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 to left ventricular dysfunction or right ventricular dysfunction, although in reality, most patients will have manifestations from both clusters ^1,2.

• left-predominant symptoms and signs
  • exertional dyspnoea and fatigue ^1,2
    • orthopnoea: dyspnoea in the recumbent position, may use multiple pillows at night ^1,2
    • 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 ^1,2
    • bendopnoea: dyspnoea while bending forward ³
  • angina ^1,2
  • syncope and cerebral dysfunction ^1,2
  • cyanosis ^1,2
  • other organ dysfunction ^1,2
  • added heart sounds ^1,2
    • S3 ‘ventricular gallop’ (occurs after S2 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 hypertrophied ventricular wall ^1,2
  • pulsus alternans ^1,2
• right-predominant symptoms and signs
  • nocturia ^1,2
  • 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 ^1,2

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

Patients with end-stage CCF may have Cheyne-Stokes respiration, hypotension, tachycardia, features of valvulopathies, 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 intrinsic cardiac or extrinsic factors. It may also be acute (acute decompensated cardiac failure) 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 is by left ventricular ejection fraction (LVEF), derived by dividing the left ventricular stroke volume by end diastolic-diastolic volume. While heart failure is not defined by the degree of left ventricular impairment, the classification is crucial for treatment decisions; 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 reduced ejection fraction (HFrEF), previously termed 'systolic heart failure'
    • ischaemic dilated cardiomyopathy ^1,2
    • non-ischaemic dilated cardiomyopathy (e.g. idiopathic, alcoholism, tachycardia-mediated cardiomyopathy, Chagas disease, Duchenne muscular dystrophy, peripartum/postpartum cardiomyopathy, hypothyroidism, cocaine use, infection, etc.) ^1,2
    • chronic hypertension ^1,2
    • obstructive valve disease (e.g. in the setting of 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 'diastolic heart failure'
    • 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
• high-output heart failure
  • 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 assessed in a complete transthoracic echocardiography exam include

• the systolic function of the left ventricle
  • the surrogate measure ejection fraction is the most popular method
• the diastolic function of the left ventricle
  • perturbations are often appreciable before the systolic function is affected
• structure of the left ventricle
  • wall thickness and left ventricular end-diastolic internal diameter may yield a derived mass, the basis of diagnosing remodellingremodeling and hypertrophy
• the right ventricular structure and function
  • more technically challenging, RV strain lacks parameters to assess to nearly the same degree as the left ventricle

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 CCF ^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, general 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: angiotensin-converting-enzyme inhibitors, angiotensin II receptor blockers, combination angiotensin receptor-neprilysin inhibitors (sacubitril/valsartan), beta-blockers (only carvedilol, bisoprolol, metoprolol succinate, nebivolol), spironolactone ^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 benefit: 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

See also

• heart failure (basic)
• high output cardiac failure