Chronic congestive heart failure

Aetiology

There are numerous and varied causes of heart failure:

 Other cardiovascular disease: coronary artery disease, cardiomyopathies,

hypertension, myocarditis, valvular heart disease, congenital heart diseases

 Pericardial disease

 Toxin-induced: heroin, alcohol, cocaine, amphetamines, lead, arsenic, cobalt,

phosphorus

 Infection: bacterial, fungal, viral (HIV), Borrelia burgdorferi (Lyme disease)

 Infiltrative diseases: amyloidosis, haemochromatosis, sarcoid

 Electrolyte imbalance: hypocalcaemia, hypophosphataemia, hypokalaemia,

hyponatraemia

 Endocrine disorders: diabetes mellitus, thyroid disease, hypoparathyroidism with

hypocalcaemia, phaeochromocytoma, acromegaly

 Systemic collagen vascular diseases: lupus, rheumatoid arthritis, systemic sclerosis,

polyarteritis nodosa, hypersensitivity vasculitis, Takayasu's syndrome, polymyositis,
Reiter's syndrome

 Drug-induced: adriamycin, cyclophosphamide, sulphonamides, some antiviral agents

 Nutritional deficiencies: thiamine, protein, selenium, L-carnitine

 Pregnancy: peripartum cardiomyopathy.

These conditions tend to increase metabolic demand, which may not be matched by a
sufficient increase in cardiac output by the failing heart. Tachyarrhythmias also decrease the
diastolic ventricular filling time and increase myocardial oxygen demand. Uncontrolled
hypertension depresses systolic function by increasing the afterload against which the failing
ventricle must pump blood, and may be the first clinical manifestation. It should be
emphasised that many of these causes may be completely reversible given appropriate and
timely treatment/intervention (e.g., revascularisation for stunned or hibernated myocardium;
standard therapy for peripartum or hypertensive cardiomyopathy; valvuloplasty or valve
replacement for valvular heart disease; standard treatment and adjunctive rate control therapy
for tachycardia-induced cardiomyopathy). Other causes, such as scarred myocardium or
dilated cardiomyopathy, are currently considered irreversible.

Classification
American College of Cardiology/American Heart Association Stages of Heart
Failure [1]

This staged classification underscores the fact that established risk factors and structural
abnormalities are necessary for the development of heart failure, recognises its progressive
nature, and superimposes treatment strategies on the fundamentals of preventative efforts.
Heart failure may progress from stage A to stage D in a given patient but generally does not
follow the path in reverse.

 Stage A: patients at high risk of developing heart failure because of the presence of
conditions that are strongly associated with the development of heart failure, for
example, hypertension, diabetes, or coronary disease; however, such patients have no
identified structural or functional abnormalities of the pericardium, myocardium, or
cardiac valves and have never shown signs or symptoms of heart failure.

 Stage B: patients who have developed structural heart disease that is strongly
associated with the development of heart failure but who have never shown signs or
symptoms of heart failure, for example, asymptomatic post-infarction left ventricular
dysfunction.

 Stage C: patients who have current or prior symptoms of heart failure associated with
underlying structural heart disease.

 Stage D: patients with advanced structural heart disease and marked symptoms of
heart failure at rest despite maximal medical therapy and who require specialised
interventions, for example, heart transplant or left ventricular assist devices.

Framingham criteria for the diagnosis of CHF [2]

Heart failure is essentially a clinical diagnosis. Clinical criteria for diagnosing heart failure,
the Framingham criteria for the diagnosis of CHF, were established before the widespread
use of echocardiographic assessment of systolic and diastolic dysfunction. The Framingham
clinical criteria, listed below, have been extremely useful for identifying heart failure
patients, both in clinical practice and in epidemiological studies, for more than 40 years.
However, since their specificity is greater than their sensitivity, it is recognised that they
probably miss mild cases of heart failure. In order to come up with a definite diagnosis of
CHF, one needs to have either 2 major criteria or the combination of 1 major and 2 minor
criteria.

Major criteria:

 Neck vein distention

 Rales

 Acute pulmonary oedema

 S3 gallop
  Increased venous pressure >16 cm of water

 Circulation time >25 seconds

 Hepatojugular reflux

 Cardiomegaly

 Paroxysmal nocturnal dyspnoea or orthopnoea.

Minor criteria:

 Ankle oedema

 Night cough

 Dyspnoea on exertion

 Hepatomegaly

 Pleural effusion

 Less than one third maximum vital capacity

 Tachycardia (HR >120 bpm).

Major or minor criteria:

 Weight loss greater than 4.5 kg in 5 days in response to treatment.

Acute exacerbation of congestive heart failure

Classification

Clinical presentations [1]

Acute CHF has been classified by The European Society of Cardiology into following
clinical groups:

1. Acute decompensated heart failure (ADHF)

 De novo or as decompensation of chronic CHF with signs and symptoms of ADHF,

which are mild and do not fulfil criteria for cardiogenic shock, pulmonary oedema, or
hypertensive crisis.

2. Hypertensive acute CHF

 Signs and symptoms of heart failure are accompanied by high BP and relatively
preserved LV function, with a CXR compatible with acute pulmonary oedema.
3. Pulmonary oedema (verified by CXR) View imageView image

 Severe respiratory distress with associated crackles on lung examination, orthopnoea,

and reduced oxygen saturation usually below 90% on room air before treatment.

4. Cardiogenic shock

 Defined as evidence of tissue hypoperfusion induced by heart failure after correction

of pre-load.

 Usually characterised by reduced BP (systolic BP <90 mmHg or a drop of mean

arterial pressure >30 mmHg) and/or low urine output (<0.5 mL/kg/hour), with a pulse
rate above 60 bpm with or without evidence of organ congestion.

 There is a continuum from low cardiac output syndrome to cardiogenic shock.

5. High output failure

 Characterised by high cardiac output, usually with high heart rate (caused by
arrhythmias, thyrotoxicosis, anaemia, Paget's disease, iatrogenic or other
mechanisms), with warm peripheries, pulmonary congestion, and sometimes with low
BP such as in septic shock.

6. Right heart failure

 Characterised by low output syndrome with increased jugular venous pressure,

increased liver size, and hypotension.

Clinical classification of acute heart failure (AHF) [2]

For simplification these patients can be classified into 3 main groups:

1. Hypertensive AHF (acute de novo heart failure or vascular failure)

 Symptoms develop rapidly against a background of hypertension with increased

sympathetic tone and neurohormonal activations.

 Left ventricular ejection fraction (LVEF) is usually preserved and there are clinical
and radiological findings of pulmonary congestion, usually without signs of systemic
congestion, for example, peripheral oedema.

 Response to therapy is rapid.

2. Normotensive AHF (acutely decompensated chronic heart failure)

 History of progressive worsening of chronic heart failure.

 BP is usually normal and symptoms and signs develop gradually with both systemic
and pulmonary congestion.
  LVEF is usually reduced.

3. Hypotensive AHF

 Presents with symptoms and signs of hypotension, organ hypoperfusion, and

cardiogenic shock.

Types of heart failure

Systolic

 Associated with LV dysfunction and characterised by cardiomegaly, third heart

sound, and volume overload with pulmonary congestion.

Diastolic

 Typically associated with normal cardiac size, hypertension, pulmonary congestion,

and a fourth heart sound.

Diagnostic criteria

Framingham criteria for CHF [32]

The Framingham criteria are the most widely accepted clinical criteria for diagnosing heart
failure. For establishing a definite diagnosis of CHF, 2 major criteria or 1 major and 2 minor
criteria must be present.

Major criteria are:

 Paroxysmal nocturnal dyspnoea or orthopnoea

 Neck-vein distention

 Rales

 Cardiomegaly

 Acute pulmonary oedema

 S3 gallop

 Increased venous pressure above 16 cm of water

 Circulation time 25 seconds or longer

 Hepatojugular reflux.

Minor criteria are:

  Ankle oedema

 Night cough

 Dyspnoea on exertion

 Hepatomegaly

 Pleural effusion

 Vital capacity reduced one third from maximum

 Tachycardia (120 bpm or more).

Major or minor criteria are:

 Weight loss of 4.5 kg or more in 5 days in response to treatment.

New York Heart Association (NYHA) clinical classification of heart failure [33]

 Class I: asymptomatic

 Class II: mild symptoms with moderate exertion

 Class III: symptoms with minimal activity

 Class IV: symptoms at rest.

Differential diagnosis

Differential Diagnosis table for Acute exacerbation of congestive heart failure

Condition Differentiating signs/symptoms Differentiating tests
 Fever, cough, productive sputum.  WCC: elevated.
 Focal signs of consolidation--  Blood cultures: positive
Pneumonia increased vocal fremitus and for organism.
bronchial breathing.  CXR: consolidation.

 Haemoptysis and sharp, pleuritic

chest pain.
 Risk factors of thromboembolism  CT pulmonary
Pulmonary (TE) include personal history of TE, angiography: clot in
embolism family history, recent trauma, pulmonary artery.
prolonged immobilisation, smoker, or
OCP use.

Asthma  Wheezing on physical examination.  Reduced peak flow.

  Spirometry: obstructive
pattern, reversibility
with beta-agonist
inhalers

 CXR: reticular infiltrate

in the late stages of
disease.
 High-resolution CT
 Progressively increasing dyspnoea.
scan: ground-glass
 Oxygen desaturation with exercise.
Interstitial appearance, reticular
lung disease  Fine bibasal crepitations with no
infiltrates,
other signs of heart failure. honeycombing, and
architectural distortion.
 Spirometry: restrictive
pattern.

Adult  CXR: diffuse infiltrates

respiratory  Severe hypoxia, fine crepitations.  Pulmonary artery wedge
distress pressure: <18 mmHg
syndrome

Treatment approach

The main goal of the treatment of acute CHF is to provide symptomatic relief.

Initial management options include a combination of oxygen, morphine, diuretics, ultra-

filtration, vasodilators and inotropes.

All patients should be admitted to the hospital. If the patient responds adequately to initial
treatment, telemetry monitoring is acceptable. Those who are hypotensive or fail to respond
to initial therapy require admission to the ICU and may need invasive monitoring if tissue
perfusion is compromised. [35] If cardiogenic shock is present, invasive evaluation is
required.

Maintenance of oxygen saturation

Oxygen therapy should be given to all patients to maintain oxygen saturation between 95% to
98%, to maximise tissue oxygenation.

Ventilation with non-invasive positive pressure ventilation (NIPPV) or CPAP may be

required if oxygen saturation cannot be maintained by oxygenation alone, and is associated
with a decreased requirement for intubation and mechanical ventilation. [1]

Mechanical ventilation is only used when other treatments, including non-invasive ventilation
methods, fail.
Haemodynamically stable

Diuretics and IV vasodilators are recommended for all patients with acute CHF who have a
systolic BP above 80 mmHg.

 Loop diuretics are the mainstay of treatment and are effective in relieving symptoms.
Non-loop diuretics, such as spironolactone and metolazone, may be added if there is
an inadequate response to loop diuretics alone.

 Glyceryl trinitrate is the first-line agent, with nesiritide considered second line.

 Although there are no large-scale studies comparing diuretics alone with glyceryl
trinitrate in patients with acute CHF, some have suggested that nitrates alone may be a
better alternative in patients with acute CHF. [36] In clinical practice both these
agents are used in combination.[B Evidence]

In patients who do not respond to initial therapy, extra-corporeal ultra-filtration is used to

reduce volume overload. [37] [A Evidence]

Haemodynamically unstable

Patients with hypotension or hypoperfusion (i.e., cold and dry, cold and wet profiles) should
be commenced on inotropic support as this may improve hemodynamics. [38] However,
positive inotropes should be used with caution because there is evidence that they result in
increased mortality, and can cause arrhythmias and worsening of coronary ischaemia. [12] [B
Evidence][B Evidence] The occurrence of sustained arrhythmias should lead to their
discontinuation. Concomitant use of amiodarone may be advisable, although there are no
large-scale data on the use of anti-arrhythmics in this setting. If the patient has symptomatic
coronary ischaemia, inotropes should be discontinued.

Patients with a systolic BP below 90 mmHg or a drop of mean arterial pressure of more than
30 mmHg with a pulse rate above 60 bpm and/or low urine output (<0.5 mL/kg/hour) are
defined as being in cardiogenic shock. Insertion of an intra-aortic balloon pump is indicated
in patients with persistent cardiogenic shock, despite inotropic therapy. (However, patients
with significant aortic regurgitation or aortic dissection are not candidates.)

Choice of inotrope depends on clinical findings. [1] Dobutamine, milrinone, or levosimendan

is recommended for patients with systolic BP 85 to 100 mmHg and no clear clinical evidence
of shock (such as cold extremities and low urine output). Levosimendan is a calcium
sensitiser. [39] [40] It may not be available in some countries. Dopamine is recommended for
patients with systolic BP <85 mmHg with clinical evidence of shock. Norepinephrine
(noradrenaline) is recommended for patients with systolic BP <85 mmHg and persistent signs
of shock.

Specific treatment of underlying cause

CAD

 IV glyceryl trinitrate is first-line treatment.

  The common adverse effect of glyceryl trinitrate is headache and hypotension. The
dose of nitrates should be reduced if systolic BP decreases below 90 to 100 mmHg,
and discontinued permanently if BP drops further. From a practical point of view, a
reduction of 10 mmHg in mean arterial BP should be achieved.

 In cases of significant CAD causing acute CHF, percutaneous revascularisation or

coronary artery bypass should be carried out.

 In the case of cardiogenic shock with acute MI, revascularisation is recommended.

Thrombolysis in this setting is not effective. [38]

Hypertensive emergency

 Use of IV beta-blockers and glyceryl trinitrate is recommended.

 If additional medicines are needed, nitroprusside is recommended in addition to other

choices.

Valvular heart disease

 In cases of severe aortic stenosis with heart failure, nitroprusside can be used,
provided the patient is not hypotensive. [41]

 The definitive treatment for aortic stenosis or mitral stenosis is valve replacement, but
in resistant heart failure a percutaneous valvotomy may be used as temporary measure
until definitive valve replacement is carried out. In mitral stenosis, percutaneous
valvuloplasty may be done if no thrombus is present on transoesophageal
echocardiogram (TOE).

 Similarly in heart failure associated with mitral regurgitation or aortic regurgitation, a

vasodilating drug such as nitroprusside should be used. A decrease in the peripheral
arterial resistance results in an increase in the cardiac output and a decrease in
regurgitant volume, which, in turn, is associated with a reduction in left ventricular
end-diastolic volume and an augmentation of the ejection fraction.

Resistance to maximal medical therapy

In cases resistant to maximal medical therapy, a left ventricular assist device should be
inserted. In some cases of non-ischaemic cardiomyopathy, sustained reversal of severe heart
failure is seen with implantation of a left ventricular assist device. [42]

Ongoing therapy

Once the patient is stabilised, definitive medical therapy for heart failure should be
commenced. Usually an ACE inhibitor [A Evidence] (or an angiotensin-II receptor antagonist
if ACE inhibitors are not tolerated)[B Evidence] is started first, followed by the addition of
beta-blockers.[A Evidence] The dose of ACE inhibitors and beta-blockers should be
increased to the maximum tolerated dose depending upon BP and heart rate. Patients who
have persistent signs of fluid overload will need ongoing diuretics. Patients with ongoing
symptoms despite this therapy should be treated as having chronic CHF.