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Congestive cardiac failure

Last revised by Dr Joachim Feger on 25 Aug 2021

Congestive cardiac failure (CCF), also known as congestive heart failure (CHF) or simply heart failure, refers to the clinical syndrome caused by inherited or acquired abnormalities of heart structure and function, causing a constellation of symptoms and signs that lead to decreased quality and quantity of life.

CCF is common, affecting 2% of all adults in developed nations, and up to 10% of adults over 65 years old 1. The condition is thought to affect up to 20 million people worldwide 1.

Clinical features traditionally associated with left and right ventricular dysfunction, respectively, may include:

  • left-predominant symptoms and signs 1,2
    • fatigue, syncope
    • dyspnea
      • subjective discomfort or difficulty breathing
    • chest pain
    • abnormal auscultatory heart sounds 1,2
      • an audible "S3" may be appreciated during early diastole and/or an "S4" in late diastole
        • the former may originate from taut mitral subvalvular structures secondary to ventricular dilation, and the latter from decreased ventricular compliance
    • pulsus alternans 1,2
  • right-predominant symptoms and signs 1,2
    • nocturia 
    • dependent, pitting edema
      • commonly bipedal or sacral
    • ascites
    • hepatomegaly 
    • jugular venous distension 

The severity of clinical presentation and functional status of a patient is often classified according to the New York Heart Association (NYHA), which assigns a grade between I and IV dependent on symptoms and on how limited the physical activity has become 1,2:

  • NYHA I: no symptoms during normal physical activity, no limitation
  • NYHA II: symptoms during ordinary physical activity, slight limitation
  • NYHA III: symptoms during less than ordinary physical activity, marked limitation (patients generally only comfortable at rest)
  • NYHA IV: symptoms even when at rest, severe limitation

In the presence of consistent symptoms and clinical signs, elevated natriuretic peptides, and the presence of diastolic dysfunction and/or structural cardiac abnormalities (e.g. left atrial dilation, left ventricular hypertrophy), patients are commonly grouped by left ventricular ejection fraction (LVEF) as follows:

  • heart failure with a reduced ejection fraction (HFrEF)
    • those with an LVEF of <40%
    • current therapy is based primarily on large clinical trials only enrolling those with ejection fractions below 40% 15
  • heart failure with a preserved ejection fraction (HFpEF)
    • an LVEF equal to or greater than 50%
  • heart failure with a midrange ejection fraction (HFmrEF)
    • those falling between the abovementioned cutoffs (40-49%)

While significant overlap exists, etiological associations may correspond to the phenotypes delineated by LVEF as follows:

A somewhat distinct entity is that of high-output heart failure in which a primary decrease in systemic vascular resistance triggers a neurohormonal cascade akin to that observed with a decreased cardiac output. Etiologies of this syndrome include:

The accuracy of interpreting chest radiographs regarding congestive cardiac failure was only around 70% according to one study 5.  

With left-sided congestive cardiac failure, the features are that of pulmonary edema which includes 1,2,4-8:

Echocardiography is the most common imaging modality used to evaluate patients with CCF 1,2. Some features assessed during a complete transthoracic echocardiography exam include:

  • left ventricular function
    • the surrogate measure ejection fraction is a common method to estimate global systolic function
    • diastolic dysfunction may also be assessed, involving spectral Doppler as well as 2D measurements
    • structure of the left ventricle
      • wall thickness and left ventricular end-diastolic internal diameter may yield a derived mass, the basis of diagnosing remodeling and hypertrophy
  • valvular anatomy and function
  • right ventricular structure and function
  • pericardial space

CT chest may demonstrate the same features as the plain radiograph but in greater detail and clarity 6,7,9. Furthermore, electrocardiograph-gated CT and cardiac CT angiography may provide estimates of cardiac function and detailed visualization of various cardiac structures 9. Mediastinal lymph node enlargement may be present in some cases 13,14.

Cardiac MRI (CMR) can provide highly accurate ejection fraction estimates and determine the presence of any structural abnormalities and is considered by many to be the gold standard imaging modality 2,9-11. Patterns of late gadolinium enhancement may be useful in delineating an etiology 10,11.

Treatment involves a multidisciplinary team and incorporates lifestyle, allied health, pharmacological, and even surgical therapies, often specific to the underlying etiology 1,2. General principles include:

  • treatment of comorbidities and complications
  • lifestyle interventions
  • pharmacotherapy 
    • depending on the clinical context, examples include angiotensin-converting-enzyme inhibitors, angiotensin II receptor blockers, beta-blockers, spironolactone, nitrates and digoxin 1,2,12
  • invasive/surgical management may include: 

Despite advances in management in recent decades, prognosis remains poor with 30-40% of patients dying within 1 year, and up to 70% dying within 5 years 1.

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Cases and figures

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