Congestive Heart Failure: Treating Failure (FL INITIAL Autonomous Practice - Differential Diagnosis)

Pathophysiology is the cascade of changes caused in a person by a disease process, in this instance, congestive heart failure. Heart failure commonly begins with an insult to the cardiac tissue such as occurs in an ischemic heart attack where blood flow to the heart muscle itself is blocked or drastically reduced. Heart cells (myocytes) die as a result of necrosis from this traumatic insult. The body's first response is to highly activate the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system in an effort to compensate for functional losses due to tissue death.² Up to this point, systems are functioning well, an orderly transient emergency boost during a time of high demand on affected and supportive tissues. The dysfunction begins when these emergency systems fail to disengage and become hyper-activated creating a cascade of ill-considered neurohormonal changes.

Hyperactive neurohormonal systems cause additional cell damage, including an increase in programmed cell death called apoptosis. Apoptosis is the method by which normal cells disengage and disintegrate when they reach the preprogrammed end of their lifespan. Cellular losses further weaken the heart and cause an intricate process known as heart remodeling to occur. Remodeling occurs when body structures change shape and/or function. In this instance, affected heart cells begin to structurally enlarge and stretch out of shape in an attempt to strengthen the weakened heart. This leads to improper gene production (expression), which stimulates further neurohormonal hyperactivity leading to increasing cellular damage and death. The eventual result is the death of the host, through pump failure, meaning the heart simply gives out.

Heart failure is not just a problem with blood flow. It is a complex disease process and includes a cascade of effects which occur even at a genetic level.

In the hemodynamic model of heart failure which provides the standard of care and treatment, there are many causes of congestion and myocardial failure. Once the heart is damaged for any reason, the same series of events almost always takes place.

When the heart muscle is damaged, cardiac output decreases which stimulates the nervous system to compensate. When blood flow through the kidneys is decreased, the juxtaglomerular cells in the kidneys secrete renin into the blood. In addition, sympathetic nerves signal directly to the juxtaglomerular cells causing these cells to release renin, whenever the sympathetic nervous system becomes activated. Renin itself via a complex chemical reaction releases a decapeptide called angiotensin I. Within a few seconds after the formation of angiotensin I, it is converted into angiotensin II almost entirely in the small vessels of the lungs.

Angiotensin II is a very strong vasoconstrictor of the arterioles and to a lesser extent the veins. Constriction of the arterioles increases the peripheral resistance and thereby raises the arterial pressure back towards normal which elevates the arterial blood pressure. Angiotensin II has a direct effect on the kidneys to cause decreased excretion of both salt and water. Angiotensin II also stimulates the secretion of aldosterone by the adrenal cortex which acts on the kidneys to cause decreased excretion of both salt and water. Both of these effects tend to elevate the blood volume thus increasing the arterial blood pressure.²

At first, these emergency compensatory mechanisms serve to sustain life. Vasoconstriction elevates the arterial blood pressure. Retaining salt and water increases the blood volume thus elevating cardiac output. Epinephrine (adrenaline) levels skyrocket, speeding up the heart, which boosts its cardiac output accordingly. This helps the heart keep up with the body's demands for oxygenated blood. However, after these compensatory mechanisms have been running for a while, the positive effects become harmful. The heart ends up working much harder than it is designed to do, and it begins to wear out, getting weaker. The weakness translates with time into the physical changes found in heart failure. This is the "standard" concept of CHF's vicious cycle.

Any number of things can cause the heart to weaken structurally, and this leads to the steps that compose the standard concept of CHF pathophysiology. The neurohormonal concept of heart failure takes up where the standard concept leaves off. In this concept, emphasis is placed on the hyperactivity of chemical messengers called neurohormones, which are busy wreaking havoc on the cellular structure of the weakened heart.²

One mechanism by which the body tells the heart what to do is by way of chemical messengers called neurohormones. These neurohormones travel through the bloodstream until they find a receptor they are attracted to. These receptors are located on the walls of cells, including heart cells. When a neurohormone finds a receptor it matches, it attaches to it. Each type of neurohormone has receptors designed just for it. When a neurohormone connects with a receptor, it has an effect on the cell. When too many of these neurohormones are active, it can dramatically change the function of the heart.³

The heart cell activity caused by these hyperactive neurohormones makes blood vessels narrower, increasing pressure. This places extra strain on the heart by 1) speeding it up too much; 2) reducing proper functioning of the cells lining the blood vessels, and 3) telling the body to retain sodium instead of filtering it out by the kidneys. All of these changes combine to result in edema. One particular neurohormone produced when the heart is weak, norepinephrine, is in itself directly toxic to heart cells.

Remodeling is a part of the neurohormonal saga in congestive heart failure. While the classic heart failure model also incorporates the process of remodeling as a sequela of tissue traumatization, the neurohormonal model helps put in place foundational effects throughout the body which contribute to the structural changes. Remodeling, in general, is the process by which the body changes the shape and/or function of an organ or bodily structure. In heart failure a structural change occurs in the shape of the left ventricle from triggers that the cells receive from the neurohormones. These structural changes result in the ventricular chamber becoming rounder and larger. Remodeling has direct effects on heart rhythm (electrical conduction) and on pumping strength. Most of us think of large muscles as making us stronger, like a bodybuilder; however, the heart does not work that way. In the enlarged heart, many things change, including changes in the chemicals produced by the body.

That brings us back to the subject of neurohormones. These chemical messengers cause the release of even more messengers through a process called gene expression. The most common expression is an atrial natriuretic peptide (ANP).³ An elevated concentration of neurohormones such as ANP in the heart during CHF worsens the heart failure. ANP’s main function is to cause the body to eliminate salt through the kidneys. It is one of the body's natural diuretics. Under normal conditions cells in the atrium of the heart make a trace amount of ANP. In heart failure, however, cells in the ventricles also begin to make ANP. This surplus of natural diuretic production is normal in unborn children, but not in adults.

In heart failure, stimulated enlargement stretches the heart’s walls (remodeling). Long-term overstimulation of heart cells results in a cascade of effects that should only happen during the normal time when these cells are supposed to be stretched, which is in the developing fetus. Elevated protein levels of these types should not be seen in the adult heart as they are designed to operate before birth, and are not meant for use in the adult body. Their effects lead to larger, weaker heart cells. This hypertrophy is devastating in the long term. It results in heart cells that do not function properly and eventually results in an increased rate of cardiac cell death.

The neurohormone called angiotensin II is a vasoconstrictor in the cardiovascular system. Its namesake, angiotensin I, is floating around inside all of us, healthy or otherwise. Angiotensin I is converted into angiotensin II by a substance in the lungs called Angiotensin Converting Enzyme (ACE). ACE is the enzyme that is blocked with ACE inhibitors. By blocking it, angiotensin I is prevented from converting into angiotensin II. A reduction in the amount of circulating angiotensin II decreases vasoconstriction which lessens the workload on the heart.

There is always a loophole it seems. Angiotensin II can also be produced in other places within the body, so ACE inhibitors cannot completely stop angiotensin II from being made. After starting an ACE inhibitor, there is typically a period where the conversion of angiotensin I to angiotensin II is almost completely eliminated. Over time, however, angiotensin II levels rise again from other production sites that compensate for the external interference we have made by introducing the pharmaceutical ACE inhibitor.

Improperly produced ANP levels increase with heart failure. Angiotensin II levels skyrocket. We also see higher levels of norepinephrine in CHF. Norepinephrine can be thought of as a relative of adrenaline. High levels are seen in heart failure patients, whether they have symptoms or not. The heart's beta-1, beta-2 and alpha-1 receptors are also affected by CHF, making the entirety of the cardiovascular control system as shaky as a bloated house of cards.²

Another group of substances that worsen heart failure is inflammatory cytokines. The best known is tumor necrosis factor – alpha (TNF-alpha). These cytokines weaken the heart's pumping action. TNF-alpha may be what causes the wasting, or cachexia seen in those individuals with some types of cancer that is also observed in some heart failure patients. A high level of TNF-alpha can be tested for and usually indicates a poor prognosis.⁴

Nitric Oxide (NO), also known as laughing gas, is made in minute traces within the body from L-arginine by an enzyme called nitric oxide synthetase (NOS). Nitric oxide causes blood vessels to relax and dilate which increases blood flow and lowers blood pressure. The cells lining our blood vessels contain a type of NOS. The presence of heart failure alters normal levels of this helpful enzyme and many other essential components of our blood, such as Endothelin.

Endothelin is a completely different and potent vasoconstrictor released by cells lining the blood vessels. Endothelin increases afterload, the resistance against which the heart must pump, by narrowing the blood vessels. It also reduces the heart's pumping strength. The worse the heart failure, the higher the endothelin level will be. Drugs to lower endothelin levels are currently in trials.

Not only do patients with heart failure die slowly from disease progression, many die from sudden cardiac death (SCD). Besides remodeling the heart musculature, electrical remodeling is also taking place. The heart's electrical pathways become progressively stretched out of shape and chemically damaged. This makes dysrhythmias much more likely.

Ventricular tachycardia (VT) or ventricular fibrillation (VF) are common causes of sudden cardiac death. There are other causes of sudden cardiac death but VT and VF seem most pervasive. To run the heart's electrical system, the body basically trades an electrolyte inside a cell for a different electrolyte outside the cell. Swapping electrical charges this way fires the heart. That is why electrolyte levels are so important. The root of the electrical remodeling problem seems to be changes in this system of electrolyte exchange. It is possible that as the heart enlarges, it stretches, causing fibrosis, which interferes with electrical pathways. There are contributing factors like decreased potassium and decreased magnesium levels caused by diuretics. An increase in digoxin levels or other class I antiarrhythmic drugs may also cause certain dysrhythmias to occur. On top of all this, there are time relationships, so there are certain times of the day when patients are more prone to dysrhythmias. Sudden cardiac death is a very complex concept.

An enlarged CHF heart can be a dramatic find. – (Standard chest x-ray)

Case Study:

Paula is a 51-year-old female who is 5’5’’ and weighs 182 pounds. She wants to have surgery to help her reduce her weight. She has a history of having a cardiac catheterization for an elevated ST segment with unrelieved chest pain. Her right coronary artery had an 85 % blockage, and a stent was placed. She is a non-smoker but enjoys eating! She has a physically demanding job, yet no exercise beyond that. She is in with her personal physician to help determine whether she is a candidate for the surgery to reduce her weight.

Her blood pressure is 130/90; the EKG shows atrial fibrillation at a rate between 88 and 100. Her respirations are non-labored at 14 breaths per minute with an oxygen saturation of 95% on room air. She appears in no distress.

The initial suspicion of heart failure most commonly occurs during a physical examination. Suspicion tends to grow as the individual begins relating their recent history, telling how they have been feeling lately and what is most concerning to them. To confirm or rule out the tentative diagnosis the first thing that is typically done is a chest X-ray to see if the heart is enlarged or if any fluid resides in the lung fields. An electrocardiogram (EKG, ECG) is generally ordered to measure the electrical impulses in the heart, looking for any suspicious changes from the norm. The EKG records the heart's rhythm, the frequency of beats, and electrical conduction in order to gather clues about why the person may have heart failure and what course of treatment would be best. An EKG may show if someone has had a heart attack in the past, if the left ventricle is thickened, or if the heart rhythm is abnormal.

The next step may be a measurement of how much blood the heart’s left ventricle pumps out with each contraction. This is called the ejection fraction. With each beat, a normal heart ejects about one-half to two-thirds of the blood volume in its left ventricle. Someone with a normal ejection fraction can still have heart failure. If the heart muscle has become so thick and stiff that the ventricle holds a smaller-than-usual volume of blood, it might still seem to pump out a normal percentage of the blood that enters it. In reality, though, the total amount of blood pumped is not enough to meet the body's needs. Based on the medical history and symptoms, the physician may order one or both of the following tests.

Echocardiography (echo) is an ultrasound that uses sound waves to examine the heart's structure and motion. During this safe, painless test, the individual lies still while a technician moves a device over the chest. It gives off a silent sound wave that bounces off the heart, creating images of the chambers and valves. The echo can tell the doctor how thick the heart muscle is and how well the heart is pumping. A two-dimensional echocardiogram coupled with Doppler flow studies is generally considered to be the most useful diagnostic test in the evaluation of individuals with heart failure, though other tests may be useful for providing information regarding the nature and severity of the failure.

Radionuclide ventriculography or multiple-gated acquisition scanning (MUGA) is a nuclear medicine test that involves injecting a small amount of radioactive dye into a vein, then taking pictures of the heart as it pumps blood. Like an echo, this test shows how much blood the heart can pump with each beat. The dye used for this test is typically iodine-based, so it is imperative to notify the technician of patient allergies to iodine, or shellfish (which contain iodine).

The above tests allow the physician to determine the nature of the problem by estimating the functioning of the heart's ventricles. These chambers may have lost some of their power to pump blood to the body, or their ability to relax and fill with blood. This information, along with the ejection fraction reading, will be used to determine what treatments would be most effective.

Angiography is a further diagnostic test that may be helpful for some clients. This examination involves injecting contrast dye into an artery or vein in the groin or arm. An x-ray is taken that will show any coronary artery blockage.

An exercise stress test is also part of a normal work-up for heart failure. This test records the heart's activity during exercise, either walking on a treadmill or pedaling a stationary bike, in order to see whether the heart responds normally to the stress of exercise.

Blood tests include a metabolic panel of sodium and potassium (electrolytes), albumin (a type of protein), and creatinine and blood urea nitrogen (kidney function). A urinalysis is also commonly ordered. All are done to check for abnormal levels that may indicate strain on the body's organs (such as the kidneys and liver) that often results from heart failure. One new test that is becoming more common is brain natriuretic peptide (BNP).³ It measures the hormone level found in the left ventricle. Being able to isolate its presence in the blood may also be used to help diagnose and grade the severity of heart failure.

Brain natriuretic peptide (BNP), now known as B-type natriuretic peptide or Ventricular Natriuretic Peptide (still BNP), is a 32-amino acid polypeptide secreted by the ventricles of the heart in response to excessive stretching of heart muscle cells (cardiomyocytes). The release of BNP is modulated by calcium ions. BNP in humans is produced mainly in the cardiac ventricles. Elevated levels of BNP in the blood show that the left ventricle is being overworked and CHF is occurring or getting worse.^4,5

The physiologic actions of BNP are similar to those of Atrial Natriuretic Peptide (ANP) and include a decrease in systemic vascular resistance and central venous pressure as well as an increase in natriuresis. Thus, the net effect of BNP and ANP is a decrease in blood volume, which lowers systemic blood pressure and afterload, yielding an increase in cardiac output, partly due to a higher ejection fraction.

Case Study:

Arthur is a 65-year-old male who has been a smoker since the age of fourteen. He is 5’10” and weighs 252 pounds. He eats a lot of pasta and enjoys any kind of meat. He “hates” vegetables and enjoys an apple once in a while. He is an accountant and works long hours sitting at a desk. He suddenly became short of breath and felt like an elephant was sitting on his chest. His skin became sweat-soaked, and he felt like he was going to die. His wife called 911, and he was immediately taken to the emergency room. In the ambulance, he was placed on oxygen at 4 liters nasal cannula since his oxygen saturation was 88%; this improved to 96%. A cardiac monitor was applied which showed an elevated ST segment and a sinus tachycardic rate of 130 beats per minute. His blood pressure was 210/110.

Once in the emergency room, he was evaluated and it was determined he needed emergency cardiac revascularization, and the catheterization team was called in. This was just the beginning of his treatment, and a thorough evaluation and treatment plan would follow. This would be the beginning of a life-long treatment plan.

CHF is being described as an epidemic, with one in eight death certificates listing heart failure as a causal factor.⁷ Be aware that despite a greater emphasis on sharing data in the health sector, difficulties arise in assessing the full magnitude of the problem due to lack of reliable population-based estimates. According to the 2017 American Heart Association Heart Disease and Stroke Statistics Update, some 6.5 million Americans currently suffer from heart failure, up from 5.7 million in the year 2012, among those 20 years of age or older.

The AHA 2017 Update goes on to report:⁷

• Annually 960,000 new heart failure cases are being diagnosed.
• In the 65-year-plus age group, 21% will develop heart failure.
• Heart failure incidence rates (in males) basically double for each 10-years during the 65 to 85 age range.
• Heart failure incidence rates (in females) basically triples for each 10-year span from age 65 to 84.
• Lifetime risk for HF is currently;
  • 30% to 42% in white males,
  • 20% to 29% in black males,
  • 32% to 39% in white females, and
  • 24% to 46% in black females.
• Five-year survival with a heart failure diagnosis after a measurable serious incident, in this case an MI, increased from 54% in 2000 to 61% in 2010.
• Despite overall treatment improvements, anticipated survival rate for heart failure remains at 50% survival five years from the time of diagnosis.

On an unfortunate note, as of 2012, the latest statistics published by the American Heart Association, annual costs of heart failure treatment topped 30.7 billion dollars. Projections place HF treatment costs in the year 2030 at around 69.7 billion dollars, or in other words, a cost of $244 dollars annually specific for one medical condition, paid by every American adult.⁷

Statistics can be cold and impersonal. They also tend to portray a singular viewpoint. An individual with a diagnosis of heart failure can live a long life given early intervention and proper ongoing treatment. The death rate is highest in the first year after an official diagnosis, possibly due to the severity of the initiating or causative medical condition leading to the diagnosis. Survival following the diagnosis of congestive heart failure is worse in black ethnic groups than it is in other groups, and high blood pressure certainly plays a factor in this. It is also worse in men than women; but, even in women, only about 20 percent survive much longer than 8 to 12 years from the time of diagnosis. In fact, the outlook for any person diagnosed with heart failure is not much better than for most forms of cancer. The fatality rate for congestive heart failure is especially high, with one of every five persons newly diagnosed dying within the first year following recognition of the condition. Of these early deaths, sudden cardiac death is common, occurring at a rate of six to nine times that of the general population.

For those with heart failure who make it through the difficult first few years following diagnosis, the causes of death broaden out somewhat, though sudden cardiac death remains a possibility. Many clients with heart failure die from complications of infections, like pneumonia, that target areas with increased vulnerability due to the comorbid condition of heart failure, although any form of infection is life-threatening to a person with a weakened heart. Attempts to get good numbers on heart failure mortality are difficult as the official cause of death may be a hodgepodge of diagnoses that exclude the root cause of heart failure. For example, a diagnosis of pulmonary edema could really mean the presence of heart failure. However it might be phrased, heart failure remains a highly lethal condition.

The two most common end of life processes in heart failure are sudden cardiac death (SCD), frequently referred to just as sudden death (SD), and progressive pump failure. One-third to one-half of those diagnosed with heart failure will die from sudden cardiac death.⁸ The chance of SCD increases for individuals with a known concurrent cardiac dysrhythmia. The longer or more often a person is in the fluid overload condition that accompanies heart failure, the more likely he/she is to develop an unstable heart rhythm. As the struggling heart enlarges, it causes electrical pathways in the heart to be over-stretched thus predisposing the client to cardiac dysrhythmias. The substances in the body that control electricity (i.e., electrolytes) also get out of balance with the wild fluid shifts and edema driven tissue damage that are occurring. As a result, if sudden cardiac death does not occur, the heart failure will progressively worsen until the lungs fill with fluid, effectively drowning the client. This is why having a comprehensive program to slow or halt the progression of the disease condition is so very important.

Despite the progressive nature of heart failure, those who have it can lead happy, productive lives. Symptomatic control with medication, lifestyle changes, and even surgical treatments can all help to slow, or even for a time, halt the progression. That makes sudden cardiac death all the more irritating, when it takes away the opportunity for quality of life. Patients with CHF do not have to wait passively to see if sudden death will strike. There are ways to minimize the occurrence of sudden death. It all starts with a good diagnostic workup.

Controlling electrolyte shifts is a major factor in dysrhythmia control in heart failure clients. Basic lab work is therefore needed on a routine basis, and a thorough cardiac workup is also an early must. Of particular interest are the results of the 12-lead EKG, both during stress and non-stress, as this will show how the heart’s electrical activity is actually functioning.

First, a quick refresher on how it should work. After all, heart muscle cells are in many ways unlike other muscle cells. It takes a nerve impulse to make a regular muscle cell contract while a heart cell can contract all by itself. The heart muscle cells that do this produce electrical signals that spread throughout the heart. It is these electrical signals that give a nice steady heartbeat.

1. The heartbeat begins with a small group of muscle cells in the upper right part of the right heart chamber - the right atrium. These cells are called the sinoatrial node (SA node), the heart's natural pacemaker.
2. Electrical impulses sent out by the SA node spread quickly throughout the upper heart chamber - so fast that all the muscle cells in the top two chambers contract pretty much at the same time.
3. The wall between the upper heart chambers and the lower heart chambers is made of a special layering of very tough tissue that even stops electrical signals. So, signals from the SA node cross this wall on a bridge made of special cells called the atrioventricular node (AV node).
4. Cells in the AV node conduct impulses more slowly, causing a delay of about 2/10 of a second before the signal gets to the ventricles. This delay gives the upper chambers (atria) time to empty into the lower chambers before the lower chambers (ventricles) start pumping blood out into the body
5. Once past the AV node, the electrical signals travel through a bunch of fibers called the bundle of His. The bundle of His passes the signals the rest of the way through the wall between the upper and lower heart chambers
6. Because the lower heart chambers - the ventricles - are so muscular, signals are not conducted through them very well. Thus the signal goes through a network of fast-conducting fibers called Purkinje fibers, splitting to travel down the right and left bundle branches to reach every part of the ventricles.
7. Now all four chambers have received the signals and have beat at the proper time - as a team. Although this seems complicated, electrical signals spread from the SA node through the entire heart in less than one second. This electrical signal journey is what an EKG records and measures.

The answer is a palpable “Pulse.”

The disorganization of heart electrical activity frequently found with heart failure often results in nonproductive, or erratic heart muscle contractions known as dysrhythmias. Of these, atrial fibrillation is the most common. Atrial fibrillation is an irregularly irregular heart rhythm that occurs when multiple foci (points of electrical stimulus or ‘pacemaker points’) in the atria fire in an uncoordinated pattern and replace the normal regular sinoatrial node firing. These fibrillatory waves, also called f waves, replace the P waves on the electrocardiogram. The atrioventricular node acts as a gatekeeper, stopping a portion of the f waves from reaching the ventricle and triggering a response.

This disorganized conduction from the atria results in chaotic conduction and an irregular and rapid response, specifically, atrial rates in excess of 350 beats per minute (bpm)-commonly, 450 to 600 bpm. Often, it results in a rapid ventricular response as well, which a heart weakened by heart failure cannot afford to make. The atria's uncoordinated activity prevents the atrial volume from fully contributing to ventricular end-diastolic volume, decreasing stroke volume and cardiac output. The effect of atrial fibrillation on the ventricles includes the loss of atrioventricular synchrony, an inappropriately rapid heart rate, and an irregular ventricular rhythm. Because diastolic filling time constantly changes, the stroke volume can vary widely. Given the atria's uncoordinated activity, microemboli may form, thus increasing the risk of stroke and putting an unbearable burden on the failing heart.⁹

Unable to cope with these rapid chaotic pressure changes, the lungs are prone to fill with fluid. Angina or chest pain from the oxygen deficit in the heart muscle itself may occur. The heart can slip into completely unproductive and acutely life-threatening dysrhythmias such as ventricular tachycardia or ventricular fibrillation, in a desperate attempt to survive.

Ventricular tachycardia or ventricular fibrillation results in sudden cardiac death. The individual experiencing either one may never feel it coming. A dysrhythmia, sometimes described as a primary dysrhythmia, deprives the heart, mind, and body of needed oxygenated blood. Without external intervention, such as cardiopulmonary resuscitation (CPR), the failing heart inevitably dies. Everyone should be encouraged to take a CPR course.

We have seen how sudden cardiac death can occur. Now we should examine the ways to prevent it. Medications are one of the primary strategies for controlling and preventing life-threatening dysrhythmias. An entire class of pharmaceuticals is devoted to dysrhythmia prevention. Digoxin, a medication commonly used for treating heart failure, has until recently been considered the first line agent of choice for control of all cases of atrial fibrillation. Due to the possibility of digoxin related inotropy, or weakening of the cardiac musculature which could potentially exacerbate heart failure symptoms, atrial ventricular node ablation with pacemaker implantation is considered the treatment of preference to control ventricular rate in those patients with good systolic functioning. Pharmacologic rate control choices currently prefer the use of beta blockers or calcium channel blockers, or a combination of the two, in preference to digoxin.¹⁰

Surgical interventions include the revascularization of any areas of the heart that are sending out distress electrical pacemaker signals, as well as the removal of areas of tissue that are blocking the rhythmic transfer of electrical impulses. Often these interventions can be accomplished by cardiac catheterization (thrombus clearing or stent placements) up to coronary artery bypass surgery. A procedure that is increasingly being used to treat heart failure patients is a selective ablation or targeted killing of aberrant pacemaker cells that cause dysrhythmias. Locating the source of the dysrhythmia and eliminating that select area of the weakened heart muscle can save much grief and heartache.

Perhaps the greatest strides of all have come in the area of implantable defibrillators that jolt a heart out of a lethal dysrhythmia and the advent of specialized pacemakers for heart failure clients. Pacemakers, in general, are small electrical generators that create rhythmic electrical pulses in order to control the heartbeat. They are often just referred to as pacers. This type of implantable aid has been in use for some time now and is frequently seen in those clients who need a pacemaker for a chronic rhythm problem. The pacemaker itself is one sealed unit that encases a battery, and circuitry. The entirely enclosed battery supplies the power needed. The circuitry is similar to a little computer, changing energy from the battery into tiny electrical impulses that go to the heart through thin wires called leads. The connector block on top of the pacemaker is plastic. That is where the leads connect to the generator unit.

One specific type of pacemaker has been shown to be a great help in about 1 in 5 heart failure patients. This style of pacemaker therapy is called ventricular resynchronization therapy (VRT) or cardiac resynchronization therapy (CRT). This pacemaker paces both of the heart’s ventricles (biventricular).

Cardiac resynchronization therapy (CRT) is used to coordinate the heart's four chambers in order for them to act together as a team, making them pump blood more efficiently.¹¹ Many CHF clients’ hearts do not have all chambers firing at just the right time to beat effectively, known as in asynchrony. Re-timing the beat of some of the chambers restores that needed teamwork and improves cardiac function. Not everyone with heart failure will improve with CRT, but studies done with end-stage CHF clients have shown some remarkable improvements. Some clients functioning at class 3 and 4 have been able to have their cardiac output boosted to a level where they can resume activities at a functional level of either 1 or 2, a dramatic and desirable change.

We will now look at the medications used to treat heart failure. The goal is to restore the maximum amount of function to the cardiovascular system with the least expense to other organs and tissues. Consistently, clients experiencing heart failure report that the major drawbacks to a good quality of life are shortness of breath and fatigue. We can control these by increasing cardiac output and thus reducing fluid retention.

Heart failure is not a simple disease, and therefore calls for a complex and integrated response using multiple medications to support the positive effects of symptom management. In general, the order of therapy may first call for initiation of loop diuretics to contain and control fluid overload in those individuals exhibiting overt heart failure symptoms such as dyspnea or peripheral edema.

Whether or not a diuretic is called for as the first line in pharmacologic intervention, the use of angiotensin converting enzyme (ACE) inhibitors are sure to be considered early on as a first-line treatment for heart failure.¹⁰ ACE inhibitors work by preventing the body from creating angiotensin, a substance in the blood that causes vessels to vasoconstrict and raise the blood pressure. ACE inhibitor patients have, in trials, consistently shown improved cardiac function, improved symptoms, and better test results. In a series of large-scale trials, use of ACE inhibitors in various phases of heart failure demonstrated a lower death rate from all causes and a decreased risk of hospitalization.⁹ Please note that while ACE inhibitors decrease some of the more visible symptoms and contribute a slowing effect, they do not seem to stop the disease progression. More studies are being conducted with some practitioners so enthused by early study returns that they are advocating that all patients with left ventricle problems be placed on an ACE inhibitor.

The antihypertensive group known as beta blockers is often prescribed in combination with ACE inhibitors. Beta-blockers block the chemical receptors known as beta-receptors. These receptors are located on the outside of heart cells and along the course of some of the major blood vessels. They aid in the process of controlling the rate at which the heart beats. There are different sub-types of beta-receptors found on heart cells. If a drug blocks all the beta-receptors it can find, it is called non-selective. If a drug blocks mainly one certain kind of beta-receptor, it is called selective. For example, of the newer medications, Coreg is non-selective and Toprol-XL is selective. There is now a huge amount of evidence supporting beta-blocker use in CHF. Beta-blocker patients have shown improved cardiac function and generally see their symptoms improve. Beta-blocker studies show that death from heart failure from all causes is lowered with less hospitalization time. The positive effects from beta blockers given in conjunction with ACE inhibitors appear to be additive, which makes them a desirable addition to heart failure treatment regimens.⁹

Diuretics are almost inevitably prescribed with heart failure at some point, often very early following diagnosis because they are THE major treatment for fluid congestion (edema). The goal of diuretics is to reduce filling pressures in the heart by causing the patient to eliminate (urinate) excess fluid. Some prescribers operate on a rigid premise that their clients with CHF need a little extra fluid to maintain an optimal preload. Preload is how far heart fibers stretch when the heart is its fullest, just before it pumps blood out into the body. This is wrong according to heart failure specialists. A wedge pressure of 20mmHg is not necessary. A wedge pressure of 12mmHg, which is normally considered low for these patients, may be perfectly fine as fluid volumes must be regulated by each individual’s needs and condition. Wedge pressure is a direct measurement of blood flow pressure obtained from a balloon-tipped flexible tube inserted through either the inferior or superior vena cava, through the heart and into the pulmonary artery.

Digoxin (Lanoxin, digitalis, and foxglove) has been a staple of heart failure treatment for over two thousand years. Would it surprise you that a few years ago it fell into disfavor as a treatment for CHF? A large drug trial known as The Digoxin Investigators Group (DIG) put 3,000 patients on a placebo and 3,000 on digoxin, then watched to see how digoxin affected end result mortality in the groups. Their findings showed that there was no difference whatsoever between digoxin users and those taking placebos. This resulted in a sudden reaction by clinicians prescribing digoxin for their heart failure clients. After all, why give something that doesn’t extend the longevity of the clients? Fortunately, this impulse reaction was recognized quickly as just that, a reaction over the wrong test criteria. Digoxin alone in heart failure patients does not noticeably lengthen a CHF sufferer’s lifespan. What it does do is help them to feel better during the course of the disease, and stay out of the hospital much more than those clients not on digoxin. It is a quality of life issue, not quantity of life.^8,12

That brings us to the shadier side of the medication spectrum. Many of the drugs used to treat heart failure actually increase the nearness of death. The patients feel and function better, but their use puts a burden on body systems, leading to a decreased lifespan. These include medications known as inotropes that make a person’s heart beat stronger.

Inotropes come under names such as milrinone, dobutamine, xamoterol and ibopamine. They are recommended for use on a short-term basis in heart failure to aid during the stabilization of patients. Basically every inotropic drug that has been studied, including in some circumstances digoxin, increases the potential for death.

Another medication class that possesses both promise and danger is vasodilators. Vasodilators cause the blood vessel walls to widen or relax, allowing blood to flow more easily. We have already looked at one type of vasodilator, called ACE inhibitors. People who cannot tolerate an ACE inhibitor are often prescribed other types of vasodilators such as isosorbide dinitrate (Isordil), hydralazine (Apresoline), or nitroglycerin to relieve symptoms and improve tolerance for exercise. Other vasodilators that take less of a toll on the body when used are currently in the drug trial study stage. Flosequinan is one that actually received FDA approval before it had to be withdrawn from the market. The use of a kinder, gentler form of vasodilator would be a great aid in the control of heart failure, so it is with mixed eagerness and trepidation that the medical community is waiting to see if any oral forms of these newest agents get off the drawing board.

One of the newest medications has the potential of jumping straight into the ranks of the first-line prescribed medications, especially in those patients who are unable to tolerate an ACE inhibitor. Angiotensin II receptor blockers (ARBs) block the AT-1 receptor, decreasing the function of the angiotensin II receptors themselves.¹³ The benefit in this is that no matter how much angiotensin II there is, it can only cause limited amounts of harm since there would be no receptors for it to connect with. Currently, candesartan and valsartan have the best evidence base for use in the treatment of heart failure, though caution in use is warranted after a surge in adverse effect reports following generic status use in the Canadian health system.¹⁵

Still another new drug to hit the market is a potent vasodilator which has shown promise in use for acute decompensated heart failure. This potent adjunct to treatment is an injectable drug known as Natrecor (nesiritide). Approved for use by the FDA in August 2001, it is the synthetic version of one of the neurohormones called BNP that the body makes naturally in the heart's ventricle. Natrecor works by dilating blood vessels, decreasing the production of other pesky neurohormones and acting as a mild diuretic. These functions reduce the load on the heart, both preload and afterload (coming and going), making the heart’s job easier. Nesiritide is typically given to patients who remain dyspneic despite the use of IV loop diuretics and who are neither hypotensive or in cardiac shock.¹⁶ Nesiritide is generally given as an intravenous bolus of 2mcg/kg followed by a continuous infusion of 0.01 mcg/kg with close monitoring of hemodynamic effects.

There are some other types of medications that are commonly used with a diagnosis of heart failure even though they have minimal or no effect on the heart. While these adjuncts to treatment are not especially heart failure medications, they are so commonly prescribed for individuals with this diagnosis that it is important to mention them here.

Blood thinners (aspirin, coumadin) are prescribed to prevent the formation of blood clots and microemboli which occur with atrial fibrillation. As the pumping pressures of the heart decrease, the risk of forming blood clots and micro-emboli increases. Be aware that there is some debate as to the advisability of prescribing every heart failure patient with coumadin. Some very well-respected practitioners feel that coumadin is not warranted unless the patient has symptomatic atrial fibrillation. Others who are just as well respected disagree. We know that good reasons exist to individualize treatment for each person with heart failure, taking into consideration their unique individual needs.

Potassium helps control heart rhythm and is essential for the normal work of the nervous system and muscles. It is important to have just the right amount of potassium in the body, especially for the heart. The kidneys control the amount of potassium in the bloodstream and eliminate any excess through the urine. Since most diuretics remove potassium from the body, there is a risk of losing too much potassium. Patients taking diuretics are encouraged to eat foods high in potassium or are prescribed potassium supplements to compensate for the potassium loss. However, ACE inhibitors can cause the body to retain potassium, so this intricate juggling act needs to be taken into account as well.

Aldactone (spironolactone) competes with aldosterone for a certain receptor site, known as the mineralocorticoid receptor, and in doing so seems to prolong the survival rate in certain individuals with heart failure. The properties of Aldactone include a diuretic effect and interference in collagen build-up. In some heart failure studies, those clients taking Aldactone had a slight slowing of disease progression that could not be attributed to other causes, especially in the area of remodeling of the heart chambers. The exact reason for this is not fully known, and it is still unclear how to use the information should further studies show that it was not just a statistical set of flukes. In light of the positive indications for use, the 2017 ACC/AHA guidelines for chronic heart failure recommend Aldactone in patients with moderate to severe heart failure while carefully monitoring renal function and maintaining normal plasma potassium levels. The goal behind spironolactone use is a reduction in the number and length of hospitalizations of those tolerating it.¹⁷

A somewhat new and exciting option is increasingly available for achieving improved oxygenation to the myocardium in sufferers of both heart failure and cardiac ischemic angina. This is the big squeeze, otherwise known as Enhanced External Counterpulsation, or EECP.

Enhanced external counterpulsation is a noninvasive treatment using carefully timed, sequential inflations of pressure cuffs placed onto the client’s calves, thighs and buttocks. Inflation and deflation of these cuffs are timed to the patient's ECG, and the effectiveness is observed by noninvasive arterial pressure waveform monitoring.¹⁸

The overall hemodynamic effect of EECP compressions is to: 1) provide diastolic augmentation and thus increase coronary perfusion pressure; 2) unload systolic cardiac workload volumes and therefore decrease myocardial oxygen demand; and 3) increase venous return and subsequently, cardiac output. This sequence of pressure shifts works to displace the pressure of flowing blood ‘backward’ into the coronary arteries during heart diastole when the cardiac tissue is in a state of relaxation and resistance to backpressure in the coronary arteries is at its lowest point.

Remarkably, coronary collateral vessel development appears to be stimulated by this noninvasive increase in artery perfusion pressures, and with time, a noticeable increase in perfusion capacities can be seen in both the new and pre-existing coronary arteries. Currently, this therapy is gaining favor as an exciting adjunct to traditional treatment of cardiac ischemic related angina, and the treatment has also been approved for use in clients experiencing heart failure. Further investigation is being done concerning EECP’s strong potential for treating other severe cardiac pathologies.

Heart failure is a complex process that results from injuries or disease processes that are severe enough to cause a functional loss in the pumping ability of the heart. The body’s attempt to compensate for the damaged myocardial cells creates a progressive structural change in the cardiac chambers that are, in the short term, somewhat beneficial, yet over the course of time, create a greater functional loss of cardiac tissue. As yet, we have no cure for heart failure. Medications, surgical revascularization procedures, and the implanting of intricate pacemakers are all beneficial for symptom control and disease management. By using carefully planned approaches, we can add both length of life and quality of life to our clients who suffer from the burden of heart failure.

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