Congestive cardiac failure

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.

Epidemiology

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 presentation

Clinical presentation varies considerably depending on the severity and aetiology of CCF ^1,2. Traditionally, symptoms can be clustered into either being attributed tofeatures traditionally associated with left ventricular dysfunction orand right ventricular dysfunction, although in realityrespectively, most patients will have manifestations from both clusters ^1,2.may include;

• left-predominant symptoms and signs
  • exertional dyspnoea and fatigue ^1,2
    • orthopnoea: dyspnoea in the recumbent positionfatigue, may use multiple pillows at night ^1,2syncope
    • paroxysmal nocturnal dyspnoea: dyspnoea that awakens the patient from sleep, usually only after 1-2 hours, and may have a chronic nocturnal cough and cardiac asthma ^1,2dyspnoea
      • subjective discomfort or difficulty breathing
      • bendopnoea: dyspnoea while bending forward ³
    • angina ^1,2chest pain
    • syncope and cerebral dysfunction ^1,2
    • cyanosis ^1,2
    • other organ dysfunction ^1,2
    • addedabnormal auscultatory heart sounds ^1,2
      • S3 ‘ventricular gallop’ (occurs after S2an 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 is due to blood slushing around in a large dilated ventricle) ^1,2
        • S4 ‘atrial gallop’ (occurs before S1 and is due to blood entering the ventricle during atrial systole hitting the stiff hypertrophiedlatter from decreased ventricular wall ^1,2compliance
    • pulsus alternans ^1,2
  • right-predominant symptoms and signs
    • nocturia ^1,2
      • nocturia 
      • dependent, pitting oedema
        • commonly bipedal or sacral
      • sacral and scrotal oedema, especially if bed bound ^1,2
      • peripheral (ankle) oedema ^1,2
      • ascites^1,2
      • hepatomegaly, may have a tender edge and gastrointestinal symptoms ^1,2
      • raised jugular venous pressure ^1,2distension 

    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

    Pathology

    Classification

    Patients with end-stage CCF may have Cheyne-Stokes respiration, hypotension, tachycardia, featuresIn the presence of valvulopathiesconsistent symptoms and clinical signs, elevated natiuretic peptides, and cardiac cachexia ^1,2. 

    Depending on the underlying aetiology, additional clinical features may also be present ^1,2. 

    Pathology

    It may be precipitated by intrinsicpresence of diastolic dysfunction and/or structural cardiac or extrinsic factorsabnormalities (e.g. It may also be acute (acute decompensated cardiac failureleft atrial dilation, left ventricular hypertrophy) or chronic (chronic congestive cardiac failure) ^1,2. Up to 40-50% of, patients have diastolic heart failure with preserved left ventricular function ⁴. 

    Classification and aetiology

    There are numerous ways of classifying CCF, the most commonly utilised being a functional classification that is based on cardiac output and ejection fraction ^1,2. In this classification, there are often overlapping aetiologies and patients can move from one classification to the other over time ^1,2.

    Another key classifier of heart failure isgrouped by left ventricular ejection fraction (LVEF) as follows:

    • heart failure with a reduced ejection fraction (LVEF(HFrEF), derived by dividing the left ventricular stroke volume by end-diastolic volume. While heart failure is not defined by the degree
      • those with an LVEF of left ventricular impairment, the classification is crucial for treatment decisions; <40%
      • current therapy is based primarily on large clinical trials only enrolling those with ejection fractions below 40%¹⁵.

        In patients with reduced systolic function the LVEF is lower and the intracardiac volumes higher. A cutoff LVEF of <40% in the presence of a suggestive clinical syndrome defines HFrEF. Intermediate ejection fractions (between 40-50%) are typically grouped in the HFrEF phenotype.

        Clinical heart failure with an ejection fraction >50% defines the HFpEF syndrome; in these patients with heart failure symptoms in whom reductions in ejection fraction do not occur, there is generally a prominent increase in the left ventricular wall thickness and progressive dilation of the left atrium.

      • low-output heart failure
    • heart failure with reduceda preserved ejection fraction (HFrEF(HFpEF), previously termed 'systolic
      • an LVEF equal to or greater than 50%
    • heart failure' with a midrange ejection fraction (HFmrEF)
      • those falling between the abovementioned cutoffs (40-49%)

    Etiology

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

    • associated with a decreased left ventricular ejection fraction 
      • ischaemic dilated cardiomyopathy ^1,2
      • non-ischaemic dilated cardiomyopathy
        • idiopathic
        • infectious
        • toxic (e.g. idiopathicsympathomimetics, alcoholism, alcohol)
      • tachycardia-mediated cardiomyopathy,
      • Chagas disease,
      • Duchenne muscular dystrophy,
      • peripartum/postpartum cardiomyopathy, 
      • hypothyroidism, cocaine use, infection, etc.)^1,2
    • regurgitant valve disease
      • aortic valve regurgitation ^1,2
      • mitral valve regurgitation
    • left-to-right shunts
      • atrial septal defect
      • ventricular septal defect
      • patent ductus arteriosus
      • Gerbode defect
      • atrioventricular septal defect^1,2
    • associated with a preserved left ventricular ejection fraction
      • chronic hypertension ^1,2
      • obstructive valve disease (e.g. in the setting of valvulopathies
        • aortic valve stenosis) ^1,2
        • regurgitant valve disease (e.g. in the setting of aortic valve regurgitation) ^1,2
        • left-to-right shunts (e.g. atrial septal defect, ventricular septal defect, patent ductus arteriosus, Gerbode defect, atrioventricular septal defect, etc.) ^1,2
    • heart failure with preserved ejection fraction (HFpEF), previously termed 'diastolicinfiltrative diseases
      • cardiac amyloidosis
      • cardiac sarcoidosis
      • endomyocardial fibrosis
      • haemochromatosis
    • ​radiation-induced heart failure'
      disease
    • hypertrophic cardiomyopathy (e.g.
      • hypertrophic obstructive cardiomyopathy,
      • Yamaguchi syndrome, chronic hypertension, obstructive valve disease, left-to-right shunts, 
    • athlete's heart,
    • Danon disease, etc.) ^1,2
    • restrictive cardiomyopathy (e.g. cardiac amyloidosis, cardiac sarcoidosis, endomyocardial fibrosis, haemochromatosis, radiation-induced heart disease, etc.) ^1,2
    • constrictive pericarditis ^1,2

• 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:

  • morbid obesity ^1,2
  • systemic arteriovenous shunts (e.g.
    • hereditary haemorrhagic telangiectasia,
    • hepatopulmonary syndrome,
    • haemodialysis fistula) ^1,2
  • chronic lung disease ^1,2
  • sepsis ^1,2
  • myeloproliferative neoplasm ^1,2
  • anaemia ^1,2
  • hyperthyroidism ^1,2
  • wet beriberi ^1,2
  • carcinoid syndrome ^1,2

Radiographic features

Plain radiograph

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 oedema which includes ^1,2,4-8:

• pulmonary venous congestion
• cephalisation of pulmonary veins
• pulmonary interstitial oedema
• pulmonary alveolar oedema
• cardiomegaly (may or may not be present depending on aetiology)
• pleural effusion

Ultrasound: echocardiography

Echocardiography is the most common imaging modality used to evaluate patients with CCF ^1,2. It is able to provide a semi-quantitative assessment of left ventricular size and function and determine the presence of valvular or wall abnormalities ^1,2.  Variables near ubiquitously Some features assessed induring a complete transthoracic echocardiography exam include:

• the systolicleft ventricular function of the left ventricle
  • the surrogate measure ejection fraction is the most populara common method
  to estimate global systolic function
• the diastolic function of the left ventricle
  • perturbations are often appreciable before the systolic function is affected
  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

CT

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 visualisation of various cardiac structures ⁹. Mediastinal lymph node enlargement may be present in some cases ^13,14.

MRI

Cardiac MRI (CMR) is able to 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 can distinguish between many aetiologies of CCF, although this is beyond the scope of this general article on CCFmay be useful in delineating an etiology ^10,11.

Treatment and prognosis

Treatment involves a multidisciplinary team and incorporates lifestyle, allied health, pharmacological, and even surgical therapies, often specific to the underlying aetiology ^1,2. An in-depth review of the treatment of CCF is beyond the scope of this article, however, generalGeneral principles include:

• treatment of comorbidities and complications (e.g. obesity, hypertension, depression, etc.) ^1,2
• lifestyle interventions: education, cessation of smoking and alcohol consumption, increase in isotonic exercise, improve diet, daily home weights ^1,2
• pharmacotherapy: 
  • mortality benefit:depending on clinical context, examples include angiotensin-converting-enzyme inhibitors, angiotensin II receptor blockers, combination angiotensin receptor-neprilysin inhibitors (sacubitril/valsartan), betabeta-blockers (only carvedilol, bisoprolol, metoprolol succinate, nebivolol), spironolactone, nitrates and digoxin^1 1,2,12
    • these medications only have a benefit in patients with HFrEF, there are no medications with a mortality benefit in HFpEF (as of December 2017) ^1,2
  • symptomatic benefit with no mortality benefitinvasive/surgical management may include: other diuretics, nitrates, digoxin, hydralazine ^1,2
• surgery: consider implantable cardioverter-defibrillators,
• cardiac resynchronisation therapy,
• ventricular assist devices, and even
• cardiac transplant, depending on the severity and aetiology ^1,2

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.

Complications

• acute decompensated heart failure and
• acute pulmonary oedema
• passive hepatic congestion
• cardiorenal syndrome
• dysrhythmias

See also

• heart failure (basic)
• high output cardiac failure
• cardiac anatomy
• echocardiography
• cardiac MRI