An abnormality of cardiac rhythm is called a cardiac arrhythmia. Arrhythmia may cause sudden death, syncope, dizziness, palpitations or no symptoms at all. Paroxysmal arrhythmias may not be detected on a single ECG record-ing. Twenty-four-hour ambulatory ECG monitoring and event recorders (p. 417) are often used to detect arrhythmias causing intermittent symptoms.
There are two main types of arrhythmia:
■ Bradycardia: the heart rate is slow (< 60 beats/min). Slower heart rates are more likely to cause symptomatic arrhythmias.
■ Tachycardia: the heart rate is fast (> 100 beats/min). Tachycardias are more likely to be symptomatic when the arrhythmia is fast and sustained. They are subdivided into supnaventricular tachycardias (SVTs), which arise from the atrium or the atrioventricular junction, and ventricular tachycardias, which arise from the ventricles.
Arrhythmias and conduction disturbances complicating acute myocardial infarction are discussed on page 456.
General principles of management of arrhythmias
Patients with adverse symptoms and signs (low cardiac output with cold clammy extremities, hypotension, impaired consciousness or severe pulmo-nary oedema) require urgent treatment of their arrhythmia. Oxygen is given to all patients, intravenous access established and serum electrolyte abnor-malities (potassium, magnesium, calcium) are corrected.
The normal cardiac pacemaker is the sinus node (p. 409) with the rate of sinus node discharge under control of the autonomic nervous system with parasympathetic predominating (resulting in slowing of the spontaneous discharge rate).
Fluctuations of autonomic tone result in phasic changes in the sinus dis-charge rate. During inspiration parasympathetic tone falls and the heart rate quickens, and on expiration the heart rate falls. This variation is normal, particularly in children and young adults, and typically results in predictable irregularities of the pulse.
Sinus bradycardia is normal during sleep and in well-trained athletes. Causes are:
■ Extrinsic to the heart. drug therapy (β-blockers, digitalis and other antiarrhythmic drugs), hypothyroidism, hypothermia, cholestatic jaun-dice, raised intracranial pressure. Treatment of symptomatic bradycardia is that of the underlying cause.
■ Intrinsic to the heart. acute ischaemia and infarction of the sinus node (as a complication of myocardial infarction) and chronic degenera-tive changes such as fibrosis of the atrium and sinus node (sick sinus syndrome) occurring in elderly people. Patients with persistent sympto-matic bradycardia are treated with a permanent cardiac pacemaker. First-line treatment in the acute situation with adverse signs (p. 420), is atropine (500 μg intravenously repeated to a maximum of 3 mg, but contraindicated in myasthenia gravis and paralytic ileus). Temporary pacing (transcutaneous, or transvenous if expertise available) is an alternative.
■ Sick sinus syndrome. Bradycardia is caused by intermittent failure of sinus node depolarization (sinus arrest) or failure of the sinus impulse to propagate through the perinodal tissue to the atria (sinoatrial block). The slow heart rate predisposes to ectopic pacemaker activity and tachyarrhythmias are common (tachy-brady syndrome). The ECG shows severe sinus bradycardia or intermittent long pauses between consecutive P waves (> 2 s, dropped P waves). Permanent pace-maker insertion is indicated in symptomatic patients. Antiarrhythmic drugs are used to treat tachycardias. Thromboembolism is common in sinus node dysfunction and patients are anticoagulated unless there is a contraindication.
■ Neutrally mediated, e.g. carotid sinus syndrome and vasovagal attacks, resulting in bradycardia and syncope.
The common causes of heart block are coronary artery disease, cardio-myopathy and, particularly in elderly people, fibrosis of the conducting tissue. Block in either the atrioventricular (AV) node or the His bundle results in AV block, whereas block lower in the conduction system (p. 411) produces right or left bundle branch block.
There are three forms:
First-degree AV block This is the result of delayed atrioventricular con-duction and reflected by a prolonged PR interval (> 0.22 s) on the ECG. No change in heart rate occurs and treatment is unnecessary.
Second-degree AV block This occurs when some atrial impulses fail to reach the ventricles.
There are several forms (Fig. 10.8):
■ Mobitz type 1 block (Wenckebach block phenomenon) is progressive PR interval prolongation until a P wave fails to conduct, i.e. absent QRS after the P wave. The PR interval then returns to normal and the cycle repeats itself.
■ Mobitz type II block occurs when a dropped QRS complex is not preceded by progressive PR prolongation. Usually the QRS complex is wide.
■ 2: 1 or 3: 1 (advanced) block occurs when only every second or third P wave conducts to the ventricles.
Progression from second-degree AV block to complete heart block occurs more frequently following acute anterior myocardial infarction and in Mobitz type II block, and treatment is with a cardiac pacemaker. Patients with Wenckebach AV block or those with second-degree block following acute inferior infarction are usually monitored.
Third-degree AV block Complete heart block occurs when all atrial activity fails to conduct to the ventricles. There is no association between atrial and ventricular activity; P waves and QRS complexes occur independ-ently of one another on the ECG. Ventricular contractions are maintained by a spontaneous escape rhythm originating below the site of the block in the:
■ His bundle (p. 411) - which gives rise to a narrow complex QRS (< 0.12 s) at a rate of 50-60 b.p.m. and is relatively reliable. Recent onset block due to transient causes, e.g. ischaemia, may respond to intravenous atropine (p. 421) without the need for pacing. Chronic narrow-complex AV block usually requires permanent pacing.
■ His-Purkinje system (i.e. distally) - gives rise to a broad QRS complex (> 0.12 s), is slow (< 40 b.p.m.), unreliable and often associated with
Fig. 10.8 Three varieties of second-degree atrioventricular (AV) block. (A) Wenckebach (Mobitz type I) AV block. The PR interval gradually prolongs until the P wave does not conduct to the ventricles (arrows). (B) Mobitz type II AV block. The P waves that do not conduct to the ventricles (arrows) are not preceded by gradual PR interval prolongation. (C) Two P waves to each QRS complex. The PR interval prior to the dropped P wave is always the same. It is not possible to define this type of AV block as type I or type II Mobitz block and it is, therefore, a third variety of second-degree AV block (arrows show P waves), not conducted to the ventricles.
dizziness and blackouts (Stokes-Adams attacks). Permanent pacemaker insertion is indicated.
Bundle branch block
Complete block of a bundle branch (Fig. 10.2) is associated with a wide QRS complex (≥ 0.12 s) with an abnormal pattern and is usually asymptomatic. The shape of the QRS depends on whether the right or the left bundle is blocked (Fig 10.9):
■ Right bundle branch block (RBBB) - the right bundle branch no longer conducts an impulse and the two ventricles do not receive an impulse
Fig 10.9 A 12-lead ECG showing (A) right bundle branch block.Note an rsR pattern with the tall R in lead V,-V2 and the broad S waves in leads I and V5 and V6. (B) left bundle branch block. The QRS duration is greater than 0.12 s. Note the broad notched R waves with ST depression in leads I, AVL and V6, and the broad QRS waves in V1-V3.
simultaneously. There is sequential spread of an impulse (i.e. first the left ventricle and then the right) resulting in a secondary R wave (RSR') in V1 and a slurred S wave in V5 and V6. RBBB occurs in normal healthy individuals, pulmonary embolus, right ventricular hypertrophy, ischaemic heart disease and congenital heart disease, e.g. atrial and ventricular septal defect and Fallot's tetralogy.
■ Left bundle branch block (LBBB) - the opposite occurs with an RSR' pattern in the left ventricular leads (I, AVL, V4-V6) and deep slurred S waves in V1 and V2. LBBB indicates underlying cardiac pathology and occurs in ischaemic heart disease, left ventricular hypertrophy, aortic valve disease and following cardiac surgery.
These arise from the atrium or the atrioventricular junction. Conduction is via the His-Purkinje system and the QRS shape during tachycardia is usually similar to that seen in the same patient during baseline rhythm.
Sinus tachycardia is a physiological response during exercise and excitement. It also occurs with fever, anaemia, heart failure, thyrotoxicosis, acute pulmo-nary embolism, hypovolaemia and drugs (e.g. catecholamines and atropine). Treatment is aimed at correction of the underlying cause. If necessary, β-blockers may be used to slow the sinus rate, e.g. in hyperthyroidism.
Atrioventricular junctional tachycardias
Tachycardia arises as a result of re-entry circuits in which there are two separate pathways for impulse conduction. They are usually referred to as paroxysmal SVTs and are often seen in young patients with no evidence of structural heart disease.
Atrioventricular nodal re-entry tachycardia (AVNRT) is the commonest type of SVT. It is due to the presence of a ‘ring' of conducting pathway in the atrioventricular (AV) node of which the ‘limbs' have differing conduction times and refractory periods. This allows a re-entry circuit and an impulse to produce a circus movement tachycardia. On the ECG, the P waves are either not visible or are seen immediately before or after the QRS complex (Fig. 10.10). The QRS complex is usually of normal shape because the ven-tricles are activated in the normal way, down the bundle of His. Occasionally
Fig. 10.10 Atrioventricular junctional tachycardia. (A) Atrioventricular nodal re-entrỵ tachycardia. The QRS complexes are narrow and the P waves cannot be seen. (B) Atrioventricular re-entrỵ tachycardia (Wolff-Parkinson-White syndrome). The tachycardia P waves (arrows) are clearly seen after narrow QRS complexes. (C) An electrocardiogram taken in a patient with Wolff-Parkinson-White (WPW) syndrome during sinus rhythm. Note the short PR interval and the
5 wave (arrow). (D) Atrial fibrillation in the WPW syndrome. Note tachycardia with broad QRS complexes with fast and irregular ventricular rate.
|Table 10.3 Clinical indicators for the identification of sustained ventricular tachycardia (12-lead ECG) in a patient presenting with wide complex tachycardia|
|Ventricular tachycardia is more likely than supraventricular tachycardia
History of ischaemic heart disease
QRS interval > 140 ms
Atrioventricular dissociation – P waves have no relationship to the QRS complexes
Capture complexes – intermittent normal QRS complex
RS interval > 100 ms
Bifid, upright QRS complex with a taller first peak in V1
Deep S wave in V6
Concordant QRS direction in leads V1-V6, i.e. all positive or all negative complexes
the QRS complex is wide, because of a rate-related bundle branch block, and it may be difficult to distinguish from ventricular tachycardia (Table 10.3).
Atrioventricular reciprocating tachycardia (AVRT) is due to the pres-ence of an accessory pathway that connects the atria and ventricles and is capable of antegrade or retrograde conduction, or in some cases both. Wolff-Parkinson-White syndrome is the best-known type of AVRT in which there is an accessory pathway (bundle of Kent) between atria and ventricles. The resting ECG in Wolff-Parkinson-White syndrome shows evidence of the pathway's existence if the path allows some of the atrial depolarization to pass quickly to the ventricle before it gets though the AV node. The early depolarization of part of the ventricle leads to a shortened PR interval and a slurred start to the QRS (delta wave). The QRS is narrow (Fig. 10.10). These patients are also prone to atrial and occasionally ventricular fibrillation.
The usual history is of rapid regular palpitations usually with abrupt onset and sudden termination. Other symptoms are dizziness, dyspnoea, Central chest pain and syncope. Exertion, coffee, tea or alcohol may aggravate the arrhythmia.
The aim of treatment is to restore and maintain sinus rhythm:
■ Unstable patient - emergency cardioversion is required in patients whose arrhythmia is accompanied by adverse symptoms and signs (p. 420).
■ Haemodynamically stable patient:
■ Increase vagal stimulation of the sinus node by the Valsalva man-oeuvre (ask the patient to blow into a 20-mL syringe with enough force to push back the plunger) or right carotid sinus massage (con-traindicated in the presence of a carotid bruit).
■ Adenosine (p. 490) is a very short-acting AV nodal-blocking drug that will terminate most junctional tachycardias. Other treatments are intravenous verapamil (p. 501) or β-blockers, e.g. metoprolol. Vera-pamil is contraindicated with β-blockers, if the QRS is wide and therefore differentiation from VT difficult or if there is AF and an accessory pathway.
Radiofrequency ablation of the accessory pathway via a cardiac catheter is successful in about 95% of cases. Flecainide, verapamil, sotalol and amio-darone are the drugs most commonly used.
Atrial fibrillation, flutter, tachycardia and ectopic beats all arise from the atrial myocardium. In some cases automaticity is acquired by damaged atrial cells. They share common aetiologies (Table 10.4). Baseline investigations in a patient with an atrial arrhythmia include an ECG, thyroid function tests and transthoracic echocardiogram.
|Table 10.4 Causes of atrial arrhythmias|
Ischaemic heart disease Rheumatic heart disease Thyrotoxicosis Cardiomyopathy
Lone atrial íibrillation (i.e. no cause discovered)
Atrial septal defect
Carcinoma of the bronchus
Acute and chronic alcohol use
Atrial fibrillation (AF)
This is the most common arrhythmia and occurs in 5-10% of patients over 65 years of age. It also occurs, particularly in a paroxysmal form, in younger patients. Atrial activity is chaotic and mechanically ineffective. The AV node conducts a proportion of the atrial impulses to produce an irregular ventricular response - giving rise to an irregularly irregular pulse. In some patients it is an incidental finding; in others symptoms range from palpitations and fatigue to acute heart failure. AF is associated with a five-fold increased risk of stroke, primarily as a result of embolism of a thrombus that has formed in the atrium. There are no clear P waves on the ECG (Fig. 10.11), only a fine oscillation of the baseline (so-called fibrillation or f waves).
When AF is caused by an acute precipitating event, such as alcohol toxicity, chest infection or hyperthyroidism, the underlying cause should be treated:
■ Haemodynamically unstable patient (p. 420) - immediate heparinization and attempted cardioversion with a synchronized DC shock (p. 489). If cardioversion fails or AF recurs, intravenous amiodarone is given (p. 491) before a further attempt at cardioversion. A second dose of amiodarone can be given.
Fig. 10.11 (A) Atrial flutter. The flutter waves are marked with an F, only half of which are transmitted to the ventricles. (B) Atrial fibrillation. There are no P waves; the ventricular response is fast and irregular.
■ Stable patient - two strategies are available for the long-term manage-ment of AF: rate control or rhythm control (i.e. conversion to, and main-taining sinus rhythm):
■ Rate control aims to reduce heart rate at rest and during exercise but the patient remains in AF. β-blockers (p. 495) or calcium antagonists (verapamil, diltiazem, p. 501) are the preferred treatment except in predominantly sedentary people where digoxin (p. 493) is used.
■ Rhythm control is generally appropriate in younger patients (i.e. < 65 years of age), patients who are highly symptomatic, patients who also have congestive heart failure, and individuals with recent onset AF (< 48 h). Conversion to sinus rhythm is achieved by electrical DC cardioversion (p. 489) and then administration of β-blockers to sup-press the arrhythmia. Other agents used depend on the presence (use amiodarone) or absence (sotalol, flecainide, propafenone) of under-lying heart disease. Catheter ablation techniques such as pulmonary vein isolation are used in patients who do not respond to antiarrhyth-mic drugs. Patients with infrequent symptomatic paroxysms of AF (< 1/month) which are haemodynamically well tolerated and whom have little underlying heart disease, are treated on an as-needed basis (‘pill in the pocket') with oral flecainide (p. 492) or propafenone.
Assessment for anticoagulation
AF is associated with an increased risk of thromboembolism, and anticoagu-lation with warfarin should be given for at least 3 weeks before (with the exception of those who require emergency cardioversion or new onset AF < 48 h duration) and 4 weeks after cardioversion. Most patients should also be anticoagulated (INR 2.0-3.0) long term; the exception being young patients (< 65 years) with lone AF, i.e. in the absence of demonstrable cardiac disease, diabetes or hypertension. This latter group has a low incidence of thromboembolism and is treated with aspirin alone.
Atrial flutter is often associated with AF. The atrial rate is typically 300 beats/ min and the AV node usually conducts every second flutter beat, giving a ventricular rate of 150 beats/min. The ECG (Fig. 10.11) characteristically shows ‘sawtooth' flutter waves (F waves), which are most clearly seen when AV conduction is transiently impaired by carotid sinus massage or drugs. The treatment of atrial flutter is similar to AF except that most cases of flutter can be cured by radiofrequency catheter ablation of the re-entry circuit.
Atrial ectopic beats
These are caused by premature discharge of an ectopic atrial focus. On the ECG this produces an early and abnormal P wave, usually followed by a normal QRS complex. Treatment is not usually required unless they cause troublesome palpitations or are responsible for provoking more significant arrhythmias when β-blockers may be effective.
Ventricular ectopic premature beats (extrasystoles)
These are asymptomatic or patients complain of extra beats, missed beats or heavy beats. The ectopic electrical activity is not conducted to the ventri-cles through the normal conducting tissue and thus the QRS complex on the ECG is widened, with a bizarre configuration (Fig. 10.12). Treatment is with β-blockers if symptomatic.
Sustained ventricular tachycardia
Ventricular tachycardia (VT) and ventricular fibrillation (VF) are usually associ-ated with underlying heart disease. The ECG in sustained VT (> 30 s) shows a rapid ventricular rhythm with broad abnormal QRS complexes. Supraven-tricular tachycardia with bundle branch block also produces a broad complex tachycardia which can usually be differentiated from VT on ECG critera (Table 10.3). However, the majority of broad complex tachycardias are VT and if in doubt treat at such. Urgent DC cardioversion is necessary if the patient is haemodynamically compromised (p. 420). If there is no haemodynamic com-promise, treatment of VT is usually with intravenous lidocaine (p. 492) or amiodarone (p. 491). Recurrence is prevented with β-blockers or an implant-able cardioverter-defibrillator (ICD). This is a small device implanted behind the rectus abdominis and connected to the heart; it recognizes VT or VF and automatically delivers a defibrillation shock to the heart.
Non-sustained ventricular tachycardia
This is defined as VT ≥ 5 consecutive beats but lasting < 30 s. It is common in patients with heart disease (and in a few individuals with normal hearts). The treatments indicated are β-blockers in symptomatic patients or an ICD
Fig. 10.12 A rhythm strip demonstrating two ventricular ectopic beats of different morphology (multimorphological).
in patients with poor left ventricular function (ejection fraction < 30%) in whom it improves survival.
Ventricular fibrillation (VF)
This is a very rapid and irregular ventricular activation (see Fig. 10.13) with no mechanical effect and hence no cardiac output. The patient is pulseless and becomes rapidly unconscious, and respiration ceases (cardiac arrest). Treatment is immediate defribrillation (Emergency Box 10.1). Survivors of VF are, in the absence of an identifiable reversible cause (e.g. during the first two days of acute myocardial infarction, severe metabolic disturbance), at high risk of sudden death and treatment is with an ICD (p. 431).
Long QT syndrome
Ventricular repolarization (QT interval) is greatly prolonged (p. 415). The causes include congenital (mutations in sodium and potassium channel genes), electrolyte disturbances (hypokalaemia, hypocalcaemia, hypomagne-saemia) and a variety of drugs (e.g. tricyclic antidepressants, phenothiazines and macrolide antibiotics). Symptoms are palpitations and syncope, as a result of a polymorphic VT (torsade de pointes, rapid irregular sharp QRS complexes that continuously change from an upright to an inverted position on the ECG), that usually terminates spontaneously but may degenerate into VF. In acquired cases treatment is that of the underlying cause and intrave-nous isoprenaline.
In cardiac arrest there is no effective cardiac output. The patient is unconscious and apnoeic with absent arterial pulses (best felt in the carotid artery in the neck). Irreversible brain damage occurs within 3 minutes if an adequate circulation is not established. Management is described in
Fig. 10.13 A rhythm strip demonstrating four beats of sinus rhythm followed by a ventricular ectopic beat that initiates ventricular fibrillation. The ST segment is elevated owing to acute myocardial infarction.
Emergency Box 10.1. Resuscitation is stopped when there is return of spon-taneous circulation and a pulse, or further attempts at resuscitation are deemed futile. Post resuscitation care centres on maintaining arterial oxygen saturation (94-98%), blood glucose values <10 mmol/L and therapeutic hypothermia.
Prognosis In many patients resuscitation is unsuccessful, particularly in those who collapse out of hospital and are brought into hospital in an arrested State. In patients who are successfully resuscitated the prognosis is often poor because they have severe underlying heart diseases. The exceptions are those who are successfully resuscitated from a VF arrest in the early stages of myocardial infarction, when the prognosis is much the same as for other patients with an infarct.
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