Right-sided heart failure

Also known as isolated right ventricular (RV) failure, or simply RV failure

References: Circulation 2008 [1][2], Rev Esp Cardiol 2010

Clinical presentation

  • Mechanisms of clinical manifestations: Decreased CO, fluid retention, atrial/ventricular arrhythmias
  • Complications: Congestive hepatopathy/cardiac cirrhosis
  • Symptoms
    • Fatigue & exercise intolerance
    • Peripheral edema, ascites, weight gain
  • P/E
    • Vitals: Hypotension
    • Head & Neck: Elevated JVP
    • Chest: Palpable RV impulse, TR murmur, clear lungs
    • Limbs: Edema


  • Causes of RV dysfunction
    1. Pressure overload
      1. Left-sided HF (most common, presents with left-sided HF s/sx)
      2.  Pulmonary hypertension (PH), chronic (e.g. PAH, cor pulmonale) or acute (e.g. PE)
      3. PS
      4. RVOT obstruction
    2. Volume overload (TR, PR, ASD, other [e.g. carcinoid])
    3. RVMI or ischemia
    4. Cardiomyopathy (e.g. ARVD)
    5. Pericardial (e.g. constrictive pericarditis)
    6. Inflow limitation (TS, SVC stenosis)
    7. Congenital heart disease (may include 1+ of above mechanisms, e.g. Eisenmenger syndrome, tetralogy of Fallot, transposition of the great arteries)


  • Goals: Characterize etiology, severity & function class, & presence/extent of end-organ damage (cardiorenal syndrome & congestive hepatopathy)
  • Echo (TTE)
    • Most commonly done 1st to assess RV function, presence/extent of TR, as well as assess for PH, congenital heart defects, valvular heart disease or left-sided disease
    • RVEF measured by 2D echo has moderate correlation (0.65-0.80) with cMRI-derived RVEF
  • cMRI
    • Most accurate way of measuring RV volume & RVEF
    • RV volume (dilatation is >101 mL/m^2)
    • RVEF (normal ~60%, >40-45%) - note: dependent on loading conditions & therefore may not reflect contractility
    • RV mass (hypertrophy is >35 g/m^2)
  • Right heart cath
    • To evaluate pulmonary pressures, PVR, CO & pulmonary vasoreactivity (in the context of PH)
  • EKG to assess rhythm, QRS duration & presence of AV block
  • Labs
    • SCr
    • ALT, albumin
    • BNP


  • Strongly associated with underlying cause
  • Factors associated with poor prognosis:
    • Decreased exercise tolerance
    • Severity of measures of RV systolic dysfunction (e.g. RVEF <35%), diastolic dysfunction
    • Chronotropic incompetence
    • Arrhythmias
    • LV systolic dysfunction
    • Serum uric acid
    • Bilirubin



  1. General principles
    • Fluid & sodium restriction
    • If using positive-pressure ventilation, avoid inspiratory pressures >30 mm Hg
  2. Treat underlying etiology, e.g.
    • Left-sided HF: Treat as per HFrEF/pEF
    • RVMI: Revasc
    • Acute PE: Anticoagulant +/- thrombolytic
    • PAH: iNO, epoprostenol & other PAH-specific agents
  3. Maintain NSR
    • Tachyarrhythmia: DC cardioversion
    • Bradyarrhythmia: Pacemaker +/- CRT
  4. Optimize RV preload (avoid hypotension as may worsen dysfunction via myocardial ischemia)
    • Low JVP/CVP/RAP? Trial 500 mL IV crystalloids
    • High? Gradual diuresis 0.5-1 kg/day, dialysis (CRRT/IHD)
  5. Not responsive to preload optimization?
    1. Optimize RV afterload: Inhaled nitric oxide, IV/inhaled epoprostenol
    2. Optimize RV contractility: IV inotropes (e.g. dobutamine) & vasopressors
    3. Others: RVAD, heart +/- lung transplant


  1. Treat underlying etiology
  2. Symptom control
    • Diuresis to manage fluid retention
  3. Maintain NSR & AV synchrony (e.g. cardioversion & rhythm control, pacemaker, RV CRT)
  4. Prevent sudden death
    • Evaluate for ICD
  5. Role of drugs used in HFrEF:
    • ACEI/BB/MRA: Unknown
    • Digoxin: No improvement in RVEF; no benefit in absence of LV systolic dysfunction
  6. Others: Cardiac rehab, RVAD, heart +/- lung transplant
  • Maximize RV preload & contractility, minimize RV afterload
  • Maintain NSR


  • "End-stage" process of impaired RV filling or systolic function caused by RV pressure/volume overload, ischemic/infarct, cardiomyopathy or pericardial disease
    • RV tolerates volume overload better than pressure overload
  • Decreased RV forward flow leads to:
    • Reduced LV preload & therefore reduced cardiac output = fatigue, exercise intolerance
    • Systemic venous fluid retention = peripheral edema, ascites, anasarca (generalized edema)
  • Ventricular interdependence is also an important feature of RV failure
    • Diastolic ventricular interdependence contributes to secondary LV systolic dysfunction in RV failure; RV enlargement shifts the interventricular septum & increases pericardial constract on the LV, leading to decreased LV preload & contractility (via reduced elastance)

Specific etiologies

  • RVMI:

    • Constellation of hypotension, elevated JVP, & clear lungs
    • Present in 20-50% of inferior-wall MI, hemodynamically significant in 10%
  • Cor pulmonale
    • RVH 2o to pulmonary disease (most commonly COPD) without left-sided HF
    • Related to hypoxemic vasoconstriction