Heart failure is a complex syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the heart to function as a pump and maintain sufficient cardiac output to meet the demands of the body. It is a common condition, with an estimated annual incidence of 10% in patients over 65 years. The long-term outcome is poor and approximately 50% of patients are dead within 5 years.
Ischaemic heart disease is the commonest cause in the developed world and hypertension is the commonest cause in Africa (Table 10.5). Any factor that increases myocardial work (arrhythmias, anaemia, hyperthyroidism, preg-nancy, obesity) may aggravate existing heart failure or initiate failure.
When the heart fails, compensatory mechanisms attempt to maintain cardiac output and peripheral perfusion. However, as heart failure progresses the mechanisms are overwhelmed and become pathophysiological. These mech-anisms involve the following:
Activation of the sympathetic nervous system
Improves ventricular function by increasing heart rate and myocardial con-tractility. Constriction of venous capacitance vessels redistributes flow cen-trally, and the increased venous return to the heart (preload) further augments ventricular function via the Starling mechanism (Fig. 10.14). Sympathetic stimulation, however, also leads to arteriolar constriction, this increasing the atterload which would eventually reduce cardiac output.
The fall in cardiac output and increased sympathetic tone lead to diminished renal perfusion, activation of the renin-angiotensin system, and hence
|Emergency Box 10.1|
Basic life support (BLS)
• Assess if patient is responsive - gently shake shoulders and ask loudly ‘are you alright?’.
• If there is no response move onto AIRWAY. Call for help and ask for AED.
• Turn the victim on his/her back on a firm surface.
• Open the airway using head tilt and chin lift - place your hand on victim’s forehead and tilt the head back and with íingertips underneath the point of the chin, lift the chin to open the airway.
• Keeping the airway open, look (chest movement), listen (breath sounds) and feel (victims expired air on your cheek) for normal breathing.
Assess for no more than 10 seconds.
• If victim is not breathing normally start chest compressions (see below).
• After 30 chest compressions, give 2 rescue breaths: use head tilt and chin lift, pinch the nose closed, take a breath and create a seal with your lips around his mouth, exhale over 1 minute. Watch for the rise and fall of the patient’s chest, indicating adequate ventilation.
• Circulation is achieved by external chest compression.
• Place the heel of one hand in the centre of the victim’s chest. Place the heel of your other hand on top of the first hand. Interlock the íingers of your hands and with straight arms press down on the sternum 5-6 cm. After each compression release all the pressure on the chest.
• Continue with chest compressions and rescue breaths in a ratio of 30:2 with 100-120 compressions per minute.
• Attach AED pads. AED assesses rhythm and delivers shock if indicated. Immediately resume CPR.
Advanced life support (ALS)
• Institute as soon as help arrives; continue cardiac massage throughout except during actual defibrillation.
• Give 100% O2 via Ambu-bag, intubate as soon as possible and initiate positive-pressure ventilation.
• Establish intravenous access and connect ECG leads.
• Drugs administered by the peripheral route should be followed by a flush of 20 mL of 0.9% saline.
• If intravenous access not possible, give drugs by the intraosseous route (tibia and humerus).
AED, Automated External Defribrillator; CPR, cardiopulmonary resuscitation; EMD,
electromechanical dissociation; VF/VT, ventricular fibrillation/ventricular tachycardia
*Reproduced by permission of the European Resuscitation Council and Laerdal
|Table 10.5 Causes of heart failure|
Ischaemic heart disease
Cardiomyopathy (hypertrophic, restrictive)
Valvular heart disease (mitral, aortic, tricuspid)
Congenital heart disease (atrial septal defect, ventricular septal defect)
Alcohol and chemotherapy, e.g. imatanib, doxorubicin
Hyperdynamic circulation (anaemia, thyrotoxicosis, Paget’s disease)
Right heart failure (RV infarct, pulmonary hypertension, pulmonary embolism, cor pulmonale, (chronic obstructive pulmonary disease))
Severe bradycardia or tachycardia
Pericardial disease (constrictive pericarditis, pericardial effusion)
Infections (Chagas’ disease)
Fig. 10.14 The Starling curve. Starling’s law states that the stroke volume is directly proportional to the diastolic filling (i.e. the preload or ventricular end-diastolic pressure). As the preload is increased, the stroke volume rises (normal). Increasing contractility (e.g. increased with sympathetic stimulation) shifts the curve upwards and to the left (z). If the ventricle is overstretched the stroke volume will fall (x). In heart failure (y) the ventricular function curve is relatively flat so that increasing the preload has only a small effect on cardiac output.
increased fluid retention. Salt and water retention further increases venous pressure and maintains stroke volume by the Starling mechanism (Fig. 10.14). As salt and water retention increases, however, peripheral and pul-monary congestion causes oedema and contributes to dyspnoea. Angiotensin II also causes arteriolar constriction, thus increasing the afterload and the work of the heart.
These are released from the atria (atrial natriuretic peptide, ANP), ventricles (brain natriuretic peptide, BNP - so called because it was first discovered in the brain) and vascular endothelium (C-type peptide). They have diuretic, natriuretic and hypotensive properties. The effect of their action may repre-sent a beneficial, albeit inadequate, compensatory response leading to reduced cardiac load (preload and afterload).
Myocardial failure leads to a reduction of the volume of blood ejected with each heartbeat, and thus an increase in the volume of blood remaining after systole. The increased diastolic volume stretches the myocardial fibres and, as Starling's law would suggest, myocardial contraction is restored. Once heart failure is established, however, the compensatory effects of cardiac dilatation become limited by the flattened contour of Starling's curve. Eventu-ally the increased venous pressure contributes to the development of pulmo-nary and peripheral oedema. In addition, as ventricular diameter increases, greater tension is required in the myocardium to expel a given volume of blood, and oxygen requirements increase.
This is a process of hypertrophy, loss of myocytes and increased interstitial fibrosis which all contribute to progressive and irreversible pump (contractile) failure. The process is multifactorial and includes apoptosis of myocytes and changes in cardiac contractile gene expression (e.g. myosin).
Most patients with heart failure present insidiously.
The clinical syndromes are:
■ Left ventricular systolic dysfunction (LVSD) - commonly caused by ischaemic heart disease, but can also occur with valvular heart disease and hypertension.
■ Right ventricular systolic dysfunction (RVSD)- occurs secondary to LVSD, with primary and secondary pulmonary hypertension, right ventricular infarction and adult congenital heart disease.
■ Diastolic heart tailure (or heart failure with normal ejection fraction) -a syndrome consisting of symptoms and signs of heart failure but with a normal or near normal left ventricular ejection fraction (above 45-50%) and evidence of diastolic dysfunction on echocardiography (e.g. abnormal left ventricular relaxation and filling, usually with left ventricular hyper-trophy). Diastolic dysfunction leads to impairment of diastolic ventricular filling and hence decreased cardiac output.
These include exertional dyspnoea, orthopnoea, paroxysmal nocturnal dysp-noea and fatigue.
There is one or more of the following: cardiomegaly with a displaced apex beat, third and fourth heart sounds, elevated JVP, tachycardia, hypotension, bi-basal lung crackles, pleural effusion, ankle oedema (plus sacral oedema in bed-bound patients), ascites and tender hepatomegaly.
The New York Heart Association classification of heart failure (Table 10.6) is useful in the assessment of severity and the response to therapy.
The aim of investigation in a patient with symptoms and signs of heart failure is to objectively show evidence of cardiac dysfunction (usually by echo-cardiography) and to establish the cause (Fig. 10.15):
■ Chest X-ray shows cardiac enlargement and features of left ventricular failure (p. 410), but can be normal.
■ ECG may show evidence of underlying causes, e.g. arrhythmias, ischae-mia, left ventricular hypertrophy in hypertension.
Table 10.6 New York Heart Association (NYHA) Classification of heart failure
No limitation. Normal physical exercise does not cause fatigue, dyspnoea or palpitations
Mild limitation. Comfortable at rest but normal physical activity produces fatigue, dyspnoea or palpitations
Marked limitation. Comfortable at rest but less gentle physical activity produces marked symptoms of heart failure
Symptoms of heart failure occur at rest and are exacerbated by any physical activity
Fig. 10.15 Algorithm for the diagnosis of heart failure. Based on the European Society of Cardiology and NICE guidelines. +Prior to BNP testing in patients with previous MI.
■ Blood tests. Full blood count (to look for anaemia which may exacerbate heart failure), liver biochemistry (may be altered due to hepatic conges-tion), blood glucose (for diabetes), urea and electrolytes (as a baseline before starting diuretics and ACE inhibitors), and thyroid function tests (in the elderly and those with atrial fibrillation). Brain natriuretic peptide (BNP) is a natriuretic hormone released from the ventricles into the cir-culation; normal plasma concentrations (< 100 mg/mL) exclude heart failure. The N terminal fragment (NTproBNP) released from pro-BNP can also be measured.
■ Echocardiography is performed in all patients with new onset heart failure. It allows an assessment of ventricular systolic and diastolic func-tion, shows regional wall motion abnormalities and may reveal the aetiology of heart failure. An ejection fraction of < 0.45 is usually accepted as evidence for systolic dysfunction.
■ Otherinvestigations. Cardiac catheterization, thallium perfusion imaging, PET scanning, cardiac MRI or dobutamine stress echocardiography (p. 419) may be of benefit in selected patients to identify those with hibernating myocardium (a region of impaired myocardial contractility due to persistently impaired coronary blood flow) in whom revasculariza-tion will improve left ventricular function and long-term prognosis.
Treatment of chronic heart failure
Treatment is aimed at relieving symptoms, control of disease leading to cardiac dysfunction, retarding disease progression and improving quality and length of survival (Table 10.7).
■ Angiotensin-converting enzyme inhibitors (ACEI, p. 497), e.g. perindopril, lisinopril and quinapril, inhibit the production of angiotensin II, a potent vasoconstrictor, and increase concentrations of the vasodilator brady-kinin. They enhance renal salt and water excretion and increase cardiac output by reducing afterload. They improve symptoms, limit the develop-ment of progressive heart failure and prolong survival, and should be given to all patients with heart failure. The major side-effect is first-dose hypotension. ACEI treatment should be introduced gradually with a low initial dose and gradual titration every 2 days to full dose with regular blood pressure monitoring and a check on serum potassium and renal function; creatinine levels normally rise by about 10-15% during ACEI therapy.
■ Angiotensin II type 1 receptor antagonists (ARA, p. 498) (e.g. losartan, ibersartan, candesartan and valsartan) block binding of angiotensin II to the type 1 receptor (AT1) and are indicated as second-line therapy in patients intolerant of ACEI. Unlike ACEI they do not affect bradykinin metabolism and do not produce a cough. Both ACEI and ARA are con-traindicated in patients with bilateral renal artery stenosis.
■ Vasodilators. Isosorbide mononitrate (vasodilator reduces preload) in combination with hydralazine (arteriolar vasodilator reduces afterload) improves symptoms and survival and is used in patients intolerant of ACEI and ARA.
β-blockers Bisoprolol, carvedilol and nebivolol (p. 495) improve symptoms and reduce cardiovascular mortality in patients with chronic stable heart failure. This effect is thought to arise through blockade of the chronically activated sympathetic system. They are started at a low dose and gradually titrated upwards.
|Table 10.7 Summary of the management of chronic heart failure|
Education of patients and family
Physical activity: reduce during exacerbations to reduce work of the heart.
Encourage low-level (e.g. 20- to 30-min walks 3–5 times weekly) with compensated heart failure
Diet and social: weight reduction if necessary, no added salt diet, avoid alcohol (negative inotropic effects), stop smoking (p. 512)
Vaccinate against pneumococcal disease and influenza
Correct aggravating factors, e.g. arrhythmias, anaemia, hypertension and pulmonary infections
Driving: unrestricted, except symptomatic heart failure disqualifies driving large lorries and buses
Sexual activity: tell patients on nitrates not to take phosphodiesterase type 5 inhibitors
ACE inhibitor (or angiotensin II receptor antagonist, ARA)*
Non-pharmacological treatment (in selected cases)
Revascularization (coronary artery bypass graft)
Cardiac resynchronization therapy (biventricular pacing)
Implantable cardioverter defibrillator
Replacement of diseased valves
Repair of congenital heart disease
Left ventricular assist device and artificial heart (bridge to transplantation)
*In all patients. ACEI (ARA) and β-blockers improve prognosis
Diuretics (Table 8.4 and p. 348) are used in patients with fluid overload. They act by promoting renal sodium excretion, with enhanced water excretion as a secondary effect. The resulting loss of fluid reduces ventricular filling pressures (preload) and thus decreases pulmonary and systemic congestion
■ Loop diuretics, e.g. furosemide (20-40 mg daily, maximum 250-500 mg daily) and bumetanide, are potent diuretics used in moderate/severe heart failure. When given intravenously, they also induce venodilatation, a beneficial action independent of their diuretic effect.
■ Thiazide diuretics, e.g. bendroflumethiazide (2.5 mg daily, max 10 mg daily), are mild diuretics that inhibit sodium reabsorption in the distal renal tubule. The exception is metolazone (2.5 mg daily, max 10 mg daily), which causes a profound diuresis and is only used in severe and resistant heart failure.
■ Aldosterone antagonists. Spironolactone and eplerenone are relatively weak diuretics with a potassium-sparing action. Spironolactone (25 mg daily) in combination with conventional treatment improves survival in patients with moderate/severe heart failure and should be given to all these patients. However, gynaecomastia or breast pain is a common side-effect. Eplerenone reduces mortality in patients with acute myocar-dial infarction and heart failure.
Digoxin is indicated in patients with heart failure and atrial fibrillation. It is also used as add-on therapy in patients in sinus rhythm who remain symptomatic despite standard treatment (vasodilators, β-blockers, diuretics).
Inotropes (p. 579) are occasionally used in patients not responding to oral medication.
Revascularization Coronary artery disease is the most common cause of heart failure. Revascularization with angioplasty and stenting or surgery can result in improvement in regional abnormalities in wall motion in up to one-third of patients and may thus have a role to play in some individuals.
Cardiac resynchronization therapy (also known as biventricular pacing) aims to improve the coordination of the atria and both ventricles. It is indicated for patients with left ventricular systolic dysfunction who have moderate or severe symptoms of heart failure and a widened QRS on ECG.
Implantable cardioverter–defibrillator (ICD) is indicated for patients with left ventricular ejection fraction < 30% on optimal medical therapy. Sudden death from ventricular tachyarrhythmias is reduced.
Cardiac transplantation is the treatment of choice for younger patients with severe intractable heart failure. The expected 1-year survival following transplantation is over 90%, with 75% alive at 5 years. Death is usually the result of operative mortality, organ rejection and overwhelming infection secondary to immunosuppressive treatment. After this time the greatest threat to health is accelerated coronary atherosclerosis, the cause of which is unknown.
There is usually a gradual deterioration necessitating increased doses of diuretics, and sometimes admission to hospital. The prognosis is poor in those with severe heart failure (i.e. breathless at rest or on minimal exertion), with a 1-year survival rate of 50%.
Acute heart failure
Acute heart failure is a medical emergency, with left or right heart failure developing over minutes or hours. Aetiology is similar to chronic heart failure and initial investigations are similar (ECG, chest X-ray, blood tests, transthoracic echocardiogram) with additional blood tests of serum troponin (for myocardial necrosis) and D-dimer (for evidence of pulmonary embolism).
Several clinical syndromes are defined:
■ Acute decompensation of chronic heart failure
■ Hypertensive heart failure - high blood pressure, preserved left ventricu-lar function, pulmonary oedema on chest X-ray
■ Acute pulmonary oedema- acutely breathless, tachycardia, profuse sweating (sympathetic overactivity), wheezes and crackles throughout the chest, hypoxia, pulmonary oedema on chest X-ray
■ Cardiogenic shock - hypotension, tachycardia, oliguria, cold extremities
■ High output cardiac failure - e.g. septic shock. Warm peripheries, pul-monary congestion, blood pressure may be low
■ Right heart failure - low cardiac output, elevated jugular venous pressure, hepatomegaly, hypotension.
In many cases the patient is so unwell that treatment (Emergency Box 10.2) must begin before the investigations are completed. Patients are managed in a high dependency unit. All require prophylactic anticoagulation, e.g. enoxaparin (p. 245). Some patients will require central venous cannulation, arterial lines and pulmonary artery cannulation for monitoring and to direct therapy. Initial therapy includes oxygen, diuretics (furosemide 50 mg i.v.) and vasodilator therapy (glyceryl trinitrate intravenous infusion 50 mg in 50 mL
0.9% saline at 2-10 mL/h) providing systolic blood pressure is > 85 mm Hg. Inotropic support can be added in patients who do not respond to initial therapy (p. 579).
1. Ethics and communication
2. Infectious diseases
3. Gastroenterology and nutrition
4. Liver, biliary tract and pancreatic disease
Liver, biliary tract and pancreatic disease
LIVER BIOCHEMISTRY AND LIVER FUNCTION TESTS
SYMPTOMS AND SIGNS OF LIVER DISEASE
NON - ALCOHOLIC FATTY LIVER DISEASE (NAFLD)
COMPLICATIONS AND EFFECTS OF CIRRHOSIS
TYPES OF CHRONIC LIVER DISEASE AND CIRRHOSIS
PRIMARY SCLEROSING CHOLANGITIS
BUDD - CHIARI SYNDROME
LIVER DISEASE IN PREGNANCY
CARCINOMA OF THE PANCREAS
NEUROENDOCRINE TUMOURS OF THE PANCREAS
5. Haematological disease
Assessment and treatment of suspected neutropenic sepsis
INHERITED HAEMOLYTIC ANAEMIAS
ACQUIRED HAEMOLYTIC ANAEMIA
THE WHITE CELL
HAEMOSTASIS AND THROMBOSIS
6. Malignant disease
COMMON INVESTIGATIONS IN MUSCULOSKELETAL DISEASE
COMMON REGIONAL MUSCULOSKELETAL PROBLEMS
THE SERONEGATIVE SPONDYLOARTHROPATHIES
Clinical features, Investigations
INFECTION OF JOINTS AND BONES
AUTOIMMUNE RHEUMATIC DISEASES
SYSTEMIC INFLAMMATORY VASCULITIS
DISEASES OF BONE
8. Water, electrolytes and acid–base balance
WATER AND ELECTROLYTE REQUIREMENTS
BODY FLUID COMPARTMENTS
REGULATION OF BODY FLUID HOMEOSTASIS
PLASMA OSMOLALITY AND DISORDERS OF SODIUM REGULATION
DISORDERS OF POTASSIUM REGULATION
DISORDERS OF MAGNESIUM REGULATION
DISORDERS OF ACID - BASE BALANCE
9. Renal disease
INVESTIGATION OF RENAL DISEASE
URINARY TRACT INFECTION
HYPERTENSION AND THE KIDNEY
RENAL CALCULI AND NEPHROCALCINOSIS
URINARY TRACT OBSTRUCTION
ACUTE RENAL FAILURE/ACUTE KIDNEY INJURY
CHRONIC KIDNEY DISEASE
RENAL REPLACEMENT THERAPY
CYSTIC RENAL DISEASE
TUMOURS OF THE KIDNEY AND GENITOURINARY TRACT
DISEASES OF THE PROSTATE GLAND
10. Cardiovascular disease
COMMON PRESENTING SYMPTOMS OF HEART DISEASE
INVESTIGATIONS IN CARDIAC DISEASE
ISCHAEMIC HEART DISEASE
VALVULAR HEART DISEASE
PULMONARY HEART DISEASE
ARTERIAL AND VENOUS DISEASE
DRUGS FOR ARRHYTHMIAS
DRUGS FOR HEART FAILURE
DRUGS AFFECTING THE RENIN - ANGIOTENSIN SYSTEM
NITRATES, CALCIUM - CHANNEL BLOCKERS AND POTASSIUM - CHANNEL ACTIVATORS
11. Respiratory disease
12. Intensive care medicine
13. Drug therapy, poisoning, and alcohol misuse
14. Endocrine disease
PITUITARY HYPERSECRETION SYNDROMES
THE THYROID AXIS
MALE REPRODUCTION AND SEX
FEMALE REPRODUCTION AND SEX
THE GLUCOCORTICOID AXIS
THE THIRST AXIS
DISORDERS OF CALCIUM METABOLISM
DISORDERS OF PHOSPHATE CONCENTRATION
ENDOCRINOLOGY OF BLOOD PRESSURE CONTROL
DISORDERS OF TEMPERATURE REGULATION
15. Diabetes mellitus and other disorders of metabolism
16. The special senses
COMMON NEUROLOGICAL SYMPTOMS
COORDINATION OF MOVEMENT
THE CRANIAL NERVES
COMMON INVESTIGATIONS IN NEUROLOGICAL DISEASE
UNCONSCIOUSNESS AND COMA
STROKE AND CEREBROVASCULAR DISEASE
EPILEPSY AND LOSS OF CONSCIOUSNESS
NERVOUS SYSTEM INFECTION AND INFLAMMATION
HEADACHE, MIGRAINE AND FACIAL PAIN
SPINAL CORD DISEASE
DEGENERATIVE NEURONAL DISEASES
DISEASES OF THE PERIPHERAL NERVES