8 Cardiovascular disease

Cardiovascular disease is the leading cause of mortality in the Western world, with most deaths arising from ischaemic heart disease. Although the incidence of ischaemic heart disease is declining in many developed countries, it continues to rise in Eastern Europe and on the Indian subcontinent. Valvular heart disease is also common, but while rheumatic fever still predominates in the Indian subcontinent, degenerative disease of the aortic valve is now the leading aetiology in developed nations. The diversity of symptoms attributable to heart disease is limited and patients often remain asymptomatic despite the presence of advanced disease. However, prompt recognition of the development of heart disease is important, as many highly effective and evidence-based treatments are available.

CLINICAL EXAMINATION OF THE CARDIOVASCULAR SYSTEM

CHRONIC EPISODIC CHEST PAIN

Angina pectoris: The pain of myocardial ischaemia is usually central and diffuse, and may radiate to the neck, jaw and arms. It is typically described as dull, heavy, squeezing or crushing but not sharp or stabbing. The sensation may be described as discomfort, breathlessness (‘angina equivalent’) or ‘indigestion’ rather than pain. It arises during (not after) exertion and may also be precipitated or exacerbated by emotion, a large meal or a cold wind. The pain builds up gradually in proportion to the intensity of exertion and is promptly relieved (<5 mins) by resting. In unstable angina (see below), similar pain may be precipitated by minimal exertion and may occur at rest. Physical examination is often unremarkable but may reveal xanthoma, gallop rhythm or evidence of arterial disease. A resting 12-lead ECG may be normal. Exercise ECG or stress radionuclide imaging helps to confirm the diagnosis and also identifies high-risk patients who require further investigation and treatment.

Oesophageal pain: Can mimic angina very closely, is sometimes precipitated by exercise and may be relieved by nitrates; however, it is usually possible to elicit a history relating chest pain to supine posture or to eating, drinking or oesophageal reflux. Upper GI endoscopy may reveal evidence of oesophagitis or hiatus hernia.

Bronchospasm: May be described by patients as exertional chest tightness and can be difficult to distinguish from ischaemic chest tightness. Persistent tightness after exercise, associated wheeze, cough or symptoms of atopy suggest the diagnosis.

Musculoskeletal chest pain: Common, with a very variable presentation. The pain may vary with posture or occur with specific movements (bending, stretching, turning). It is sometimes accompanied by local tenderness over a rib or costal cartilage. Causes include minor soft tissue injuries, arthritis, costochondritis and Coxsackie viral infection.

ACUTE CHEST PAIN

Acute coronary syndromes: Prolonged and severe ischaemic chest pain may be due to unstable angina (which comprises recent-onset limiting angina, rapidly worsening or crescendo angina, and angina at rest) or acute myocardial infarction (MI); these are known collectively as the acute coronary syndromes. Although there may be a history of antecedent chronic stable angina, an episode of chest pain at rest is often the first presentation of coronary disease. The pain of MI typically takes several minutes to develop, is very severe and is often accompanied by autonomic disturbance including sweating, nausea and vomiting. Physical examination may reveal signs of important comorbidity (e.g. peripheral and/or cerebrovascular disease), autonomic disturbances, arrhythmia or heart failure. A 12-lead ECG may show features of ischaemia (ST elevation or depression, T-wave inversion) and helps guide initial treatment. An ECG obtained during the episode of pain is particularly useful. Plasma troponin concentrations should be measured and, if these are normal, the test should be repeated a minimum of 12 hrs after the onset of symptoms. If these tests are negative, an exercise test can help to confirm or refute a diagnosis of underlying coronary disease.

Arrhythmia: In patients with underlying coronary artery disease, the onset of a tachyarrhythmia may result in ischaemic chest pain at rest and can mimic an acute coronary syndrome.

Aortic dissection: An important differential diagnosis of acute coronary syndrome. The pain is severe, sharp and tearing, often felt in or penetrates through to the back, and is typically very sudden in onset. CXR may show a widened mediastinum but is normal in 10% of cases; transoesophageal echocardiography, CT or MRI can provide a definitive diagnosis.

Massive pulmonary embolism: May produce severe central chest pain with breathlessness and autonomic disturbance and can mimic MI. Sudden onset is typical. ECG may show right heart strain, and echocardiography right heart dilatation. CXR is frequently normal.

Myocarditis and pericarditis: Produce pain that is characteristically felt retrosternally, to the left of the sternum, or in the left or right shoulder. It varies in intensity with movement and with phase of respiration. It is usually described as ‘sharp’ and may ‘catch’ the patient during inspiration or coughing; there is occasionally a history of a prodromal viral illness.

The differential diagnosis of dyspnoea is wide and includes many respiratory disorders (p. 271). However, both acute and chronic dyspnoea may have a cardiac aetiology. Acute left heart failure with pulmonary oedema is a common cause of the former. With pulmonary oedema:

• Patients are typically distressed, agitated and sweaty, and may produce frothy pink sputum.

• There is often a history of chronic heart failure or MI.

• Extensive crepitations are audible in the chest and signs of right heart failure (e.g. elevated jugular venous pulse (JVP), peripheral oedema) may be evident.

• CXR confirms the presence of pulmonary oedema.

• Underlying causes may be revealed by ECG (e.g. MI, arrhythmia) and echocardiography (e.g. acute valvular regurgitation).

Arrhythmias can also cause acute breathlessness, but usually do so only if the heart is structurally abnormal (e.g. onset of atrial fibrillation in a patient with mitral stenosis).

Chronic exertional dyspnoea is the predominant symptom in chronic heart failure. Lying down increases venous return to the heart so patients may also complain of breathlessness on lying flat (orthopnoea) or of waking up during the night profoundly breathless (paroxysmal nocturnal dyspnoea). There may be a history of ischaemic heart disease, hypertension or valvular disorders.

• Relevant physical signs include an elevated JVP, displaced apex beat and cardiac murmurs.

• Echocardiography permits assessment of left ventricular (LV) function and is the key investigation.

Breathlessness may also be the dominant or sole feature of myocardial ischaemia (‘angina equivalent’). Patients sometimes describe chest tightness as ‘breathlessness’ but ischaemia may also cause dyspnoea by inducing transient LV dysfunction. Associated chest tightness, close correlation of symptoms with exercise, and objective evidence of myocardial ischaemia from stress testing may all help to establish the diagnosis.

SYNCOPE AND PRESYNCOPE

Cardiovascular disorders that cause an abrupt fall in cerebral perfusion may lead to recurrent or isolated episodes of syncope (sudden loss of consciousness) and presyncope (lightheadedness and near-collapse). Other causes of blackouts and ‘funny turns’ include seizure, hyperventilation and hypoglycaemia; dizziness, in the form of vertigo, may also result from labyrinthine or central vestibular dysfunction (p. 619). An accurate description of events from the patient and a witness is invaluable and helps to guide investigations. In cardiac syncope (i.e. secondary to arrhythmia or structural heart disease), onset is usually sudden and recovery rapid. In contrast, patients with vasovagal syncope often feel nauseated and unwell for several minutes before and after the episode. Patients with seizures may exhibit abnormal movements, usually take many minutes to recover and are confused on recovery.

Arrhythmias: May cause lightheadedness or blackouts, the latter with profound bradycardia or malignant ventricular tachyarrhythmias. Ambulatory ECG recordings may establish the diagnosis, although a close temporal relationship must be demonstrated between symptoms and a recorded arrhythmia. Patient-activated ECG recorders are useful for patients with recurrent dizziness but clearly unhelpful in sudden collapse. Where necessary, an implantable ‘loop recorder’ can be placed beneath the skin of the upper chest under local anaesthesia. This device continuously records an ECG, storing arrhythmic events in its digital memory for subsequent analysis.

Structural heart disease: Severe aortic stenosis, hypertrophic obstructive cardiomyopathy and severe coronary artery disease can cause lightheadedness or syncope on exertion. Profound hypotension occurs when cardiac output fails to rise normally as peripheral vascular resistance falls during exercise. Syncope may also result from an arrhythmia in these conditions. Echocardiography demonstrates the presence of structural heart disease. Exercise testing may reveal myocardial ischaemia, arrhythmia or an abnormal haemodynamic response during exertion.

Vasovagal syncope: Usually triggered by a reduction in venous return due to prolonged standing, excessive heat or a large meal. Initial sympathetic activation leads to vigorous contraction of the relatively underfilled ventricles. This stimulates ventricular mechanoreceptors, causing rebound parasympathetic activation and sympathetic withdrawal leading to bradycardia, vasodilatation or both. Often the diagnosis is clear from the history, but for repeated problematic episodes, head-up tilt testing (the patient lies on a table tilted to an angle of 70° for up to 45 mins with monitoring of ECG and BP) assists the diagnosis. In severe cases β-blockers or disopyramide may be helpful.

Carotid sinus hypersensitivity: May cause lightheadedness or syncope through inappropriate bradycardia and vasodilatation. Monitoring of the ECG and BP during carotid sinus massage can establish the diagnosis but should not be performed in patients with suspected carotid vascular disease (risk of a transient ischaemic attack).

Postural hypotension: May result from hypovolaemia (e.g. excessive diuretic therapy), sympathetic degeneration (e.g. diabetes mellitus, ageing) and drug therapy (e.g. vasodilators, antidepressants). Withdrawal of unnecessary medication, graduated elastic stockings and, in some cases, treatment with fludrocortisone may be helpful.

PALPITATION

The term ‘palpitation’ may be used to describe a variety of sensations, including an erratic, fast, slow or forceful heart beat. A detailed description is essential (Box 8.2) and patients should be asked to tap out the heart beat on the table.

• Recurrent but short-lived bouts of an irregular heart beat, such as dropped or missed beats, are usually due to atrial or ventricular extrasystoles.

• Poorly defined attacks of a pounding, forceful, fast heart beat are a common manifestation of anxiety but may also occur in anaemia, pregnancy and thyrotoxicosis.

• Discrete bouts of a very rapid (>120/min) heart beat suggest a paroxysmal arrhythmia.

• Atrial fibrillation typically presents with a completely irregular tachycardia.

An ECG recording during an attack of palpitation (ambulatory monitoring or patient-activated recorder) may be necessary to establish a definitive diagnosis. Most cases are due to an awareness of the normal heart beat, sinus tachycardia or benign extrasystoles triggered by stress, intercurrent illness, caffeine or alcohol. In such cases, careful explanation and reassurance will often suffice but a low-dose β-blocker may be helpful in patients with distressing symptoms. Arrhythmia management is described on pages 215–225.

ABNORMAL HEART SOUNDS AND MURMURS

The first clinical manifestation of heart disease may be the incidental discovery of an abnormal sound on auscultation. Clinical evaluation is helpful (Box 8.3) but an echocardiogram is often necessary to confirm the nature of an abnormal heart sound or murmur. Some added sounds are physiological but may also occur in pathological conditions; for example, a third sound is common in young people and in pregnancy but is also a feature of heart failure. Similarly, an ejection systolic murmur may occur in hyperdynamic states (e.g. anaemia, pregnancy) but also in aortic stenosis. Benign murmurs do not occur in diastole and systolic murmurs that radiate or are associated with a thrill are almost always pathological. Individual murmurs are dealt with below (pp. 254–260).

8.3 AUSCULTATORY FEATURES OF HEART MURMURS

When does it occur?

• Time the murmur using heart sounds, carotid pulse and apex beat. Is it systolic or diastolic?

• Does the murmur extend throughout systole or diastole or is it confined to a shorter part of the cardiac cycle?

Where is it heard best? (location)

• Listen over the apex and base of the heart, including the aortic and pulmonary areas

Where does it radiate?

• Evaluate radiation to the neck, axilla or back

What does it sound like? (pitch and quality)

• Pitch is determined by flow (high pitch indicates high-velocity flow)

• Is the intensity constant or variable?

DISORDERS OF HEART RATE, RHYTHM AND CONDUCTION

Arrhythmias can cause palpitation, dizziness, syncope, chest pain or breathlessness, and trigger heart failure or even sudden death. They are generally classified as either tachycardias (heart rate >100/min) or bradycardias (heart rate <60/min).

• ‘Supraventricular’ (sinus, atrial or junctional) arrhythmias usually produce narrow QRS complexes because the ventricles are depolarised via normal pathways.

• Ventricular arrhythmias give rise to broad QRS complexes because the ventricles are activated in an abnormal sequence.

SINUS RHYTHMS

Sinus arrhythmia: Refers to a physiological increase of the sinus rate during inspiration and slowing during expiration. It is mediated by the parasympathetic nervous system and may be pronounced in children.

Sinus bradycardia: May occur in healthy people at rest, especially athletes. Pathological causes include MI (sinus node ischaemia), raised intracranial pressure, hypothermia, hypothyroidism, cholestatic jaundice and drug therapy (e.g. β-blockers, verapamil, digoxin). Asymptomatic sinus bradycardia requires no treatment; symptomatic patients usually respond to i.v. atropine.

Sinus tachycardia: Usually due to an increase in sympathetic activity with exercise or emotion. Pathological causes include anaemia, fever, thyrotoxicosis, phaeochromocytoma, cardiac failure, shock and drug therapy (e.g. inhaled β-agonists).

TACHYARRHYTHMIAS

There are two main mechanisms of tachycardia:

Increased automaticity: The tachycardia is produced by repeated spontaneous depolarisation of an ectopic focus, often in response to catecholamines.

Re-entry: Occurs when there are two alternative pathways with different conducting properties (e.g. an area of normal tissue and an area of ischaemic tissue). In sinus rhythm each impulse passes down both pathways before entering a common distal pathway. However, owing to different refractory periods, a premature impulse may travel selectively down one pathway then retrogradely up the alternative pathway, establishing a closed loop or re-entry circuit and thus initiating a tachycardia.

ATRIAL TACHYARRHYTHMIAS

Atrial ectopic beats (extrasystoles): Usually cause no symptoms but can give the sensation of a missed beat or abnormally strong beat. The ECG shows a premature but otherwise normal QRS complex; the preceding P wave has a different morphology because the atria activate from an abnormal site. Treatment is rarely necessary.

Atrial tachycardia: Produces a narrow complex tachycardia with abnormal P-wave morphology caused by increased atrial automaticity, sinoatrial disease or digoxin toxicity. It may respond to β-blockers, which reduce automaticity, or class I or III anti-arrhythmic drugs (p. 760).

Atrial flutter: Results from a large re-entry circuit within the right atrium. The atrial rate is approximately 300/min, but associated 2 : 1, 3 : 1 or 4 : 1 atrioventricular (AV) block usually produces a ventricular heart rate of 150, 100 or 75/min. The ECG shows saw-toothed flutter waves. With regular 2 : 1 AV block these may be buried in the QRS complexes and T-waves but can be revealed by transiently increasing the degree of AV block through carotid sinus massage (Fig. 8.1) or i.v. adenosine. Digoxin, β-blockers or verapamil can limit the ventricular rate but electrical or chemical cardioversion is often preferable. In addition to restoring sinus rhythm, flecainide, amiodarone or propafenone may prevent recurrent episodes of atrial flutter, though catheter ablation is now the treatment of choice for patients with persistent and troublesome symptoms.

Fig. 8.1 Atrial flutter with 2:1 block; flutter waves revealed by carotid sinus massage.

‘SUPRAVENTRICULAR’ TACHYCARDIAS

AV NODAL RE-ENTRY TACHYCARDIA (AVNRT)

This is due to re-entry in the right atrium and AV node, and tends to occur in hearts that are otherwise normal. It produces episodes of regular tachycardia with a rate of 140–220/min that last from a few seconds to many hours.

• The patient is usually aware of a fast heart beat and may feel faint or breathless.

• Polyuria may occur, and also angina if there is underlying coronary disease.

• The ECG (Fig. 8.3) usually shows a regular tachycardia with normal QRS complexes but occasionally there may be rate-dependent bundle branch block.

• Attacks may be terminated by carotid sinus pressure or Valsalva manoeuvre, but if not, i.v. adenosine or verapamil will restore sinus rhythm in most cases.

• When there is severe haemodynamic compromise, the tachycardia should be terminated by DC cardioversion (p. 226).

• If attacks are frequent or disabling, prophylactic oral therapy (e.g. β-blocker, verapamil) may be indicated but catheter ablation (p. 228) offers a very high chance of complete cure and is usually preferable to long-term drug treatment.

Fig. 8.3 Supraventricular tachycardia. The rate is 180/min and the QRS complexes are normal.

ATRIOVENTRICULAR RE-ENTRANT TACHYCARDIA (AVRT) AND WOLFF–PARKINSON–WHITE SYNDROME

An abnormal band of rapidly conducting tissue (‘accessory pathway’) connects the atria and ventricles. In around half of cases, premature activation of ventricular tissue via the pathway produces a short PR interval and a ‘slurring’ of the QRS complex, called a delta wave (Fig. 8.4). As the AV node and bypass tract have different conduction speeds and refractory periods, a re-entry circuit can develop, causing tachycardia; when associated with symptoms, the condition is known as Wolff–Parkinson–White syndrome.

• The ECG appearance of AVRT may be indistinguishable from that of AVNRT.

• Carotid sinus pressure, Valsalva manoeuvre or i.v. adenosine can terminate the tachycardia.

• If AF occurs, it may produce a dangerously rapid ventricular rate (since the accessory pathway lacks the rate-limiting properties of the AV node) and should be treated as an emergency, usually with DC cardioversion.

• Digoxin and verapamil shorten the refractory period of the accessory pathway and must be avoided.

• Prophylactic treatment is only indicated in symptomatic patients; catheter ablation (p. 228) of the accessory pathway is now preferred to drug therapy (flecainide or amiodarone).

Fig. 8.4 Wolff–Parkinson–White syndrome. A strip of accessory conducting tissue allows electricity to bypass the AV node and spread from atria to ventricles without delay. When ventricular activation occurs through the AV node (1), the ECG is normal; however, when it occurs through the accessory pathway (2), a very short PR interval and a broad QRS complex are seen. In sinus rhythm, ventricular activation occurs by both paths, causing the characteristic short PR and slurring of the upstroke of the QRS complex (delta wave). The proportion of activation occurring via the accessory pathway may vary; therefore, at times, the ECG can look normal.

VENTRICULAR TACHYARRHYTHMIAS

VENTRICULAR TACHYCARDIA (VT)

VT usually occurs in patients with coronary heart disease or cardiomyopathies and may cause haemodynamic compromise or degenerate into ventricular fibrillation (p. 221). The ECG shows tachycardia with broad, abnormal QRS complexes and a rate >120/min (Fig. 8.5). VT is by far the most common cause of a broad-complex tachycardia but may be difficult to distinguish from supraventricular tachycardia with bundle branch block or Wolff–Parkinson–White syndrome. When there is doubt, it is safer to manage the problem as VT.

• Emergency DC cardioversion is required if systolic BP is <90 mmHg, but if VT is well tolerated then i.v. amiodarone or lidocaine may be tried.

• Hypokalaemia, hypomagnesaemia, acidosis and hypoxaemia must be corrected.

• β-blockers and/or amiodarone may be effective for subsequent prophylaxis.

• Long-term treatment with class I anti-arrhythmic drugs is dangerous in patients with ischaemic heart disease.

• An implantable cardiac defibrillator may be indicated in patients with refractory VT or at high risk of arrhythmic death (e.g. poor LV function, associated haemodynamic compromise).

• VT occasionally occurs in patients with otherwise healthy hearts; in such cases prognosis is good and catheter ablation can be curative.

Fig. 8.5 Ventricular tachycardia: rhythm strip. Typical broad bizarre QRS complexes with a rate of 160/min.

TORSADES DE POINTES (TWISTING POINTS)

This form of VT complicates prolonged ventricular repolarisation (prolonged QT interval), which may be congenital or secondary to drugs (e.g. class Ia and class III anti-arrhythmics, macrolide antibiotics, tricyclic antidepressants, phenothiazines) or electrolyte disturbance (↓Ca²+, ↓Mg²+, ↓K+). The ECG shows rapid irregular complexes that oscillate from an upright to an inverted position, seeming to twist around the baseline. It is typically non-sustained but may degenerate into ventricular fibrillation. The ECG in sinus rhythm shows a prolonged QT interval.

• I.v. magnesium should be given in all cases.

• Atrial pacing or i.v. isoprenaline shortens the QT interval by increasing heart rate.

• Otherwise, treatment is directed at the underlying cause.

• Patients with congenital long QT syndrome often require an implantable cardiac defibrillator.

CARDIAC ARREST

Cardiac arrest describes the sudden, complete loss of cardiac output. The patient is unconscious, pulseless and apnoeic. Death is inevitable without prompt effective treatment.

ASYSTOLE AND PULSELESS ELECTRICAL ACTIVITY (PEA)

Asystole occurs when there is no electrical activity within the ventricles due to failure of the conducting tissue or massive ventricular damage. PEA refers to the absence of cardiac output despite the presence of organised electrical activity, often due to a catastrophic event such as cardiac rupture. These rhythms do not respond to defibrillation; treatment consists of cardiopulmonary resuscitation (CPR) with the additional support of atropine and adrenaline (epinephrine) whilst seeking potentially reversible causes; prognosis is poor.

MANAGEMENT OF CARDIAC ARREST

The management of cardiac arrest is shown in Figure 8.7.

• Basic life support (BLS) encompasses manoeuvres that attempt to maintain a low level of circulation pending more definitive treatment with advanced life support (ALS).

• ALS aims to restore cardiac output by defibrillation or correction of other reversible causes of cardiac arrest.

Fig. 8.7 Algorithm for basic and adult advanced life support. For further information see www.resus.org.uk. (BLS = basic life support; CPR = cardiopulmonary resuscitation; PEA = pulseless electrical activity; VF = ventricular fibrillation; VT = pulseless ventricular tachycardia)

In the absence of an identifiable, treatable cause (e.g. ischaemia, aortic stenosis), survivors of VT or VF arrest should be considered for anti-arrhythmic therapy or an implantable cardiac defibrillator (p. 226). • Patients who survive cardiac arrest in the context of acute MI require no specific additional treatment.

BRADYARRHYTHMIAS

SINOATRIAL DISEASE (SICK SINUS SYNDROME)

Sinoatrial disease results from degeneration of the sinus node and is common in the elderly. It may present with palpitation, dizzy spells or syncope, due to intermittent tachycardia, bradycardia, or pauses with no atrial or ventricular activity (sinus arrest or sinoatrial block). A permanent pacemaker may benefit patients with symptomatic bradycardias but is not indicated in asymptomatic patients.

ATRIOVENTRICULAR (AV) BLOCK

AV block may be congenital or result from:

• Idiopathic fibrosis.

• Myocardial infarction/ischaemia.

• Trauma (e.g. cardiac surgery).

• Inflammation (e.g. sarcoidoisis).

• Drugs (e.g. verapamil, digoxin or β-blockers).

First-degree AV block

AV conduction is delayed, producing a prolonged PR interval (>0.20 secs). It rarely causes symptoms.

Second-degree AV block

In second-degree AV block some atrial impulses fail to conduct to the ventricles resulting in dropped beats.

Mobitz type I block (‘Wenckebach’s phenomenon’): There are repeated cycles of progressively lengthening PR intervals culminating in a dropped beat. It is sometimes observed at rest or during sleep in athletic young adults with high vagal tone.

Mobitz type II block (Fig. 8.8): The PR interval of conducted impulses remains constant but some P waves are not conducted. It is usually caused by disease of the His–Purkinje system and carries a risk of asystole. In 2 : 1 AV block alternate P waves are conducted, so it is impossible to distinguish between Mobitz type I and type II block.

Fig. 8.8 Second-degree AV block (Mobitz type II). The PR interval of conducted beats is normal but some P waves are not conducted. The constant PR interval distinguishes this from Wenckebach’s phenomenon.

Third-degree (complete) AV block

AV conduction fails completely, the atria and ventricles beat independently (AV dissociation, Fig. 8.9), and ventricular activity is maintained by an escape rhythm arising in the AV node or bundle of His (narrow QRS complexes) or the distal Purkinje tissues (broad QRS complexes). Distal escape rhythms are completely regular but slower and less reliable. Cannon waves may be visible in the neck, and the intensity of the first heart sound varies due to the loss of AV synchrony.

Fig. 8.9 Complete (third-degree) AV block. There is complete dissociation of atrial and ventricular complexes. The atrial rate is 80/min and the ventricular rate is 38/min.

Stokes–Adams attacks

Episodes of ventricular asystole may complicate complete heart block, Mobitz type II second-degree AV block and sinoatrial disease, resulting in recurrent syncope (‘Stokes–Adams’ attacks). Episodes are characterised by a sudden loss of consciousness, typically without warning, which may result in a fall. Convulsions (due to cerebral ischaemia) can occur if asystole is prolonged. There is pallor and a death-like appearance during the attack, but when the heart starts beating again there may be a characteristic flush. In contrast to epilepsy, recovery is rapid.

Management

AV block complicating acute MI: Acute inferior MI is often complicated by transient AV block because the right coronary artery supplies the AV junction. There is usually a reliable escape rhythm, and if the patient remains well, no treatment is required. Symptomatic second-degree or complete heart block may respond to i.v. atropine or, if this fails, a temporary pacemaker. In most cases the AV block will resolve within 7–10 days. Second-degree or complete heart block complicating acute anterior MI is usually a sign of extensive ventricular damage involving both bundle branches and carries a poor prognosis. Asystole may ensue and a temporary pacemaker should be inserted as soon as possible. If the patient presents with asystole, i.v. atropine (3 mg) or i.v. isoprenaline (2 mg in 500 ml 5% dextrose, infused at 10–60 ml/hr) may help to maintain the circulation until a temporary pacing electrode can be inserted.

Chronic AV block: Patients with symptomatic bradyarrhythmias associated with AV block should receive a permanent pacemaker. Asympto-matic first-degree or Mobitz type I second-degree AV block does not require treatment, but a permanent pacemaker is usually indicated in patients with asymptomatic Mobitz type II second-degree or complete heart block on prognostic grounds.

BUNDLE BRANCH BLOCK AND HEMIBLOCK

Interruption of the right or left branch of the bundle of His delays activation of the corresponding ventricle, broadens the QRS complex (≥0.12 secs) and produces characteristic alterations in QRS morphology (Figs 8.10 and 8.11). Right bundle branch block (RBBB) can be a normal variant but left bundle branch block (LBBB) usually signifies important underlying heart disease (Box 8.6).

Fig. 8.10 Right bundle branch block. Note the wide QRS complexes with ‘M’-shaped configuration in leads V₁ and V₂ and a wide S wave in lead I.

Fig. 8.11 Left bundle branch block. Note the wide QRS complexes with the loss of the Q wave or septal vector in lead I and ‘M’-shaped QRS complexes in V₅ and V₆.

THERAPEUTIC PROCEDURES

EXTERNAL DEFIBRILLATION AND CARDIOVERSION

The heart can be depolarised by passing an electrical current through it from an external source. This will interrupt any arrhythmia and produce a brief period of asystole, usually followed by the resumption of normal sinus rhythm. Elective cardioversion requires a general anaesthetic. In this situation, a low-amplitude shock synchronised to occur 0.02 secs after the R wave peak is used. Patients with long-standing atrial arrhythmias are at risk of systemic embolism before and after cardioversion, so should be adequately anticoagulated for at least 4 wks either side of the procedure.

IMPLANTABLE CARDIAC DEFIBRILLATORS (ICDs)

These devices sense rhythm and deliver current through leads implanted in the heart via the subclavian or cephalic vein. They automatically sense and terminate life-threatening ventricular arrhythmias. ICDs have all of the functions of a pacemaker (to deal with bradycardias) but in addition can treat ventricular tachyarrhythmias using overdrive pacing, synchronised cardioversion, or defibrillation. ICD implantation is subject to similar complications as pacemaker implantation (see below). Indications for ICDs are shown in Box 8.7.

CATHETER ABLATION

Catheter ablation therapy has become the treatment of choice for many patients with recurrent arrhythmias (e.g. AV nodal and AV re-entry tachycardias), as it offers the prospect of a lifetime cure without the need for long-term drug therapy. A series of catheter electrodes are inserted into the heart via the venous system and used to record the activation sequence of the heart in sinus rhythm, during tachycardia and after pacing manoeuvres. Once the arrhythmia focus or circuit is identified, a catheter is placed into this critical zone and the culprit tissue is selectively ablated using radio-frequency current or cryoablation. Serious complications are rare (<1%) but include inadvertent complete heart block requiring pacemaker implantation, and cardiac tamponade.

TEMPORARY AND PERMANENT PACEMAKERS

Temporary pacemakers

Transcutaneous pacing: Administered by delivering an electrical stimulus sufficient to induce cardiac contraction through two adhesive gel pad electrodes placed externally over the apex and upper right sternal edge. It is easy and quick to set up, but causes significant discomfort.

Transvenous pacing: Delivered by positioning a pacing electrode at the apex of the right ventricle via the internal jugular, subclavian or femoral vein using fluoroscopic imaging. The electrode is then connected to an external pulse generator which can be adjusted to alter the energy output or pacing rate. Temporary pacing may be indicated in the management of transient heart block or of other causes of transient bradycardia (e.g. drug overdose), or as a prelude to permanent pacing. Complications include:

• Pneumothorax.

• Brachial plexus or subclavian artery injury.

• Infection (usually Staphylococcus aureus).

• Pericarditis.

Permanent pacemakers

Permanent pacemakers utilise the same principles but the pulse generator is implanted under the skin. Electrodes can be placed in the right ventricular apex, the right atrial appendage or both (dual-chamber). Atrial pa-cing may be appropriate for patients with sinoatrial disease without AV block. In dual-chamber pacing the atrial electrode can be used to detect spontaneous atrial activity and trigger ventricular pacing, thereby preserving AV synchrony and allowing the ventricular rate to increase together with the atrial rate during exercise, leading to improved exercise tolerance. A code is used to signify the pacing mode (Box 8.8). Most dual-chamber pacemakers are programmed to a mode termed DDD. Rate-responsive pacemakers trigger a rise in heart rate in response to movement or increased respiratory rate and are used in patients unable to mount an increase in heart rate during exercise. Early complications of permanent pacing include:

8.8 INTERNATIONAL GENERIC PACEMAKER CODE

Chamber paced	Chamber sensed	Response to sensing
O = none	O = none	O = none
A = atrium	A = atrium	T = triggered
V = ventricle	V = ventricle	I = inhibited
D = both	D = both	D = both

Late complications include:

• Infection.

• Erosion of the generator or lead.

• Lead fracture due to mechanical fatigue.

CARDIAC RESYNCHRONISATION THERAPY (CRT)

CRT is a new treatment for selected patients with heart failure and LBBB. This conduction defect is associated with uncoordinated LV contraction, which may exacerbate heart failure. CRT devices carry an additional lead that is placed via the coronary sinus into one of the veins on the epicardial surface of the left ventricle. Simultaneous septal and LV epicardial pacing resynchronises LV contraction, improving exercise tolerance in selected patients.

CORONARY HEART DISEASE (CHD)

CHD, also known as ischaemic heart disease, is the leading cause of premature death in the developed world and is estimated to become, by 2020, the major cause of death world-wide. In the UK 1 in 3 men and 1 in 4 women die from CHD. Disease of the coronary arteries is almost always due to atherosclerosis and its complications, particularly thrombosis. Atherosclerosis is a progressive inflammatory disorder of the arterial wall, characterised by focal lipid-rich deposits of atheroma that remain clinically silent until they become large enough to impair arterial perfusion or until disruption of the lesion results in thrombotic occlusion or embolisation of the affected vessel. The pathogenesis of atherosclerosis is complex but several risk factors have been identified:

Age and sex: Age is the most powerful independent risk factor for atherosclerosis. Pre-menopausal women have much lower rates of disease than age- and risk-matched males but thereafter risk is similar.

Family history: A ‘positive’ family history is present when clinical problems occur in first-degree relatives aged <50 yrs (male) or <55 yrs (female). Increased risk reflects a combination of shared genetic and environmental (e.g. smoking, exercise, diet) factors.

Hypertension: The incidence of atherosclerosis increases as BP (systolic and diastolic) rises. Antihypertensive therapy reduces coronary mortality and stroke.

Hypercholesterolaemia: The risk of CHD and other atherosclerotic vascular disease rises with plasma cholesterol concentration, especially the ratio of total cholesterol to high-density lipoprotein (HDL) cholesterol. A weaker correlation exists with plasma triglyceride concentration. Lowering low-density lipoprotein (LDL) and total cholesterol concentrations reduces the risk of cardiovascular events.

Diabetes mellitus: A potent risk factor for all forms of atherosclero-sis and is often associated with diffuse disease. Insulin resistance (normal glucose homeostasis with high levels of insulin) is also a risk factor for CHD.

Lifestyle factors: There is a strong, dose-linked relationship between cigarette smoking and CHD. Physical inactivity and obesity are associated with other risk factors (hypertension, diabetes) but are both independent risk factors for atherosclerosis. Diets deficient in fresh fruit, vegetables and polyunsaturated fatty acids are associated with an increased risk of vascular disease. Regular exercise appears to have a protective effect.

STABLE ANGINA

Stable angina occurs when coronary blood flow is impaired by fixed or stable atheroma of the coronary arteries. During exertion, an imbalance between myocardial oxygen supply and demand causes transient myocardial ischaemia. Coronary atheroma is by far the most common cause of angina; however, the symptom may also be a manifestation of other forms of heart disease such as aortic valve disease, hypertrophic cardiomyopathy or coronary vasopasm (Prinzmetal’s angina). Occasionally, the coronary arteries are involved in other disorders such as polyarteritis and other connective tissue disorders.

Clinical features

The history is by far the most important factor in making the diagnosis of stable angina (p. 209). The condition is characterised by central chest pain, discomfort or breathlessness that is precipitated by exertion or other forms of stress, and is promptly relieved by rest. Physical examination is frequently negative but may reveal evidence of:

• Aortic stenosis (an occasional cause of angina).

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Tags: Davidsons Essentials of Medicine

Apr 3, 2017 | Posted by admin in GENERAL & FAMILY MEDICINE | Comments Off

Class I	No limitation during ordinary activity
Class II	Slight limitation during ordinary activity
Class III	Marked limitation of normal activities without symptoms at rest
Class IV	Unable to undertake physical activity without symptoms; symptoms may be present at rest

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