What is heart failure? |

Causes and Symptoms

The circulation of the blood has many functions. It is essential for the delivery of oxygen, nutrients, and elements of the immune system to tissues. It also contributes to regulation and communication between different parts of the body by moving chemical messengers from where they are produced to where they have a biological effect. The delivery of warm blood to the surface of the skin is one essential element in temperature control. The blood pressure determines how much water can move across the exchange surfaces in the kidneys, thus affecting water balance in the body. The movement of blood through the kidneys, the lungs, and all tissues is important for waste removal.

All these functions depend on the ability of the heart to contract and eject blood. Blood is pumped, in two serial circuits, from the right heart through the lungs into the left heart and from the left heart around the body back to the right heart. In each circuit, the blood travels through large arteries, then to smaller arterioles, to capillaries (where exchange takes place), and back via small venules and veins to the heart. Heart failure describes the situation in which heart function is reduced. While still able to beat, the heart is unable to meet the circulatory needs of the body. That is, the heart muscle is unable to contract enough to pump the blood adequately.

The severity of the heart failure can be gauged by the ejection fraction, a measure of the pumping capacity of the heart. It is the percentage calculated from the stroke volume (the volume of blood leaving a heart chamber with each beat) divided by the residual volume (the volume left in the heart chamber at the end of a heartbeat). Thus, the ejection fraction measures how much blood in the heart chamber can actually leave when the heartbeat occurs. In normal, healthy hearts, this value is 100 percent: the amount that stays in the heart is approximately equal to the amount that leaves it. In mild or moderate heart failure, it ranges approximately between 15 and 40 percent: Less blood leaves the heart with each beat, and more blood remains behind.

The pressure inside the heart at the end of a heartbeat is another index of heart performance. If the heart is failing and more blood is left behind in the heart at the end of a beat, the pressure inside the heart at the end of the beat will be increased. In cases of severe failure, the pressure in the arteries outside the heart will fall.

In failure, the heart cannot supply enough blood for all the functions of the circulation. This fact accounts for the variety of symptoms that accompany heart failure: labored breathing; light-headedness; generalized weakness; cold, pale, or even bluish skin tone; and accumulation of fluid in the extremities and/or lungs. Other possible symptoms include distended neck veins, accumulation of fluid in the abdomen, abnormal heart rate and rhythm, and chest pain.

The specific symptoms of the condition depend on the type of failure, its severity, its underlying causes, and the ways in which the body attempts to compensate. There are several ways to categorize types of heart failure: acute or chronic, forward or backward, and right-sided or left-sided.

Acute heart failure refers to a sudden decrease in heart function. It can be caused by toxic quantities of drugs, anesthetics, or metals or by certain disease states, such as infections. Most often, however, it is caused by a sudden blockage of the coronary arteries supplying the heart muscle. A sudden blockage caused by a blood clot can induce a heart attack and subsequent heart failure, causing chest pain and often abnormal heart rate or rhythm. These effects are sometimes so rapid that there is little time for the body to attempt compensation.

Chronic heart failure is a progressive reduction in heart function that develops over time. It can be caused by inherited or acquired diseases, allergic reactions, connective tissue or metabolic abnormalities, high blood pressure, and anatomical defects. The most common cause, however, is coronary artery disease. This disease narrows blood vessels and leads to a reduction in the amount of blood reaching the heart muscle. It causes reduced oxygen availability and, eventually, a reduction in the ability of the heart muscle to contract.

In the early stages of chronic failure, the hormone and nervous systems promote compensation in the heart, blood vessels, and kidneys to help the heart continue to pump enough blood. These systems stimulate the heart muscle directly to make it beat harder. They also take advantage of the fact that modest stretching of the heart muscle increases its ability to contract. By stimulating the blood vessels to contract, more blood moves back toward the heart, causing a cold, pale, or even bluish skin tone. Stimulation of the kidney to retain water and sodium results in an increase in blood volume, which also moves more blood back to the heart. In each case, the heart muscle is stretched by these increases and, therefore, can contract harder.

Yet these reactions do not constitute a long-term solution. The heart muscle can become fatigued from overwork and can become overstretched. A resulting accumulation of fluid in the heart reduces its ability to contract. Compensation fails, and the additional fluid in the blood starts to back up in the circulation. This condition is called backward heart failure. At the same time, the heart is unable to pump hard enough to move the blood forward against the higher resistance caused by the contraction of the blood vessels. This condition is termed forward heart failure. Congestive heart failure is the stage that occurs when the backup of pressure is worsened by fluid retention and blood vessel contraction. The congestion, or accumulation of fluid, occurs in the veins and tissues.

Left-sided or right-sided heart failure can occur alone or together. The right side of the heart pumps blood to the lungs to be oxygenated, and the left side of the heart pumps oxygenated blood to the organs of the body. Normally, these two sides are well matched so that the same volume moves through each side. When the right heart cannot contract properly, however, blood accumulates upstream in the veins and somewhat less blood reaches the lungs to pick up oxygen, resulting in distended veins and shortness of breath. It is primarily a backward heart failure. Fluid can back up in the veins and increase pressure in the capillaries so that it starts to leak out of the circulation into the surrounding tissues. This leads to an accumulation of fluid (called
edema), especially in the liver and lower extremities. In isolated right-sided heart failure, this pressure rarely backs up to such an extent that it causes problems through the rest of the circulation to the left side of the heart.

In contrast, when the left side of the heart cannot contract properly, it can back up pressure so badly that it creates a pressure overload against which the right side of the heart must pump. This increase in the workload on the right side of the heart frequently leads to two-sided heart failure. This outcome is especially common since the disease conditions that exist in the left side are likely to exist on the right as well. In left-sided heart failure, blood accumulates upstream in the lungs, increasing pressure enough to cause a leakage of fluid into the lungs (pulmonary edema). This leakage interferes with oxygen uptake and therefore causes shortness of breath. It also results in inadequate blood flow to the body’s tissues, including the muscles and brain, resulting in generalized weakness and light-headedness. Left-sided heart failure is thus both a backward and a forward failure.

Treatment and Therapy

Treatments for cardiac failure, like its symptoms, depend on a variety of factors. The first goal of treatment is to avoid any obvious precipitating causes of the failure, such as alcohol, drugs, the cessation of nonessential medications, acute stress, a salt-loaded diet, overexercise, infection, illness, or surgery. The next approach is to take the simplest measures to reduce distension of the heart by controlling salt and water retention and to decrease the workload of the heart by altering the circulatory needs of the tissues. The former can be achieved by dietary salt restriction, restriction of fluid consumption, or mechanical removal of fluid accumulating around the lungs or abdomen. The latter can be accomplished with bed rest and weight loss.

Typically, drug therapy is also required in order to treat heart failure. No single agent meets all the requirements for optimal treatment, which includes rapid relief of labored breathing and edema, enhanced heart performance, reduced mortality, reduced progression of the underlying disease, safety, and minimal side effects. Therefore, drugs are used in combination to achieve control over sodium and water retention, improve heart contraction, reduce heart work, and protect against blood clots.

The purpose of therapy with diuretic drugs (drugs that increase salt and water loss through the kidneys) is threefold: to reduce the pooling of fluid that can take place in the lungs, abdomen, and lower extremities; to minimize the buildup of back pressure from the accumulation of blood in the veins; and to reduce the circulating blood volume. All these things will lessen the overstretch of the heart muscle and bring it to a level of stretch that is closer to its optimum. Care must be taken, however, not to reduce severely the water content of the blood, which could reduce the stretch on the heart muscle to below the optimum and consequently impair heart contraction. One way to monitor how much water is lost or retained is for patients to empty their bladders and then weigh themselves each day before breakfast. If weight changes steadily or suddenly, then sodium and water loss may be too great or too little. In either case, an adjustment is in order. Some generic diuretic drugs used to treat heart failure include furosemide, ethacrynic acid, the thiazides, and spironolactone.

The purpose of therapy with inotropic drugs (drugs that increase the contractile ability of heart muscle) is to improve the pumping action of the heart. This effect causes an increase in stroke volume (more blood moves out of the heart per beat) and helps compensate for forward failure. The increased output also reduces the backup of blood returning to the heart and thus also compensates for backward failure.

Digitalis, a derivative of the foxglove plant which originated as a Welsh folk remedy, is still the most frequently used inotropic drug for the treatment of chronic heart failure. Because it improves heart muscle contraction, it reverses to some extent all the symptoms of heart failure. Digitalis exerts its effects by increasing the accumulation of calcium inside the heart muscle cells. Calcium interacts with the structure of the shortening apparatus inside the cell to make more contractile interactions within the cell possible. Its disadvantages are that it becomes toxic in high doses and that it can severely damage performance of an already healthy heart.

Other inotropic agents also act to improve contraction by increasing calcium levels within the heart muscle cells. Some of them mimic the naturally produced hormones and neurotransmitters that are released and depleted in early stages of heart failure. These are called the sympathomimetic drugs. They include drugs such as dopamine, terbutaline, and levodopa. While these drugs improve heart performance, they can have serious side effects: increased heart rate, palpitations, and nervousness. One group of inotropic agents improves cardiac contraction while relaxing blood vessels. These drugs, called phosphodiesterase inhibitors, stop the breakdown of an essential cellular messenger molecule which helps to manage calcium levels and other events inside both heart cells and blood vessel cells. Examples of these drugs include amrinone and milrinone. Their use is not common because they can cause stomach upset and fatigue and because they are not clearly superior to other treatments.

The purpose of therapy with
vasodilator drugs (drugs that relax the blood vessels) is to decrease the work of the heart. The resulting expansion of the blood vessels makes it easier for blood to be pumped through them. It also leaves room for pooling some of the blood in the veins, decreasing the amount of blood returning to the heart and so reducing overstretching as well. Some of the vasodilators, such as hydralazine, pinacidil, dipyridamole, and the nitrates, act directly on the blood vessels. Other vasodilators, such as angiotensin-converting enzyme (ACE) inhibitors and adrenergic inhibitors, inhibit the release of naturally produced substances that would make the blood vessels contract. Sometimes it is hard to predict the effects of vasodilators because they may act differently in different blood vessels and the body may attempt to offset the effects of the drug by releasing substances that contract blood vessels. Vasodilator drug therapy is usually added to other treatments when the symptoms of heart failure persist after digitalis and diuretic therapy are used.

The purpose of therapy with antithrombotics (blood clot inhibitors) is to prevent any further obstruction of the circulation with blood clots. Because heart failure changes the mechanics of blood flow and is the result of damaged heart muscle, it can increase the formation of blood clots. When blood clots form an obstruction in the large blood vessels of the lungs, it is often fatal. Clots can also lodge in the heart, causing further damage to heart muscle, or in the brain, where they could cause a stroke. Both the short-acting clot inhibitor heparin and oral agents such as aspirin are used to prevent these effects.

The combination of all these drug therapies, while unable to reverse the permanent damage of heart failure, makes it possible to treat the condition. Individuals treated for heart failure can lead comfortable, productive lives.

If the heart failure progresses to acutely life-threatening proportions and the patient is in all other ways healthy, the next alternative is surgical
replacement of the heart. Artificial hearts are sometimes used as a transition to heart transplant while a donor is sought. Yet transplantation is not a perfect solution. Transplanted hearts do not have the nervous system input of a normal heart and so their control from moment to moment is different. They are also subject to rejection. Nevertheless, they provide an enormous improvement in quality of life for severe heart failure patients.

Perspective and Prospects

The vital significance of the pulse and heartbeat have been part of human knowledge since long before recorded history. Pulse taking and herbal treatments for poor heartbeat have been recorded in ancient Chinese, Egyptian, and Greek histories. Digitalis has been used in treatment for at least two hundred years. It was first formally introduced to the medical community in 1785 by the English botanist and physician William Withering. He learned of it from a female folk healer named Hutton, who used it with other extracts to treat more than one kind of swelling. Withering identified the foxglove plant as the source of its active ingredient and characterized it as having effects on the pulse as well as on fluid retention. The plant is indigenous to both the United Kingdom and Europe and may well have been employed as a folk remedy for far longer.

The developments in physiology and medicine during the nineteenth century set the stage for greater understanding and further treatments of heart failure. It was then that the stethoscope and blood pressure cuff were created for diagnostic purposes. In basic science, cell theory, hormone theory, and kidney physiology led to a better understanding of how heart muscle contraction and fluid balance might be coordinated in the body. The concepts and techniques required to keep organs and tissues alive outside the body with an artificial circulation system were conceived and introduced. Anesthesia and sterile techniques essential for cardiac surgery were developed.

These ideas and accomplishments contributed to important discoveries in the early twentieth century that greatly enhanced the understanding of the early compensatory responses to heart failure. For example, it was found that when heart muscle is stretched, it will contract with greater force on the next beat and that heart muscle usually operates at a muscle length that is less than optimal. Thus, when the amount of blood returning to the heart increases and stretches the muscle in the walls of the heart, the heart will contract with greater force, ejecting a greater volume of blood. This phenomenon, called the Frank-Starling mechanism, was first demonstrated in isolated heart muscle by the German physiologist Otto Frank and in functional hearts by the British physiologist Ernest Henry Starling in 1914.

Subsequent developments in the second half of the twentieth century, such as more specific vasodilator and diuretic drugs as well as the heart-lung machine, have led to the options of more complete drug therapy, artificial hearts (first introduced to replace a human heart by William DeVries in 1982), and heart transplant (first performed by Christiaan Barnard in 1967) as options for the treatment of heart failure. Researchers have begun clinical trials to assess the viability of using gene therapy for increasing blood flow in patients with advanced heart failure. Though treating heart failure is an ongoing challenge for the medical profession, diagnosing the ailment is becoming easier than before through preventative methods such as annual blood tests and breath tests, findings for the latter of which were published in the Journal of the American College of Cardiology in 2013. Furthermore, ongoing stem-cell research may lead to greater advances in the treatment of heart failure.

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