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Congestive Heart Failure is a syndrome affecting the entire body and caused by a poorly functioning heart. If the heart cannot deliver enough blood to meet the body's needs, the organs respond, often making things worse. The word "congestion" refers to a variety of symptoms and signs seen in this disorder which are due to excessive fluid accumulation. There is edema in the feet and legs and even in the lungs, filling the air spaces. Not all patients have congestive symptoms. About one-quarter have only exercise intolerance, shortness of breath and/or weakness as their primary symptoms. This group might be better termed "chronic" heart failure. Many patients have a mixture of all of the symptoms mentioned. |
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CHF Causes Disability and Death |
CHF is a cause of significant disability. Five million Americans are living disabled lives due to this disorder. Six hundred thousand people are hospitalized because of it each year. This number is more than twice as many admissions as all other cardiac disorders combined, and more than any other cause of hospitalization for any reason. 1
Although deaths due to coronary artery disease and hypertension have declined significantly, deaths due to CHF have increased fourfold in the last thirty years. 2 In the past, the five year survival rate from the time of diagnosis was only 25% for men and 35% for women.3 Several recent studies using older therapy protocols have shown no improvement: 62% survival at one year after hospitalization for CHF and only 16-25% at 6-10 years. 4,5,6
As bad as these numbers may seem, none of them reflect the improved prognosis expected with modern aggressive therapy. Nor do they reflect the improved survival expected from treatment strategies aimed at preventing loss of heart muscle function before CHF appears. |
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The Normal Heart: Follow The Blood |
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The normal heart has four pumping chambers and four valves. "Used" or venous blood returns from the veins and enters the right atrium. It then is pumped through the tricuspid valve into the right ventricle. The right ventricle pumps it through the pulmonic valve into the lungs where it picks up oxygen and gives off carbon dioxide. This "new" blood then returns to the left atrium which pumps it through the mitral valve to the left ventricle.
The left ventricle is the main pumping chamber of the heart. It is the largest and has the thickest muscle because it pumps blood to the entire body. It is the chamber damaged by heart attacks. When it squeezes, it usually empties 50-70% of its contents.
This percentage is often called the Ejection Fraction. When blood leaves it exits through the aortic valve and goes out the aorta to all the arteries of the body.
The normal heart has tremendous reserve. Its output is measured in liters per minute and the cardiac output can increase up to six times over resting levels. That is why an athlete can run a mile or a marathon, with the heart delivering much more blood to working muscles. This reserve is also why a malfunctioning heart can go undetected for many years. A bad valve or weak heart muscle calls upon this extra reserve capacity for cardiac performance at rest and at low levels of daily activity. Only more strenuous exertion might reveal impairment of function.
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Understanding CHF: Causes |
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Primary causes of CHF can be roughly divided into diseases affecting the heart muscle, valves, pericardial sac around the heart and abnormal heart rhythms. Some of these primary causes overlap. For example, a leaking valve may cause such a degree of overwork for the heart muscle that it gets weaker and weaker over time.
- Heart Muscle Disease: Heart muscle provides the pumping function of the heart. Heart attacks cause muscle death and scar formation and are the commonest cause of muscle dysfunction. Certain viruses can infect heart muscle and destroy it. These problems cause the heart to enlarge and are called Dilated Cardiomyopathies. Heart muscle can inappropriately thicken due to genetic disorders or high blood pressure. This can cause Hypertrophic Cardiomyopathy. Certain substances like iron or amyloid can deposit in the heart causing dysfunction. These are termed Infiltrative Cardiomyopathies. Finally, the left ventricle can weaken over time due to other conditions such as valve diseases which cause extra pressure or volume work. The heart enlarges (dilates) and loses muscle power. After a certain point this adaption to extra work becomes permanent and the heart will not return to normal even if the valve is fixed. This is a Secondary Cardiomyopathy due to another primary cause.
- Valve Diseases: Valves can slowly narrow over time in response to an ongoing disease process. This obstructs blood flow and results in "stenosis" of the valve. Stenosis causes extra pumping work for heart muscle and it often thickens in order to adapt. As the valve gets worse, the adaption fails and the heart muscle weakens. The heart then dilates and heart failure symptoms begin to occur. Valves can commonly leak and this is termed "regurgitation". As this worsens, the heart muscle adapts but can enlarge and eventually fails. Chronic valve disease can be caused by rheumatic fever in childhood or degeneration and calcification later in life. Certain specific conditions can be involved such as infection (endocarditis) or valve tissue breakdown (mitral valve prolapse).
- Pericardial Disease: The heart moves within a sac called the pericardium. Rarely, chronic inflammation can cause scarring and thickening of the pericardium restricting the heart and resulting in a unique form of heart failure (constriction). Acute inflammation can result in a rapid accumulation of fluid in the pericardial sac, resulting in impairment of cardiac filling and performance and acute heart failure (tamponade).
- Heart Rhythm Disorders: Certain chronic heart rhythm disorders have recently been identified as causes of cardiac deterioration. Sustained high heart rates due to abnormal atrial rhythms such as atrial fibrillation or atrial tachycardia can eventually lead to heart muscle "exhaustion", enlargement and heart failure. One abnormality of activation of the heart muscle called left bundle branch block can cause a moderate deterioration in heart muscle performance in some patients.
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Understanding CHF: The Body's Response |
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The entire body adapts or responds to the presence of poor cardiac performance. Much of this adaption makes things worse for the heart and creates some of the obvious symptoms.
- The Heart Adapts: Enlargement of the heart is the classic response of working heart muscle to heart failure. The left ventricle dilates or enlarges when dealing with too much volume work or pressure work. This helps to maintain the efficiency of the weaker muscle. It is a sign that heart failure has begun.
- The Nervous and Endocrine Systems Adapt: The "neurohumeral" response" involves a higher tone of the sympathetic nervous system, secretion of certain hormones from the heart itself and changes in secretion of other hormones.7 Much of this makes the resistance to arterial blood flow higher and results in more work for a weakened heart. In this sense, these neurohumeral changes are maladaptive.
- The Kidneys Adapt: The kidneys respond to receiving less cardiac output as they would if the body had lost blood or was dehydrated. They retain salt and conserve water. This is a truly maladaptive response since salt and water balance are normal to begin with. Fluid accumulation and edema appears in the legs and when severe enough edema reaches the abdomen and the lungs.
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Symptoms only appear when function has deteriorated severely. The most common are the classic congestive symptoms and signs:
- Shortness of breath with exertion.
- Shortness of breath lying flat.
- Swelling or edema of feet, ankles and legs.
- Weight gain due to fluid accumulation.
- Weakness and fatigue.
Other symptoms can occur less commonly and include increased abdominal girth, loss of appetite, decreased urination in the daytime, increased urination at night.
The problem may be obvious if symptoms and signs worsen over time and are present every day. CHF may be less obvious if certain symptoms come and go. Some may occur only with exertion. These symptoms can be confusing since other diseases can cause them as well. |
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The Importance of Early Diagnosis of CHF |
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Untreated CHF continues a downward spiral of heart muscle function. The earlier it is recognized, the earlier it can be treated and the better is the future for cardiac function.
The poor survival results of the past have been improved with modern treatment. 7 Thus symptoms and signs must be recognized early on and appropriate treatment begun to gain the most benefit from current medical therapy. |
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Avoiding Acute Exacerbations of CHF |
If CHF worsens badly enough to result in hospitalization, the heart and kidneys do not always return to the same level of function after successful hospital treatment. The stress of worsened congestion damages the heart and kidneys and they do not return to the previous stable state. Thus prognosis can worsen after each hospitalization or period of deterioration.8
Every effort must be made to avoid exacerbations of heart failure. The most common causes are noncompliance with dietary salt restriction and not taking cardiac medications properly.9 Close supervision and support are thus critical to obtaining the best treatment outcome. |
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Prevention of CHF is Possible |
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Recent studies have conclusively proven that strategies used to preserve heart muscle function can help delay or prevent the syndrome of congestive heart failure. If cardiac diagnostic studies (echo, nuclear, angiography) are used to identify asymptomatic patients with significant problems, they can be treated with certain strategies to reduce or delay the onset of left ventricular enlargement and dysfunction.
Asymptomatic patients with significant valvular regurgitation have been helped in this way.10 Great benefit is seen with treatment of patients having heart muscle dysfunction preventing further deterioration.11,12
The first step is identification of a heart problem which will potentially lead to heart failure. Then a plan of treatment and observation can begin to prevent CHF from occurring. In certain disorders, surgery is required to repair or replace a valve or deal with coronary artery disease. If done early enough it can prevent CHF from ever developing. This preventive strategy will ensure the best long term outcome. |
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Treatment: The Five Principles |
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1. Start treatment early enough to prevent progression, deterioration and complications.
2. Treat with appropriate doses of the best medications to achieve improved cardiac function. Unfortunately, only a minority of patients are now treated with enough medicine to reach maximum benefit.13
3. Learn to live within prescribed limits of variation in body weight, salt intake, fluid intake, exercise and medication use. "Falling off the wagon" by noncompliance with the treatment plan is the commonest cause of deterioration and repeat hospitalization.9
4. Learn to recognize symptoms and signs of early deterioration such as weight gain, intolerance of activity, and shortness of breath. Develop a plan with your doctor and heart failure team to respond to these changes.
5. Develop a close working relationship with the doctors and nurses who help care for your CHF. Communication with them and their intimate knowledge of you and your problem is the most valuable treatment tool available. |
A wide variety of medicines are used to treat CHF. Choice among them is governed by the primary cause of each person's problem. Most patients are on a combination of drugs. The main categories are:
- Angiotensin converting-enzyme (ACE) inhibitors (Capoten, Vasotec, Zestril, Prinivil, Monopril, and others). These medicines are now the mainstay of treatment, particularly for those with established left ventricular heart muscle dysfunction.
- Diuretics (Lasix, Furosemide, Aldactone, Zaroxolyn, Demedex, and others). These medicines treat the symptoms of congestion by helping the kidneys eliminate salt and water. Addition of the aldosterone-antagonist spironolactone (Aldactone) to other diuretics provides added survival benefit. 14
- Digoxin (Lanoxin). This old time medicine is still a standard. With the two above, they constitute the standard "triple therapy" for congestive heart failure.15,16 Digoxin acts by affecting the autonomic (vagal) nervous system and by strengthening the heart muscle slightly.
- Beta Blockers (Coreg, Tenormin, Lopressor, and others). These medications are now used as additional therapy for primary heart muscle disease in CHF. There is evidence that they improve muscle function and long term prognosis.17
- Nitroglycerine drugs (Isordil, Imdur, Ismo, and others). These are used to help patients with coronary heart disease and can provide some added relief for symptoms of pulmonary congestion.
- Other hypertension drugs (Cardura, Calcium channel blockers, and others). Diuretics, ACE inhibitors and beta blockers are all used for blood pressure control. If the pressure remains high, cardiac workload remains elevated and this makes heart failure worse. These other hypertension medications can provide added help.
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Treatment: Lifestyle Changes |
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• Diet: Restriction of salt in the diet is a mainstay of therapy. Dietary salt intake is balanced against the dose of diuretics which help eliminate it. One of the most common causes of acute exacerbation of CHF is an increase in dietary salt. A few restaurant meals can do it. Learning to read food labels and making menu choices wisely is essential.
• Exercise: An efficient body makes far fewer demands on a weakened heart. Regular, low to moderate level aerobic exercise improves muscular efficiency and preserves vascular reflexes.18 A program should be prescribed and supervised by your physician or heart failure team.
• Rest: Adequate rest periods between activities is very helpful. Spacing physical activity 30-60 minutes after mealtimes is a good idea. Adequate sleep is important as well. |
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Treatment: A Team Approach Gets Better Results |
Your personal physician should always supervise your overall care. A team approach to disease management of heart failure has been shown to achieve better compliance with treatment and better long term outcomes.19
A cardiologist is the most useful specialist to involve from the onset of congestive heart failure.20 Recent studies establish the value of additional specialty nurses, dietitians and others. 21 This team of professionals, working with a cardiologist at a heart failure center, closely supervises the treatment plan. Frequent communication by phone with nurses greatly helps in the day to day management of medicines, changes in symptoms, body weight and other problems. This approach will reduce readmissions to hospital and provide better quality of life outcomes.19 |
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References - Understanding Congestive Heart Failure |
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1. Field, JL. Beyond Four Walls: Research Summary for Clinicians and Administrators on CHF Management. Cardiology Pre-Eminence Round Table. 1994; 11.
2. Kannel, WB et al. Changing Epidemiologic Features of Cardiac Failure. BHF 1994; 72 (2 Suppl): S3- S9.
3. Kalon, KL et al. Survival After the Onset of Congestive Heart Failure in Framingham Heart Study Subjects. Circ 1993; 88: 107-118.
4. Jaagosild, P et al. Outcomes of Acute Exacerbation of Severe Congestive Heart Failure. Arch Int Med 1998; 158: 1081-1089.
5. Croft, JB et al. Heart Failure Survival Among Older Adults in the United States. Arc Int Med 1999; 159: 505-510.
6. Serni, M et al. Congestive Heart Failure in the Community. Arc Int Med 1999; 159: 29-34.
7. Swedberg, K et al. Hormones Regulating Cardiovascular Function in Patients with Severe Congestive Heart Failure. Circ 82; 1990: 1730-1735.
8. Anderson, B et al. Spectrum and Outcomes of Congestive Heart Failure in a Hospitalized Population. Am Heart J. 1993; 126: 632-640.
9. Michaelson, A et at. Prospective Study of Heart Failure Patients.
10. Scognamiglio, R et al. Nifedipine in Asymptomatic Patients with Severe Aortic Regurgitation and Normal Left Ventricular Function. NEJM 1994; 331: 689-694.
11. CONSENSUS Trial Study Group. Effects of Enalapril of Mortality in Severe Congestive Heart Failure: Results of the Cooperative North Scandinavian Enalapril Survival Study. NEJM 1987; 316: 1429- 1438.
12. SOLVD Investigators. Effect of Enalapril on Survival of Patients with Reduced Left Ventricular Ejection Fraction and Congestive Heart Failure. NEJM 1991; 325: 293-302.
13. Levine, BT. Reverse Remodeling in Heart Failure with Intensification of Vasodilator Therapy. Clin Cardiol 1997; 20: 697-702.
14. Pitt, B et al. RALES Study 1998.
15. Parker, M et al. For the RADIANCE Study. Withdrawal of Digoxin from Patients with Chronic Heart Failure Treated with Angiotensin Converting-Enzyme Inhibitors. NEJM 1993; 329: 1-7.
16. Young, JB et al. Superiority of "Triple" Drug Therapy in Congestive Heart Failure: insights from the PROVED and RADIANCE trials. First International Meeting of the Working Group on Heart Failure Proceedings. 1998; 829: 54 Abstract.
17. Packer, M et al. Effect of Carvedilol on Morbidity and Mortality in Patients with Chronic Heart Failure. NEJM 1996; 334: 1349-1355.
18. McKelvie, RS et al. Effects of Exercise Training in Patients with Congestive Heart Failure. J. Am. Coll. Cardiol. 1995; 25: 789-796.
19. Stewart, S et al. Effects of a Home-Based Intervention Among Patients with Congestive Heart Failure Discharged from an Acute Care Hospital. Arch Int Med 1998; 158: 1067-1072.
20. Reis, SE et al. Treatment of Patients Admitted to the Hospital with CHF: specialty related disparities in practice patterns and outcomes. J. Am Coll Cardiol 1997; 30: 733-738.
21. Noyes, DA et al. Outcomes of an Advanced Practice Nurse Home Care Program for Heart Failure Patients. Circ 1998; I-483. |
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