Congestive heart failure (CHF) is a condition in which the heart's function as a pump is inadequate to deliver oxygen rich blood to the body. Congestive heart failure can be caused by:
The heart has two atria (right atrium and left atrium) that make up the upper chambers of the heart, and two ventricles (left ventricle and right ventricle) that make up the lower chambers of the heart. The ventricles are muscular chambers that pump blood when the muscles contract. The contraction of the ventricle muscles is called systole.
Many diseases can impair the pumping action of the ventricles. For example, the muscles of the ventricles can be weakened by heart attacks or infections (myocarditis). The diminished pumping ability of the ventricles due to muscle weakening is called systolic dysfunction. After each ventricular contraction (systole) the ventricle muscles need to relax to allow blood from the atria to fill the ventricles. This relaxation of the ventricles is called diastole.
Diseases such as hemochromatosis (iron overload) or amyloidosis can cause stiffening of the heart muscle and impair the ventricles' capacity to relax and fill; this is referred to as diastolic dysfunction. The most common cause of this is longstanding high blood pressure resulting in a thickened (hypertrophied) heart. Additionally, in some patients, although the pumping action and filling capacity of the heart may be normal, abnormally high oxygen demand by the body's tissues (for example, with hyperthyroidism or anemia) may make it difficult for the heart to supply an adequate blood flow (called high output heart failure).
In some individuals one or more of these factors can be present to cause congestive heart failure. The remainder of this article will focus primarily on congestive heart failure that is due to heart muscle weakness, systolic dysfunction.
Congestive heart failure can affect many organs of the body. For example:
Eventually, untreated, worsening congestive heart failure will affect virtually every organ in the body.
Many disease processes can impair the pumping efficiency of the heart to cause congestive heart failure. In the United States, the most common causes of congestive heart failure are:
Less common causes include viral infections of the stiffening of the heart muscle, thyroid disorders, disorders of the heart rhythm, and many others.
It should also be noted that in patients with underlying heart disease, taking certain medications can lead to the development or worsening of congestive heart failure. This is especially true for those drugs that can cause sodium retention or affect the power of the heart muscle. Examples of such medications are the commonly used nonsteroidal antiinflammatory drugs (NSAIDs), which include ibuprofen (Motrin and others) and naproxen (Aleve and others) as well as certain steroids, some medication for diabetes (such as rosiglitazone [Avandia] or pioglitazone [Actos]), and some calcium channel blockers.
The symptoms of congestive heart failure vary among individuals according to the particular organ systems involved and depending on the degree to which the rest of the body has "compensated" for the heart muscle weakness.
The diagnosis of congestive heart failure is most often a clinical one that is based on knowledge of the patient's pertinent medical history, a careful physical examination, and selected laboratory tests.
A thorough patient history may disclose the presence of one or more of the symptoms of congestive heart failure described above. In addition, a history of significant coronary artery disease, prior heart attack, hypertension, diabetes, or significant alcohol use can be clues.
The physical examination is focused on detecting the presence of extra fluid in the body (breath sounds, leg swelling, or neck veins) as well as carefully characterizing the condition of the heart (pulse, heart size, heart sounds, and murmurs).
Useful diagnostic tests include the electrocardiogram (ECG) and chest X-ray to detect previous heart attacks, arrhythmia, heart enlargement, and fluid in and around the lungs. Perhaps the single most useful diagnostic test is the echocardiogram, in which ultrasound is used to image the heart muscle, valve structures, and blood flow patterns. The echocardiogram is very helpful in diagnosing heart muscle weakness. In addition, the test can suggest possible causes for the heart muscle weakness (for example, prior heart attack, and severe valve abnormalities). Virtually all patients in whom the diagnosis of congestive heart failure is suspected should ideally undergo echocardiography early in their assessment.
Nuclear medicine studies assess the overall pumping capability of the heart and examine the possibility of inadequate blood flow to the heart muscle. Heart catheterization allows the arteries to the heart to be visualized with angiography (using dye inside of the blood vessels that can be seen using X-ray methods). During catheterization the pressures in and around the heart can be measured and the heart's performance assessed. In rare cases, a biopsy of the heart tissue may be recommended to diagnose specific diseases. This biopsy can often be accomplished through the use of a special catheter device that is inserted into a vein and maneuvered into the right side of the heart.
Another helpful diagnostic test is a blood test called a BNP or brain natriuretic peptide level. This level can vary with age and gender but is typically elevated from heart failure and can aid in the diagnosis, and can be useful in following the response to treatment of congestive heart failure.
The choice of tests depends on each patient's case and is based on the suspected diagnoses.
After congestive heart failure is diagnosed, treatment should be started immediately. Perhaps the most important and yet most neglected aspect of treatment involves lifestyle modifications. Sodium causes an increase in fluid accumulation in the body's tissues. Because the body is often congested with excess fluid, patients become very sensitive to the levels of intake of sodium and water. Restricting salt and fluid intake is often recommended because of the tendency of fluid to accumulate in the lungs and surrounding tissues. An American "no added salt" diet can still contain 4 to 6 grams (4000 to 6000 milligrams) of sodium per day. In individuals with congestive heart failure, an intake of no more than 2 grams (2000 milligrams) of sodium per day is generally advised. Reading food labels and paying close attention to total sodium intake is very important.
Likewise, the total amount of fluid consumed must be regulated. Although many people with congestive heart failure take diuretics to aid in the elimination of excess fluid, the action of these medications can be overwhelmed by an excess intake of water and other fluids. The maxim that "drinking eight glasses of water a day is healthy" certainly does not apply to patients with congestive heart failure. In fact, patients with more advanced cases of congestive heart failure are often advised to limit their total daily fluid intake from all sources to 2 quarts. The above guidelines for sodium and fluid intake may vary depending on the severity of congestive heart failure in any given individual and should be discussed with their physician.
An important tool for monitoring an appropriate fluid balance is the frequent measurement of body weight. An early sign of fluid accumulation is an increase in body weight. This may occur even before shortness of breath or swelling in the legs and other body tissues (edema) is detected. A weight gain of two to three pounds over two to three days should prompt a call to the physician, who may order an increase in the dose of diuretics or other methods designed to stop the early stages of fluid accumulation before it becomes more severe.
Aerobic exercise, once discouraged for congestive heart failure patients, has been shown to be beneficial in maintaining overall functional capacity, quality of life, and perhaps even improving survival. Each person's body has its own unique ability to compensate for the failing heart. Given the same degree of heart muscle weakness, individuals may display widely varying degrees of limitation of function. Regular exercise, when tailored to the person's tolerance level, appears to provide significant benefits and should be used only when the individual is compensated and stable.
Addressing potentially reversible factors
Depending on the underlying cause of congestive heart failure, potentially reversible factors should be explored. For example:
Until recently, the selection of medications available for the treatment of congestive heart failure was frustratingly limited and focused mainly on controlling the symptoms. Medications have now been developed that both improve symptoms, and, importantly, prolong survival.
Angiotensin Converting Enzyme (ACE) Inhibitors
ACE inhibitors have been used for the treatment of hypertension for more than 20 years. This class of drugs has also been extensively studied in the treatment of congestive heart failure. These medications block the formation of angiotensin II, a hormone with many potentially adverse effects on the heart and circulation in patients with heart failure. In multiple studies of thousands of patients, these drugs have demonstrated a remarkable improvement of symptoms in patients, prevention of clinical deterioration, and prolongation of survival. In addition, they have been recently been shown to prevent the development of heart failure and heart attacks. The wealth of the evidence supporting the use of these agents in heart failure is so strong that ACE inhibitors should be considered in all patients with heart failure, especially those with heart muscle weakness.
Possible side effects of these drugs include:
When used carefully with proper monitoring, however, the majority of individuals with congestive heart failure tolerate these medications without significant problems. Examples of ACE inhibitors include:
For those individuals who are unable to tolerate the ACE inhibitors, an alternative group of drugs, called the angiotensin receptor blockers (ARBs), may be used. These drugs act on the same hormonal pathway as the ACE inhibitors, but instead block the action of angiotensin II at its receptor site directly. A small, early study of one of these agents suggested a greater survival benefit in elderly congestive heart failure patients as compared to an ACE inhibitor. However, a larger, follow-up study failed to demonstrate the superiority of the ARBs over the ACE inhibitors. Further studies are underway to explore the use of these agents in congestive heart failure both alone and in combination with the ACE inhibitors.
Possible side effects of these drugs are similar to those associated with the ACE inhibitors, although the dry cough is much less common. Examples of this class of medications include:
Beta-blockers
Certain hormones, such as epinephrine (adrenaline), norepinephrine, and other similar hormones, act on the beta receptor's of various body tissues and produce a stimulative effect. The effect of these hormones on the beta receptors of the heart is a more forceful contraction of the heart muscle. Beta-blockers are agents that block the action of these stimulating hormones on the beta receptors of the body's tissues. Since it was assumed that blocking the beta receptors further depressed the function of the heart, beta-blockers have traditionally not been used in persons with congestive heart failure. In congestive heart failure, however, the stimulating effect of these hormones, while initially useful in maintaining heart function, appears to have detrimental effects on the heart muscle over time.
However, studies have demonstrated an impressive clinical benefit of beta-blockers in improving heart function and survival in individuals with congestive heart failure who are already taking ACE inhibitors. It appears that the key to success in using beta-blockers in congestive heart failure is to start with a low dose and increase the dose very slowly. At first, patients may even feel a little worse and other medications may need to be adjusted.
Possible side effects include:
Beta-blockers should generally not be used in people with certain significant diseases of the airways (for example, asthma, emphysema) or very low resting heart rates. While carvedilol (Coreg) has been the most thoroughly studied drug in the setting of congestive heart failure, studies of other beta-blockers have also been promising. Research comparing carvedilol directly with other beta-blockers in the treatment of congestive heart failure is ongoing. Long acting metoprolol (Toprol XL) is also very effective in individuals with congestive heart failure.
Digoxin
Digoxin (Lanoxin) has been used in the treatment of congestive heart failure for hundreds of years. It is naturally produced by the foxglove flowering plant. Digoxin stimulates the heart muscle to contract more forcefully. It also has other actions, which are not completely understood, that improve congestive heart failure symptoms and can prevent further heart failure. However, a large-scale randomized study failed to demonstrate any effect of digoxin on mortality.
Digoxin is useful for many patients with significant congestive heart failure symptoms, even though long-term survival may not be affected. Potential side effects include:
These side effects, however, are generally a result of toxic levels in the blood and can be monitored by blood tests. The dose of digoxin may also need to be adjusted in patients with significant kidney impairment.
Diuretics
Diuretics are often an important component of the treatment of congestive heart failure to prevent or alleviate the symptoms of fluid retention. These drugs help keep fluid from building up in the lungs and other tissues by promoting the flow of fluid through the kidneys. Although they are effective in relieving symptoms such as shortness of breath and leg swelling, they have not been demonstrated to positively impact long-term survival.
Nevertheless, diuretics remain key in preventing deterioration of the patient's condition thereby requiring hospitalization. When hospitalization is required, diuretics are often administered intravenously because the ability to absorb oral diuretics may be impaired, when congestive heart failure is severe. Potential side effects of diuretics include:
It is important to prevent low potassium levels by taking supplements, when appropriate. Such electrolyte disturbances may make patients susceptible to serious heart rhythm disturbances. Examples of various classes of diuretics include:
One particular diuretic has been demonstrated to have surprisingly favorable effects on survival in congestive heart failure patients with relatively advanced symptoms. Spironolactone (Aldactone) has been used for many years as a relatively weak diuretic in the treatment of various diseases. Among other things, this drug blocks the action of the hormone aldosterone.
Aldosterone has many theoretical detrimental effects on the heart and circulation in congestive heart failure. Its release is stimulated in part by angiotensin II (see ACE inhibitors, above). In patients taking ACE inhibitors, however, there is an "escape" phenomenon in which aldosterone levels can increase despite low levels of angiotensin II. Medical researchers have found that spironolactone (Aldactone) can improve the survival rate of patients with congestive heart failure. In that the doses used in the study were relatively small, it has been theorized that the benefit of the drug was in its ability to block the effects of aldosterone rather than its relatively weak action as a diuretic (water pill). Possible side effects of this drug include elevated potassium levels and, in males, breast tissue growth (gynecomastia).
Another aldosterone inhibitor is eplerenone (Inspra).
In some cases, despite the use of optimal therapies as described above, the patient's condition continues to deteriorate due to progressive heart failure. In selected patients, heart transplantation is a viable treatment option. Candidates for heart transplantation are generally under age 70 and do not have severe or irreversible diseases affecting the other organs. Additionally, a transplant is done only when it is clear that the patient's prognosis is poor with continued medical treatment of the heart condition. Transplant patients require close medical follow-up while taking the necessary drugs that suppress the immune system, and because of the risk of rejection of the transplanted heart. They also must be monitored for possible development of coronary artery disease in the transplanted heart.
Although there are thousands of patients on waiting lists for a heart transplant at any given time, the number of operations performed each year is limited by the number of available donor organs. For these reasons, heart transplantation is a realistic option in only a small subset of the large numbers of patients with congestive heart failure.
Given the limitations associated with heart transplantation, much attention has recently been directed towards the development of mechanical assist devices that are designed to assume part or all of the pumping function of the heart. There are several devices available for clinical use and many more are actively being developed. For instance, there are currently left ventricular assist devices that are approved for use as a temporary mode of circulatory support in very ill patients until a transplant can be performed. Studies examining the possible role of these mechanical assist devices on a long term basis as permanent self-contained implants are ongoing. The current major limitation of these devices is the risk of infection, especially at the site where the device exits the body through the skin to communicate with its external power source.
A less invasive modality, which can be placed without surgery, is the biventricular pacemaker. This device has proved valuable in appropriate types of patients with heart failure and impaired ventricles by improving the synchrony of contraction.
Congestive heart failure is generally a progressive disease with periods of stability punctuated by episodic clinical exacerbations. The course of the disease in any given individual, however, is extremely variable. Factors involved in determining the long term outlook (prognosis) for a given patient include:
With the availability of newer drugs to potentially favorably affect the progression of disease, the prognosis in congestive heart failure is generally more favorable than that observed just 10 years ago. In some cases, especially when the heart muscle dysfunction has recently developed, a significant spontaneous improvement is not uncommonly observed, even to the point where heart function becomes normal.
Heart failure is often graded on a scale of I to IV based on the patient's ability to function.
The prognosis of heart failure patients is very closely associated with the functional class.
An important issue in congestive heart failure is the risk of heart rhythm disturbances (arrhythmias). Of those deaths that occur in individuals with congestive heart failure, approximately 50% are related to progressive heart failure. Importantly, the other half are thought to be related to serious arrhythmias. A major advance has been the finding that nonsurgical placement of automatic implantable cardioverter/defibrillators (AICD) in individuals with severe congestive heart failure (defined by an ejection fraction below 30%-35%) can significantly improve survival, and has become the standard of care in most such individuals.
In some people with severe heart failure and certain ECG abnormalities, the left and right side of the heart don't beat in rhythm, and inserting a device called a biventricular pacer can significantly reduce symptoms.
Despite the significant advances in drug therapy for congestive heart failure over the past 20 years, many exciting developments are under active study. New classes of medications are being tested in clinical trials, including the calcium sensitizing agents, vasopeptidase inhibitors, and natriuretic peptides. As was the case with the ACE inhibitors and beta-blockers, the potential use of these drugs is based on theoretical considerations that have resulted from an increased understanding of the processes both underlying and resulting from heart failure. Additionally, gene therapy that is targeted toward certain genes thought to contribute to heart failure is being tested.
These developments have justified an unprecedented optimism in the treatment of congestive heart failure. The majority of individuals, with appropriate lifestyle measures and medical regimens, can maintain active, fulfilling lifestyles. The range of treatment options has been significantly strengthened by drugs such as the ACE inhibitors and beta-blockers. In the future, we will surely see the addition of many more and equally potent interventions.
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