Congestive Heart Failure 101

Heart failure, or congestive heart failure (CHF), is a very common disease, afflicting approximately 4.8 million Americans. While many other forms of heart disease have become less common in recent years, CHF has been increasing steadily. This may be because more people with other forms of heart disease survive longer but are left with damaged hearts, which leads to CHF. Also, as the elderly population increases, there are more people at high risk of developing CHF. Approximately 400,000 new CHF cases occur each year, and it is the most common diagnosis in hospital patients over 65.

In this article, we will discuss congestive heart failure -- its causes, its warning signs and how it can be treated.

The purpose of the heart is to pump blood, which contains oxygen and nutrients, to the rest of the body. CHF is simply the failure of the heart to perform this main function adequately. Of course, a lack of blood pumped to the body is only considered CHF if the heart actually receives a sufficient volume of blood from the incoming vessels in the first place (i.e., normal filling pressures). When there is not enough blood for the heart to pump out, the problem is not CHF.

CHF occurs when the flow of blood from the heart (cardiac output) decreases, or fluid backs-up behind the failing ventricle, or both. Physicians have several different ways of describing heart failure:

Unilateral heart failure: Because the heart is basically two pumps (right side, left side) in one, either side can fail independently of the other.

  • Left-sided heart failure: When the left ventricle can't pump out enough blood, it gets backed-up in the lungs (behind the left ventricle), causing pulmonary edema, a build-up of fluid in the lungs. Among other things, this brings about shortness of breath. Left-sided heart failure often leads to right-sided heart failure.
  • Right-sided heart failure: The right ventricle cannot pump out enough blood, causing fluid to back up in the veins and then in capillaries of the body (behind the right ventricle). Because of the back-up, fluid leaks out of the capillaries and builds up in the tissues, a condition called systemic edema. Edema is especially noticeable in the legs because the lower half of the body drains into the right side of the heart .

Directional heart failure:

  • Backwards heart failure: The ventricle is not pumping out all the blood that comes into it. This increases the ventricular filling pressure and systemic or pulmonary edema. In fact, the heart can only meet the needs of the body if the ventricular filling pressure is high.
  • Forward heart failure: The heart is not pumping out enough blood to meet the needs of the body. Because less blood reaches the kidneys, they conserve salt and water, which contributes to excess fluid retention and edema. Forward failure also decreases the blood flow to various organs, causing weakness and fatigue.

Time-dependent heart failure:

  • Acute heart failure: This describes heart failure that occurs suddenly. A heart attack can cause acute heart failure if a large enough part of the heart muscle dies. When this happens, the heart cannot pump out enough blood, causing heart failure and pulmonary edema. This makes breathing very difficult and can lead to death. Acute heart failure can also occur when a heart valve suddenly stops functioning or the chordae tendineae, the muscle and cord that helps the mitral valve function properly, suddenly ruptures.
  • Chronic heart failure: This describes heart failure that develops gradually. The symptoms are subtle at first but become more acute over time.

Phasic heart failure: The heart can fail in either of the two phases of the cardiac cycle -- contraction (systole) and rest (diastole).

  • Systolic heart failure: The heart has difficulty contracting and pumping out enough blood. This causes weakness, fatigue and decreased ability to exercise.
  • Diastolic heart failure: The heart is unable to fill properly during diastole, usually due to increased filling pressure. This causes systemic or pulmonary edema or both.

Output vs. demand heart failure:

  • High-output heart failure Cardiac output is normal or a little bit high, but demand for blood flow is abnormally high (hyperthyroidism, anemia, severe infections). The heart is unable to deliver the increased amount of blood and fails.
  • Low-output failure Cardiac output is low, but demand for blood flow is normal. The heart is unable to meet this demand and fails. Low-output failure is more common than high-output failure.


Causes of CHF

Blood Flow Through the Heart
  • Oxygen-depleted blood from the veins enters the right side of the heart
  • The right ventricle pumps that blood to the lungs where it picks up oxygen
  • Blood returning from the lungs enters the left side of the heart
  • The left ventricle pumps that blood through the arteries to the body
  • CHF is not a specific diagnosis, but is a result of another underlying condition. Finding the underlying condition is important because the treatment often depends on what that condition is. Many conditions can lead to CHF:

    • High blood pressure (hypertension) increases the work of the heart. The heart has to pump blood against higher resistance and must therefore generate more force. The added strain on the heart muscle can cause failure. This is one of the most common causes of CHF in the United States.
    • Coronary artery disease causes ischemia, inadequate oxygen supply to the heart muscle, which can damage or destroy heart muscle tissue, leading to failure. Coronary artery disease is the other most common cause of CHF in the United States.
    • Valvular heart disease causes improper blood flow through the heart, which increases the heart's workload. There are three main types of faulty heart valves:

    Narrow (stenotic) valves restrict the flow of blood. To generate enough pressure to pump blood through a narrow valve, the heart has to work much harder.
    Leaky (regurgitant) valves
    allow blood to flow back through after it has been pumped out. The heart must pump more blood with each heartbeat (the blood coming in normally plus blood leaking back), greatly increasing its workload.
    Endocarditis is an infection of the heart valves that can damage them.

    • Abnormal heart rhythms (arrhythmias) interrupt the normal filling and pumping cycle. If the heart beats too slow (bradycardia), then not enough blood gets pumped out. If the heart beats too fast (tachycardia), then there is not enough time for the heart to fill with blood. In either case, cardiac output is reduced causing the heart to fail.
    • Overactive thyroid gland (hyperthyroidism) increases the overall rate of metabolism in the body. The heart must circulate blood more frequently so that the body's tissues get an adequate amount of oxygen. This increased work can cause the heart to fail.
    • A severe decrease in red blood cells (anemia) reduces the supply of oxygen in circulated blood (blood cells carry oxygen). To provide adequate amounts of oxygen to bodily tissues, the heart must circulate blood more frequently. This extra work can cause the heart to fail.
    • Diseases that affect the heart muscle itself (cardiomyopathy) result in inadequate contraction of the heart. This decreases the cardiac output, which leads to CHF. Technically, cardiomyopathy only means diseases that originate and primarily affect the myocardium. However, many physicians also use the term in "ischemic cardiomyopathy," a condition resulting from the scarring caused by coronary artery disease. Diseases that cause cardiomyopathy include:

    Infections (viral, bacterial, AIDS, Lyme disease, rheumatic fever, etc.)
    Toxins (alcohol, cocaine, radiation, chemotherapy, etc.)
    Nutritional deficiencies (thiamine deficiency causing beri-beri)
    Connective tissue disorders (lupus, rheumatoid arthritis, etc.)
    Neuromuscular diseases (muscular dystrophy)
    Infiltrative (amyloidosis, sarcoidosis, cancer)
    Idiopathic (unknown)
    Peripartum cardiomyopathy

    • Diseases that affect the pericardium (the sac surrounding the heart) restrict the ability of the heart to stretch when it fills. The filling is reduced, thereby diminishing cardiac output. A thickened or scarred sac (constrictive pericarditis) or fluid within the sac (pericardial tamponade) both reduce the ability of the heart to fill.
    • Birth defects in the formation of the heart (congenital heart disease) produce an additional workload on the heart eventually causing it to fail. These defects involve abnormal formation of the walls between different chambers of the heart (hole in the heart), abnormal formation of the heart valves, or abnormal positions of the blood vessels that bring blood to or from the heart.


    Precipitating Factors

    Many other factors, called precipitating factors, place an extra burden on a failed heart. Identifying the precipitating factor, as well as the initial cause of CHF, is important for directing proper treatment. Precipitating factors include:
    • Stopping prescribed medications
    • Excessive intake of fluids or salt
    • Uncontrolled hypertension
    • Infection
    • Heart attack
    • Ischemia (lack of blood to heart muscle)
    • Cardiac arrhythmia (abnormal heart rhythm)
    • Anemia
    • Pulmonary embolus (blood clot in lung)
    • Hyperthyroidism (overactive thyroid)
    • Hypoxia (low level of oxygen in blood usually due to lung disease)
    • New heart valve malfunction

    CHF often develops slowly over many years. As the heart fails, the body compensates to maintain the cardiac output and blood flow to the organs. Although these compensatory mechanisms are useful, they often cause further heart damage and worsen CHF. This compensation usually delays the development of CHF symptoms.

    Sympathetic Nervous System
    The sympathetic nervous system is part of the autonomic nervous system, which works at the subconscious level and controls the workings of many organs (e.g., heart, blood vessels, glands, intestines and bladder). Sympathetic nerves secrete a chemical called norepinephrine, which belongs to a class of chemicals called catecholamines or adrenergics. Norepinephrine binds to different receptors on various organs and can have a number of effects on those organs. These receptors are:
    • Alpha-adrenergic receptors These receptors constrict blood vessels (arteries, veins) and enlarge (dilate) pupils.
    • Beta-1-adrenergic receptors These receptors increase both the heart's rate and the force of the heart's contraction.
    • Beta-2-adrenergic receptors These receptors dilate both cardiac blood vessels and bronchial air passages.

    When the heart begins to fail, the first thing the body does is activate the sympathetic nervous system. Sympathetic nerve stimulation increases the heart rate and the force of contraction and constricts the body's veins. These factors work together to increase cardiac output. However, sympathetic nerve stimulation also constricts arteries, which increases blood pressure. The increase in pressure forces the heart to work harder and use more oxygen, which is thought to cause further deterioration of the heart over time.

    The body then decreases the blood flow to the kidneys. This activates the renin-angiotensin-aldosterone system. The decreased blood flow causes the kidney to release an enzyme called renin. Renin converts an inactive plasma protein, angiotensinogen, into an active hormone called angiotensin II. Angiotensin II is a powerful constrictor of both arteries and veins and stimulates the adrenal gland to secrete a hormone called aldosterone. Aldosterone causes the kidneys to retain salt and water which increases blood volume. The increased blood volume helps to maintain cardiac output by increasing the filling of the heart. However, the increased blood volume, along with the vasoconstriction, also increases blood pressure. This increased pressure causes edema and an increased workload, which may further weaken the heart.

    The body also increases the secretion of a hormone in the pituitary gland called anti-diuretic hormone (ADH). This causes the kidney to retain more fluid, which increases blood volume and helps cardiac output, but also increases blood pressure, which makes the weakened heart work even harder.

    There are also changes in the heart muscle itself. The thickness of the muscle layer increases (hypertrophy), enabling the heart to contract with greater force to maintain cardiac output. This increases the need for oxygen, however, and eventually leads to further deterioration. The heart can also enlarge by stretching and thinning its walls (dilation). Initially this may help increase output by increasing the amount of blood that the heart can hold, but the dilation eventually fails and leads to further worsening of the disease.


    Symptoms of Congestive Heart Failure

    • Shortness of breath or difficulty breathing (dyspnea) This is the most common symptom of CHF and is caused by pulmonary edema. Many different types of dyspnea may be encountered:

    Shortness of breath only with exertion (dyspnea on exertion) -- As the disease progresses, the amount of exertion needed to produce dyspnea becomes less.

    Shortness of breath while at rest

    Shortness of breath when lying down (orthopnea) -- When lying down, blood from the elevated legs returns to the heart and causes pulmonary edema. Sitting up usually repeves this symptom. Many people sleep on several pillows to avoid this effect. As the disease progresses, some people even need to sleep sitting in a chair.

    Intermittent shortness of breath at night (paroxysmal nocturnal dyspnea) -- This is caused by pulmonary edema and by depression of breathing during the sleep state.

    • Cough
    • Edema This occurs most often in the legs. Edema in the legs usually increases during the day because gravity increases the amount and pressure of blood in the veins of the leg, which pushes more fluid out. It improves at night when the legs are elevated. Edema is usually treated with diuretics (fluid pills) to eliminate the excess fluid. Edema can occur in many other areas, including the abdominal cavity, the space between the lungs and the chest cavity, the pericardium, and the stomach and intestines (causing nausea and loss of appetite).
    • Weight gain Fluid retention often increases a CHF sufferer's weight.
    • Fatigue This is a common symptom and may be related to reduced blood flow to many of the organs and muscles. Occasionally, CHF may reduce blood flow to the brain and cause confusion, especially in the elderly.
    • Chest pain This is a symptom of angina and heart attacks, both leading causes of CHF.
    • Acute pulmonary edema This is a severe and abrupt onset or worsening of CHF. This condition leads to a dangerously low level of oxygen in the blood, which can be life threatening. Symptoms of acute pulmonary edema include severe shortness of breath, a cough that is sometimes blood tinged (hemoptysis), profuse sweating, and anxiety. Acute pulmonary edema must be treated immediately.

    CHF Symptoms and Associated Physical Activity
    • Class 1: Physical activity is not limited. Symptoms are nonexistent or mild.
    • Class 2: Physical activity is limited slightly. Symptoms are mild to moderate with activity but at a comfortable level while at rest.
    • Class 3: Physical activity is markedly limited. Symptoms are moderate to severe.
    • Class 4: Any physical activity causes discomfort. Symptoms are severe and may be present at rest.

    Source: New York Heart Association

    When a physician examines someone with CHF, he or she may find the following:

    • Enlargement of the heart (cardiomegaly)
    • A third heart sound (S3) -- Normally, the heart makes two sounds (S1 and S2) often described as "lub dub, lub dub." In CHF there is a third sound, which is also called an S3 gallop because the three sounds are reminiscent of a horse galloping.
    • Sound of fluid in the lungs during inspiration (Rales)
    • Enlargement of the jugular vein in the neck (jugular venous distention) -- This occurs because CHF causes an increase in the amount of blood and pressure in veins.
    • Enlargement of the liver (hepatomegaly) -- This is caused by a back-up of blood from the heart.
    • Hepatojugular reflex -- When the liver is depressed, more blood travels into the jugular veins, causing them to become even more enlarged.
    • Edema -- This is usually located in the legs, ankles, feet. The term "pitting edema" is often used because applying slight fingertip pressure produces a temporary pit which resolves quickly.
    • Fast heart rate (tachycardia)
    • Increased rate of breathing (tachypnea)
    • High blood pressure (hypertension)
    • Low blood pressure (hypotension) -- When the cardiac output is severely decreased, then low blood pressure occurs. This is obviously an ominous sign and may mean death is imminent. This is also called cardiogenic shock.
    • Fluid in the abdominal cavity (ascites)
    • Fluid in the space between the lungs and the ribs (pleural effusion)

    The following are useful diagnostic tests for CHF:

    • A chest X-ray (CXR) is a very useful test in CHF. It can detect pulmonary edema, an enlarged heart and pleural effusion.
    • An electrocardiogram (EKG) is helpful because it can detect the presence of a heart attack, cardiac ischemia, abnormal heart rhythms or an enlarged heart.
    • An echocardiogram can determine the amount of blood ejected from the heart with each heartbeat (ejection fraction). An ejection fraction is a way to quantify how well or efficient the heart is beating and to determine the severity of CHF. Normally, the ejection fraction is 55 to 75 percent. In addition, an echocardiogram can help determine the cause of CHF by detecting heart valve abnormalities, pericardial abnormalities, congenital heart disease or an enlarged heart. An echocardiogram can show if the heart is contracting abnormally (wall motion abnormalities), which is a sign of coronary artery disease.


    Treatment of CHF

    The goal of treatment in CHF is to control the symptoms and treat the underlying cause as well as the precipitating cause. Before prescribing medications, your physician may want you to lose weight and stop smoking. These measures may reduce the workload on the heart as well as control some of the causes of CHF (high blood pressure, coronary artery disease). In addition, reducing the intake of salt and water can improve symptoms and may reduce the need of some medications. Exercise may be helpful to improve overall fitness. However, when CHF is severe, bed rest may be required.


    Diuretics (water pills) are medications used to increase the amount of sodium (Na+) and water excreted by the kidneys. This reduces the blood volume and the amount of blood that the heart has to pump, thereby reducing its workload. The goal is to maintain ideal weight by eliminating edema. Diuretics include:

    • hydrochlorothiazide
    • chlorothalidone
    • metalazone (Zaroxolyn)
    • furosemide (Lasix)
    • bumetanide (Bumex)
    • trimeratene
    • spironolactone

    A major side effect is a low potassium (K+) level, which can cause muscle cramping and abnormal heart rhythms. Potassium supplements or potassium-sparing diuretics can be used either alone or in combination with other diuretics.

    Vasodilators are groups of medications that dilate or enlarge blood vessels. During CHF, the blood vessels are often constricted due to the activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system. When vasodilators are used, they decrease the resistance and blood pressure against which the heart must beat, thus increasing the cardiac output. Angiotensin converting enzyme inhibitors (ACE inhibitors) are very effective vasodilators. This is one of the few medications that have actually been shown to prolong life in CHF patients. ACE inhibitors reduce blood pressure and fluid retention by preventing the renin-angiotensin-aldosterone system from working. ACE inhibitors include:

    • captopril (Capoten)
    • enalapril (Vasotec)
    • lisinopril (Zestril, Prinivil)
    • benazepril (Lotensin)
    • fosinopril (Monopril)
    • quinapril (Accupril)

    Side effects include cough and occasionally a rash.

    Angiotensin receptor blockers block the effects of angiotensin instead of blocking its production. Angiotensin receptor blockers include:

    • losartan (Cozaar)
    • irbesartan (Avapro)
    • valsartan (Diovan)

    These medications do not cause the side effect of cough produced by ACE inhibitors.

    Nitroglycerin dilates veins and can be taken under the tongue (Nitrostat), intravenously, by mouth (Isosordil, Sorbitrate, ISMO), or by skin patches (Nitro-Dur, Transderm-Nitro). 

    Calcium channel blockers dilate blood vessels and are sometimes used to treat CHF, especially when ischemia is present. These drugs also tend to decrease the force of the heart's contraction, however, and so can worsen CHF. Calcium channel blockers include:

    • nifedipine (Procardia XL, Adalat CC)
    • diltiazem (Cardizem)
    • verapamil (Calan, Isoptin)
    • amlodipine (Norvasc)
    • felodipine (Plendil)
    • nisoldipine (Sular)

    Side effects include low blood pressure, headache, edema, and constipation. 

    Hydralazine is a vasodilator that acts on arteries. It is used less frequently since ACE inhibitors have been found to be more effective.

    Alpha blockers block the alpha-adrenergic receptors of the sympathetic nervous system, thereby dilating blood vessels. Alpha blockers include prazocin (Minipress) and doxazosin (Cardura). Side effects include rapid heartbeat and low blood pressure. 

    Digitalis medications (digoxin, Lanoxin) increase the force of contraction of the heart muscle and also control abnormal heart rhythms, especially atrial fibrillation and atrial flutter. Therefore, digitalis is most useful when someone with atrial fibrillation or atrial flutter has CHF (a fairly common scenario). It improves heart function without increasing mortality. It has many side effects, including nausea, vomiting, many types of abnormal heart rhythms, confusion and negative interactions with other medications.

    Beta blockers have been found to be useful for CHF. By blocking the beta-adrenergic receptors of the sympathetic nervous system, the heart rate and force of contraction are decreased. Of course, this must be done carefully because decreasing these two things can actually worsen CHF. Beta blockers include:
    metoprolol (Lopressor, Toprol-XL) atenolol (Tenormin) carvedilol (Coreg) 

    Sympathomimetic medications act similarly to the sympathetic nervous system and are used when CHF is severe, such as in cardiogenic shock. They treat CHF by increasing the force of the heart's contraction. Sympathomimetic drugs include dopamine (Inotropin) and dobutamine (Dobutrex). Because they must be taken intravenously and are extremely strong, these medications are used mainly when CHF has become life threatening. They can cause abnormal heart rhythms and ischemia.

    Occasionally, there are circumstances when surgery can treat CHF. The most common surgical procedures are:

    • Heart valve replacement When a heart valve malfunctions, valve replacement can reverse the symptoms. In some cases, this can be a life-saving procedure. 
    • Congenital heart defect correction Surgical repair of congenital heart defects is frequently used to restore normal functioning as much as possible.
    • Coronary artery bypass If Coronary artery disease (CAD) is the cause of CHF, then correcting the CAD with coronary artery bypass grafts can be useful.
    • Heart transplant When CHF persists and worsens despite maximum therapy, then a heart transplant can be an option. Patients considered for transplants usually suffer from severe symptoms (Class 4 on the New York Heart Association's scale), have ejection fractions of 15 to 20 percent and have one year survival rates of 50 percent. The improvement in anti-rejection drugs (especially cyclosporine) have increased survival from this procedure. There are also some devices that assist the severely failed heart, such as an intra-aortic balloon pump and a left ventricular assist device. These are used as bridges to keep a person alive until a donor heart can be found.


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    About the Author
    Carl Bianco, M.D., is an emergency physician practicing at Dorchester General Hospital in Cambridge, MD, located on the Eastern Shore of Maryland. Dr. Bianco attended Medical school at Georgetown University School of Medicine and received his undergraduate degree from Georgetown University majoring in nursing and pre-med. He Completed an internship and residency in Emergency Medicine at Akron City Hospital in Akron, Ohio.