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Ashley EA, Niebauer J. Cardiology Explained. London: Remedica; 2004.

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Cardiology Explained.

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Chapter 7Heart failure


The survival rate for myocardial infarction (MI) has greatly increased in recent years due to the success of thrombolysis and primary angioplasty. However, the ensuing epidemic of heart failure has created a major public health problem. Data from the UK suggest that heart failure affects approximately 2% of the population. Furthermore, the prognosis for chronic heart failure (CHF) is poor: a patient admitted to hospital with pulmonary edema has a poorer prognosis (the 5-year mortality rate is around 50%) than a patient presenting with a carcinoma in any organ other than the lung.

The many causes of heart failure (see Table 1) operate through the central mechanism of reduced ventricular function. As a consequence, the heart is unable to perfuse the tissues adequately. The resulting clinical syndrome (see Table 2) can be explained by compensatory measures, such as cardiac hypertrophy and activation of the sympathetic nervous system and the renin–angiotensin system.

Table 1. Causes of heart failure.

Table 1

Causes of heart failure.

Table 2. The multiorgan symptoms of heart failure.

Table 2

The multiorgan symptoms of heart failure.

Heart failure is categorized as either systolic or diastolic. Systolic dysfunction is due to poor left ventricular (LV) contraction, usually expressed as ejection fraction (EF). Heart failure patients with diastolic dysfunction (more common in the elderly) have normal LV ejection fraction; the defect seems to lie in relaxation of the left ventricle and is associated with delayed filling. For the generalist, one clue to diastolic dysfunction lies in the chest x-ray (CXR), which can show signs of congestion without significant LV dilatation. However, echocardiography is required for a firm diagnosis (see Chapter 4, Understanding the echocardiogram).


The approach to heart failure has changed enormously over the past few years (see Figure 1). Earlier thinking focused on inadequate pump function and the accepted therapeutic wisdom was to bolster it with β-agonist inotropes. The idea of treating heart failure by blocking the sympathetic nervous system would have been regarded as heretical and dangerous. However, it has now been realized that most CHF pathology is a result of the body's own compensatory mechanisms (see Figure 2) and that interrupting these neurohumoral pathways achieves more than attempting to "overdrive" the failing heart. The exception is acute decompensation (acute heart failure, pulmonary edema, cardiogenic shock), where the focus is on short-term survival; although the primary aim is still the reduction of preload and afterload using diuretics and vasodilators, inotropes in the form of β-agonists are also used.

Figure 1. Treatment of heart failure according to (a) old and (b) new paradigms.

Figure 1

Treatment of heart failure according to (a) old and (b) new paradigms. ADH: antidiuretic hormone (vasopressin).

Figure 2. Chronic heart failure.

Figure 2

Chronic heart failure. TNF: tumor necrosis factor.

Clinical history and examination

The hallmark of heart failure is dyspnea. The classic combination of raised jugular venous pressure (JVP), peripheral edema, palpable liver, basal crepitations, tachycardia, and a third heart sound is well known. Orthopnea (shortness of breath when lying flat) and paroxysmal nocturnal dyspnea (acute nocturnal shortness of breath) are both manifestations of decompensation of ventricular function – precipitated by diurnal susceptibility and increased venous return resulting from adoption of the supine position.

In an elderly person, the cause of acute shortness of breath can often be difficult to diagnose, and the chest may reveal nothing but coarse breath sounds throughout. In this situation, two factors are helpful: the JVP and overt sympathetic overactivation (cold peripheries and profuse sweating).



The electrocardiogram of a patient with heart failure often shows LV hypertrophy (LVH). This may show a "strain" pattern (LVH plus ST depression), most commonly in the lateral chest leads. Arrhythmias are also common in heart failure.

Chest x-ray

Classic signs on CXRs are common only for acute heart failure. Typically, some of the following signs are seen (see Figure 3):

Figure 3. (a) Classic signs of acute heart failure that can be seen on a chest x-ray of left ventricular failure.

Figure 3

(a) Classic signs of acute heart failure that can be seen on a chest x-ray of left ventricular failure. (b) Pleural effusion on a chest x-ray.

  • cardiomegaly (see Figure 4)
  • upper lobe blood diversion
  • "bat's wing" alveolar edema
  • pleural effusions
  • Kerley B lines (lymphatics)

Figure 4. Cardiomegaly and pleural effusion (on the right side) in a patient with heart failure.

Figure 4

Cardiomegaly and pleural effusion (on the right side) in a patient with heart failure.


This is the investigation of choice and can identify and quantify LVH and dysfunction (both systolic and diastolic) as well as examine causes of heart failure, such as valve abnormalities.

Blood tests

The measurement of natriuretic peptides for the diagnosis of heart failure is not yet routine. However, other blood tests can contribute to the clinical picture. The sodium concentration is often low (<130 mmol/L, despite high total body sodium) as a result of dilution and is a strong prognostic indicator. The potassium level is altered by many of the therapeutic agents and should be kept in the mid to high normal range (4.25–5 mmol/L) to minimize the risk of arrhythmia. If the pulse is of full volume, investigative blood tests for anemia and thyroid function should be carried out. If echo suggests restrictive cardiomyopathy, further tests can be carried out for iron storage disease, amyloidosis, or sarcoidosis.

Management: acute heart failure

The approach to the management of acute decompensation is different from that to CHF. Acute pulmonary edema should be managed by:

  • sitting the patient up
  • giving high-flow oxygen
  • giving diamorphine (2.5–5 mg intravenous [IV])
  • giving nitrates (sublingual at first, then isosorbide mononitrate 2–10 mg/hour IV)
  • giving loop diuretics (eg, furosemide [frusemide] 40–80 mg slow IV)

Blood pressure is a key measurement and should be considered when deciding the rate of a nitrate infusion or whether to use β-agonists. If the systolic blood pressure drops below 100 mm Hg, consideration should be given to replacing the nitrate infusion with one containing dobutamine (2–10 μg/kg/min). Although the effect of an IV diuretic can often be dramatic (probably due to an early effect on pulmonary venous dilatation), nitrates are preferred because, in addition to decreasing preload, they also decrease peripheral resistance and do not reduce cardiac output.

It is also important to take the precipitating factor into account. If, for example, a patient is in atrial fibrillation, slowing the ventricular rate may be more effective than a combination of more general measures. Similarly, if a patient has suffered an MI then thrombolysis or intervention may be the key to their recovery.

Management: cardiogenic shock

Cardiogenic shock, which has a 90% mortality rate, is the most severe form of acute heart failure. It is diagnosed when acute heart failure and hypotension are resistant to the measures described above and there is evidence of tissue hypoxia. Treatment, which should be in the coronary care unit of a specialist center, involves inotropic support, invasive monitoring equipment, intra-aortic balloon pumping, and, in the setting of MI, cardiac catheterization.

Intra-aortic balloon pump counterpulsation

Intra-aortic balloon pump (IABP) counterpulsation was developed in the early 1960s. A balloon is inserted, via the femoral artery, into the descending aorta (see Figure 5). Using electrocardiography for synchronization, the balloon is almost instantaneously, automatically inflated with helium at the onset of diastole, then deflated just prior to systole. This serves a dual purpose:

Figure 5. (a) Insertion of an intra-aortic balloon pump and (b) the corresponding arterial pressure waveform.

Figure 5

(a) Insertion of an intra-aortic balloon pump and (b) the corresponding arterial pressure waveform.

  • it improves coronary blood flow by increasing the perfusion pressure in the ascending aorta during diastole
  • it encourages systemic perfusion by reducing impedance to ventricular ejection at the point of balloon deflation (it creates a negative pressure which helps to "suck" the blood out)

Contraindications to IABP include severe aortic regurgitation and aortic dissection.

Management: chronic heart failure

The chronic form of heart failure is a condition that most generalists treat every day. When referring these patients, it is useful to classify the severity of heart failure. This is facilitated by a very simple scale: the New York Heart Association (NYHA) functional classification (see Table 3). It is straightforward and provides a common language that is understood by cardiologists worldwide.

Table 3. The New York Heart Association functional classification of chronic heart failure.

Table 3

The New York Heart Association functional classification of chronic heart failure.

Diagnosis and assessment

The initial diagnosis and assessment of the severity and progression of CHF can be made using echo and exercise testing with gas analysis. The most commonly used echo measure is the EF. This is rated as:

  • 45%–70%, normal
  • 35%–45%, mildly impaired
  • 25%–35%, moderately impaired
  • <25%, severely impaired
  • <15%, end-stage/transplant candidates
  • 5% is compatible with life, but not long life

The single best exercise-testing measurement is the maximum rate of oxygen consumption (VO2 max). In a situation where cardiac and respiratory causes of dyspnea coexist, exercise testing with gas analysis can be particularly useful in discerning which is the greater problem.


The first step in the management of CHF is patient education. It is easy for physicians to forget (since they use the term every day) that, to most patients, heart "failure" sounds significantly worse than "myocardial infarction", "heart attack", or even "cardiac arrest". Educating patients about their condition – by giving them information about avoiding excessive salt intake and teaching them how to use their daily weight to monitor fluid balance – will pay dividends in long-term management.

Historical Hearts

Hippocrates believed that the left side of the heart and its associated arteries were conduits for air rather than blood. Galen (ad 138–201) thought that blood passed through invisible pores in the ventricular septum. Such was his influence on Roman medical thinking that this idea remained in place until the 15th century when an embargo on the dissection of human cadavers was lifted by the Pope. Not long after this, Leonardo da Vinci and others began to produce detailed anatomical drawings, and William Harvey finally described the function of the heart as a pump that pushed blood through a circulatory system, beat by beat.

Spironolactone, angiotensin-converting enzyme inhibitors (ACEIs), and β-blockers are the only agents that have been shown to reduce heart failure mortality, and all are now widely used in the community. However, their use requires caution. Although not strictly necessary, most practitioners use short-acting preparations (eg, captopril, metoprolol) when first starting these treatments.


Although diuretics are the mainstay of CHF management, their main role is in symptom control – they may even increase neurohumoral activation. An approach that allows patients to take control of their own diuretic dosage and alter it according to their daily weight (in much the same way as diabetics alter their insulin dosage) may be successful in many patients. It is recommended that diuretics should always be used with an ACEI. In addition, the skillful use of diuretics with complementary actions (see Figure 6, Tables 4 and 5) can aid diuresis and even avoid hospital admission if the balance is upset. Given the choice between increasing the dose of a loop diuretic or adding another agent, it is usually best to add another agent.

Figure 6. The mechanism of action of diuretics in chronic heart failure management.

Figure 6

The mechanism of action of diuretics in chronic heart failure management.

Table 4. Diuretics used in the treatment of heart failure.

Table 4

Diuretics used in the treatment of heart failure.

Table 5. Treatment of heart failure with diuretics (loop diuretics, thiazides, metolazone).

Table 5

Treatment of heart failure with diuretics (loop diuretics, thiazides, metolazone).

Spironolactone has been shown to improve outcomes in stage III–IV heart failure with an effect equivalent to that of ACE inhibition (25 mg spironolactone has a beneficial effect on remodeling, but essentially no effect on potassium levels and diuresis).

Metolazone is a thiazide-like diuretic that has a powerful synergistic action with loop diuretics, so should be used in the community only as a last resort, for short periods, and be accompanied by daily electrolyte checks.

Defining Hearts

Pulmonary edema was first explained by Henry Welch, who showed that it could be reproduced by obstructing the outflow of the left ventricle. However, the first definition of heart failure was provided by Theophile Bonet (1620–1689), who published clinico-pathological studies linking the effects of valvular disease and cardiac chamber size to the clinical features of dyspnea and edema.

Angiotensin-converting enzyme inhibitors

ACEIs were the first agents shown to reduce mortality in heart failure. Angiotensin receptor blockers (ARBs) are currently reserved for those patients with an ACE cough. Guidelines for starting ACEIs are outlined in Table 6.

Table 6. The recommended procedure for starting an angiotensin-converting enzyme inhibitor (ACEI).

Table 6

The recommended procedure for starting an angiotensin-converting enzyme inhibitor (ACEI).


Much of the early work on β-blockers used carvedilol – a nonselective β-blocker, α-antagonist, and antioxidant. However, although its significant effect appeared to result from β-blockade resulting in many different β-blocking agents being used, recent trials have suggested there may be effects over and above that of β-blockade. Beneficial effects of β-blockade include a reduction in heart rate (which increases myocardial perfusion), regression of LVH (probably related to inhibition of the deleterious effects of excess catecholamines), and a reduction in sudden death (probably related to a reduction in ventricular fibrillation – 50% of heart failure deaths are due to arrhythmia).


Digoxin has perhaps the longest history of any of the treatments for heart failure. However, being a positive inotrope, it occupies a controversial place overarching the old and new paradigms for the treatment of sinus rhythm heart failure. It works by increasing cellular calcium via inhibition of Na+/K+ ATPase and consequent reduction of Ca2+ extrusion via Na+/Ca2+ exchange (see Figure 7). As K+ "competes" with digoxin at the ATPase site, digoxin can become toxic in hypokalemic patients. Symptoms of digoxin toxicity are gastrointestinal upset and (more rarely) visual disturbances and headache. However, despite its widespread use, there have been no large, prospective, placebo-controlled trials to determine the efficacy of digoxin in reducing mortality (although it has been shown to reduce hospital admissions).

Figure 7. Mechanism of action of digoxin.

Figure 7

Mechanism of action of digoxin. Digoxin inhibits Na+/K+ ATPase. As a consequence of an increased intercellular Na+ concentration, Ca2+ extrusion (via Na+/Ca2+ exchange) is reduced. The result is an increase in cellular Ca2+.

Hydralazine and nitrates

The vasodilator combination of hydralazine (up to 300 mg) and nitrates (160 mg isosorbide dinitrate) has been tested with digoxin and diuretics in several large trials and has been associated with mortality reductions in heart failure. However, the advent of ARBs is likely to offer a better alternative to ACEIs than this drug combination.

Future directions

Areas of controversy still exist in the management of CHF. For example, aspirin is known to be effective as an aid to secondary prevention of coronary artery disease. However, it can reduce the efficacy of ACEIs. Also, despite the high rate of heart failure deaths due to arrhythmia (50%), amiodarone is the only antiarrhythmic (so far) that has been shown to reduce mortality.

New agents currently being investigated in trials include:

  • calcium sensitizers (increase contractile response to intracellular Ca2+)
  • endothelin antagonists (there are increased levels of endothelin – a potent vasoconstrictor – in heart failure); results of all recent trials have been negative or neutral at best
  • TNF-α antibodies; recent trials all produced negative results
  • neutral endopeptidase inhibitors (neutral endopeptidase breaks down atrial natriuretic peptide and brain natriuretic peptide – peptides with diuretic, natriuretic, and vasodilator properties)

Heart failure treatments, according to NYHA classification, are outlined in Table 7.

Table 7. Treatment of heart failure according to the New York Heart Association (NYHA) functional classification of congestive heart failure.

Table 7

Treatment of heart failure according to the New York Heart Association (NYHA) functional classification of congestive heart failure.


Recent evidence suggests that individualized exercise training programs can be beneficial in stable, mild to moderate heart failure. Like most other aspects of the treatment of heart failure, today's advice (exercise) is the opposite of that from 30 years ago (bed rest).

Early Treatments

The first breakthrough in the treatment of heart failure was by William Withering (1741–1799), who published observations of the therapeutic use of digitalis (foxglove). Ironically, he believed its main mechanism of action was diuretic. Until the discovery of digitalis, treatment for heart failure had remained unchanged since Egyptian times: bed rest, fluid restriction, and weak herbal diuretics were combined with starvation, laxatives, and venesection. Patients can perhaps derive some solace from the fact they are living today, rather than 200 years ago.

Revascularization of patients with heart failure is being considered increasingly as it is realized that chronic LV dysfunction does not necessarily mean permanent or irreversible cell damage. Myocardium that has suffered low-level ischemia and no longer contributes significantly to ventricular function (hibernating myocardium) remains viable, and therefore potentially rescuable. It can be detected by cardiovascular magnetic resonance imaging, perfusion imaging, low-dose dobutamine stress echo, or PET scanning (perfusion metabolism mismatch).

Many patients with systolic heart failure exhibit significant intra- or interventricular conduction delays (IVCDs) that cause ventricular dysynchrony, recognized by a wide QRS complex on the ECG (typically, a left bundle branch block morphology). Ventricular dysynchrony has several important consequences for cardiac performance, which include abnormal interventricular septal wall motion, reduced diastolic filling time, and prolonged mitral regurgitation duration. In addition, there is a proportional increase in mortality with increasing QRS duration. Cardiac resynchronization therapy (CRT) provides atrial-synchronized, biventricular pacing using standard pacing technology combined with a special third lead. This third lead is implanted via the coronary sinus and positioned in a cardiac vein to sense and pace the left ventricle. Following a sensed atrial contraction, both ventricles are stimulated to contract simultaneously. The resulting resynchronization of ventricular contraction reduces mitral regurgitation and optimizes left ventricular filling, thereby improving cardiac function.

Transplantation and ventricular assist devices are options for end-stage disease. Local availability and guidelines vary. Indications are:

  • severe LV dysfunction (eg, EF <20% as demonstrated by radionuclide ventriculography)
  • VO2 max <14 mL/kg/min (patients with values above this tend to have a better prognosis without surgery)

Contraindications center on comorbidities, eg, vasculopathy, diabetes mellitus with target-organ damage, or pulmonary hypertension. In addition, few centers will transplant patients over the age of 60 years.

Several studies have shown clear benefit from a multidisciplinary approach to heart failure treatment. Specialist nurses who visit patients in the community can significantly reduce the rate of hospitalization by helping with exercise, symptom control, and fluid balance, and by alerting the medical team early to any potential deterioration.

Palliative care

The very poor prognosis associated with heart failure begs the question of the availability of hospice care and end-of-life support for this population. The irony remains that while cancer patients receive end-of-life support and often report dyspnea as an equivalent problem to pain, many more heart failure patients whose chief symptom is dyspnea have a poorer prognosis and go unattended. The management of these patients is an area deserving of more investigation and analysis. For example, what is the place of drugs that are known to help symptoms but which might increase the risk of sudden death (eg, inotropes)? Does "dual-intent" apply? What are the wishes of the patient? As cardiology becomes more technological there is less focus on patients and more on their lesions and the tools used to treat them. Generalists are almost certainly better than cardiologists at practising holistic care.

Unfortunately, conventional drugs for the treatment of heart failure do not adequately control the most common symptoms of fatigue and dyspnea. The latter is the most common distressing symptom in refractory heart failure. Maintaining a very close control of plasma volume is facilitated by regular weighing and adjustment of diuresis, but this rarely provides full symptom control. Fortunately, relief is possible through the use of opiates. These drugs reduce preload and afterload, dampen the central respiratory drive, and relieve distress through a central narcotic action. Thus, they are well suited for use in this situation. Drawbacks, such as tolerance and dependence, should not deter their use as studies suggest that they are minimal in this setting. Physical dependence is inevitable, but only relevant in the case of discontinuation of therapy, in which case it can be managed by gradual withdrawal. Morphine can be given at a dose of 2.5 mg 4 hourly and as required, with the 4-hourly dose readjusted after 48 hours to take account of interim dosing. Control of constipation should always accompany chronic opioid treatment.

Further reading

  1. Jong P, Demers C, McKelvie RS. et al. Angiotensin receptor blockers in heart failure: meta-analysis of randomized controlled trials. J Am Coll Cardiol. 2002;39:463–70. [PubMed: 11823085]
  2. Krumholz HM, Baker DW, Ashton CM. et al. Evaluating quality of care for patients with heart failure. Circulation. 2000;101:E122–40. [PubMed: 10736303]
  3. Niebauer J, Volk HD, Kemp M. et al. Endotoxin and immune activation in chronic heart failure: a prospective cohort study. Lancet. 1999;353:1838–42. [PubMed: 10359409]
  4. Nolan J. A historical review of heart failure. Scott Med J. 1993;38:53–7. [PubMed: 8502981]
  5. Task Force of the Working Group on Heart Failure of the European Society of Cardiology. The treatment of heart failure. Eur Heart J. 1997;18:736–53. [PubMed: 9152644]
Copyright © 2004, Remedica.
Bookshelf ID: NBK2218
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