Chronic heart failure

What is chronic heart failure?

Chronic heart failure is an ongoing process in which the heart is unable to pump out an amount of blood that is adequate for the needs of the body. Commonly, it follows a relapsing and remitting course. During the periods of stability, patients feel much better but during the episodes of instability, symptoms are worsen and may necessitate hospitalization.


The main causes of chronic heart failure are:

1. Previous myocardial infarction (also called heart attack)

It is the most common cause.  After myocardial infarction, the area of damage tissue in heart muscle is healed with fibrous tissue. This healed fibrous tissue is less functional and contract poorly, and impede the function of normal heart muscle by distorting their contraction and relaxation patterns that lead to chronic heart failure.

2.  Ischemic heart disease

Ischemic heart disease means the heart muscle get a small amount of oxygen rich blood caused by the partial obstruction or stenosis of one or more of the coronary arteries by atherosclerotic plaque. Chronically inadequate blood supply to the heart muscle may lead to a reduction in contractility and causes chronic heart failure.

3. Hypertension (high blood pressure)

Hypertension places a pressure load on the heart. In long term uncontrolled hypertension, this pressure load produces changes in the heart muscle that lead to failure.

4. Valvular heart disease

In valvular heart disease, valve may be stenotic (narrowed) or regurgitant (leaking). Narrowed heart valve can obstruct the flow of blood in the heart. This obstruction increases the stress on the heart muscle and secondary changes take place that lead to chronic heart failure. In leaking valve, heart works harder to deal with the extra volume of blood that may lead to failure.

5. Cardiomyopathy

It is a disease of the heart muscle. It may be familial or due to alcohol misuse, adriamycin intake (use in cancer treatment), viral infection (Coxsackie virus, HIV), hemochromatosis, sarcoidosis, hyperthyroidism and thiamine deficiency. Cardiomyopathy causes the heart to enlarge and become weaker that ultimately lead to failure.

6. Congenital heart disease

It present at birth.  Usually, manifests in childhood or adult life. Ventricular septal defect and atrial septal defect are the most common congenital heart disease that may cause chronic heart failure.


At first chronic heart failure begins after an index event such as myocardial infarction, ischemic heart disease, hypertension, cardiomyopathy, valvular heart disease or congenital heart disease. It produces an initial decline in the pumping capacity of the heart. At this stage, most of the patients remain asymptomatic or minimally symptomatic. This initial decline in the pumping capacity of the heart activates a variety of compensatory mechanisms including the renin-angiotensin-aldosterone system and sympathetic nervous system. Activation of the renin-angiotensin-aldosterone system can maintains cardiac output through increased retention of sodium and water, and activation of the sympathetic nervous system can maintains cardiac output through increased myocardial contractility. In addition, there is activation of atrial natriuretic peptide, brain natriuretic peptide, prostaglandins, and nitric oxide that offset the excessive peripheral vasoconstriction. For a period of years, these systems are able to restore heart function to a normal homeostatic range and patients remain asymptomatic or minimally symptomatic. However, with time the sustained activation of these systems can cause secondary end-organ damage within the heart that excessively decline in the pumping capacity of the heart and patients become overtly symptomatic.


Shortness of breath – It first appear on moderate exertion such as walking up a steep hill. As heart failure progresses, the shortness of breath are provoked by mild exertion and ultimately the patient breathless walking from room to room, dressing, washing or trying to hold a conversation.

Orthopnea – Some patients with chronic heart failure develop breathing difficulty in lying position. This condition is called orthopnea. It is due to excess pooling of blood in lying position from periphery that accumulates in the lung. To prevent this condition, patient may sleep in a semi-upright position with extra pillows.

Fatigue, weakness and poor effort tolerance – In chronic heart failure, less amount of blood is going to the vital organs and skeletal muscles that cause fatigue, weakness and poor effort tolerance.

Swelling of body (edema) – Generalized high pressure is developed within the venous system in chronic heart failure. This may cause leak out fluid from the blood vessels to the interstitial tissue spaces of the body and develops edema.

Low urine output – A poor blood supply to the kidney may leads to low urine output.

Weight loss – Some patients with chronic heart failure may lose weight. It is due to loss of appetite, impaired absorption of food due to gastrointestinal fluid retention, poor tissue perfusion due to a low cardiac output and muscle atrophy due to less physical activity. Sometimes marked weight loss occurs and this condition is known as cardiac cachexia.

New York Heart Association (NYHA) functional classification for classes of chronic heart failure:

According to severity of the patient’s symptoms, it classify the heart failure into four categories. This classification guide the treatment plan and also give an idea about the patient prognosis.

Class I: No limitation during ordinary activity (such as walking, climbing stairs).

Class II: Slight limitation during ordinary activity. Patient comforts at rest but fatigue, palpitation or breathing difficulty develop during ordinary activity.

Class III: Marked limitation of normal activities. Patient comforts at rest but fatigue, palpitation or breathing difficulty develop during less than ordinary activity.

Class IV: Unable to undertake any physical activity without symptoms; symptoms may be present at rest.


For diagnosis, following investigations are done in patients with chronic heart failure:

Electrocardiogram (ECG):  Look for evidence of ischemia, previous myocardial infarction, arrhythmia and left ventricular hypertrophy.

Echocardiography:  It is very useful investigation to establish the cause.

Chest X-ray: Look for evidence of enlarged heart, heart contour (may give clue to etiology) and lung congestion.

Brain natriuretic peptide (BNP): It is a type of hormone and elevated in blood in patients with chronic heart failure.

Thyroid function test: It is done to exclude hyperthyroidism and hypothyroidism. Both may cause and exacerbate chronic heart failure.

Hemoglobin level: It is done to see anemia. Anemia may exacerbate failure.

Serum urea, creatinine and electrolytes: These may help to detect any complications.


1. General measures


Good general nutrition should be maintained. Eat a healthy diet that rich in vegetables, fruits, monounsaturated fatty acids (main sources are olive oil, canola oil and safflower oil) and omega-3 polyunsaturated fatty acids (main sources are fish oils and some nut), but low in saturated fatty acids (main sources are dairy products, meat products, palm oil and coconut oil). Patients avoid high salt foods and added salt. Salt causes retention of fluid in the body and aggravates chronic heart failure.


As usual fluid intake is recommended. Drinking too much fluid can increase heart’s workload and worsen heart failure. Usually, fluid restriction is not necessary unless the patient develop peripheral edema or hyponatremia (plasma sodium concentration falls below 125 mmol/L). If these develop, patient should intake 1 to 1.5 liters of fluid per day. Some patients may need to weigh themselves at the same time each morning, preferably before breakfast and after voiding, as a measure of fluid load and adjust their diuretic therapy (water pill) accordingly to excrete extra water and sodium.


Weight reduction is required in obese persons and extra caloric supplementation is recommended for patients losing their weight due to advanced chronic heart failure. Usually, patients maintain an ideal body weight.


It is better to avoid drink alcohol. If the chronic heart failure is caused by alcohol-induced cardiomyopathy, patients should not drink it at all.


Smoking should be stopped. Cessation of smoking can reduce the further risk of heart disease.


Regular moderate aerobic exercise within limits of symptoms is beneficial.


Patients with chronic heart failure are at increased risk of developing influenza and streptococcal pneumoniae infection. Therefore, annually Influenza and at least 5-yearly pneumococcal vaccination should be given.

Sexual activity

Many patients with chronic heart failure can still be sexually active. For sexual activity, patients choose a time when feeling rested and free from stresses. In men with compensated chronic heart failure who developed erectile dysfunction, treatment with a cyclic guanine mono-phosphate phosphodiesterase type-5 inhibitor (sildenafil, tadalafil) can be given, but these drugs must not be taken within 24        hours of prior nitrate  use, and nitrate must not be re-started for at least 24 hours afterward.

2. Drug therapy

There are many drugs for chronic heart failure that can relief symptoms and expand life longevity. Commonly, the following drugs are used to treat chronic heart failure.


Diuretic produces an increase in urinary salt and water excretion, leading to a reduction in excess body fluid and relief symptoms. Commonly used diuretics are

(a) Loop diuretics – Usually, furosemide 40 to 120 mg once daily or bumetanide 1 to 4 mg once daily relief symptoms. Dose is titrated on the clinical response including symptom improvement and resolution of excess body fluid. Hypokalaemia (decrease plasma potassium level) is a common side effect of loop diuretics. To minimize this side effect, potassium-sparing diuretics such as amiloride 5 to 10 mg once daily or spironolactone 50 to 200 mg twice daily can be co-prescribed.

(b) Potassium-sparing diuretics – Also called aldosterone receptor antagonists that include amiloride, spironolactone and eplerenone. They directly block the salt and water retaining effect of aldosterone from the kidney and improve long-term clinical outcome in patients with chronic heart failure. They may cause hyperkalaemia (increase plasma potassium level). Data from Randomized Aldactone Evaluation Study show that low dose spironolactone (25 once daily) reduces mortality in patients with chronic heart failure.

(c) Thiazide diuretics – They include hydrochlorthiazide, bendroflumethiazide and metolazone. In some patients with severe chronic heart failure, edema may persist despite loop diuretics. In such patients the combination of a loop diuretic and a thiazide diuretic (hydrochlorthiazide 25 mg daily or bendroflumethiazide 5 mg daily or metolazone 5 mg daily) may improve symptoms by producing an excessive diuresis.

ACE (angiotensin converting enzyme) inhibitors

They include captopril, enalapril, lisinopril, ramipril etc. ACE inhibitors prevent peripheral vasoconstriction, aldosterone induced salt and water retention, and sympathetic nervous system activation. By these mechanisms, they can produce a substantial improvement in effort tolerance, prevent the onset of overt heart failure and improve the long term outcome in chronic heart failure. Some patients are unable to tolerate an ACE inhibitor because of its side effect (persistent dry cough). In these cases, an angiotensin receptor blocker (ARB) may be alternative.

Angiotensin receptor blockers (ARBs)

They include losartan, valsartan, candesartan, olmesartan etc. ARBs produce similar beneficial effects to that of ACE inhibitors but are generally better tolerated. Sometimes, the combination of an ARB and an ACE inhibitor are used in patients with recurrent hospitalizations with severe chronic heart failure.


Digoxin helps the heart to pump more effectively by increasing the force of contraction. It also regulates an irregular heart rhythm and used in patients with chronic heart failure and atrial fibrillation. In severe chronic heart failure, digoxin reduces the hospitalizations, although it has no effect on long- term survival.


They include carvedilol, metoprolol, bisoprolol, nebivolol. Beta-blockers should be started with very low doses and increased gradually to a target maintenance dose. They counteract the harmful effects of excessive activation of the sympathetic nervous system. They improve left ventricular function, reduce the risk of arrhythmias, improve symptoms, reduce the frequency of hospital admission and strikingly improve survival in chronic heart failure.

Vasodilators (nitrate and hydralazine)

Nitrate reduces preload (degree to which heart is stretched) and hydralazine reduces after load (resistance against which heart pump). Their use is limited because nitrate causes tolerance and hydralazine causes severe hypotension. The combination of these two drugs is valuable in chronic heart failure, when ACE inhibitor or ARB is contraindicated (in kidney failure) or intolerance (due to side effect).

3.Device therapy  

Implantable cardioverter defibrillator (ICD)

An ICD is a small device that is implanted under the skin in the chest area with either one or two leads are placed in the right side of the heart. About half of the patients with chronic heart failure die suddenly, mainly as the result of a ventricular arrhythmia (abnormally fast, life-threatening heart rhythm). Anti-arrhythmic drugs are less effective in this condition. ICD can detect and terminates life-threatening ventricular arrhythmia and improves survival. It should be considered for all patients with NYHA Class II or class III heart failure (irrespective of cause of chronic heart failure) with left ventricular ejection fraction (LVEF) of 35% or less for the primary prevention of mortality. If a patient previously not received an ICD but develops ventricular arrhythmia, ICD is also strongly recommended as a secondary prevention of mortality.

Cardiac resynchronization therapy (CRT)

In chronic heart failure, an abnormality in the electrical conducting system of the heart may develop that causes the left ventricle to pump in a dysynchronous fashion. This dysynchrony markedly reduces the efficiency of the left ventricle and aggravates chronic heart failure. A CRT has an additional lead that is placed in the left ventricle to make the heart pump in a coordinated way by resynchronizing the left ventricular contraction. CRT is considered in patients with NYHA Class III or class IV heart failure ,  left ventricular ejection fraction (LVEF) of 35% or less, and a wide QRS complex in ECG (120 milliseconds or more, usually manifest with left bundle branch block). CRT improves contractile performance of the heart, relieves symptoms, and reduces morbidity and mortality in chronic heart failure. Now CRT-D (CRT – defibrillator) is more preferable than CRT alone. This device incorporates a CRT with an ICD. CRT can improve the ability of the heart to pump out blood to the body and ICD can stop the life-threatening ventricular arrhythmia by delivering an electrical shock called defibrillation.

Ventricular assist devices (VADs)

Ventricular assist devices aid the heart’s pumping function. It can provide a short but significant prolongation of survival in patients who have end-stage chronic heart failure.  But it’s wide spread use is limited due to high complication rates like bleeding, infection, systemic embolism etc.

4. Revascularization surgery

Chronic heart failure due to coronary artery disease (myocardial infarction or ischemic heart disease) may improve with coronary artery bypass surgery or percutaneous coronary intervention who present with hibernating myocardium. Hibernating myocardium are the areas of viable non-contracting heart muscle.  These areas can be detected by magnetic  resonance imaging, positron   emission tomographic scanning or stress echocardiography. After surgery, the hibernating myocardium gets an appropriate amount of oxygen rich blood and become active that improves heart function.

5. Heart transplantation

It is an established treatment for patients with end-stage chronic heart failure when above measures failed. But its use is limited due to lack of donor hearts.


In chronic heart failure, the following complications may occur:

Kidney failure – Less amount of blood is going to the kidney that may cause kidney failure.

Liver problem – It is caused by poor blood supply to liver and hepatic venous congestion. This may cause mild jaundice and abnormal liver function tests.

Hypokalaemia (low serum potassium) – It is due to treatment with potassium-losing diuretics (furosemide, bumetanide) or hyperaldosteronism (increase the level of body aldosterone hormone).

Hyperkalaemia (high serum potassium) – It is due to the effects of ACE inhibitors, ARBs or potassium-sparing diuretics which promote the re-absorption of potassium from kidney.

Hyponatraemia (low serum sodium) – It is a feature of severe chronic heart failure and is a poor prognostic sign. It is due to diuretic therapy, high ADH (anti-diuretic hormone) or failure of the cell membrane ion pump.

Thromboembolism – Pulmonary embolism and deep vein thrombosis may occur due to low cardiac output.

Heart arrhythmia – Heart arrhythmia is a disturbance of the electrical rhythm of the heart. It is due to underlying heart disease or electrolyte imbalance.


The prognosis of patients with chronic heart failure is poor despite advances in therapy. It is difficult to predict the prognosis of individual patient. Patients with symptoms at rest (NYHA class IV) have a 30 to 50% annual mortality rate, patients who are symptomatic with mild activity (NYHA class III) have mortality rate of 10 to 20% annually, and patients with symptoms only with moderate activity (NYHA class II) have a 5 to 10% annual mortality rate. Mortality rates are higher in older patients, patients with a reduced left ventricular ejection fraction (LVEF), diabetes mellitus, chronic kidney disease or patients with an underlying coronary artery disease.