Right Heart Failure

  • Right Heart Failure is a clinical syndrome which occurs due to an inability of the right heart heart to meet physiological demands. A variety of etiological processes can result in right heart failure; however, common pathophysiologic and clinical sequelae often result as discussed below.
  • Overview
    • As discussed in the Pathogenesis section below, Right Heart Failure is ultimately caused by pathological increases in the afterload of the right heart. The etiologies which can enhance right-sided afterload can be broadly categorized into two groups. The first group of etiologies are due to diseases of the heart itself whereas the second group are due to primary diseases of the pulmonary circulation. When right-sided failure occurs due to primary disease in the pulmonary circulation, this is often termed "Cor Pulmonale".
  • Cardiac Causes
    • Left Heart Failure: Left heart failure results in pulmonary hypertension over time, thus increasing the right heart's afterload. Indeed, left heart failure is the most common cause of right-sided failure and results in a combination of their respective clinical syndromes termed "Congestive Heart Failure".
    • Pulmonic Valve Stenosis: Stenosis of the pulmonic valve increases the resistance felt by the right heart during ventricular ejection and thus increases the right heart's afterload.
    • Myocardial Infarction of right heart: This is an exception to the general rule that right-sided failure is caused by pathological increases in right heart afterload. Indeed, ischemic injury to the right heart can result in right-sided failure due to direct damage to right heart cardiomyoctyes.
  • Cor Pulmonale
  • Initiation
    • The Right Heart is a relatively thin-walled chamber that is poorly adapted to eject against high afterloads. Consequently, conditions which increase right-sided afterload are particularly problematic and often result in failure of the right heart to eject sufficient blood to meet physiological demands. Initially, a set of compensatory processes are able to maintain sufficient cardiac output through the right heart; however, over time these processes become maladaptive and hasten progressive failure of the right heart.
  • Compensation
    • Reduced volume ejection of the right heart in the context of normal venous return results in an increased Ventricular End Diastolic Volume (VEDV) and thus enhanced preload. Courtesy of the Frank-Starling Relationship this will improve ventricular ejection a certain amount but usually not enough to overcome the high afterload. Over time, in cases of chronic right heart failure, the right ventricle will begin to physically remodel to counteract chronically increased afterloads. Initially, this will manifest as concentric, right-sided ventricular hypertrophy allowing thickening of the ventricular wall and thus improving the capacity of the right ventricle to push against large afterloads. However, overtime right-sided hypertrophy takes on an eccentric pattern, resulting in dilation of the right ventricle and a reduced capacity to push against large afterloads.
  • Sequelae
    • In cases of chronic right heart failure, long-term inability of the right heart to eject ventricular volume will result in backup of blood into the right atrium and systemic veins. This increases right atrial pressure and overtime may lead to right atrial dilation and derangements of atrial electrophysiology, manifesting as right atrial fibrillation. Backup of blood into the venous system leads to symptomology of venous congestion described below.
Clinical Consequences
  • Overview
    • In general, symptomology of right heart failure rarely occurs in isolation and presents within the context of the primary cardiac or pulmonary disease which induces right-sided failure. The clinical contribution of right-sided failure is primarily dominated by sequelae from Congestion of the systemic veins due to backup of blood from the failing right heart. However, remodeling of the heart can also result in important physical signs.
  • Congestion
    • Elevated jugular venous pressure: Due to backup of blood into the jugular veins
    • Peripheral Edema: Due to congestion of veins in the extremities, especially legs
    • Acute hepatic congestion or chronic hepatic congestion: Due to backup of blood into the hepatic sinusoidal capillaries. May manifest as hepatomegaly.
  • Cardiac Remodeling
    • Atrial Fibrillation: Due to dilation of the right atrium
    • Tricuspid Valve Regurgitation: May occur in a late stage due to dilation of the right ventricle.