Heart disease is the No. 1 cause of death in the world and the leading cause of death in the United States, killing approximately 380,000 Americans a year. Heart disease accounts for 1 in 6 deaths in the U.S. A person dies from heart disease about once in every 90 seconds (AHA, CDC, NIH, 2013).
Each year an estimated 550,000 new cases of heart failure, also called congestive heart failure (CHF), both terms used interchangeably throughout this program, are diagnosed. Half of all newly diagnosed cases will die within five years of diagnosis. It is time to focus on recognition and management of the number one killer of our time, CHF. This course is an update and overview of congestive heart failure, or heart failure which simply exists when the effective cardiac output is not sufficient to meet the metabolic demands of the body.
After completing this course, the student will be able to:
Congestive heart failure (CHF), also called heart failure, is a life-threatening condition in which the heart can no longer pump enough blood to meet the metabolic needs of the body. The very name echoes with the sound of doom. To the person being informed that they have it, the term CHF possesses an impact equal to cancer as a diagnosis. Nearly 5 million Americans live with CHF, with 550,000 new cases diagnosed each year. Of those hearing these words applied to them for the first time, nearly half will die of complications related to this condition within the first 5 years after diagnosis, bringing the annual death rate to nearly 380,000 cases in the United States each and every year.
Despite such horrendous statistics, new studies show that the actual number of Americans receiving a new diagnosis of CHF is very slightly on the decline! Over the past 10 years for which statistics are available, the death rate from heart disease has fallen about 39 percent (AHA, CDC, NIH, 2013). As though to balance this, however, the continuing increase in the aging population has brought the total number of those who are struggling to live with CHF to new, record highs. (Preidt, 2008; Cohen 2014).
At this time, there is no cure for CHF. Treatment relies on early recognition and management of this life-threatening condition. The recognition of early signs and symptoms of this disease process allows interventions to be implemented as early as possible to manage the physiologic disease changes that occur. To add to the complexity, disease management simply does not get any more complex than with CHF. Recent studies show that gains are being achieved in the treatment of CHF, and that with knowledge, determination and the compassionate provision of care, even CHF can be managed.
Congestive heart failure is the end stage for all diseases affecting the heart and as such is a major cause of sickness and death. CHF by simple definition is the inability of the heart to pump enough blood to meet the body's needs. The term CHF does not mean that the heart as an organ has failed completely, but rather infers that the functioning of the heart is not sufficient or strong enough to meet the body's needs at times of stress or increased activity. This inability to pump effectively is the reason for the descriptive word Congestive, as in congestive heart failure or CHF, which is one of the more commonly used terms associated with this condition.
The reasoning behind associating the term congestive with the disease process of CHF begins with the left ventricle of the heart that normally receives blood from the lungs before pushing this blood through the arteries to the brain, internal organs, and extremities. When the left ventricle is weak, the effected person may experience symptoms of dropsy or show that they possess a weak heart. Both of these are older terms referring to the diminishment in cardiac output with its associated feelings of fatigue and dizziness, along with symptoms of fluid congestion partially related to the lack of oxygenated blood flow to the kidneys, which prevents the functional removal of excess fluid.
Excesses of fluid accumulate wherever it can, mainly in the feet, legs, abdomen and lungs. Often this accumulation of fluid is combined with shortness of breath on exertion, the inability to breathe while lying flat, and the tendency to awaken during sleep with shortness of breath. If the congestion of CHF becomes severe, excess fluid will accumulate in the lungs causing a life-threatening condition known as pulmonary edema which is accompanied by severe respiratory difficulties. As the disease progresses to the point where the right ventricle of the heart also fails, the patient will have an increase in the symptoms of low cardiac output and experience fluid build-up in the tissues of the body, resulting in leg swelling and fluid congestion of the internal organs.
Diagram of the heart
Congestive heart failure is by no means a new disease. Descriptions of CHF exist in writings from ancient Egypt, Greece, and India. The Romans were known to use the plant foxglove (Digitalis, Digoxin, Lanoxin) as a medicine to treat the condition. Widespread understanding of the nature of CHF seems to have been scarce until William Harvey first published a detailed description of the circulation in 1628. Roentgens discovery of the principles of x-rays and the coinciding development by Einthoven of electrocardiography around the 1890s led to vast improvements in the ongoing investigation into CHF. The more modern advents of echocardiography, cardiac catheterization and nuclear medicine have much improved early diagnosis and investigation into the causes and treatment of CHF.
Strong suspicion exists among scholars that the historical practice of bloodletting and leeches were primarily intended to be a specific treatment for the symptoms resulting from increased vascular load from CHF, that is, before popularization of the practice resulted in the use of bloodletting as the aspirin equivalent throughout medieval Europe. It should be acknowledged that ancient medical practitioners did achieve varying degrees of success in the treatment of CHF for centuries. William Withering published the documented benefits of digitalis on dropsy or CHF in 1785. He merely set into the newly available format of the printing press the treatment that had been in use since the days of Rome. In the 19th and early 20th centuries, CHF associated with fluid retention was treated with those horrid yet effective replacements of the leech known as Southey's tubes, which were inserted into edematous peripheries, allowing a limited drainage of fluid.
Southey's tubes are big bore needles with blunt - extended bevel tips for insertion directly into edematous tissue in order to allow release of trapped edema. The visual impression they give to the eyes of modern health professionals is somewhat like an early Frankenstein relative of the modern vacutainer.
The practice of medicine in the 20th century brought with it new forms of medications that have proven to be revolutionary in the treatment of CHF. The first mercurial based generations of diuretics, though effective, were associated with substantial toxicity, a risk greatly diminished in their replacements, the thiazide diuretics that were introduced in the 1950s. The use of vasodilators in the treatment of CHF did not truly begin until the development of angiotensin-converting enzyme inhibitors in the 1970s. By using these new families of medications in combination with other agents possessing a more direct effect on the cardiac system, todays treatments are more effective for the control of this, as of yet, incurable disease process.
Diagram of a heart, internal view
The normal function of the heart is to provide a gentle pulsatile pressure, which propels a stream of blood carrying oxygen and nutrients to the living cells of the body. This repetitive process ensures, with its bellows-like action that the flow of blood delivers oxygen and nutrients to the cells and carries away waste materials from the cells. Both at rest and during exercise, this pulsating pressure known as cardiac output (CO) continues, providing just enough force to keep blood moving in the pulse-by-pulse journey of cellular life. Cardiac output, distribution of oxygenated blood to the tissues and venous return are all delicately balanced by neurohumoral and intrinsic cardiac factors.
The disease condition known as CHF is the failure of the heart to carry out its function. It has no simple cause. It also has no simple treatment. CHF is the end result of most, if not all, of the disease processes and conditions that affect the heart. CHF can involve the heart's left side, right side, or, as in most cases, both sides and is manifested by systolic or diastolic dysfunction or both. The combination of systolic and diastolic abnormalities is common in CHF.
In systolic dysfunction (primarily a problem of ventricular contraction), the heart fails to provide enough blood flow to insure the delivery of oxygen and nutrients to the tissues. This is a problem of inadequate cardiac output resulting both in terms of oxygen and nutrients a wide variety of problems with energy utilization, energy supply, electrophysiological functions and cellular contractile element interaction. This last bit appears to reflect abnormalities in intracellular Calcium++ ion modulation and cyclic adenosine monophosphate (or cAMP) production. (Merck Manual, 2005; 2014).
Diastolic dysfunction (resistance to ventricular filling) accounts for 20% to 40% of cases of CHF. It is generally associated with prolonged ventricular relaxation time as measured during isovolumic relaxation (the time between aortic valve closure and mitral valve opening when ventricular pressure falls rapidly). Resistance to filling (ventricular stiffness) relates directly to ventricular diastolic pressure. This resistance appears to increase with age, probably reflecting myocyte loss. Myocytes are the special muscle cells that make up the heart muscle and increased interstitial collagen deposition. Diastolic dysfunction is presumed to be dominant in hypertrophic cardiomyopathy where the ventricles of the heart expand to replace damaged tissues, circumstances with marked ventricular hypertrophy (e.g., hypertension, advanced aortic stenosis), and amyloid infiltration of the myocardium. (Merck Manual, 2005; 2014).
High output failure is CHF associated with a persistent high cardiac output that eventually results in ventricular dysfunction, literally wearing the heart muscle out. Conditions associated with high cardiac output include anemia, beriberi, thyrotoxicosis, pregnancy, advanced Paget's disease and arteriovenous fistula. CHF that develops in response to high-output states is often reversible by early, aggressive treatment of the underlying cause. Cardiac output is elevated in various forms of cirrhosis and the onset of congestion reflects cardiac and hepatic mechanisms of fluid retention. (Merck Manual, 2005; 2014).
The left side of the heart is made up of two chambers starting with the left atrium (or upper chamber) and the larger left ventricle (or lower chamber). The left atrium receives oxygenated blood from the left and right superior and inferior pulmonary veins draining the left and right lungs respectively. The left atrium pumps the blood through the mitral valve into the left ventricle. The left ventricle during ventricular systole then pumps the blood through the aortic valve into the aorta which disperses it throughout the circulation.
If the left ventricle loses its ability to forcefully contract (called systolic failure), it cannot exert enough force to pump the volume of blood that is needed through the circulatory system. If the left ventricle loses its ability to relax (diastolic failure) because the left ventricular muscle has become stiff, it cannot properly fill with blood during the resting period between each beat. This is an important distinction because the treatments for each type of failure, left or right can be different.
Blood flow through the Left Heart chambers and vessels
In left ventricular failure, cardiac output decreases and pulmonary venous pressures increase. The elevation of pulmonary capillary pressures can rise to levels that exceed the functional pressure of the plasma proteins that form the barrier between vascular fluids and atmospheric gases, about 24 mm Hg. This leads to increased fluid in the lungs, reduced pulmonary compliance and a rise in the oxygen cost of the work of breathing. This high vascular pressure, known as pulmonary venous hypertension, along with the pulmonary edema resulting from left ventricular failure significantly alters the function of the lungs and those tricky ventilation perfusion relationships. Air hunger therefore correlates with elevated pulmonary venous pressure and the resultant increased work of breathing, although the precise relationship is still being debated.
Due to the vascular layout of the pulmonary system, pleural effusions characteristically accumulate in the right hemithorax, though they later manifest bilaterally. In an effort to deal with this fluid crisis, lymphatic drainage is greatly enhanced, but cannot overcome the increase in fluid in the lungs. Unoxygenated pulmonary arterial blood ends up being shunted past nonaerated alveoli, decreasing mixed pulmonary capillary PO2. These changes often progress to the point where an arterial blood gas analysis reveals an increased pH and a reduced PaO2 (pulmonary oxygen concentration), that is to say, a respiratory alkalosis. A PaCO2 (pulmonary carbon dioxide concentration) above normal signifies alveolar hypoventilation, possibly due to respiratory muscle failure and typically requires urgent ventilatory support. (Merck Manual, 2005; 2014).
Mimi is a 42 year old female who started walking 30 minutes a day to decrease her weight and to build up her physical tolerance. She is 54 and weighs 185 pounds. She has been exercising for only a week. She is a non-smoker. Drinks at least 10 cups of coffee a day at work. A year ago she had developed hypertension and is a border line diabetic. She can tell when her blood sugar gets low because she gets an odd taste in her mouth. She carries peanut butter crackers with her and that seems to bring her blood sugar up.
Last week her shoes started to get tight and she noticed her ankles swelling. Mimi attributed this to being on her feet all the time at work. She loves her job, and is a hard working waitress, who works on limited sleep and works odd hours. She developed chest pain a few weeks ago and attributed it to moving boxes of food supplies. She suddenly felt weak, dizzy, and short of breath at work. Her manager called 911 when Mimi became pale, very short of breath (SOB) and started to pass out. He had to ease her to the floor.
When the ambulance came Mimi had a blood pressure of 200/100, respirations were 28 with an oxygen saturation of 88%. She was extremely SOB. Her heart rate was 140 and she was in sinus tachycardia. Her temperature was 97.6 F. Her blood glucose was 90. She had no chest pain only palpitations which scared her.
The ambulance paramedic placed her on a cardiac monitor, started her on oxygen 4 liters per minutes via a nasal cannula which increased her Oxygen saturation to 96%. A peripheral IV was started with normal saline. Her EKG revealed a normal sinus rhythm to a narrow complex sinus tachycardia ranging from 98 to 130. A non encoated ASA was given. A cardiologist read the EKG and would be evaluating her once she arrived in the emergency room.
Individuals with left ventricular failure generally present to health care practitioners in one of three ways:
Should either systolic or diastolic failures occur, blood coming into the left side of the heart from the lungs will congest or back up, the pressure difference from this increase in congestion causing fluid or lung water as it is sometimes referred to, to exude into the lung fields. This is, of course, pulmonary hypertension. This form of hypertension is incredibly damaging to the pulmonary tissues and sets up the conditions that are needed for the dreaded pulmonary edema, also at times referred to as drowning in your own fluid. As the heart's ability to effectively pump decreases, peripheral blood flow slows down, typically causing fluid to build up in tissues throughout the body (generalized edema). It is because of this excess of fluid or congestion that the descriptive term congestive heart failure is a bit more widely used than the more correct term, heart failure.
The right atrium is the receiving chamber for venous (unoxygenated) blood from the systemic circulation-from the arms, head, abdomen, and legs. It receives blood that returns to the heart through the superior vena cava (draining blood from the head and upper extremities), inferior vena cava (draining blood from the abdominal viscera and the lower extremities), the coronary sinus (draining blood from the circulation of the heart) and the many tiny Thebeisian veins (draining small amounts of blood directly from the atrial wall itself). The blood is then propelled through the tricuspid valve during right atrial systole into the right ventricle where it then is ejected through the pulmonic valve into the left and right pulmonary arteries and into the lungs where the blood is replenished with oxygen.
Right-sided ventricular failure usually, but not always, is secondary to left-sided heart failure. The reason both the left and right ventricles tend to be affected in a domino fashion is that when the left ventricle fails, increased fluid pressure is, in effect, transferred back through the lungs, ultimately damaging the heart's right side. When the right side loses pumping power, blood backs up in the body's veins. This usually causes that unsightly and medically hazardous swelling in the legs and ankles.
Blood flow through the Right Heart (i.e. from the body into the lungs)
The most common cause of right ventricular heart failure is prior left-sided heart failure which increases pulmonary venous pressure. Increased pulmonary venous pressure leads to a state of generalized pulmonary arterial hypertension which results in a thickening of the muscular walls of the right atrium and ventricle. In a similar fashion, tricuspid regurgitation may also result in right ventricular failure. The force of blood being pushed backward past an incompetent tricuspid valve can set up conditions for pulmonary hypertension and right ventricular heart failure. This is just one example of why it is so important that a complete diagnostic workup be completed. Other causes of strictly right-sided failure can be mitral stenosis, primary pulmonary hypertension, multiple pulmonary emboli, pulmonary artery or valve stenosis, and right ventricular myocardial infarction. (Merck Manual, 2005; 2014).
Right-sided ventricular failure is closely associated with the development of systemic venous congestive symptoms. The sluggish venous congestion in turn leads to a moderate hepatic dysfunction that is common in CHF secondary to right-sided heart failure. The ailing liver manifests with what are usually modest increases in both conjugated and unconjugated bilirubin, prothrombin time, and in hepatic enzymes (e.g. alkaline phosphatase, AST, ALT). None of these abnormal laboratory values by themselves is particularly diagnostic for CHF however. As circulation becomes increasingly compromised, red flags such as markedly reduced splanchnic blood flow and hypotension occur. When these are present, a state of central necrosis begins to form around the hepatic veins causing inflammation and acute symptoms that may be severe enough to suggest hepatitis with acute liver failure. If that is not enough, hepatic circulation slows down directly contributing to a reduced aldosterone breakdown by the impaired liver. This is very important, as it further contributes to overall fluid retention. (Merck Manual, 2005; 2014).
Do be aware that generalized volume overload and increased systemic venous pressure can occur in polycythemia, over-perfusion of blood products, acute renal failure with over hydration, or in obstruction of either vena cava. If these conditions occur, they can readily simulate CHF. Myocardial function may be completely normal, merely masked by what is occurring throughout the rest of the vascular system.
Be alert to the fact that the presence of peripheral edema is not a reliable sign of CHF. The presence of an observable jugular venous distention and hepatojugular reflex are a very good visual indication that something is wrong with that individual's heart pumping pressures. The hepatojugular reflex is an elevation of venous pressure visible in the jugular veins. It can be demonstrated when there is either active or impending right-sided heart failure by applying firm pressure with the flat hand over the person's liver or upper abdomen. (Merck Manual, 2005; 2014).
Notice the thickening of both ventricle walls in an effort to increase strength of heartbeat
Congestive heart failure is, largely, a chronic disease process. Lifestyle choices and the effects of other predisposing disease processes set up the conditions that gradually worsen, with intervals of acute crisis. By the time a person is diagnosed with CHF, chances are very good that the heart has been losing pumping capacity little by little for quite some time.
At first, the heart tries to make up for the loss of effective pumping capacity by:
The heart is not in this alone. The rest of the body also tries to compensate for the loss of cardiac output.
The results of these temporary measures achieve little more than to mask the symptoms of CHF. They do not solve the problem. This is why many people are not aware of their condition until years after their heart becomes about as effective as a soggy sponge. Inevitably, the efforts to compensate made by the heart and body just cannot keep up with the demands placed on them, and the person experiences fatigue, breathing problems or other symptoms that prompt a trip to the doctor.
Congestive heart failure results in hypoperfusion of oxygenated blood to the tissues and the inability to effectively carry away the flood pools of waste-filled, spent blood.
Perhaps the number one effect of CHF is the feeling of shortness of breath or difficulty breathing (i.e. dyspnea). This occurs as blood and fluid backs up in the left and right pulmonary veins due to failure of the left side of the heart. This backpressure causes fluid to leak into the lungs resulting in an unpleasant feeling of breathlessness during activity (most commonly), at rest, or while sleeping. This breathless feeling may come on suddenly and be intense enough to wake a person up gasping for air. Those with CHF often have difficulty breathing while lying flat and may need to prop the upper body and head up on two or more pillows. They commonly complain of waking up tired or feeling anxious and restless, a complaint that should clue a healthcare provider that CHF may be lurking.
A companion symptom of lung congestion is the presence of persistent coughing or wheezing not related to another disease process such as the flu or a cold. This occurs as the fluid builds up in the lung tissues due to the congestion of the pulmonary vasculature. Generally, any long, ongoing bouts of coughing that consistently produce white or pink blood-tinged phlegm should be suggestive of CHF.
The buildup of excess fluid in body tissues, i.e. edema, is a sign of a definite circulatory problem and possibly CHF. This edema comes about as blood flow out of the heart slows, causing blood returning to the right side of the heart through the veins to back up. This back up is much more serious than a spoiled commute however as it is causing fluid to build up in the body tissues, areas not designed for excess fluid storage. The kidneys, for example, are less able to dispose of sodium and water when bogged down and the necessary brisk flow of blood is unavailable. This in turn causes additional fluid retention in the tissues, marked by swelling in the feet, ankles, legs or abdomen and fluid weight gain. So if your shoes are suddenly feeling a bit tight, there might be more going on than too much salt on last night's popcorn!
Forceful pump pressures falter leaving fluid further from the heart to puddle along
All this thinking about CHF making you tired? Maybe it is because your heart cannot pump enough blood to meet the needs of your body tissues. With CHF, unexplained fatigue is a major symptom of trouble ahead. The body starts diverting blood away from less vital organs, particularly muscles in the limbs, in order to send it to the heart and brain. When a person starts feeling tired all the time and has difficulty with everyday activities such as shopping, climbing stairs, carrying groceries, or walking, it is time to go visit the local healthcare professional. A body should not need to be performing daily activities dependent on emergency systems. The resulting wear and tear trashes vital organs in a most unappealing manner.
Directly related to this robbing of the blood supply are the symptoms of lack of appetite and/or nausea. When blood flow is being diverted to the brain and lungs, the digestive system receives less oxygen rich blood and problems with digestion compound. One such feeling that occurs is that of being both full and simultaneously nauseous. Cyanosis, or observable discoloration in the extremities due to the lack of oxygenated blood flow, may occur with any form of CHF. The cause in CHF can be considered central and may reflect hypoxemia. A quick way to tell if the cause is central or peripheral is when improved color of the nail bed can be regained with vigorous massage. This is strongly suggestive of peripheral cyanosis. A cyanosis of central origin, in contrast, cannot be altered by increasing the local blood flow with massage, warming, or by any other peripheral means. (Merck Manual, 2005; 2014).The brain is the organ that is receiving the most attention during CHF. Confusion and impaired thinking are common companions of CHF. Changing levels of certain substances in the blood, such as sodium, can contribute to the confusion, memory loss, and feelings of disorientation. Remember those poor bogged down kidneys? All of the organ systems interlock. No injury to one occurs without a cascade of effects influencing all the rest. An interesting side note to the confusion and sluggish thought processes that result with CHF is that family or friends are the ones that often seek help for the patient. Perhaps the very evolution of the disease condition itself makes it harder for an individual to know that they are in need of medical assistance.
Of the actual physical changes occurring to the heart in its attempt to compensate for decreased pumping ability, the only one likely to get noticed by the individual is the increased heart rate. This increase in rate is directly connected to an attempt to make up for the loss in pumping capacity. In order to increase capacity, the heart beats faster. This may be reflected in cardiac palpitations, which feel like the heart is racing or throbbing.
Diagram of dynamic circulatory flow patterns
Acute pulmonary edema is a life-threatening manifestation of left-sided heart failure, most often secondary to the sudden onset of pulmonary venous hypertension. A sudden rise in left ventricular filling pressure results in rapid movement of plasma fluid through the pulmonary capillaries and into the interstitial spaces and alveoli. This symptom of CHF is in reality a medical disaster in its own right, and presents with extreme dyspnea, deep cyanosis, tachypnea, hyperpnea, restlessness and anxiety, accompanied by a sense of suffocation. Pallor and diaphoresis in this medical emergency are common. The pulse may be thready and a blood pressure difficult to obtain. Respirations are labored, and rales are widely dispersed over both lung fields anteriorly and posteriorly. Some individuals manifest with marked bronchospasm or wheezing (cardiac asthma). Noisy respiratory efforts often render cardiac auscultation difficult, but a summation gallop, merger of S3 and S4 sounds may be heard. Hypoxemia is severe. CO2 retention in this emergency state is a late, ominous manifestation of secondary hypoventilation and requires immediate attention. (Merck Manual, 2005; 2014).
Congestive heart failure can be tricky. Even though more Americans die from diseases of the heart and circulatory system than from any other cause, it is often a complete surprise when they receive the diagnosis. Often this is due to the progressive nature of the condition, and the nature in which the body attempts to compensate. Those who have advanced heart disease, i.e. heart failure, tend to have episodes of serious symptoms, then long periods in which nothing seems to happen. These compensatory periods are filled with happenings-it is just that they are difficult to feel or discern. One vital way of tracking change is careful monitoring of physical activity limitations. Even though the individual may feel back to snuff, in reality the continuing insufficient vascular perfusion works to diminish strength and physiologic responsiveness one functional piece at a time. For this reason, the degree to which a person's physical activity is limited provides a valuable means of determining the effect that the condition is having on that individual. A well-accepted classification scale known as the New York Heart Association Functional Classification has been formatted and is in use to standardize these categories of Functional Heart Class. (Bolton, 2005).
November 8, 2001, the American College of Cardiology in collaboration with the American Heart Association released a new class system for heart failure patients. This new system is designed for use along with functional class systems such as the New York system described above. The new system classifies heart failure in stages A through D. Only stage C and D patients actually have the physical changes that are manifested by CHF. Do be cautious when using the new system until it gets familiar as it measures progression more in the manner of cancer classes. That is to say, even though treatment may make cancer disappear, the patient is still classified as a cancer patient. In the new heart failure system, patients who develop into stage C always remain in stage C even if they get better and their symptoms disappear. Their functional class would improve to class one but they would remain in stage C anyway. Confused? Do not be. Once you become familiar with the change, the benefits of this style of classification system become obvious. For any in-depth questions, the entire guidelines are available from the American Heart Association or at their website. (Circulation, 2005).
|Agnes Miller is a 47-year-old female with a mixed heritage of Pacific Islander and West African black. She is a working person, who has been complaining to her husband about not feeling well for several months. She had gone to an urgent care center two weeks previously with a persistent cough that just would not go away, and shortness of breath on exertion. At this time, she had been started on a general antibiotic. She now follows up with her family practitioner, who she has not visited in the last two years, her husband accompanies her. Her stated purpose is to get another cycle of antibiotics as she still has the cough and shortness of breath.|
|On questioning, it is revealed that she continues to smoke, 3 packs a day. Early last year she experienced a prolonged bout of the flu, characterized by severe abdominal gas pains that kept her in bed for over a week. Since that time, she has been feeling fatigued and having intermittent episodes of difficulty concentrating at work where she is a high-level actuary for an international insurance provider. Her job consists of desk and paperwork, with little physical activity, and includes many missed meals and late work nights.|
|Physical exam reveals faint right lower lung field crackles, a blood pressure of 190/120, pulse of 110, respiration of 22, and tympanic temperature of 99.7. She is hesitant about lying flat on her back, complaining of "snoring troubles" at home when she rests in this position. By palpitation it is evident that her liver is somewhat enlarged and a positive hepatojugular response is present.|
|Due to the findings of the physical exam and Mrs. Millers report, the initial impression is that of Class C, Functional Level 3 - Heart Failure, and not an infectious process, though that will be ruled out by laboratory testing.|
|The initial plan is to inform Mrs. and Mr. Miller that there may be more going on than another course of antibiotic will resolve, and gain their cooperation in further diagnostic testing, starting with a CXR, laboratory testing, then proceeding on as warranted.|
|Discussion Mrs. Millers reported symptoms fall directly in line with developing and possibly advanced Heart Failure, of the Congestive type. In women, Myocardial Infarctions are often manifested as dyspnea with or without abdominal pain and discomfort, instead of left arm pain as is more typical in men. Her heritage and lifestyle as she reports it also falls in line with an increased risk for cardiac disease. Right-sided heart failure, where the pulmonary vascular pressures are high, often manifests with night coughs and crackles in the lung fields due to the presence of fluid in the lungs forced out of the vascular beds by pressure. The increase in overall blood pressure, as well as pulse, may be a compensatory mechanism by which the body is trying to deal with the heart failure forced on it by ischemic heart changes post myocardial infarction. The heightened respiratory rate may also be a compensation for vascular changes as well as overall lack of blood oxygenation.|
Prognosis, grim.Should diagnostic testing confirm the suspicion of advanced Heart Failure, immediate targeted treatment will need to be initiated. Due to the potentially advanced state of the condition, as it manifests, the Millers will be faced with hard choices as far as life style changes and therapeutic options.
Prevention is the best means of dealing with CHF. As the condition is the end result of stresses and damage to the vascular system, and not caused by an exclusive disease process, it becomes difficult to form preventive measures that would be specific to CHF. As the heart ages, for instance, some of the blood-pumping ability of the heart muscle naturally decreases. The serious loss of vascular ability called CHF is the result of stress to our heart from a wide variety of health conditions that either damage the heart muscle itself, or create conditions that lead to the work that the heart is doing being so difficult that the heart damages itself. All of the behaviors associated with heart disease such as smoking, being overweight, eating foods high in fat and cholesterol, and lack of exercise contribute to CHF. In some individuals however, lifestyle has been shown to have absolutely nothing to do with the formation of CHF. For instance, some people who go on to develop CHF are born with structural heart defects, while in others a virus or other infectious process has damaged the heart muscle. Any measure of prevention therefore must be aimed at maintaining an overall healthy lifestyle, though it does seem prudent to institute preventive measures aimed at known disease processes that cause damage to the heart and vascular system.
|(Uddin, 2007) (Merck Manual, 2005).|
The following is a discussion of some of the conditions most commonly associated with being causes of CHF. (Merck Manual, 2005; 2014) (Circulation, 2005).
Ischemic Heart Disease robs the heart muscle of the vitality it needs to function, it attempts to compensate by making structural changes
The most common reported cause of CHF is ischemic heart disease. Ischemia is reduced blood flow, usually caused by blocked arteries. It accounts for about 70% of CHF cases in the US.
Diabetes is the next most common cause of CHF. Extra strain is placed on the heart, and diabetes has been identified as the causative factor in about 13% of CHF cases. People with diabetes also tend to be overweight and have high blood pressure and high cholesterol, all of which make the heart work harder.
Hypertension is often considered the third most common cause of CHF, occurring as a cause in approximately 7% of cases, although it is a slippery one to pin down as it often accompanies other causes in a sick sort of supporting role. It is known that uncontrolled high blood pressure increases a person's risk of developing CHF by two to three times. When pressure in the blood vessels is too high, the heart has to pump harder than normal to keep the blood circulating. This takes a toll on the heart, and over time, the chambers get larger and weaker.
Myocardial infarction is a frequent cause of CHF. A heart attack occurs when an artery that supplies blood to the heart fails (which blurs with ischemic heart disease). The loss of oxygen and nutrients damages the heart's muscle tissue. Part of it essentially dies. The remaining healthy tissue has to pump even harder to keep up. This cause again overlaps, as a history of myocardial infarctions plays an integral role in the formation of ischemic heart disease, hypertension and coronary artery disease.
Ischemia, necrosis and heart failure, oh my! Heart attacks do damage that is significant even when they are survived
When cholesterol and fatty deposits build up in the heart's arteries, less blood reaches the heart muscle. This damages the muscle, and the healthy heart tissue that remains is forced to work harder.
Heart valve problems can result from disease, infection or a defect present at birth. When the valves do not open or close completely during each heartbeat, the heart muscle has to pump harder to keep the blood moving. If the workload becomes too great, CHF results.
Cardiomyopathy or inflammation of the heart (myocarditis), are terms used to label heart muscle disease states. Any damage to the heart muscle whether due to drug or alcohol use, viral infections or unknown reasons increases the risk of CHF. Cocaine, as well as, methamphetamine use produce an accumulative toll of heart damage. Alcohol is by far the most common culprit.
Heart defects present at birth are still another initiating stress that creates the conditions necessary for CHF to occur. If the heart and its chambers fail to develop correctly, the healthy parts have to work harder to make up for it. This hyperplasia of the heart muscle progresses on into remodeling and CHF with every subsequent beat.
When the lungs do not work properly, the heart has to work harder to get available oxygen to the rest of the body. This results in heart muscles stretching, growing to compensate, which in turn leads to neurohormonal release from cardiac muscle cells, and the process of heart chamber remodeling begins its inevitable cascade out of control.
Low red blood cell counts such as occur is disease states such as anemia force the body to hustle around the available blood cells. When there are not enough red blood cells to carry oxygen, the heart tries to move the small number of cells at a faster heart rate. It can become overtaxed from extended effort. An interesting side-note is that sickle cell anemia is occasionally linked to CHF as well.
An overactive thyroid gland (hyperthyroidism) is the jet fuel of CHF. This condition causes the body to work at a faster pace, and the heart can be overworked trying to keep up.
Kidney damage or disease not related to diabetes initiates the process that results in CHF. The overall stress placed on the heart and vascular system by lack of kidney function is tremendous. The results of this wearing damage manifest in many disease conditions and processes, CHF being just one of many.
This is a very uncommon disease of unknown cause involving the medium and small pulmonary arteries. It results in right ventricular failure or fatal syncope generally within 2 to 5 years after detection. Women are affected twice as often as men, with the median age at diagnosis around 35 years old. Younger individuals who have been diagnosed with this condition have a worse overall prognosis. Thickening of the blood vessel wall known as Intimal Hyperplasia, and the consequent narrowing of the vessel lumen, is present in this disease. Areas of medial hypertrophy and hyperplasia, irreversible plexiform lesions, and necrotizing arteritis (plexogenic arteriopathy) occur in more advanced cases. Similar vascular lesions and clinical course have been observed in some patients with cirrhosis and in a few patients taking the once popular appetite suppressant drug combination dexfenfluramine-phentermine (fen-phen), which is no longer marketed in the United States. (Merck Manual, 2005; 2014).
Abnormal heart rhythms (arrhythmia or dysrhythmia) contribute increased levels of stress and strain on the tissues of the heart. When the heart beats too quickly, too slowly, or in an irregular fashion, it may not be able to pump enough blood to meet all the body's needs. While dysrhythmias may contribute to or even cause CHF, their presence can be a result of having existing CHF!
Those conditions that affect the tough membranous sac that surrounds the heart (the pericardium) are known as pericardial diseases. Disease processes that produce fluid accumulation (effusion), infection/inflammation (pericarditis), or abnormal thickening (constriction) are the more common ones. As expected, given the nature of the disease process present with pericardial conditions, they add greatly to the labor and stress of the heart, often long after the acute disease process is resolved.
Congestive heart failure has plagued humankind for as long as recorded history. Only in recent years have we been able to recognize it as a condition brought about by disease, trauma, and even congenital abnormalities, anything that causes the heart itself to function in an abnormal and stressful manner for extended lengths of time. Now we can predict its development by recognizing the conditions that cause it to occur. We even have the screening tools to measure it, such as the New York Functional Assessment and the American Heart Association/American College of Cardiology Heart Failure Staging Tool, so we can better focus on early treatment and aggressive control with medications, invasive procedures, and especially with life style changes. These areas will be discussed in detail in sections two and three of this special three part series on the Recognition and Management of Congestive Heart Failure.
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Colucci, Wilson. (September 14, 2012). Evaluation and management of asymptomatic left ventricular systolic dysfunction. Retrieved February 1, 2014 from UptoDate.com.
Colucci, Wilson. (June 7, 2013) Overview of the therapy of heart failure due to systolic dysfunction. Retrieved February 13, 2014 from UptoDate.com.
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This course is applicable for the following professions:
Advanced Registered Nurse Practitioner (ARNP), Certified Registered Nurse Anesthetist (CRNA), Clinical Nurse Specialist (CNS), Licensed Practical Nurse (LPN), Licensed Vocational Nurses (LVN), Midwife (MW), Registered Nurse (RN)
Cardiology, CPD: Practice Effectively, Critical Care / Emergency Care, Geriatrics, Medical Surgical