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Clinical manifestations, diagnosis, and management of high-output heart failure

Clinical manifestations, diagnosis, and management of high-output heart failure
Literature review current through: Jan 2024.
This topic last updated: Sep 21, 2022.

INTRODUCTION — While most patients with heart failure (HF), with either reduced or preserved ejection fraction, have low or normal cardiac output accompanied by elevated systemic vascular resistance, a minority of patients with HF present with a high-output state with low systemic vascular resistance.

This topic will discuss the clinical manifestations, diagnosis, and management of high-output HF. The causes and pathophysiology of high-output HF are discussed separately. (See "Causes and pathophysiology of high-output heart failure".)

CLINICAL MANIFESTATIONS — Symptoms and signs in patients with high-output HF include general findings related to the hemodynamic disorder as well as specific findings related to particular causes of high-output HF.

General symptoms and signs — Patients with high-output HF may develop symptoms and signs classically associated with the more common "low-output" HF; specifically, they may develop symptoms and signs of pulmonary and/or systemic venous congestion, such as dyspnea, tachypnea, abdominal bloating, and peripheral edema; and signs of pleural effusion, in addition to generalized fatigue.

Several characteristic findings are sometimes seen on physical examination in patients with high-output HF:

The heart rate is typically between 85 and 105 beats per minute, but it may be higher with some causes (eg, thyrotoxicosis). Tachycardia is present during rest, sleep, and exercise.

The extremities may be warm and well-perfused (good capillary refill) due to peripheral vasodilation.

Examination of the arteries may display signs related to increased left ventricular (LV) stroke volume. The pulse is usually bounding with a quick upstroke, followed by a rapid collapse (Corrigan or water hammer pulse), and the pulse pressure (systolic minus the diastolic pressure) is typically wide. Pistol-shot sounds may be auscultated over the femoral arteries (Traube sign), subungual capillary pulsations (Quincke pulse) may be seen, and a systolic bruit may be heard over the carotid arteries. The differential diagnosis of these findings is discussed below. (See 'Differential diagnosis' below.)

Examination of the systemic veins may reveal a cervical venous hum, heard best over the internal jugular veins, particularly on the right side. Less often, a venous hum may be appreciated over the femoral veins.

Cardiac examination may reveal a hyperdynamic precordium; an enlarged apical impulse; a loud first heart sound, occasionally with a "scratchy" midsystolic murmur (Means-Lerman scratch) in the second and third left intercostal spaces (resulting from the rubbing together of the normal pleural and pericardial surfaces); and a third heart sound, which is due to the increased rate of ventricular filling. (See "Auscultation of cardiac murmurs in adults" and "Auscultation of heart sounds".)

Manifestations of specific disorders — Patients with high-output HF commonly present with a disease condition (eg, obesity, liver disease, arteriovenous shunt, lung disease, or myeloproliferative disorder) that causes low systemic vascular resistance and sometimes an increased metabolic rate that results in a high cardiac output state. In some cases, HF may be the presenting symptom of an occult cause of a high-output state (such as an arteriovenous fistula). Clinical manifestations of these disorders are discussed in separate topic reviews for these conditions. Clinical manifestations of some key causes are summarized here. (See "Causes and pathophysiology of high-output heart failure".)

Obesity — Obesity was the most common cause of high-output HF in one series [1]. In adults, obesity is generally defined by a body mass index (BMI) ≥30 kg/m2. (See "Obesity in adults: Prevalence, screening, and evaluation", section on 'Measurements'.)

Arteriovenous fistula — A patient with an acquired arteriovenous fistula may have a history of a traumatic injury, may have undergone a vascular or other percutaneous or open procedure, or may have a highly vascular condition or tumor.

Large (>7 cm) congenital hemangiomas may cause high-output HF in infants [2]. Congenital hemangiomas are present and fully grown at birth, unlike infantile hemangiomas. Infantile hepatic hemangiomas most commonly occur in the presence of multiple skin hemangiomas; multifocal hepatic hemangiomas may cause HF. Hereditary hemorrhagic telangiectasia (also called Osler-Weber-Rendu syndrome) is associated with epistaxis, gastrointestinal bleeding, and mucocutaneous telangiectasia [3]. (See "Congenital hemangiomas: Rapidly involuting congenital hemangioma (RICH), noninvoluting congenital hemangioma (NICH), and partially involuting congenital hemangioma (PICH)" and "Infantile hemangiomas: Epidemiology, pathogenesis, clinical features, and complications" and "Clinical manifestations and diagnosis of hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome)".)

In some cases, HF may be the initial clinical presentation of an acquired or congenital fistula [4-7].

Vein of Galen aneurysmal malformation (VGAM) is a rare anomaly associated with poor outcomes from high-output cardiac failure and neurologic complications. Fetal echocardiography can be used to visualize vena cava dilation and reversal of diastolic flow in the transverse aortic arch associated with biventricular dysfunction. In a single-center retrospective review, combined cardiac index was higher in nonsurvivors than in survivors [8].

The clinical manifestations of HF associated with hemodialysis arteriovenous access are discussed separately [9,10]. (See "Evaluation and management of heart failure caused by hemodialysis arteriovenous access".)

In patients with a chronic skeletal disorder such as Paget disease, the high-output state is usually well tolerated for years. The main clinical manifestations of Paget disease are pain and deformities in the affected areas of bone. As with most causes of high-output HF, clinical manifestations of HF are not typically seen in the absence of underlying heart disease. (See "Clinical manifestations and diagnosis of Paget disease of bone", section on 'Clinical manifestations'.)

Cirrhosis — The clinical manifestations of cirrhosis include nonspecific symptoms (eg, fatigue) as well as symptoms and signs of hepatic decompensation (eg, jaundice, abdominal distention from ascites) and hyperammonemia (eg, altered mental status, asterixis). (See "Cirrhosis in adults: Etiologies, clinical manifestations, and diagnosis", section on 'Clinical manifestations'.)

Erythroderma — Erythroderma presents with diffuse erythema and scaling involving all or most of the skin surface area (most commonly defined as ≥90 percent). The widespread lesions are warm and red. (See "Psoriasis: Epidemiology, clinical manifestations, and diagnosis".)

Myeloproliferative disorders — Myeloproliferative disorders with extramedullary hematopoiesis that may result in high-output HF may present with a variety of symptoms and signs including fatigue and splenomegaly. Examination of peripheral blood and bone marrow reveals pathologic features of the specific disorders, as discussed separately. (See "Clinical manifestations and diagnosis of primary myelofibrosis", section on 'Clinical manifestations' and "Clinical manifestations and diagnosis of chronic myeloid leukemia", section on 'Clinical manifestations'.)

Hyperthyroidism — Hyperthyroidism, even in the absence of high-output HF, is associated with palpitations, due to both tachycardia and more forceful cardiac contraction, and exertional dyspnea, which is due to increased oxygen consumption and carbon dioxide production and respiratory muscle weakness. Other physical exam findings of hyperthyroidism include stare, lid lag, proptosis, and fine tremor of the outstretched hands. The skin may be moist and warm as a result of cutaneous vasodilation; blood flow to the skin in hyperthyroid patients can be increased three times or greater than that in euthyroid controls due to enhanced endothelium-dependent vasodilation [11]. Among individuals with hyperthyroidism, the thyroid examination varies according to the cause (ranging from nonpalpable to enlarged and tender; a palpable nodule may or may not be present). (See "Overview of the clinical manifestations of hyperthyroidism in adults" and "Diagnosis of hyperthyroidism", section on 'Physical examination'.)

It is important to be aware of apathetic hyperthyroidism, a condition in older patients, in which many of the usual manifestations of thyrotoxicosis may be absent [12]. Such patients may present with unexplained HF or unexplained atrial fibrillation (AF). Clues to thyrotoxicosis in older patients include anxiety and emotional lability in the presence of a widened pulse pressure and either AF or unexplained sinus tachycardia. Tachycardia is commonly absent in older patients due to the presence of coexistent conduction system disease. Hyperthyroidism is more likely to lead to HF in older patients who often have underlying cardiac disease [13]. (See "Overview of the clinical manifestations of hyperthyroidism in adults", section on 'Geriatric hyperthyroidism'.)

Clinically significant hyperthyroidism should also be ruled out in patients with HF and reduced ejection fraction receiving amiodarone for prophylaxis against arrhythmias who present with recurrence of arrhythmias (eg, AF with rapid ventricular response, electrical storm) after a period of stability. (See "Amiodarone and thyroid dysfunction".)

Sepsis — Patients with sepsis typically present with hypotension, tachycardia, fever, and leukocytosis. Additional clinical manifestations are discussed separately. The acute vasodilation and concomitant increased cardiac index may initially mask the relative myocardial dysfunction in sepsis. (See "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis", section on 'Clinical presentation'.)

Beriberi — Beriberi is uncommon in developed countries except in malnourished individuals, such as those with severe alcohol use disorder, individuals on fad diets [14,15], individuals who have undergone weight-loss surgery, and patients receiving total parenteral nutrition if adequate thiamine supplements are not provided. Beriberi has also been reported in patients with HF on prolonged diuretic regimens, although the frequency of significant thiamine deficiency in this population is uncertain [16]. The combination of thiamine deficiency with chronic alcohol use disorder may result in the concomitant presence of alcohol-induced cardiomyopathy and depression in LV systolic function due to thiamine deficiency [17]. (See "Overview of water-soluble vitamins" and "Alcohol-induced cardiomyopathy".)

Beriberi heart disease is due to severe thiamine (vitamin B1) deficiency. Beriberi disease in adults is classically divided into two types: a "dry" form (which may present with a burning sensation in the extremities, weakness, and falls associated with symmetrical peripheral neuropathies with both sensory and motor components) and a "wet" form (which may present with tachycardia, dyspnea, and peripheral edema associated with cardiomyopathy and high-output HF). Painful glossitis may be caused by thiamine deficiency. Anemia may be present if there is concomitant iron and/or folate deficiency. Wernicke encephalopathy is rarely accompanied by overt beriberi heart disease but may be accompanied by some signs of a high-output state. (See "Overview of water-soluble vitamins", section on 'Deficiency' and "Wernicke encephalopathy", section on 'Other signs'.)

Anemia — The presentation of patients with anemia depends upon the severity of anemia and the time course of its development, as discussed separately. Slow development of chronic anemia is well tolerated and frequently overlooked for some time. While mild anemia is common among patients with high-output HF (eg, related to hemodilution or chronic kidney disease), only profound anemia (eg, prolonged reduction in hemoglobin to approximately 6 g/dL) is likely to be the cause of high-output HF.

Chronic pulmonary disease — Chronic obstructive pulmonary disease (COPD) and other chronic lung diseases are associated with high-output HF, including isolated right HF. COPD typically presents with dyspnea, chronic cough, and sputum production, often with a history of cigarette smoking. Other symptoms and signs are discussed separately [18,19]. (See "Chronic obstructive pulmonary disease: Diagnosis and staging", section on 'Clinical Presentation'.)

DIAGNOSTIC EVALUATION

When to suspect high-output heart failure — High-output HF should be suspected in patients with conditions that may cause low systemic vascular resistance or high metabolic rate that may lead to HF as well as in others who present with symptoms and signs of HF but have well-perfused extremities; bounding pulses and a hyperkinetic precordium may or may not be present.

Approach to diagnosis — The diagnostic evaluation of high-output HF involves the following steps:

Diagnosis of the HF syndrome – A diagnosis of HF is made based upon identification of a constellation of clinical symptoms, signs, and test results (including elevated natriuretic peptide levels when the diagnosis of HF is uncertain), as discussed in detail separately. (See "Heart failure: Clinical manifestations and diagnosis in adults" and "Natriuretic peptide measurement in heart failure".)

Of note, in patients with high-output HF, natriuretic peptide levels are generally elevated (as in low-output HF). In a study of 120 patients with high-output HF, the mean N-terminal pro B-type natriuretic peptide level was 734 (range 327 to 2253) compared with a mean level of 76 (38 to 228) in controls without HF [1].

Confirming the presence of a high-output state – In patients suspected of having high-output HF, the presence of high output is typically suggested by echocardiography and confirmed with invasive hemodynamics:

Initial evaluation with echocardiography We recommend obtaining a comprehensive echocardiogram (ie, with assessment of LV ejection fraction [LVEF] and estimated cardiac output). The presence of one or more of the following echocardiographic findings is suggestive of high-output HF: estimated cardiac index ≥4 L/min, dilation of the inferior vena cava, right ventricular enlargement or dysfunction, elevation in estimated pulmonary artery pressures, or LV enlargement. Of note, LVEF can be normal or reduced in patients with high-output HF. (See "Tests to evaluate left ventricular systolic function".)

Further evaluation for echocardiographic signs of high output – For patients with new or worsening HF with supportive findings on echocardiography, we generally suggest invasive evaluation of cardiac hemodynamics by right heart catheterization. This allows for definitive assessment of volume status, and direct determination of cardiac output and pulmonary artery pressures. Echocardiography is sufficient for diagnosis only for selected cases with high-quality echocardiographic evidence of high cardiac index (CI). (See "Pulmonary artery catheterization: Interpretation of hemodynamic values and waveforms in adults".)

In the cardiac catheterization laboratory, we assess cardiac output indexed for body surface area (CI) but do not use a strict threshold CI to identify a high-output state (such as resting CI ≥4 L/min/m2). High-output HF has traditionally been defined as symptoms in the setting of a cardiac output greater than 8 L/min or a CI greater than 4 L/min/m2 [1,20]; however, this is not an absolute threshold since a CI that one patient may tolerate without problems may be excessive for another having decreased cardiac reserve. In addition to elevated CI, demonstration of elevated left-sided cardiac filling pressure (pulmonary capillary wedge pressure >14 mmHg or LV end-diastolic pressure >16 mmHg) is generally required, as normal values should make one question the diagnosis.

Clinical judgment is required in diagnosing high-output HF in patients with elevated CI on cardiac catheterization. Some patients may have a transient high-output state (eg, due to anxiety or pain) that may not be the cause of HF. (See 'Differential diagnosis' below.)

Since increased cardiac output is physiologic during pregnancy, the presence of high-output HF in a pregnant woman should prompt evaluation for other causes of heart disease. (See "Management of heart failure during pregnancy".)

Identifying the cause of high-output HF A clinical evaluation including history, physical examination, echocardiography, and other cardiovascular testing as needed is helpful in identifying the likely cause of high-output HF. Our initial evaluation for the cause of high-output HF includes the following tests:

Complete blood count

Laboratory assessment of kidney and liver function

Thyroid function tests (thyroid stimulating hormone, free T4)

Vitamin B level

Liver ultrasound

Diagnostic criteria for diseases that cause high-output HF are described in their respective topics:

Obesity. (See "Obesity in adults: Prevalence, screening, and evaluation", section on 'Measurements'.)

Arteriovenous fistula. (See "Congenital hemangiomas: Rapidly involuting congenital hemangioma (RICH), noninvoluting congenital hemangioma (NICH), and partially involuting congenital hemangioma (PICH)" and "Infantile hemangiomas: Epidemiology, pathogenesis, clinical features, and complications" and "Clinical manifestations and diagnosis of hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome)".)

Cirrhosis. (See "Cirrhosis in adults: Etiologies, clinical manifestations, and diagnosis", section on 'Clinical manifestations'.)

Erythroderma. (See "Psoriasis: Epidemiology, clinical manifestations, and diagnosis".)

Myeloproliferative disorders. (See "Clinical manifestations and diagnosis of primary myelofibrosis", section on 'Clinical manifestations' and "Clinical manifestations and diagnosis of chronic myeloid leukemia", section on 'Clinical manifestations'.)

Hyperthyroidism. (See "Overview of the clinical manifestations of hyperthyroidism in adults" and "Diagnosis of hyperthyroidism", section on 'Physical examination'.)

Beri beri. (See "Overview of water-soluble vitamins" and "Alcohol-induced cardiomyopathy".)

Anemia. (See "Diagnostic approach to anemia in adults".)

Chronic obstructive pulmonary disease. (See "Chronic obstructive pulmonary disease: Diagnosis and staging", section on 'Clinical Presentation'.)

Sepsis. (See "Sepsis syndromes in adults: Epidemiology, definitions, clinical presentation, diagnosis, and prognosis".)

Assessing the response to therapy – The diagnosis of high-output HF is confirmed if improvement is observed following treatment of the cause to reverse the high-output state. (See 'Management' below.)

Differential diagnosis — High-output HF should be distinguished from other causes of HF and other conditions that cause symptoms and signs of HF. The main condition that should be distinguished from high-output HF is HF with preserved ejection fraction (HFpEF), especially in patients with obesity [21,22]. High-output HF is best distinguished from HFpEF by the finding of elevated CI and elevated N-terminal pro-B-type natriuretic peptide level. (See 'Approach to diagnosis' above.)

If estimated CI is elevated using the Fick equation (eg, due to elevated pulmonary artery saturation), a careful assessment of saturations should be performed to rule out left-to-right shunting. (See "Pulmonary artery catheterization: Interpretation of hemodynamic values and waveforms in adults", section on 'Detection of left-to-right shunts'.)

The differential diagnosis of high CI at cardiac catheterization includes a transient response to anxiety or pain (which may resolve with treatment of these conditions), so these conditions should be considered and excluded in patients with sinus tachycardia.

MANAGEMENT — Management includes supportive care as well as specific therapy aimed at effectively correcting the cause of the high-output and/or low systemic vascular resistance state; specific therapy can sometimes dramatically reverse the HF.

General management — For all patients, volume overload is treated with sodium restriction and judicious use of diuretics [23].

Acute HF is treated as described separately. Patients with symptomatic hypotension (systolic blood pressure <90 mmHg) are treated with vasopressor support as needed. (See "Treatment of acute decompensated heart failure: General considerations" and "Treatment of acute decompensated heart failure: Specific therapies".)

Management of stable patients with mild high-output HF who have HF with reduced LVEF (≤40 percent), also known as HFrEF, includes standard evidence-based therapy for HFrEF (eg, renin-angiotensin-aldosterone system antagonists, beta blockers, and sodium-glucose co-transporter 2 inhibitors), as tolerated. Some patients who have low systemic vascular resistance prior to therapy may not tolerate higher doses of HF medications with vasodilating properties (eg, angiotensin converting enzyme inhibitors or angiotensin receptor-neprilysin inhibitors) due to hypotension. (See "Overview of the management of heart failure with reduced ejection fraction in adults".)

Management of high-output HF during pregnancy is discussed below. (See 'Management during pregnancy' below.)

Management of specific causes — In most cases, treatment of the cause of high-output HF will reverse symptoms and signs of HF. If there is more than one cause of high-output state, it may be helpful to treat the individual components. However, some cardiac abnormalities may not resolve with treatment of the cause of the high-output state.

Obesity — Management of patients with obesity, including counseling on diet, exercise, and goals for weight management, as well as criteria for drug therapy and surgery, is discussed separately. (See "Obesity in adults: Overview of management".)

Arteriovenous fistula

Acquired fistulas — Management of patients with HF due to hemodialysis arteriovenous fistula and treatment of acquired fistulas of the lower extremity are discussed separately. Surgical or endovascular repair of the fistula can be associated with rapid resolution of high-output HF. (See "Evaluation and management of heart failure caused by hemodialysis arteriovenous access" and "Acquired arteriovenous fistula of the lower extremity", section on 'Management'.)

In a study of 11 patients with high fistula flows (>3000 mL/min) and elevated natriuretic peptide levels, a novel vascular repair procedure ("secondary extension technique") resulted in a median flow decrease of 58 percent, which correlated with a decrease in pro-B-type natriuretic peptide of 70 percent and resolution of high-output HF symptoms [24].

In most patients with Paget disease with high-output HF, treatment with a bisphosphonate or calcitonin leads to normalization of the cardiac index (CI) within six months [25]. (See "Treatment of Paget disease of bone".)

Congenital fistulas — For infants with hemangiomas who develop HF, options include embolization, surgical excision of the tumor, and medical therapy (eg, glucocorticoids). (See "Infantile hemangiomas: Management", section on 'High-output failure' and "Congenital hemangiomas: Rapidly involuting congenital hemangioma (RICH), noninvoluting congenital hemangioma (NICH), and partially involuting congenital hemangioma (PICH)", section on 'Treatment of complications'.)

The treatment of high-output HF in patients with hereditary hemorrhagic telangiectasia poses a clinical challenge, as discussed separately. (See "Hepatic hemangioma", section on 'Management' and "Clinical manifestations and diagnosis of hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome)", section on 'Clinical features' and "Hereditary hemorrhagic telangiectasia (HHT): Evaluation and therapy for specific vascular lesions", section on 'Hepatic AVMs'.)

Cirrhosis — For patients with cirrhosis, liver transplantation may normalize the cardiac output [26]. In one study, the CI decreased by a mean of 35 percent after liver transplantation [27]. Hyperdynamic circulation may persist longer in patients with alcohol-associated cirrhosis compared with those with postviral disease [28,29]. (See "Cirrhosis in adults: Overview of complications, general management, and prognosis".)

Erythroderma — The treatment is that of the primary skin disorder. As the lesions heal and warmth disappears, there is a concomitant reduction in the elevated cardiac output. (See "Treatment of psoriasis in adults".)

Myeloproliferative disorders — Management of myeloproliferative disorders is discussed separately. (See "Myelofibrosis (MF): Management of primary MF and secondary MF" and "Overview of the treatment of chronic myeloid leukemia".)

Hyperthyroidism — The appropriate treatment for HF due to hyperthyroidism is to return the patient to a euthyroid state, usually with an antithyroid drug or radioactive iodine. The restoration of euthyroidism typically leads to normalization of the heart rate, arterial pulse pressure, cardiac output, LVEF, and a reduction in LV diameter [30]. (See "Graves' hyperthyroidism in nonpregnant adults: Overview of treatment".)

Beta blockers may be beneficial by slowing the heart rate, but they should be administered cautiously since there may be a further reduction in myocardial contractility in patients with impaired LV systolic function [31,32]. Beta blockers are particularly helpful in patients with sinus tachycardia or atrial fibrillation due to hyperthyroidism but may be contraindicated in patients with acute HF and low cardiac output.

Sepsis — Management of sepsis is discussed separately. (See "Evaluation and management of suspected sepsis and septic shock in adults".)

Anemia — The management of HF associated with anemia depends upon the type and severity of the anemia. Diagnostic tests for determining the type of anemia should be carried out immediately. (See "Diagnostic approach to anemia in adults".)

The treatment for HF due to chronic anemia should be specific for the cause and severity of the anemia. A restrictive red blood cell transfusion strategy (eg, trigger hemoglobin threshold of 7 to 8 g/dL) is generally suggested in patients with HF. Individualized transfusion decisions are based upon clinical judgment, including whether the patient appears to have symptoms from anemia. (See "Diagnostic approach to anemia in adults".)

If the anemia is acute, bed rest and oxygen by nasal cannula are appropriate. If transfusion is indicated, transfusion of packed red blood cells must be done cautiously and slowly to avoid further volume overload and worsening HF. Transfusion should be performed at a rate of one-half unit given over three or four hours, and the patient should be monitored for dyspnea and signs of pulmonary edema. Diuretic therapy, beginning with an intravenous loop diuretic (eg, 20 to 40 mg furosemide), can be used to treat volume overload. Vasodilator therapy has no role because of the marked reduction in systemic vascular resistance.

The cause of anemia should be treated when possible, as discussed separately. (See "Evaluation and management of anemia and iron deficiency in adults with heart failure", section on 'Treatment' and "Treatment of iron deficiency anemia in adults" and "Treatment of vitamin B12 and folate deficiencies".)

Beriberi — With appropriate treatment, the CI and heart rate are reduced, and there is an increase in systemic vascular resistance [33,34]. Treatment of concomitant nutritional anemia may also be required.

Patients with concomitant alcohol-induced cardiomyopathy and LV systolic dysfunction due to thiamine deficiency [17] do not respond well standard treatment of HF; a diagnosis of thiamine deficiency must therefore be considered so that specific therapy with thiamine can be given. The initial loading doses of thiamine are in the range of 100 to 500 mg intravenously, followed by 25 to 100 mg/day orally for at least two weeks. (See "Alcohol-induced cardiomyopathy".)

Patients with furosemide-associated thiamine depletion maintain their ability to absorb thiamine and respond to thiamine repletion with improved LV function and effective diuresis [35,36]. Magnesium may have to be coadministered with thiamine, particularly in magnesium-depleted patients [37,38]. In animal models, magnesium depletion alone leads to a blunted response to thiamine supplementation and loss of thiamine from tissues [39]. The mechanism for this relationship is unknown, although it has been proposed that magnesium depletion may interfere with the activation of transketolase.

Management during pregnancy

General management during pregnancy — The treatment of high-output HF during pregnancy depends on the severity of the HF and its etiology. As noted above, other potential causes of HF should be identified and treated. In mild cases, bed rest and a loop diuretic may be effective, but often no specific therapy is necessary; the cardiac output generally normalizes between two days to two weeks postpartum, although one study demonstrated a gradual fall in cardiac output from 7.4 L/min to 5.0 L/min at 24 weeks postpartum [40].

Acute HF during pregnancy is managed with supplemental oxygen therapy, pharmacologic therapy (including diuretic therapy in patients with pulmonary and/or systemic venous congestion), and venous thromboembolism prophylaxis. The management of anticoagulation during pregnancy (eg, for women with or at risk of thromboembolism) is best performed with a multidisciplinary approach (including input from cardiology/vascular medicine, obstetrics/maternal-fetal medicine, hematology, and/or pharmacy). (See "Management of heart failure during pregnancy", section on 'Acute heart failure' and "Treatment of acute decompensated heart failure: Specific therapies" and "Use of anticoagulants during pregnancy and postpartum".)

Drugs used to treat chronic HFrEF during pregnancy are discussed separately. (See "Management of heart failure during pregnancy" and "Adverse effects of angiotensin converting enzyme inhibitors and receptor blockers in pregnancy".)

Management of the cause during pregnancy — Decisions on management of the cause of the high-output state during pregnancy are based upon assessment of the maternal and fetal risks and benefits.

Management of hyperthyroidism during pregnancy is discussed separately. (See "Hyperthyroidism during pregnancy: Treatment".)

In some cases of arteriovenous malformations, surgical resection or embolization of the fistula has been performed during or immediately following pregnancy with resolution of the HF symptoms. In more severe cases, emergency termination of the pregnancy has been required [41].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Heart failure in adults".)

SUMMARY AND RECOMMENDATIONS

Clinical manifestations – The clinical manifestations of high-output heart failure (HF) include dyspnea, fatigue, tachycardia at rest, warm extremities, wide pulse pressure, bounding pulses, and a hyperkinetic precordium, although physical examination can also be relatively normal. (See 'Clinical manifestations' above.)

Manifestations of specific disorders – Patients with high-output HF commonly present with a disease condition (eg, obesity, liver disease, arteriovenous shunt, lung disease, or myeloproliferative disorder) that causes a high cardiac output state. In some cases, HF may be the presenting symptom of an occult cause of a high-output state (such as an arteriovenous fistula). (See 'Manifestations of specific disorders' above.)

When to suspect high-output HF – High-output HF should be suspected in patients with conditions that may lead to low systemic vascular resistance and/or increased metabolism as well as in others who present with symptoms and signs of HF but have well-perfused extremities, bounding pulses, and a hyperkinetic precordium. (See 'When to suspect high-output heart failure' above.)

Approach to diagnosis – The approach to diagnosis of high-output HF involves: establishing a diagnosis of HF based upon identification of a constellation of clinical symptoms, signs, and test results; identifying hemodynamic parameters of a high-output state (by a high-quality echocardiogram or by right heart catheterization); and identifying the cause of high-output HF. (See 'Approach to diagnosis' above.)

Management – Management of high-output HF includes supportive care (including treatment of volume overload with diuretics) and treatment of the cause of the high-output state. (See 'Management' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Amir Haghighat, MD, FACC, who contributed to earlier versions of this topic review.

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Topic 113041 Version 11.0

References

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