Chronic heart failure

It is clinically useful to divide heart failure into the syndromes of right, left and biventricular (congestive) heart failure, but it is rare for any part of the heart to fail in isolation.

Right heart failure:

This syndrome occurs in association with:

• Chronic lung disease (cor pulmonale)
• PE or pulmonary HT
• Tricuspid valve disease
• Left-to-right shunts (e.g. ASD and VSD)

The most frequent cause of right heart failure is secondary to left heart failure

Symptoms and signs of right heart failure:

Symptoms:

• Fatigue
• Breathlessness
• Anorexia
• Nausea

Signs:

• Increased JVP
• Tender, smooth hepatomegaly
• Dependent pitting oedema
• Ascites
• Pleural transudates (commonly right-sided)

Left heart failure:

Causes include:

• IHD (the most common cause)
• HT
• Mitral/aortic valve disease
• Cardiomyopathies

Mitral stenosis causes left atrial HT and signs of left heart failure but does not itself cause failure of the left ventricle

Symptoms and signs of left heart failure:

Symptoms:

• Fatigue
• Exertional dyspnoea
• Orthopnoea
• Paroxysmal nocturnal dyspnoea (PND)

Signs are few and not prominent until a late stage or if the ventricular failure is acute:

• Cardiomegaly
• Displaced apex
• Left ventricular 3^rd or 4^th heart sound that, with a tachycardia, is described as a gallop rhythm
• Functional mitral regurgitation (caused by dilatation of the mitral annulus)
• Bi-basal lung crackles with possible pulmonary oedema

Congestive (biventricular) heart failure:

This term is best restricted to cases where right heart failure is secondary to left heart failure. The physical signs are thus a combination of the above syndromes

General/diagnostic investigations:

• CXR
• Echocardiography
• Blood tests:
• FBC
• LFTs
• U&Es
• TFTs

• Cardiac catheterisation

Functional/prognostic investigations:

• Cardiopulmonary exercise testing
• Resting and stress radionucleotide angiography
• Ambulatory ECG monitoring for 24-28 hours (if an arrhythmia is suspected)
• Serum ANP levels (a measure of left ventricular systolic dysfunction)

General treatment:

• Moderate physical exercise
• Weight loss (if appropriate)
• Salt restriction
• Alcohol abstinence (as alcohol has a negatively inotropic effect)

Drug management:

Relies on the following categories of drugs:

• Diuretics
• Vasodilators
• Positive inotropic agents
• Digitalis glycosides
• Anti-arrhythmic agents

Diuretics:

All act by promoting the renal excretion of salt and water. The resulting loss of fluid reduces preload and produces consistent haemodynamic and symptomatic benefits in patients with HF and rapidly removes dyspnoea and peripheral oedema.

Loop diuretics:

• E.g. frusemide, bumetanide
• Act by reducing sodium and chloride reabsorption in the ascending limb of the loop of Henle
• Cause a brisk and short-lived diuresis
• Produce marked K⁺ loss and hyperuricaemia

Thiazide diuretics:

• E.g. bendrofluazide
• Effect the distal convoluted tubule, reducing sodium reabsorption
• Mild diuretic action
• Less effective in patients with a reduced GFR
• Again, promote K⁺ loss
• Metolazone is a powerful thiazide diuretic, producing a profound diuresis acting synergistically with loop diuretics

Potassium-sparing diuretics:

• Spironolactone:
• Competitive aldosterone antagonist
• Weak diuretic
• Has a potassium-sparing action (since aldosterone promotes the excretion of potassium)
• Amiloride, triamterene:
• Act at the distal tubule, preventing potassium secretion in exchange for sodium
• Weak diuretics
• Should be avoided in patients with renal failure and those taking ACEIs (as both lead to potassium retention)

Vasodilator therapy:

Arteriolar vasodilators:

• α-adrenoreceptor antagonists (e.g. prazosin)
• Direct smooth muscle relaxants (e.g. hydralazine)
• Calcium-channel blockers (e.g. amlodipine)

Venodilators:

• Short-acting nitrates (e.g. GTN)
• Long-acting nitrates (e.g. isosorbide mononitrate)

With chronic use, tolerance develops

Angiotensin converting enzyme inhibitors (ACEIs):

• E.g. enalapril
• Decrease TPR and reduce circulating levels of catecholamines
• Should be carefully introduced to patients due to risk of first-dose hypotension
• Concomitant potassium-sparing diuretics should be discontinued (since ACEIs can lead to potassium retention)
• ACEIs are contraindicated in patients with bilateral renal artery stenosis
• Between 10-15% of patients develop a cough, owing to the inhibition of bradykinin metabolism

Angiotensin II receptor antagonist:

• E.g. losartan
• Similar haemodynamic effects to ACEIs
• Do not affect bradykinin metabolism or produce a cough

ß-blockers:

• E.g. metoprolol

Inotropic agents – usually acute heart failure:

Digitalis glycosides:

• Is a competitive inhibitor of Na⁺-K⁺-ATPase, therefore, producing high levels of intracellular sodium. This is then exchanged for calcium – leads to increased cardiac contractility
• Digoxin is administered orally (1mg loading dose and 0.125-0.25mg daily according to body mass and renal function)
• Digoxin toxicity (levels >2.5nmol/L) leads to:
• Anorexia, nausea, altered vision
• Arrhythmia (e.g. ventricular premature beats, VT and AV block)

Anticoagulants:

• HF is associated with a 4x risk of stroke
• Oral anticoagulants are recommended in patients with:
• Atrial fibrillation
• A previous history of thromboembolism

Treatment summary:

• All patients with clinical HF should receive treatment with diuretics and an ACEI
• Patients in AF should be digitalized but patients in sinus rhythm may also be improved by the addition of digoxin or a ß-blocker