipose HFpEF, and hyperkinetic circulation due to anxiety. Elevated pressures and a demonstrated cause separate the syndrome from flow signs alone.

Functional assessment uses a walk test or cardiopulmonary exercise testing, but high cardiac output does not guarantee high peak VO2 if extraction, anemia, or the lungs are limiting. The relationship between delivery and consumption can be defined with invasive hemodynamics in complex cases; monitoring tracks cardiac output, resistance, pressures, dimensions, rhythm, and cause. In dialysis access, changes in flow and symptoms are more useful than a single threshold; in thyrotoxicosis, biochemical control is also followed; documentation should specify the dominant cause, hemodynamic state, and degree of reversibility. A generic label without etiological investigation exposes the patient to symptomatic therapy alone.

Treatment and prognosis

Diuretics control edema and pressures, but vasodilation maintains sodium-retaining activation. Dose and combinations are adapted to blood pressure, kidney function, and cause; excessive depletion may produce hypotension without normalizing the source of increased flow. Oxygen is used in hypoxemia and transfusion in anemia according to severity, symptoms, and context; overly rapid correction or a high transfusion volume may cause circulatory overload, making the cause and pace of correction essential. Vasoconstrictors and inotropes are reserved for shock and are not chronic therapy; sepsis requires antibiotics, source control, and individualized resuscitation.

In a symptomatic high-flow fistula, banding, revision, flow reduction, or ligation is considered; the goal is to reduce shunting while preserving access if possible; after the procedure, cardiac output, blood pressure, dialysis, and symptoms are checked. Definitive ligation requires a convincing causal relationship and a plan for alternative access. Kidney transplant recipients with persistent fistulas may show regression of cardiac mass after closure, but the decision remains individual. Arteriovenous malformations may be embolized or operated on according to location. In hepatic involvement of hereditary telangiectasia, inappropriate procedures may be dangerous, and transplantation is reserved for selected cases.

Hyperthyroidism is treated with antithyroid drugs, radioiodine, or surgery according to etiology. Beta-blockers control symptoms and heart rate, but in thyrotoxic shock with severe dysfunction they require caution and titratable agents; hormone control is the treatment of the cause. Anemia requires iron, vitamins, bleeding control, or hematological therapy; normalization of hemoglobin must follow guidelines for the condition, particularly in kidney disease, where targets and erythropoiesis-stimulating agents carry risks. Thiamine is administered promptly before or together with glucose in at-risk individuals; improvement in lactate and circulation may be rapid, but does not exclude other concomitant causes.

In cirrhosis, sodium and ascites are controlled with diuretics, paracentesis, and albumin according to hepatological indications; TIPS is reassessed if the shunt precipitates heart failure. Liver transplantation may correct the hyperdynamic circulation, but cardiomyopathy and pulmonary hypertension modify eligibility; weight loss in obesity reduces demand and volume but must preserve muscle mass. Nutritional approaches, exercise, drugs, and metabolic surgery are selected with attention to congestive status and perioperative risk. Sleep apnea and hypoventilation require nocturnal ventilation, oxygen when indicated, and weight management; improvement in right ventricular afterload may take months.

Bisphosphonates treat active Paget disease and may reduce bone blood flow. Myeloproliferative neoplasms or tumors require specific therapy; control of the clone or mass may reverse the physiology. HFrEF therapy is applied when a truly reduced ejection fraction exists, but potent vasodilators may be poorly tolerated with already low resistance; phenotype-based prescribing distinguishes treatment of myocardial dysfunction from treatment of the shunt. Fibrillation is managed with rhythm or rate control and anticoagulation according to risk. Eliminating tachycardia reduces demand, but excessive bradycardia may reduce the cardiac output required before correction of the cause.

Prognosis in the contemporary study was worse than in controls, with marked differences by cause; obesity, liver disease, and arteriovenous shunts were important phenotypes. Right heart damage, kidney dysfunction, blood pressure, and hospitalizations increase risk; remodeling is reversible if the load is removed before established fibrosis and valvular regurgitation. Echocardiography and clinical assessment verify regression after treatment; cardiac output that normalizes while perfusion and ejection fraction worsen is not necessarily a success: it may indicate myocardial exhaustion. Longitudinal interpretation avoids false reassurance.

Complications

Chronic congestion causes pulmonary edema, ascites, effusions, and diuretic resistance. The kidneys and liver experience both high venous pressure and low effective arterial blood volume; creatinine and sodium may worsen despite high cardiac output; tricuspid regurgitation progresses with right ventricular dilation and further increases ineffective return. Atrial fibrillation and annular dilation form a cycle that may persist after partial correction of the cause. High-flow pulmonary hypertension may develop vascular remodeling and right heart dysfunction; delay in removing the shunt reduces reversibility.

Fibrillation, flutter, and persistent tachycardia may transform the hyperdynamic state into cardiomyopathy with reduced ejection fraction. Demand ischemia and secondary myocardial infarction are possible in anemia, thyrotoxicosis, and sepsis; high-output shock combines severe vasodilation and inadequate oxygen delivery; warm extremities and high venous oxygen saturation do not guarantee cellular oxygenation. Lactate may result from hypoperfusion, catecholamines, or metabolic deficiencies; a subsequent cold phase signals loss of reserve and requires critical care support without forgetting treatment of the cause.

Fistula procedures may cause thrombosis, loss of access, ischemia, or insufficient flow reduction; extensive closure rapidly modifies blood pressure and afterload. Vascular and cardiac surveillance prevents new imbalances. TIPS may precipitate edema or right heart failure; shunt reduction risks recurrence of portal hypertension; the multidisciplinary decision balances two pathological circulations. Transfusions may cause TACO, while unmonitored correction of thyrotoxicosis or aggressive beta-blockade may destabilize cardiac output.

Malnutrition and thiamine deficiency may be both cause and consequence. Intestinal edema and diuretics maintain deficiencies; supplementation alone does not correct alcohol use, malabsorption, or diet. Sarcopenic obesity conceals muscle loss and increases frailty; rapid weight reduction requires distinction among diuresis, adipose tissue, and lean mass. Cirrhosis adds encephalopathy, infections, bleeding, and hepatorenal syndrome; these complications may dominate prognosis more than the cardiac output measurement.

Late diagnosis exposes the patient to repeated symptomatic interventions without removal of the cause; follow-up must verify that anemia, thyroid function, access flow, or shunting remains controlled and that the ventricle recovers. When the cause is irreversible, the phenotype may progress to advanced heart failure with low reserve, organ damage, and hospitalizations; assessment for heart, liver, or combined transplantation depends on the site of disease. Integrated palliative care is appropriate in uncorrectable terminal forms and addresses dyspnea, edema, and goals without confusing high cardiac output with a favorable prognosis.