24
CHAPTER 5
Chronic heart failure Dr Michael Cripwell, MRCGP Dr David Patterson, MD, FRCP
SUMMARY 1. The common symptoms and signs of chronic heart failure are dyspnoea, ankle swelling, raised jugular venous pressure and basal crepitations. Other conditions may be confused with chronic heart failure, including dependent oedema or oedema due to renal or hepatic disease. Shortness of breath may be due to respiratory disease or severe anaemia. Heart failure secondary to lung disease (cor pulmonale) should be distinguished from congestive cardiac failure. Heart failure may also present with less common symptoms including: cough, anorexia and weight loss, hepatic capsule pain and confusion. 2. Once heart failure is recognized, an attempt should be made to determine the underlying cause which may include valvular abnormalities, altered cardiac rhythm, specific heart muscle disease, coronary artery disease and hypertension. 3. Investigations initiated by the general practitioner include ECG, chest x-ray, full blood count (FBC), mean corpuscular volume (MCV), gamma transferase (G77T), creatinine and electrolytes, thyroxine. 4. If no underlying cause is found then referral should be considered in those under 75 and those aged 75 and over who fail to respond to treatment. 5. It is important to encourage patients to stop smoking, reduce weight and, where appropriate, alcohol consumption. Added salt should be avoided. 6. Digoxin should be prescribed to control the ventricular rate in those with atrial fibrillation. Renal function and potassium should be checked beforehand and the dose of digoxin adjusted to take into account any renal impairment. 7. Bendrofluazide is recommended in doses of not more than 10 mg (5 mg in the elderly). Potassium supplements may be requiredfor those at high riskfrom hypokalaemia, including patients taking digoxin. Amiloride can be added if the heart failure is not adequately controlled. 8. For more severe heart failure a loop diuretic such as frusemide (starting at 40 mg daily) will be required. Potassium supplements or amiloride will probably be 9 needed. 9. Vasodilators are the next line of treatment. The angiotensin converting enzyme (ACE) inhibitors are very effective and have been shown to increase life expectancy. They may cause severe hypotension following the first dose, particularly in patients taking diuretics. Thus, if diuretics cannot be stoppedfor at least a day, hospital admission may be needed.
10. Regular follow-up is necessary to check the efficacy of treatment. Regular weighing is useful and urea and electrolytes should be checked, the frequency depending on the severity, drugs used and renal function. 11. Patients should be encouraged to lead as normal a life as is possible within the constraints of their symptoms.
Introduction These guidelines consider the management of chronic but not acute heart failure. Diagnosis Chronic heart failure is not a diagnosis in itself. It is a condition that results from the impaired function of the heart together with a failure of the compensating mechanisms. The heart is unable to provide sufficient blood for the tissues' metabolic needs. The common symptoms and signs of chronic heart failure are: tiredness or lack of energy, dyspnoea, ankle swelling, raised jugular venous pressure and basal crepitations. There are however some important diagnostic pitfalls: 1. Ankle oedema is an unreliable sign of heart failure; it may simply be dependent oedema or due to renal or hepatic disease. 2. Shortness of breath may be caused by heart failure but it can also be the result of respiratory disease, severe anaemia or an unfit patient. The possibility of hyperventilation due to metabolic acidosis also needs to be kept in mind. 3. It is important to distinguish heart failure which is secondary to lung disease (cor pulmonale) from heart failure secondary to left heart failure since the management will differ. Left heart failure may exist for several years before it progresses to right heart failure with the signs of oedema and elevated jugular venous pressure (JVP). 4. After a period of bed rest there may be a normal JVP despite severe heart failure. Less common presentations of heart failure include: 1. Persistent dry cough, especially in young adults. 2. Anorexia and weight loss (due to engorgement of the splanchnic circulation). 3. Hepatic capsule pain (due to a distended liver) when occurring on exertion may be wrongly diagnosed as angina. The tenderness in the right upper abdominal quadrant and may lead to misdiagnosis of gall bladder disease.
25 4. Confusion and personality change (secondary to poor cerebral circulation). 5. Cold peripheries (due to vasoconstriction). 6. General malaise and weakness. The diagnosis can more confidently be made when there is clear evidence of increased atrial filling pressure, namely elevated JVP and/or congestive changes on chest x-ray. In many cases, however, the complete pattern of symptoms and signs together with the results of investigations need to be considered when reaching a diagnosis.
Assessment The New York Heart Association has classified heart failure according to the severity of symptoms (Goldman et al., 1981): No limitation of physical activity Class I: Class II: Symptoms with ordinary daily activity Class III: Symptoms of minimal exertion Class IV: Symptoms at rest. This classification is useful in recording the functional state of the patient over a prolonged follow-up period and also for communicating the severity of disability. The classification can be quite helpful in monitoring the progress of a patient. Once heart failure is recognized, assessment should include an attempt to identify an underlying cause. Major causes include: * Valvular abnormalities * Congenital heart disease * Specific heart muscle disease * Altered cardiac rhythm * Coronary artery disease * Cardiomyopathy * Lung disease * Systemic hypertension. Rarer causes include: * Recurrent pulmonary emboli * Myocarditis * Thyrotoxicosis * Endocarditis. A number of drugs may contribute to the development of heart failure, for example beta blockers, some calcium antagonists, and salt and water retaining drugs such as carbenoxolone and non-steroidal anti-inflammatory drugs. Similarly pregnancy, infections and anaemia associated with other factors may precipitate heart failure. Microvascular and macrovascular disease in diabetes may also contribute.
Investigations initiated by the general practitioner The main aim of investigation is to pick out cases that may be amenable to specific medical or surgical treatment: 1. ECG may indicate ischaemia or infarction, arrhythmias or atrial and ventricular hypertrophy. 2. Chest x-ray will show heart size and evidence of pulmonary congestion or pleural effusions.
3. FBC, MCV and gamma GT may be raised in those patients where there is alcohol excess. 4. Urea, creatinine and electrolytes. 5. Serum thyroxine if there is any clinical evidence of
thyrotoxicosis. If the symptoms, signs or investigations suggest a cause that is treatable by surgery then the patient should be referred to a cardiologist without delay. For example, heart failure secondary to aortic valve disease has a high mortality at one year; the absence of cardiomegaly should not be a reason for delaying an operation. Other surgically treatable causes include: mitral valve disease, septal defects secondary to myocardial infarction, and left ventricular aneurysm. If the investigations initiated by the general practitioner do not indicate any apparent underlying cause then a non-urgent cardiologist's opinion should be sought in those under 75. Cardiology department investigations may include echocardiography, doppler-cardiography, cardiac catheterization, angiography and 24-hour ambulatory ECG. (Echo cardiography and 24-hour ambulatory ECG are now available by direct access for general practitioners in Bloomsbury and Islington District who have attended a training session.) In those aged 75 and over, indications for referral are the possibility of aortic stenosis, significant arrhythmias, possible pulmonary emboli and failure to respond to diuretics and digoxin, or if their condition prohibits introduction of vasodilators at home (see below).
Treatment In this section it is assumed that surgically treatable lesions have been excluded.
Non-drug therapy In newly diagnosed chronic heart failure there is some value in bed rest for a few days. This reduces workload and may increase renal perfusion leading to diuresis. However, the period of bed rest for patients at home should probably be for only one or two days because the benefit must be balanced against the increased risks of venous thrombosis. Heart failure carries a poor long-term prognosis (Wilson, 1984) and it is vital that as many as possible of the risk factors for relapse and progression are reduced (Cleland et al., 1987). It is therefore particularly important for patients to stop smoking, reduce weight if overweight, and reduce alcohol consumption. Adjustments may need to be made in lifestyle to reduce, as far as possible, chronic stress and fatigue. Restrictions may need to be placed on strenuous physical activity but patients should be encouraged to maintain a reasonable fitness by regular exercise. Patients should be advised to avoid adding salt to their food. Drug treatment The cause of the heart failure as well as its severity should be considered when planning drug treatment. When atrial fibrillation is one of the precipitating causes, digoxin is effective in controlling the ventricular rate. The evidence that it exerts any long-term inotropic effect on the heart muscle is controversial (Chamberlain, 1985); some patients
26
in sinus rhythm do derive some benefit and it does, therefore, have a role in these patients but in view of its increasing toxicity with age, it is probably best prescribed only for its anti-arrhythmic effects in the elderly. Before prescribing digoxin assess renal function and serum potassium (the elderly may have normal serum creatinine despite a significantly reduced glomerular filtration rate). A formula corrected for age and weight gives a more accurate prediction of renal function (see Weatherell et al., 1987). In the presence of severe renal impairment (ie reduction of glomerular filtration rate to less than 10 ml per minute) the daily dosage of digoxin may need to be as low as 62.5 mcg. Serum digoxin levels are of limited value because of the considerable overlap between the therapeutic and toxic values. They are of some use when trying to establish whether the dosage is adequate. The principal long-term drugs for treating established heart failure used to be diuretics. However there are now a number of alternative possibilities. The following scheme of treatment is suggested: 1. Bendrofluazide 5 mg (2.5 mg in the elderly) increasing to 10 mg daily (5 mg in the elderly). Urea and electrolytes need to be monitored as hyponatraemia and hypokalaemia may develop. Potassium supplements may be required for those most at risk from hypokalaemia. These include those on digoxin, antidepressants, and tranquillizers. Potassium supplements may lead to hyperkalaemia in those with renal impairment. 2. If heart failure is not adequately controlled by 10 mg of bendrofluazide then 5-10 mg of amiloride can be added (more conveniently taken as a combination tablet, eg hydrochlorothiazide 50 mg and amiloride 5 mg - Moduretic). The potassium-sparing amiloride has the advantage of making potassium supplements unnecessary but may lead to hyponatraemia. 3. For more severe heart failure a loop diuretic will be required such as frusemide, starting at 40 mg daily. Potassium supplements will probably be required; alternatively, amiloride can be added (frusemide 40 mg plus amiloride 5 mg is available as a combination tablet - Frumil). The dose may be doubled to 80 mg of frusemide and 10 mg of amiloride daily if necessary. The potassium-sparing aldosterone antagonist spironolactone in a dose of 100-200 mg daily may be used in place of amiloride. Traditionally, spironolactone has been considered particularly useful when features of right heart failure predominate with hepatic congestion and possible secondary hyperaldosteronism. It takes about three days for this drug to exert its full diuretic effect. But in view of recent reports of possible carcinogenicity this drug should be used only if alternative drug treatment has failed. If heart failure is still not controlled on 80 mg daily of frusemide plus amiloride or spironolactone, then the underlying diagnosis needs to be reconsidered and probably a cardiologist's opinion sought before adding further treatment. Some of the reasons for progression and relapse of heart failure will be considered below and further treatment will need to be directed at these developments. 4. The next step in treatment of severe cardiac failure is the use of vasodilators. These act by reducing preload (or end diastolic ventricular volume) and afterload (which is a measure of the resistance which the ventricle must overcome
to eject its stroke volume). By reducing one or both, the vasodilators enhance myocardial function (Table 1). Vasodilators have to be used with caution since, if they are given to a patient in heart failure who is hypovolaemic, they will reduce cardiac output and this may render the patient very ill. The use of nitrates is limited by a compensating tachycardia. Prazosin is an effective drug and can be used when heart failure is not being controlled with diuretics. Nifedipine has a negative inotropic effect but is still useful particularly when the patient has angina or hypertension. Table 1
Vasodilator drugs used in heart failure.
Drug
Isosorbide dinitrate Isosorbide mononitrate Prazosin Nifedipine Enalapril Captopril Lisinopril
Main effect
Initial dose
Maintenance dose
V
10 mg tds
up to 40 mg tds
V
5 mg tds 0.5 mg tds 5 mg tds 2.5 mg 6.25-12.5 mg 2.5 mg
up to 20 mg tds up to 8 mg tds up to 20 mg bd up to 20 mg bd up to 25 mg tds up to 20 mg daily
A A V&A V&A V&A
V=predominant veno-dilator A=predominant arterio-dilator
The ACE inhibitors captopril, enalapril or lisinopril are mixed arteriolar and venodilators which have proved very effective in severe heart failure. They improve well-being and exercise capacity and have been shown to increase life expectancy in these patients (Cooperative North Scandinavian Enalapril Survival Study, 1987). There is a possibility, however, of severe hypotension following the first dose particularly in patients taking diuretics and thus patients should be closely monitored for several hours following initiation of therapy. Where possible, diuretics should be stopped for at least one day before commencing the drug. If the severity of the chronic heart failure precludes stopping diuretics, ACE inhibitors are best initiated in hospital. If hypotension does occur then it will probably happen within an hour or so of taking the first dose. It can usually be effectively treated by putting the patient in a head down position and raising the legs. Occasionally intravenous fluids have to be given rapidly to correct the hypotension. It takes up to four weeks for ACE inhibitors to exert their maximum effect. The principal side-effects of the ACE inhibitors are worsening of renal function and hyperkalaemia. Urea and electrolytes should be measured twice-weekly when a patient is being started on these drugs. The danger of hyperkalaemia is increased if amiloride or a prostaglandin synthetase inhibitor such as indomethacin is being prescribed. Other side-effects include neutropenia, loss of taste and dry cough. Although vasodilators are effective in treatment of the patient with heart failure secondary to mitral incompetence, they are dangerous if used in a patient with aortic or mitral stenosis. An as yet unanswered question is whether ACE inhibitors should continue to be used only when diuretics fail or whether they should be introduced earlier in the course of the disease. Diuretic therapy will continue to be required in patients on ACE inhibitors; usually the potassium-sparing diuretic can be stopped.
27
Monitoring and follow-up All patients on an established regimen of treatment for chronic heart failure will need to be seen at 2-3 monthly intervals to assess continuing efficacy of treatment. Checks on blood urea and electrolytes will usually need to be performed about every six months. The frequency of blood tests will depend on the severity of the heart failure, renal function and the drugs being used. Any patient on diuretics for chronic heart failure should probably have annual urea and electrolyte checks. If changes are being made to treatment they will need to be seen more frequently. Regular measurement of weight can be a good guide to increasing fluid overload due to heart failure. Relapse is common and the five likely causes are: 1. Poor compliance with treatment (common particularly in the elderly) 2. Incorrect dose of drugs, for example too much digoxin leading to toxicity or too much frusemide leading to hypovolaemia which stimulates the renin-angiotensinaldosterone axis resulting in secondary hyperaldosteronism and salt and water, retention 3. Effects of other medication, for example beta blockers, anti-arrhythmics such as verapamil and salt- and waterretaining drugs such as NSAIDs or carbenoxolone 4. New pathology, for example silent myocardial infarction, pulmonary embolism and arrhythmias 5. Complications of CCF, for example impaired hepatic function leading to impaired albumen synthesis and impaired aldosterone and renin degradation. The patient should be advised to see his or her general practitioner if there is a return of such symptoms as increasing dyspnoea or ankle oedema. In view of the poor prognosis of chronic heart failure and the success of newer treatments, a periodic review is necessary. Monitoring of repeat prescriptions enables periodic follow-up to be arranged, although those who stop taking medication altogether may only be picked up by regular review of a disease register. It is helpful when monitoring the patient with heart failure if both positive and negative findings on examination are recorded in the notes. For example, the entry that there was no murmur on a previous examination is very valuable if the patient relapses and this time a murmur is present.
Information for the patient and family The term 'heart failure' may be taken by a patient to imply a terminal illness; despair is a normal reaction to chronic heart disease. Time needs to be spent explaining that there are
effective treatments; emphasis needs to be given to the importance of lifestyle and compliance with drug treatment. Most patients should be encouraged to live as normal a life as possible within the constraints of the symptoms and to continue with activities until tired, when they should rest. The question of sexual relationships needs to be discussed bearing in mind that symptoms of heart failure include exertional dyspnoea and orthopnoea. The possibility of impotence in men resulting from treatment (for example high doses of thiazides) needs to be considered. The patient will need to be reassured that moderate levels of activity including sexual intercourse does not lead to worsening of heart failure. In severe heart failure which precludes penetrative intercourse patients may need to be encouraged to express affection by other forms of physical contact. Sufficient time must be allowed in follow-up appointments to enable patients to express their fears about the illness while at the same time offering on-going support and advice.
Audit points The following groups are suitable subjects for audit: 1. The proportion of patients with chronic heart failure in whom there is evidence that an underlying cause has been looked for 2. The proportion of patients who have been reviewed in the last six months and have had recordings of weight, pulse, blood pressure, auscultation of the lungs and functional capacity 3. The proportion of those on diuretics who have had their electrolytes measured in the last year 4. The proportion of patients with severe heart failure (NY Heart Association Class 3 or 4) who are being treated with ACE inhibitors.
References Chamberlain D A ( 1985) Digitalis where are we now? British Heart Journal 54, 227-33. Cleland W and Dargie F (1987) Mortality in heart failure: clinical variables of prognostic value. British Heart Journal 58, 572-82. Cooperative North Scandinavian Enalapril Survival Study (1987) Effects of enalapril on mortality in severe congestive heart failure. New England Journal of Medicine 316, 1429-34. Goldman L, Hashimoto B, Cook EF et al. (1981) Comparative reproducability and validity of systems for assessing cardiovascular functional class: advantages of a new specific activity scale. Circulation 64, 1227-30. Weatherell D J, Ledingham J G G and Warrell D A (Eds) (1987) Oxford Textbook of Medicine. London, OUP. Wilson J R (1984) How and why patients with chronic heart failure die. International Journal of Cardiology 6, 255-8.
CHAPTER 5
Chronic heart failure Dr Michael Cripwell, MRCGP Dr David Patterson, MD, FRCP
SUMMARY 1. The common symptoms and signs of chronic heart failure are dyspnoea, ankle swelling, raised jugular venous pressure and basal crepitations. Other conditions may be confused with chronic heart failure, including dependent oedema or oedema due to renal or hepatic disease. Shortness of breath may be due to respiratory disease or severe anaemia. Heart failure secondary to lung disease (cor pulmonale) should be distinguished from congestive cardiac failure. Heart failure may also present with less common symptoms including: cough, anorexia and weight loss, hepatic capsule pain and confusion. 2. Once heart failure is recognized, an attempt should be made to determine the underlying cause which may include valvular abnormalities, altered cardiac rhythm, specific heart muscle disease, coronary artery disease and hypertension. 3. Investigations initiated by the general practitioner include ECG, chest x-ray, full blood count (FBC), mean corpuscular volume (MCV), gamma transferase (G77T), creatinine and electrolytes, thyroxine. 4. If no underlying cause is found then referral should be considered in those under 75 and those aged 75 and over who fail to respond to treatment. 5. It is important to encourage patients to stop smoking, reduce weight and, where appropriate, alcohol consumption. Added salt should be avoided. 6. Digoxin should be prescribed to control the ventricular rate in those with atrial fibrillation. Renal function and potassium should be checked beforehand and the dose of digoxin adjusted to take into account any renal impairment. 7. Bendrofluazide is recommended in doses of not more than 10 mg (5 mg in the elderly). Potassium supplements may be requiredfor those at high riskfrom hypokalaemia, including patients taking digoxin. Amiloride can be added if the heart failure is not adequately controlled. 8. For more severe heart failure a loop diuretic such as frusemide (starting at 40 mg daily) will be required. Potassium supplements or amiloride will probably be 9 needed. 9. Vasodilators are the next line of treatment. The angiotensin converting enzyme (ACE) inhibitors are very effective and have been shown to increase life expectancy. They may cause severe hypotension following the first dose, particularly in patients taking diuretics. Thus, if diuretics cannot be stoppedfor at least a day, hospital admission may be needed.
10. Regular follow-up is necessary to check the efficacy of treatment. Regular weighing is useful and urea and electrolytes should be checked, the frequency depending on the severity, drugs used and renal function. 11. Patients should be encouraged to lead as normal a life as is possible within the constraints of their symptoms.
Introduction These guidelines consider the management of chronic but not acute heart failure. Diagnosis Chronic heart failure is not a diagnosis in itself. It is a condition that results from the impaired function of the heart together with a failure of the compensating mechanisms. The heart is unable to provide sufficient blood for the tissues' metabolic needs. The common symptoms and signs of chronic heart failure are: tiredness or lack of energy, dyspnoea, ankle swelling, raised jugular venous pressure and basal crepitations. There are however some important diagnostic pitfalls: 1. Ankle oedema is an unreliable sign of heart failure; it may simply be dependent oedema or due to renal or hepatic disease. 2. Shortness of breath may be caused by heart failure but it can also be the result of respiratory disease, severe anaemia or an unfit patient. The possibility of hyperventilation due to metabolic acidosis also needs to be kept in mind. 3. It is important to distinguish heart failure which is secondary to lung disease (cor pulmonale) from heart failure secondary to left heart failure since the management will differ. Left heart failure may exist for several years before it progresses to right heart failure with the signs of oedema and elevated jugular venous pressure (JVP). 4. After a period of bed rest there may be a normal JVP despite severe heart failure. Less common presentations of heart failure include: 1. Persistent dry cough, especially in young adults. 2. Anorexia and weight loss (due to engorgement of the splanchnic circulation). 3. Hepatic capsule pain (due to a distended liver) when occurring on exertion may be wrongly diagnosed as angina. The tenderness in the right upper abdominal quadrant and may lead to misdiagnosis of gall bladder disease.
25 4. Confusion and personality change (secondary to poor cerebral circulation). 5. Cold peripheries (due to vasoconstriction). 6. General malaise and weakness. The diagnosis can more confidently be made when there is clear evidence of increased atrial filling pressure, namely elevated JVP and/or congestive changes on chest x-ray. In many cases, however, the complete pattern of symptoms and signs together with the results of investigations need to be considered when reaching a diagnosis.
Assessment The New York Heart Association has classified heart failure according to the severity of symptoms (Goldman et al., 1981): No limitation of physical activity Class I: Class II: Symptoms with ordinary daily activity Class III: Symptoms of minimal exertion Class IV: Symptoms at rest. This classification is useful in recording the functional state of the patient over a prolonged follow-up period and also for communicating the severity of disability. The classification can be quite helpful in monitoring the progress of a patient. Once heart failure is recognized, assessment should include an attempt to identify an underlying cause. Major causes include: * Valvular abnormalities * Congenital heart disease * Specific heart muscle disease * Altered cardiac rhythm * Coronary artery disease * Cardiomyopathy * Lung disease * Systemic hypertension. Rarer causes include: * Recurrent pulmonary emboli * Myocarditis * Thyrotoxicosis * Endocarditis. A number of drugs may contribute to the development of heart failure, for example beta blockers, some calcium antagonists, and salt and water retaining drugs such as carbenoxolone and non-steroidal anti-inflammatory drugs. Similarly pregnancy, infections and anaemia associated with other factors may precipitate heart failure. Microvascular and macrovascular disease in diabetes may also contribute.
Investigations initiated by the general practitioner The main aim of investigation is to pick out cases that may be amenable to specific medical or surgical treatment: 1. ECG may indicate ischaemia or infarction, arrhythmias or atrial and ventricular hypertrophy. 2. Chest x-ray will show heart size and evidence of pulmonary congestion or pleural effusions.
3. FBC, MCV and gamma GT may be raised in those patients where there is alcohol excess. 4. Urea, creatinine and electrolytes. 5. Serum thyroxine if there is any clinical evidence of
thyrotoxicosis. If the symptoms, signs or investigations suggest a cause that is treatable by surgery then the patient should be referred to a cardiologist without delay. For example, heart failure secondary to aortic valve disease has a high mortality at one year; the absence of cardiomegaly should not be a reason for delaying an operation. Other surgically treatable causes include: mitral valve disease, septal defects secondary to myocardial infarction, and left ventricular aneurysm. If the investigations initiated by the general practitioner do not indicate any apparent underlying cause then a non-urgent cardiologist's opinion should be sought in those under 75. Cardiology department investigations may include echocardiography, doppler-cardiography, cardiac catheterization, angiography and 24-hour ambulatory ECG. (Echo cardiography and 24-hour ambulatory ECG are now available by direct access for general practitioners in Bloomsbury and Islington District who have attended a training session.) In those aged 75 and over, indications for referral are the possibility of aortic stenosis, significant arrhythmias, possible pulmonary emboli and failure to respond to diuretics and digoxin, or if their condition prohibits introduction of vasodilators at home (see below).
Treatment In this section it is assumed that surgically treatable lesions have been excluded.
Non-drug therapy In newly diagnosed chronic heart failure there is some value in bed rest for a few days. This reduces workload and may increase renal perfusion leading to diuresis. However, the period of bed rest for patients at home should probably be for only one or two days because the benefit must be balanced against the increased risks of venous thrombosis. Heart failure carries a poor long-term prognosis (Wilson, 1984) and it is vital that as many as possible of the risk factors for relapse and progression are reduced (Cleland et al., 1987). It is therefore particularly important for patients to stop smoking, reduce weight if overweight, and reduce alcohol consumption. Adjustments may need to be made in lifestyle to reduce, as far as possible, chronic stress and fatigue. Restrictions may need to be placed on strenuous physical activity but patients should be encouraged to maintain a reasonable fitness by regular exercise. Patients should be advised to avoid adding salt to their food. Drug treatment The cause of the heart failure as well as its severity should be considered when planning drug treatment. When atrial fibrillation is one of the precipitating causes, digoxin is effective in controlling the ventricular rate. The evidence that it exerts any long-term inotropic effect on the heart muscle is controversial (Chamberlain, 1985); some patients
26
in sinus rhythm do derive some benefit and it does, therefore, have a role in these patients but in view of its increasing toxicity with age, it is probably best prescribed only for its anti-arrhythmic effects in the elderly. Before prescribing digoxin assess renal function and serum potassium (the elderly may have normal serum creatinine despite a significantly reduced glomerular filtration rate). A formula corrected for age and weight gives a more accurate prediction of renal function (see Weatherell et al., 1987). In the presence of severe renal impairment (ie reduction of glomerular filtration rate to less than 10 ml per minute) the daily dosage of digoxin may need to be as low as 62.5 mcg. Serum digoxin levels are of limited value because of the considerable overlap between the therapeutic and toxic values. They are of some use when trying to establish whether the dosage is adequate. The principal long-term drugs for treating established heart failure used to be diuretics. However there are now a number of alternative possibilities. The following scheme of treatment is suggested: 1. Bendrofluazide 5 mg (2.5 mg in the elderly) increasing to 10 mg daily (5 mg in the elderly). Urea and electrolytes need to be monitored as hyponatraemia and hypokalaemia may develop. Potassium supplements may be required for those most at risk from hypokalaemia. These include those on digoxin, antidepressants, and tranquillizers. Potassium supplements may lead to hyperkalaemia in those with renal impairment. 2. If heart failure is not adequately controlled by 10 mg of bendrofluazide then 5-10 mg of amiloride can be added (more conveniently taken as a combination tablet, eg hydrochlorothiazide 50 mg and amiloride 5 mg - Moduretic). The potassium-sparing amiloride has the advantage of making potassium supplements unnecessary but may lead to hyponatraemia. 3. For more severe heart failure a loop diuretic will be required such as frusemide, starting at 40 mg daily. Potassium supplements will probably be required; alternatively, amiloride can be added (frusemide 40 mg plus amiloride 5 mg is available as a combination tablet - Frumil). The dose may be doubled to 80 mg of frusemide and 10 mg of amiloride daily if necessary. The potassium-sparing aldosterone antagonist spironolactone in a dose of 100-200 mg daily may be used in place of amiloride. Traditionally, spironolactone has been considered particularly useful when features of right heart failure predominate with hepatic congestion and possible secondary hyperaldosteronism. It takes about three days for this drug to exert its full diuretic effect. But in view of recent reports of possible carcinogenicity this drug should be used only if alternative drug treatment has failed. If heart failure is still not controlled on 80 mg daily of frusemide plus amiloride or spironolactone, then the underlying diagnosis needs to be reconsidered and probably a cardiologist's opinion sought before adding further treatment. Some of the reasons for progression and relapse of heart failure will be considered below and further treatment will need to be directed at these developments. 4. The next step in treatment of severe cardiac failure is the use of vasodilators. These act by reducing preload (or end diastolic ventricular volume) and afterload (which is a measure of the resistance which the ventricle must overcome
to eject its stroke volume). By reducing one or both, the vasodilators enhance myocardial function (Table 1). Vasodilators have to be used with caution since, if they are given to a patient in heart failure who is hypovolaemic, they will reduce cardiac output and this may render the patient very ill. The use of nitrates is limited by a compensating tachycardia. Prazosin is an effective drug and can be used when heart failure is not being controlled with diuretics. Nifedipine has a negative inotropic effect but is still useful particularly when the patient has angina or hypertension. Table 1
Vasodilator drugs used in heart failure.
Drug
Isosorbide dinitrate Isosorbide mononitrate Prazosin Nifedipine Enalapril Captopril Lisinopril
Main effect
Initial dose
Maintenance dose
V
10 mg tds
up to 40 mg tds
V
5 mg tds 0.5 mg tds 5 mg tds 2.5 mg 6.25-12.5 mg 2.5 mg
up to 20 mg tds up to 8 mg tds up to 20 mg bd up to 20 mg bd up to 25 mg tds up to 20 mg daily
A A V&A V&A V&A
V=predominant veno-dilator A=predominant arterio-dilator
The ACE inhibitors captopril, enalapril or lisinopril are mixed arteriolar and venodilators which have proved very effective in severe heart failure. They improve well-being and exercise capacity and have been shown to increase life expectancy in these patients (Cooperative North Scandinavian Enalapril Survival Study, 1987). There is a possibility, however, of severe hypotension following the first dose particularly in patients taking diuretics and thus patients should be closely monitored for several hours following initiation of therapy. Where possible, diuretics should be stopped for at least one day before commencing the drug. If the severity of the chronic heart failure precludes stopping diuretics, ACE inhibitors are best initiated in hospital. If hypotension does occur then it will probably happen within an hour or so of taking the first dose. It can usually be effectively treated by putting the patient in a head down position and raising the legs. Occasionally intravenous fluids have to be given rapidly to correct the hypotension. It takes up to four weeks for ACE inhibitors to exert their maximum effect. The principal side-effects of the ACE inhibitors are worsening of renal function and hyperkalaemia. Urea and electrolytes should be measured twice-weekly when a patient is being started on these drugs. The danger of hyperkalaemia is increased if amiloride or a prostaglandin synthetase inhibitor such as indomethacin is being prescribed. Other side-effects include neutropenia, loss of taste and dry cough. Although vasodilators are effective in treatment of the patient with heart failure secondary to mitral incompetence, they are dangerous if used in a patient with aortic or mitral stenosis. An as yet unanswered question is whether ACE inhibitors should continue to be used only when diuretics fail or whether they should be introduced earlier in the course of the disease. Diuretic therapy will continue to be required in patients on ACE inhibitors; usually the potassium-sparing diuretic can be stopped.
27
Monitoring and follow-up All patients on an established regimen of treatment for chronic heart failure will need to be seen at 2-3 monthly intervals to assess continuing efficacy of treatment. Checks on blood urea and electrolytes will usually need to be performed about every six months. The frequency of blood tests will depend on the severity of the heart failure, renal function and the drugs being used. Any patient on diuretics for chronic heart failure should probably have annual urea and electrolyte checks. If changes are being made to treatment they will need to be seen more frequently. Regular measurement of weight can be a good guide to increasing fluid overload due to heart failure. Relapse is common and the five likely causes are: 1. Poor compliance with treatment (common particularly in the elderly) 2. Incorrect dose of drugs, for example too much digoxin leading to toxicity or too much frusemide leading to hypovolaemia which stimulates the renin-angiotensinaldosterone axis resulting in secondary hyperaldosteronism and salt and water, retention 3. Effects of other medication, for example beta blockers, anti-arrhythmics such as verapamil and salt- and waterretaining drugs such as NSAIDs or carbenoxolone 4. New pathology, for example silent myocardial infarction, pulmonary embolism and arrhythmias 5. Complications of CCF, for example impaired hepatic function leading to impaired albumen synthesis and impaired aldosterone and renin degradation. The patient should be advised to see his or her general practitioner if there is a return of such symptoms as increasing dyspnoea or ankle oedema. In view of the poor prognosis of chronic heart failure and the success of newer treatments, a periodic review is necessary. Monitoring of repeat prescriptions enables periodic follow-up to be arranged, although those who stop taking medication altogether may only be picked up by regular review of a disease register. It is helpful when monitoring the patient with heart failure if both positive and negative findings on examination are recorded in the notes. For example, the entry that there was no murmur on a previous examination is very valuable if the patient relapses and this time a murmur is present.
Information for the patient and family The term 'heart failure' may be taken by a patient to imply a terminal illness; despair is a normal reaction to chronic heart disease. Time needs to be spent explaining that there are
effective treatments; emphasis needs to be given to the importance of lifestyle and compliance with drug treatment. Most patients should be encouraged to live as normal a life as possible within the constraints of the symptoms and to continue with activities until tired, when they should rest. The question of sexual relationships needs to be discussed bearing in mind that symptoms of heart failure include exertional dyspnoea and orthopnoea. The possibility of impotence in men resulting from treatment (for example high doses of thiazides) needs to be considered. The patient will need to be reassured that moderate levels of activity including sexual intercourse does not lead to worsening of heart failure. In severe heart failure which precludes penetrative intercourse patients may need to be encouraged to express affection by other forms of physical contact. Sufficient time must be allowed in follow-up appointments to enable patients to express their fears about the illness while at the same time offering on-going support and advice.
Audit points The following groups are suitable subjects for audit: 1. The proportion of patients with chronic heart failure in whom there is evidence that an underlying cause has been looked for 2. The proportion of patients who have been reviewed in the last six months and have had recordings of weight, pulse, blood pressure, auscultation of the lungs and functional capacity 3. The proportion of those on diuretics who have had their electrolytes measured in the last year 4. The proportion of patients with severe heart failure (NY Heart Association Class 3 or 4) who are being treated with ACE inhibitors.
References Chamberlain D A ( 1985) Digitalis where are we now? British Heart Journal 54, 227-33. Cleland W and Dargie F (1987) Mortality in heart failure: clinical variables of prognostic value. British Heart Journal 58, 572-82. Cooperative North Scandinavian Enalapril Survival Study (1987) Effects of enalapril on mortality in severe congestive heart failure. New England Journal of Medicine 316, 1429-34. Goldman L, Hashimoto B, Cook EF et al. (1981) Comparative reproducability and validity of systems for assessing cardiovascular functional class: advantages of a new specific activity scale. Circulation 64, 1227-30. Weatherell D J, Ledingham J G G and Warrell D A (Eds) (1987) Oxford Textbook of Medicine. London, OUP. Wilson J R (1984) How and why patients with chronic heart failure die. International Journal of Cardiology 6, 255-8.
