Cardiology > High Output Heart Failure 

Background   

High Output Heart Failure (HOHF) is a rare clinical syndrome where cardiac output is elevated (typically >8 L/min) due to increased metabolic demands or peripheral vasodilation, yet the heart still fails to meet systemic requirements. Despite the elevated cardiac output, patients develop typical heart failure symptoms due to circulatory overload and neurohormonal activation. 

II) Classification/Types

• • Primary HOHF – Caused by intrinsic conditions that increase metabolic demand or reduce systemic vascular resistance. 

• • Secondary HOHF – Occurs in preexisting cardiac disease (e.g., HFrEF) exacerbated by high-output states. 

III) Epidemiology 

• • Sex: Affects both genders equally, depending on the underlying etiology. 

• • Age: Most often seen in adults, but can occur in children (e.g., AV malformations). 

• • Region: Prevalence depends on endemic diseases (e.g., thiamine deficiency in developing countries). 

• • Risk groups: Patients with chronic illnesses (e.g., cirrhosis, severe anemia, thyrotoxicosis). 

Etiology

I) Causes

• • Anemia – Reduced oxygen-carrying capacity → increased cardiac output. 

• • Thyrotoxicosis – Increases basal metabolic rate and HR/contractility. 

• • Arteriovenous (AV) Fistulas – Bypass resistance vessels, increasing preload. 

• • Beriberi (Thiamine deficiency) – Impairs myocardial energy utilization. 

• • Paget’s disease of bone – Increased vascularity raises cardiac workload. 

• • Cirrhosis – Splanchnic vasodilation leads to reduced SVR and hyperdynamic state. 

• • Sepsis – Inflammatory vasodilation and increased tissue demand. 

• • Obesity – Elevated metabolic demands and increased blood volume. 

• • Pregnancy – Physiological high-output state may decompensate if cardiac reserve is limited. 

II) Risk Factors

• • Chronic anemia 

• • Hyperthyroidism 

• • AV malformations (e.g., dialysis fistulas) 

• • Nutritional deficiencies (especially B1) 

• • Liver disease 

• • Chronic infection or inflammation  

Clinical Presentation

I) History (Symptoms)

• • Dyspnea on exertion – Most common presenting symptom 

• • Fatigue and weakness – Due to decreased tissue perfusion 

• • Palpitations – From tachycardia 

• • Orthopnea, PND – If pulmonary congestion develops 

• • Peripheral edema – From volume overload 

• • Warm extremities – Classic sign, differentiates from low-output HF 

• • Bounding pulses and wide pulse pressure 

II) Physical Exam (Signs)

Vital Signs: 

• • Tachycardia 

• • Wide pulse pressure 

• • Elevated systolic BP, low or normal diastolic 

• • Warm, flushed extremities 

• • O2 saturation – Look for high venous oxygen content (from AV shunts)  

Cardiovascular: 

• • S3 gallop 

• • Displaced apical impulse 

• • Jugular venous distension (JVD) 

• • Bounding peripheral pulses 

Pulmonary: 

• • Rales or crackles if pulmonary congestion present 

Abdomen: 

• • Hepatomegaly, possible ascites in cirrhosis 

Peripheral: 

• • Edema, particularly in dependent areas 

• • AV bruit (in AV fistulas or shunts) 

Differential Diagnosis (DDx)

• • Low-output heart failure (HFrEF, HFpEF) 

• • Thyrotoxic cardiomyopathy 

• • Septic shock 

• • Severe anemia without HF 

• • Cirrhosis without cardiac involvement 

• • Arteriovenous malformation 

• • Beriberi (wet vs. dry) 

 Diagnostic Tests

Initial Tests 

• • Echocardiogram (Transthoracic) – Hyperdynamic LV function, EF >70%, elevated filling pressures 

• • EKG – Sinus tachycardia, possible LVH or signs of strain 

• • Chest X-ray – Cardiomegaly, pulmonary vascular congestion 

Additional Tests 

• • Cardiac output measurement (via right heart catheter): Output >8 L/min 

• • Systemic vascular resistance (SVR) – Low (<800 dynes/sec/cm⁵) 

Lab Tests 

• • CBC – To detect anemia 

• • TSH, Free T4 – Evaluate for thyrotoxicosis 

• • BNP/NT-proBNP – Often elevated 

• • CMP – Liver/kidney function 

• • Thiamine level – If beriberi suspected 

• • Lactate – To evaluate for hypoperfusion 

• • Arterial blood gases – May show metabolic acidosis 

Treatment

I) Treat Underlying Cause

• • Anemia – Transfuse or treat underlying cause 

• • Hyperthyroidism – Antithyroid drugs (methimazole, PTU), beta-blockers 

• • AV fistula – Surgical correction or embolization 

• • Beriberi – High-dose thiamine replacement 

• • Cirrhosis – Optimize volume, consider liver transplant 

• • Obesity – Weight loss and manage comorbidities 

II) Symptomatic Treatment (if volume overload)

• • Diuretics – Loop diuretics (e.g., furosemide) 

• • Beta-blockers – Reduce HR, improve filling time 

• • Afterload reduction – Cautious use if hypertension present 

• • Salt restriction and fluid restriction if significant edema  

III) Avoid 

• • Inotropes – Typically not indicated due to already high cardiac output 

• • Excessive diuresis – May worsen perfusion if SVR is low 

Consults

• • Cardiology – For diagnosis confirmation, echo/cath, and management 

• • Endocrinology – If thyrotoxicosis or metabolic causes 

• • Hematology – For anemia work-up 

• • Nutritionist – Thiamine deficiency, weight loss strategies 

• • Interventional radiology/surgery – For AV malformations 

Patient Education

• • Educate on symptoms of worsening HF (weight gain, edema, fatigue) 

• • Importance of treating underlying conditions (e.g., thyroid disease) 

• • Avoid excessive salt or fluid intake 

• • Encourage smoking cessation and healthy diet 

• • Screen for alcohol use and nutritional deficiencies 

• • Vaccines: 

• • Annual influenza vaccine 

• • Pneumococcal vaccine per age and risk group 

• • COVID-19 vaccination as indicated 

Follow-Up

• • Regular monitoring of symptoms, weight, and volume status 

• • Periodic echocardiography 

• • Re-evaluate for resolution of underlying cause 

• • Close follow-up after initiation of treatment to prevent readmissions