Sinoatrial node The SAN sits high in the lateral right atrium (RA) just below the superior vena cava (SVC). It is 1 \200\2232 cm in length, 2 \200\2233 mm wide, and less than 1 mm fr om the epicardial surface. It is the dominant site of impulse generation; impulses are cond ucted out of the sinus node to depolarize the surrounding RA. The SAN is richly innervated with both adrenergic and cholinergic receptors, which alter the rate of depolarization henc e controlling the heart rate. Activation spreads out from the SAN to the rest of the RA and left atrium (LA) via specialized interatrial connections including Bachmann \200\231s bund le. Atrioventricular node The atrioventricular node (AVN) is found in the RA anterior to the mo uth of the coronary sinus and directly above the insertion of the septal lea \202 et of th e tricuspid valve. It is the only electrical connection to the ventricle, via the bundle of His, which, like the SAN it is also densely innervated with sympathetic and parasympatheti c \201 bres. His \200\223Purkinje system The electrical impulse conducts rapidly through the bundle of H is into the upper part of the interventricular septum, where it splits into two branches: t he right bundle branch, which continues down the right side of the septum to the apex of th e right ventricle and the base of the anterior papillary muscle, and the left bundle branch , which further splits into two fascicles, anterior and posterior. The terminal Purkinje \201 bres connect with the ends of the bundle branches, forming an interweaving network on the endocardial surface so that a cardiac impulse is transmitted almost simultaneously to t he entire right and left ventricles. THE CARDIAC CONDUCTION SYSTEM 479 1 2 0 3 \200\22360 mV 4 \200\22380 mV Fig. 10.1 The cardiac action potential . The action potential has \201 ve parts: 0 rapid in \202 ux of Na + causing fast depolarization 1 rapid early repolarization due to ef \202 ux of Na + 2 plateau phase where repolarization is slowed by an in \202 ux of Ca 2 + 3 repolarization due to the the ef \202 ux of K + 4 diastole with a steady-state resting t ransmembrane voltage. The plateau phase distinguishes the cardiac from neuronal action pote ntial. The release of Ca 2 + during phase 2 triggers mechanical contraction of the cell. SAN AVN MV His bundle TV Left bundle branch Right bundle branch Left anterior and posterior hemi fasicles Fig. 10.2 Anatomy of the normal conduction system. AVN = atrioventricular node; MV = mitral valve;. SAN = sinoatrial node; TV = tricuspid valve. 480 CHAPTER 10 Arrhythmias Bradycardia: general approach \200 Ask speci \201 cally about previous cardiac disease, palpitations, blackouts, dizziness, chest pain, symptoms of heart failure, current medicati on. Examine carefully, noting the blood pressure (BP), jugular venous pressure (JVP) waveform (?cannon waves), heart sounds and murmurs, and signs of heart failu re. Investigations 12-lead electrocardiogram (ECG) and rhythm strip Look speci \201 cally for the relationship between P waves and QRS complex. A long rhythm strip is sometimes necessary to detect complete heart block if atrial and ventricular rates are similar Blood tests Full blood count (FBC), biochemistry, glucose (urgently) Ca 2 + , Mg2 + (especially if on d iuretics) Biochemical markers of cardiac injury Where appropriate Blood cultures, C-reactive protein (CRP), erythrocyte sedimentation rate (ESR) Thyroid func tion tests (TFTs) Drug levels. Arterial blood gasses Chest x-ray Heart size ?Signs of pulmonary oedema Emergency nanagement Haemodynamically unstable patients \200 Severe haemodynamic compromi se (cardiac arrest, asystole, systolic blood pressure (SBP)<90 mmHg, severe pulmonary oedema, evidence of cerebral hypoperfusion) needs immediate treatment. \200 Give oxygen via face mask if the patient is hypoxic on ai r. \200 Keep nil by mouth (NBM) until de \201 nitive therapy has been started, to reduce the risk of aspiration in case of cardiac arrest or when the patient lies supine for temporary wire insertion. Secure peripheral venous access. \200 Give atropine 1 mg IV (MiniJet ) bolus; repeat i f necessary up to a maximum 3 mg. Give isoprenaline 0.2 mg IV (MiniJet ) if there is a delay in pacing and the patient rem ains unstable. Set up an infusion (1 mg in 100 mL 1 M saline starting at 1 mL/min titrating to heart rate (HR)). Insert temporary pacing wire (technique described in b Temporary ventricular pacing, p. 808 ). If this is not possible immediately, set up an external pacing system and transfer to a screening room for trans- venous pacing. Look for and treat reversible causes ; drug overdose ( B -blockers, verapamil, diltiazem, digoxin), hypothyroidism, hypothermia, myocardial infarction (MI), in fective endocarditis). BRADYCARDIA: GENERAL APPROACH 481 Haemodynamically stable patients \200 Admit to the coronary care unit (CCU) with continuo us ECG monitoring. Keep atropine drawn up and ready in case of acute deterioration. \200 Avoid temporary pac ing wire unless there is haemodynamic deterioration. Long-term management \200 Ensure all possible underlying causes have been identi \201 ed and removed. \200 Regardless of etiology if symptomatic bradycardia remains refer for permanent pacing (see b p. 530). Complete heart block should always be referred for a permanent pacemaker, whether symptomatic or not. External cardiac pacing \200 In emergencies, external cardiac pacing (via an external de \201 brillator that can pace) may be used \201 rst, but this is only a temporary measure until a more \200\230de \201 nitive \200\231 transvenous pacing wire can be inserted. The de \201 brillator ECG electrodes need to be attached. \200 Attach the de \201 brill ation patches to the anterior and posterior chest wall. Turn the output up (in volts or amp eres) until ventricular capture with QRS complexes is seen. This will also cause extremely unpleasant thoracic muscular capture, so the patient must be sedated with benzodiazepam External cardiac pacing is useful as a standby in patients, e.g. post-MI, when the risks of prophylactic transvenous pacing after thrombolysis are high. Haemodynamically stable patients with anterior MI and bifasicular block may be managed simp ly by application of the external pacing electrodes and having the pulse generator ready if necessary. Familiarize yourself with the machine in your hospital when you have some time \200\224 a cardiac arrest is not the time to read the manual for the apparatus! 482 CHAPTER 10 Arrhythmias Sinus bradycardia In sinus bradycardia, the SAN discharges <60/min. P waves are normal but slow. It may be normal (e.g. in sleep, healthy resting hearts). Causes \200 Young athletic individual \200 Healthy resting heart, e.g. sleep \200 Chr onic degeneration of sinus or AV nodes or atria \200 Drugs \200\224 B -blockers, morphin e, amiodarone, calcium-channel blockers, lithium, propafenone, clonidine Increased vagal tone \200 vasovagal attack \200 nausea or vomiting \200 carotid sinus hypersensitivity Hypothyroidism \200 Hypothermia \200 MI or ischaemia of the sinus node \200 Cholestat ic jaundice \200 Raised intracranial pressure Sinus pause The SAN fails to generate impulses (sinus arrest) or the impulses are not condu cted to the atria (SA exit block). A single dropped P wave with a PP interval that is a mul tiple of the basic PP interval suggests exit block. A period of absent P waves suggests sin us arrest. Causes include, excess vagal tone, acute myocarditis, MI, aging ( \201 brosis), stroke, digoxin toxicity, and anti-arrhythmic drugs. Sick sinus syndrome This syndrome encompasses a number of conduction system problems: per- sistent sinus bradycardia not caused by drugs, sinus pauses, AV conduction disturbances, an d paroxysms of atrial arrythmias. It is usually diagnosed by ambulatory cardiac monitoring. ATRIOVENTRICULAR BLOCK 483 Atrioventricular block This can occur at the AVN (nodal) or His \200\223Purkinje system (in franodal). Common causes are ischaemic heart disease (IHD), conduction system \201 brosis (aging), calci \201 c aortic stenosis, congenital, cardiomyopathy, hypo- thermia, hypothy roidism, trauma, radiotherapy, infection, connective tissue disease, sarcoidosis, and anti- arrhythmic drugs. AV block is further classi \201 ed: First-degree AV block Every impulse conducts to the ventricle but the conduction time is pr o- longed. Every P wave is followed by a QRS but with a prolonged PR interval ( > 200 ms). If the QRS width is normal then the block is at the AV node, if the QRS shows aberration (r ight (RBBB) or left bundle branch block (LBBB)), then the block may be at the AV node or th e His \200\223Purkinje system. Second-degree AV block \200 Mobitz 1 (Wenckebach): ECG shows the PR interval prolongs unt il a P wave is not conducted. The PR interval following the dropped P wave must be the shor test. The RR interval is therefore irregular. This block is characteristic of the AVN. Mobitz 2: ECG shows a \201 xed P to QRS ratio of 2:1, 3:1, or 4:1. Block is predominantly at the His bundle and there is often an aberrant pattern to the QRS complex. Third-degree AV block (complete heart block) There is no conduction to the ventricle. The E CG shows dissociation between the P and QRS complexes. An escape pacemaker rhythm takes ove r. A narrow QRS indicates AVN block, and the His bundle is the pace- maker, which is faster and more stable than more distal sites. A wide QRS indicates infranodal block and a distal ventricular pacemaker site. Asystole may occur; therefore, this carries a worse prognosis. This type of heart block always requires implantation of a permanent pacemaker. Causes of atrioventricular block \200 Conduction system \201 brosis (aging) Myocarditis (diphtheria, rheumatic fever, viral, Chagas \200\231 disease) \200 Associated with neuromuscular disease, i.e. m yotonic dystrophy. \200 Collagen vascular disease (systemic Associated with acute myocardial infarction or ischaemia Drugs ( B -blockers, digitalis, Ca 2 + -channel blockers) lupus eryhtematosus (SLE), rheumatoid arthritis (RA), scleroderma) \200 Cardiomyopathies Increased vagal tone \200 Trauma or following cardiac surgery/catheter ablation (haemochromotosis, amyloidosis) \200 Granulomatous disease (sarcoid) \200 Congenital he art block \200 Congenital heart disease (atrial septal defect (ASD), Ebstein \200\231s, p atent ductus arteriosus (PDA)). Calci \201 c aortic stenosis \200 Infective endocarditis \200 Hypothyroidism \200 Hy pothermia 484 CHAPTER 10 Arrhythmias Bundle branch block This is due to disease in the His \200\223Purkinje system causing a QRS > 120 ms. Common causes are conduction system \201 brosis (aging), IHD, hyperten- sion, cardiomyopathies, cardiac surgery, in \201 ltrative diseases (e.g. amyloid). \200 LBBB ( Fig. 10.3 ): LV depolarization is delayed, giving a wide QRS, large notched R waves in leads I and V 6 , and a deep S wave (may be preceded by small R wave) in V 1 . Block con \201 ned to the anterior or posterior fascicles of the left bundle gives left-axis or right-axis deviation respectively on the ECG. BBB leads to asynchronous contra ction of the left and right ventricle, which reduces cardiac output, important in heart fai lure. \200 RBBB: RV depolarization is delayed, giving wide QRS, an RSR pattern in V 1 , a nd a slurred S wave in I and V 6 . This can be a normal variant but more commonly as a resu lt of causes listed above and, in addition, ASD, pulmonary embolism (PE), cor pulmonale. Bifasicular block (Fig. 10.4 ) = RBBB + left anterior hemiblock (left-axis deviation on ECG), RBBB + left posterior hemiblock (right-axis deviation on ECG), or LBBB. All of these may progress to complete AV block. Trifasicular block = bifasicular block + 1st-degree AV block. Management \200 Conventional teaching is that LBBB is always pathological, and thorough investigation for an underlying cause is needed (echocardiogram, cardiac MR, coronary angio graphy); however, a cause may not be found. RBBB may occur in otherwise completely normal h earts. Permanent pacing is not normally needed for isolated RBBB or LBBB, unless associated with more advanced levels of block (bi- or trifasicular block), symptomat ic bradycardia, syncope. Common causes of bundle branch block \200 IHD \200 Hypertensive heart disease \200 Va lve disease (especially aortic stenosis) \200 Conduction system \201 brosis (aging) \200 Myocarditis or endocarditis \200 Cardiomyopathies \200 Pulmonary hypertension \200 Trauma or post-cardiac surgery \200 Neuromuscular disorders (myotonic dystrophy) \200 Polymyositis. BUNDLE BRANCH BLOCK 485 Fig. 10.3 ECG showing LBBB. There is a wide QRS complex with large notched R waves in leads I and V 6 and a deep S wave in V 1 . Fig. 10.4 ECG showing bifasicular block. There is a wide QRS complex with an rSr pattern in V 1 and deep slurred S wave in V 6 (=RBBB). The QRS in lead 1 is positive and lead aVF neg ative (=left anterior hemiblock). There is also 2nd-degree AV nodal block (Mobitz type 1 or Wenkebach). Observing the rhythm strip from the \201 rst P wave, there is a gradually pr olonging PR interval and the P wave that follows the 6th QRS complex is blocked. 486 CHAPTER 10 Arrhythmias Tachycardia: general approach Tachyarrhythmias may present with signi \201 cant symptoms a nd haemo- dynamic compromise. The approach to patients depends upon the following factors: The effect of the rhythm on the patient \200 Patients with cardiac arrest \200\224 immed iate unsynchronized DC shock (follow advanced life support (ALS) guidelines) Patients with signs of severe haemodynamic compromise : shock; low BP, cool peripheries, sweating \200 cerebral hypoperfusion; confusion, agitate d, depressed conscious level pulmonary oedema \200 chest pain Record an ECG/rhythm strip and treat immediately with synchronized DC shock \200 Patients without haemodynamic compromise : record an ECG and diagnose tachyarrhythmia. Follow the treatment algorithm outlined here. If they deteriorate , treat as above. Diagnosing the arrhythmia The main distinctions to make are: \200 tachy- ( > 120/min) vs. brady- (<60/min) arrhythmia \200 narrow ( \211 120 ms or 3 small squares) vs. broad QR S complex \200 regular vs. irregular rhythm. Investigations for patients with tachyarrhythmias Regular vs. irregular rhythm \200 Narrow vs. broad QRS complex \200 FBC, biochemistry, glucose (urgently) \200 Ca 2 + , Mg 2 + (especially if on diuretics) \200 Biochemical m arkers of myocardial injury \200 Blood cultures, CRP, ESR \200 Thyroid function tests \200 Drug levels \200 Arterial blood gasses \200 Heart size \200 Evidence of pulmona ry oedema \200 Other pathology (e.g. Ca 2 + bronchuslAF, pericardial 12-lead ECG and rhythm strip Blood tests Where appropriate Chest X-ray (CXR) effusionlsinus tachycardia, hypotension 9 AF) This page intentionally left blank 488 CHAPTER 10 Arrhythmias Tachycardia: emergency management History Previous cardiac disease, palpitations, dizziness , chest pain, symptoms of heart failure and recent medication. Ask speci \201 cally about conditions known to be associated with certain cardiac arrhythmias (e.g. AF \200\224 alcoh ol, thyrotoxicosis, mitral valve disease, IHD, pericarditis; VT \200\224 previous MI, LV a neurysm). Examination BP, heart sounds and murmurs, signs of heart failure, carotid bruits. Management (Fig. 10.5 ) Haemodynamically unstable patients Tachyarrhythmias causing severe haemodynamic compromise require urgent correction, usually with external de \201 brillatio n. Drug therapy requires time and haemodynamic stability. \200 The only exception is a pa tient in chronic AF with an uncontrolled ventricular rate \200\224 de \201 brillation is unlikely to cardiovert to sinus rhythm (S R). Rate control and treatment of precipitant is \201 rst-line. Sedate awake patients with midazolam (2.5 \200\22310 mg IV) diamorphine (2.5 \200\2235 m g IV + metoclopramide 10 mg IV) for analgesia. Beware respiratory depression and have \202 umazenil and naloxone to hand. \200 Formal anesthesia with propofol is preferred, bu t remember the patient may not have an empty stomach and precautions should be taken to pre vent aspiration (e.g. cricoid pressure, endotracheal (ET) intubation). Start at 200 J synchronized shock and increase as required. \200 If tachyarrhythmia recur s or is unresponsive try to correct d P a O 2 (partial pressure of oxygen in the arterial b lood), i P a CO 2 (partial pressure of carbon dioxide in the arterial blood), acidosis or d K + . Give Mg 2 + (8 mmol IV stat) and shock again. Amiodarone 150 \200\223300 mg bolus IV may also be used. \200 If there is ongoing ventricular tachycardia (VT) in the context o f cardiac arrest or recurrent VT episodes, causing haemodynamic compromise, requiring repea ted DC cardioversions then give IV amiodarone (300 mg IV bolus, followed by 1.2 g IV over 2 4 hours via central venous line). Follow Resuscitation Council periarrest arrhythmia guidel ines. 1 Haemodynamically stable patients \200 Admit and arrange for continuous ECG monitoring and 12-lead ECG. \200 Try vagotonic maneuvers (e.g. Valsalva/carotid sinus massage). \200 If diagnosis is clear, introduce appropriate treatment. \200 If there is doubt regarding diagnosis, give adenosine 6 mg as a fast IV bolus followed by 5 mL saline \202 ush. If th ere is no response, try 9, 12, and 18 mg in succession with continuous ECG rhythm strip. \200 De \201 nitive treatment should start as soon as diagnosis is known (see b Treatment options in tachyarrhythmias, p. 721). \200 First episodes of atrioventri cular node re-entrant tachycardia (AVNRT), atrioventricular re-entrant tachycardia (AVRT), or focal atrial tachycardia may ne ed no further treatment. All other diagnoses and Wolff \200\223Parkinson \200\223White synd rome (WPW) should be referred to a cardiologist for further investigation and management. 1 Resuscitation Council (UK) guidelines Y www.resus.org.uk. TACHYCARDIA: EMERGENCY MANAGEMENT 489 Patient with tachycardia Is patient in shock? Yes No 12 lead ECG, UEs, TFTs Emergency DC cardioversion No Yes Is rhythm regular? QRS > 120 ms No Treat as VT. Ignore possibility of SVT. Try lidocaine 50 \200\223100 mg. If fails arrange D C CV. Refer to cardiology. Treat as AF. Control rate with -blocker or verapamil. Start anticoagulation with heparin. If <48 hours since onset consider Yes Normal P waves visible? Yes No Consider sinus tachy- cardia. Look for under- lying cause. If no cause found proceed to ade nosine Give iv adenosine (or vera- pamil if contraindication) while recording 12 lead ECG continuo usly No Yes Tachycardia terminated? Underlying P-wave rate >tachycardia rate? Yes No Likely diagnosis AVRT or AVNRT. Look at SR ECG, if evidence of WPW discuss with cardiologis t. If normal refer to cardiology as outpatient. If episodes are recurrent start verapamil o r -blocker Focal atrial tachycardia. If episodes are recurrent start verapamil or -blocker. If patie nt is well refer as outpatient, otherwise inpatient Atrial flutter. Treat as for AF Fig. 10.5 Guidelines to the safe management of arrhythmias in the emergency department (ada pted from Barts and the London NHS Trust A + E guidelines). CV = cardioversion; UEs = urea and electrolytes. 490 CHAPTER 10 Arrhythmias Tachyarrhythmias: classi \201 cation Fast heart rates can be classi \201 ed in various wa ys; however, an anatomical approach should be used, which can then be subdivided mechanisti cally. This provides a simple foundation for understanding the ECG appearance and the tachy cardia mechanism. Atrial tachyarrhythmias These are contained completely in the atria (or SAN) and are charac ter- ized by: \200 sinus tachycardia \200 sinus node re-entrant tachycardia (SNRT) \200 atrial \201 brillation (AF) \200 atrial tachycardia focal atrial tachycardia \200 macro-re-entrant atrial tachycardia (=atrial \202 utter). Atrioventricular tachyarrhythmias These are dependent on activation between the atrium and ventricle (or AV node). They are characterized by: \200 AVRT \200 AVNRT \200 junction al tachycardia. Ventricular tachyarrhythmias These are contained completely in the ventricle and are charac terized by: \200 VT monomorphic VT. \200 polymorphic VT (torsades de pointes) . ventricular \201 brillation (VF). Features of a broad complex tachycardia suggesting ventricular origin \200 AV dissociatio n (NB: VA conduction may be present during VT). independent P waves. \200 capture and fusion beats QRS width > 140 ms (if RBBB appearance) or > 160 ms (if LBBB appearance) QRS axis < \210\222 30 or > + 90. \200 Concordance of QRS complexes in precordial leads (all positive or all negative) Absence of RS or RS > 100 ms in precordial leads Supraventricular causes of a broad complex tachycardia \200 SVT + aberrancy (bundle branc h block) \200 SVT + pre-excitation (activation of the ventricle over a pathway other than the AV node) Antidromic AVRT \200 SVT + class 1c drug ( \202 ecainide). This page intentionally left blank 492 CHAPTER 10 Arrhythmias ECG diagnosis of tachyarrhythmias By following simple rules when interpreting the ECG, any tachycardia can be classi \201 ed to the categories described earlier; however, the ECG sh ould always be considered in the clinical context. A broad complex tachycardia (BCT) must a lways be diagnosed as VT in the acute setting, as treating such patients incorrectly may be fatal. View the ECG in both tachycardia and the patients \200\231 usual rhythm to make a d iagnosis (e.g. may see features of WPW). For narrow complex tachycardias (NCTs), use caroti d sinus massage or adenosine boluses to see the underlying atrial rhythm. A simple approach follows (Fig. 10.6 ): 1. Is the tachycardia regular? Grossly irregular RR intervals regardless of other ECG featu res indicate AF (or VF; however expect the patient to be unconscious!). A slight irregulari ty can occur in other tachycardias, particularly at their onset. Alternatively, multiple at rial and/or ventricular ectopic beats or atrial tachy cardia with variable AV block can giv e irregularity. 2. Is the QRS complex broad ( > 120 ms)? Yes \200\224 ventricular in origin, no \200\224 supraventricular. SVT should only be considered for a BCT when there is strong clinical suspicion (e.g. young patient, no previous cardiac history, normal RV and LV function, no accompanying cardiovas cular compromise) and after discussion with senior colleagues. NB: Look at the SR ECG (if a vailable) for pre-existing bundle branch block or pre-excitation (suggesting an accessory p athway). 3. Identify P waves, their morphology and P:R ratio \200 1:1 P:R, normal P-wave morpholog y : sinus tachycardia, focal atrial tachycardia originating from close to the SA node (high crista terminalis or right superior pulmonary vein) or, rarely, SNRT. 1:1 P:R, abnormal P-wave morphology : focal atrial tachycardia. AVRT or AVNRT (if slow activation from ventricle to atrium = long RP tachycardia). \200 P waves n ot visible: AVRT or AVNRT (with fast activation from ventricle to atrium). Compare QRS morp hology in tachycardia with SR, as a slight de \202 ection in the tachycardia QRS complex n ot seen in SR may represent the P wave, P:R 2:1,3:1 or greater: focal or macro-re-entrant atrial tachycardia with AV nodal block . P-wave rate > 250/min : this de \201 nes atrial \202 utter (macro-re-entrant atrial tach ycardia). Usually there will be 2:1 or 3:1 P:R ratio. In typical atrial \202 utter, a cha racteristic saw-tooth baseline is seen in the inferior leads. 4. Response to AV block (adenosine or carotid massage) If a rapid P-wave rate persists desp ite induced AV nodal block, then the tachycardia is independent of the AV node, i.e. macro- re-entrant or focal atrial tachycardia and SNRT. If tachycardia is terminated by AV nodal b lock, it is either AVRT or AVNRT (rarely, junctional tachycardia). Focal atrial tachycardia and SNRT may also be terminated by adenosine, not due to AV nodal block, but because they are adenosine sensitive. ECG DIAGNOSIS OF TACHYARRHYTHMIAS 493 Tachycardia Irregular RR intervals? Yes No Yes AF \200 Multiple ectopics (A or V) \200 Atrial tachycardia with \200 Variable AV bloc k No QRS > 120 ms VT Yes No P waves visible? No Yes P:R 1:1 ratio? AVNRT \200 AVRT Focal atrial tachycardia \200 Atrial flutter P wave morphology normal? (upright in I, II, III, aVF) No Yes Sinus tachycardia \200 SNRT \200 Focal atrial tachycardia originating close to SA node RP distance > PR? No Yes Focal atrial tachycardia \200 Atypical AVNRT \200 AVRT via slow accessory pathway AVRT \200 AVNRT Fig. 10.6 ECG diagnosis of tachycardia. 494 CHAPTER 10 Arrhythmias Supraventricular tachycardia (see Fig. 10.7) This section deals with the diagnosis and phar macological management of individual SVTs. Their mechanisms and ablation are discussed in d etail in Chapter 11. Atrial tachycardia (ectopic focus re-entry) Atrioventricular re-entry tachycardia (AVRT) Sinus node AV node re-entry tachycardia (AVNRT) AV node Fig. 10.7 Types of supraventricular tachycardia. Reproduced with permission from Ramrakha P , Moore K, and Sam M (2010). Oxford Handbook of Acute Medicine . 3rd ed. Oxford: Oxford Uni versity Press. Sinus tachycardia De \201 ned as a sinus rate > 100/min, this may be physiological (e.g. e xercise or emotion) or pathological. Look for and treat the underlying cause \200\224 anem ia, drug related (e.g. caffeine, cocaine, salbutamol, etc.) hyperthy- roidism, pain, hypoxi a, pyrexia, or hypovolaemia. If no underlying cause is found, consider SNRT or focal atrial tachycardia as alternative diagnoses. These will be paroxysmal in nature, have sudden onse t or offset and are usually terminated by IV adenosine. If no underlying cause is found, it may be termed inappropriate sinus tachycardia. B -blockers are useful for symp- tomatic pe rsistent inappropriate sinus tachycardia, and vital in controlling the sinus rate in hypert hyroidism or heart failure, or post MI. SINUS NODAL RE-ENTRANT TACHYCARDIA 495 Sinus nodal re-entrant tachycardia This is a rare cause of narrow complex tachycardia due t o a micro re-entry circuit within the SAN. ECG is identical to sinus tachycardia, making di ag- nosis dif \201 cult. B -blockers or calcium-channel antagonists are the \201 rst-lin e treatment. Modi \201 cation of the SA node by radiofrequency ablation (RFA) is reserved for drug-refractory cases or those not wishing to take drugs. Regular tachycardia Irregular tachycardia Atrial \201 brillation (see b Atrial \201 brillation, p. 500) \200 Atrial \202 utte r with variable Sinus tachycardia \200 SNRT \200 Atrial tachycardia ( see b Atrial AV block tachycardia, p. 496). \200 focal atrial tachycardia \200 macro-re-entrant atrial tachyc ardia SR with frequent atrial or ventricular ectopic beats (atrial \202 utter). AVRT (i.e. with accessory path, e.g. WPW) (see b Atrioventricular re-entrant tachycardia (AVRT), p. 498) AVNRT (see b Atrioventicular nodal re-entrant tachycardia (AVNRT), p. 498) 496 CHAPTER 10 Arrhythmias Atrial tachycardia The term atrial tachycardia describes all regular atrial rhythms with a P rate > 100/min, regardless of the mechanism, and this should be pre \201 xed by either f ocal or macro-re-entrant, unless the mechanism is unknown. Focal atrial tachycardia This is due to an automatic focus of atrial cells \201 ring fast er than the SA node. The P-wave morphology and axis during tachycardia can be used to predi ct the location of the source. They are characteristically paroxysmal with short bursts at a rate of 150 \200\223250/min, but may be incessant, risking tachycardia-induced cardiomyop athy. They occur in normal hearts but are also associated with many forms of cardiac diseas e. It may be terminated with IV adenosine. Treatment is needed only for symptomatic patients or incessant tachycardia. B -blockers and calcium-channel antagonists can be used to slow the atrial rate and the ventricular respon se by AV nodal blockade. Class 1c ( \202 ecainide and propafenone) or class 3 (amiodarone and sotalol) may suppress the tachycardia, but their use is limited by toxicity. RFA is the most effective therapy and is a cure. Macro-re-entrant atrial tachycardia (atrial \202 utter) Atrial \202 utter (AFL) is an E CG de \201 nition of a P-wave rate > 240/min, and an absence of an isoelectric baseline be tween de \202 ections. It is caused by a re-entry circuit over large areas of the right or left atrium (see b Atrial arrhythmias: mechanism, p. 564). The circuit is not in \202 uen ced by adeno- sine, and the AVN block reveals the underlying rhythm. It is usually (but not always) associated with structural heart disease. AFL exacerbates heart failure symptoms a nd, if incessant, will worsen LV function. DC cardioversion effectively restores SR, but AFL often recurs. Drug therapy is not very ef fective. AVN blockade is dif \201 cult to achieve and the high doses of B -blockers, calci um-channels antagonists, and digoxin required may have unwanted side-effects. Class 1c drug s are used to maintain SR; however, propafenone and \202 ecainide can paradoxically accel erate the ventricular rate in AFL by slowing the tachycardia rate down suf \201 ciently to allow the AVN to conduct 1:1. They should always be used in combination with an AVN-blocki ng agent. Amiodarone is an alternative agent, particularly if LV function is impaired. RFA is the most effective way of maintaining SR and is a cure. If curative ablation is not possible, and effective rate control is not possible with drugs, then ablation of the AV no de and a pacemaker is a permanent palliative solution. Anticoagulation recommendations for patients with AFL are identical to those for patients with AF. 1 1 Blomstrom-Lundqvist C, Scheinman MM, Aliot EM et al. (2003). ACC/AHA/ESC guidelines for t he management of patients with supraventricular arrhythmias J Am Coll Cardiol 42 : 1493 \200\223531. This page intentionally left blank 498 CHAPTER 10 Arrhythmias Atrioventricular nodal re-entrant tachycardia (AVNRT) (see Figs. 10.8 and 10.9 ) This is th e commonest cause of a narrow complex tachycardia in patients with normal hearts, typically in young adults, commoner in women. It characteristically causes paroxysms of severe palpi tations, with a pounding in the neck (due to re \202 ux of blood into the jugular veins ca used by the simultanous atrial and ventricular contraction). It has a benign prognosis and may require no treatment. The ECG in SR is usually normal. The tachycardia is terminated by IV adenosine or vagal maneuvers. The underlying re-entry c ircuit is entirely within the AV node and therefore can be controlled long term with B -blo ckers, verapamil, or diltiazem. Alternative effective, but second-line agents are \202 ec ainide, propafenone, or sotalol. The \201 rst-line treatment for recurrent symptomatic ep isodes however is RFA, which is a cure. When symptoms are very infrequent, a \200\230pill in the pocket \200\231 approach is sometimes helpful, i.e. a large oral dose of, e.g., vera pamil is taken to terminate the event. Atrioventricular re-entrant tachycardia (AVRT) (see Figs. 10.8 and 10.9 ) This is due to an AV re-entry circuit involving a connection other than the AV node. As these accessory path ways are congenital, arrhythmias usually present much younger than AVNRT (infancy or childh ood). Rapid par- oxysmal palpitations are the usual symptom. It is usually a NCT (ortho- dr omic), as the ventricle is activated via the AVN; however, a BCT is also possible if the ve ntricle activates via the accessory pathway (antidromic). The prognosis may not be benign a nd specialist referral is mandatory. RFA is the treatment of choice. The most useful drugs are \202 ecainide and propafenone, which slow conduction in the accessory pathway without slowing the AV node. Verapamil, diltiazem, and digoxin should be avoided only when ventric ular pre-excitation is present. Junctional tachycardia This term should only be used for focal tachycardias that originate from the AV nodal tissue directly, and are in fact rare in adult cardiology. Distinction fr om other forms of NCT is only possible at the electrophysi- ology (EP) study. RFA is high r isk as the AV may be damaged. B -blockers and \202 ecainide are effective. Further reading Blomstrom-Lundqvist C , Scheinman MM , Aliot EM , et al. ( 2003 ). ACC/AHA/ ESC guidelines for the management of patients with supraventricular arrhythmias . J Am Coll Cardiol 42 : 1493 \200\223 531 . JUNCTIONAL TACHYCARDIA 499 I aVR V1 V4 II aVL V2 V5 III avF V6 V3 II Fig. 10.8 Typical presenting ECG of AVNRT or AVRT. A narrow complex tachycardia without vis ible P waves. FP AVN SP Left side AP Fig. 10.9 Mechanism of AVNRT and AVRT. Both AVNRT and AVRT have re-entry mechanisms. Orthod romic AVRT via a left-sided accessory pathway (AP) (left). Activation from A to V is down t he atrioventricular node (AVN), then across the ventricular myocardium and back from V to A up the AP, thus completing the circuit. The ventricle therefore is an essential part of th e circuit. Antidromic AVRT (not shown) would activate in the opposite direction. Typical AV NRT (right) acti- vates from the atrium to the AVN via the slow pathway (SP) and from the A VN to the atrium via the fast pathway (FP), thus completing the circuit. The ventricle is a ctivated as a bystander via the bundle of His and is not an essential part of the circuit. Atypical AVNRT (not shown) activates in the opposite direction. 500 CHAPTER 10 Arrhythmias Atrial \201 brillation Atrial \201 brillation (AF) is the most common sustained cardiac arrhythmia, with a prevalence of 0.5 \200\2231 % in the general population but 10-fold gre ater in those aged over 65 years. It is an atrial arrhythmia where uniform acti- vation is replaced by chaos, such that co-ordinated contractile function is lost and the atria dilate . It is characterized by an ECG lacking any con- sistent P waves, and a rapid, irregular ve ntricular rate. Classi \201 cation Previously, many terms have been used to pre \201 x AF; however, an in ter- national consensus on nomenclature has now been reached. 1 This allows the correct sel ection of management options for patients. All episodes of AF lasting greater than 30 s sho uld be described as: \200 \201 rst detected or a recurrent episode \200 self-terminat ing or not self-terminating \200 symptomatic or asymptomatic . \200 paroxysmal (if self -terminating within 7 days) \200 persistent (if cardioverted to SR by any means or lasts > 7 days regardless of how it terminates) permanent (if cardioversion to SR is not possible or is not undertaken) \200 lone (in the absence of underlying structural heart disease), or idiopathic (in the absence of any disease). Causes AF is a common end-point for many forms of cardiac disease where atrial myocytes are damaged or subject to adverse stress generated by ischaemia, cyanosis, or elevated intraca vity or pericardial pressures. These changes alter the conduction properties of the myocard ium, facilitating \201 brillation (see Table 10.1 ). Table 10.1 Causes of atrial \201 brillation Common causes Potentially reversible causes Rare causes Hypertension \200 Left ventricular (LV) failure (any cause) \200 Coronary artery diseas e (CAD) \200 Mitral or tricuspid valve disease \200 Hypertrophic obstructive cardiomyop athy (HOCM) Alcohol binge \200 Pneumonia \200 Hyperthyroidism \200 Acute MI \200 Acute pericard itis \200 Myocarditis \200 Exacerbation of Congenital heart disease Autonomic \200\230vagal \200\231 overactivity Pericardial effusion \200 Cardiac metastases \200 Myocardial in \201 ltrative diseases (e.g. amyloid) \200 Atrial myxoma pulmonary disease \200 Pulmonary embolism \200 Cardiac surgery 1 Levy S, Camm AJ, Saksena S, et al. (2003). International consensus on nomenclature and cl assi \201 cation of atrial \201 brillation. J Cardiovasc Electrophysiol 14: 443 \200\223 5. ATRIAL FIBRILLATION 501 Symptoms and signs Palpitations, dyspnoea, fatigue, presyncope, syncope, and chest pain are common; however, 30 % of patients present with AF as an incidental \201 nding only. Ambu latory monitoring reveals that even patients with symp- tomatic paroxysmal AF have many asy mptomatic episodes. Physical \201 nd- ings are an irregular pulse (which if rapid will be faster at the apex than the wrist), variable intensity of the \201 rst heart sound, and absent \200\230a \200\231 waves in the JVP. 502 CHAPTER 10 Arrhythmias Atrial \201 brillation: investigations A reversible cause should be identi \201 ed early to allow appropriate treat- ment. The most important investigations are:1 \200 ECG : irr egular ventricular rate and absence of P waves. V rate depends on intact AV nodal function. In the presence of complete AV nodal block, a slow regular ventricular escape rhythm is pr esent. The QRS will be broad if there is aberrant conduction; ST \200\223T-wave changes may be due to rapid rate, digoxin, or underlying cardiac disease. ECHO transoesophageal echocardiography (TOE) : for LV function, valve lesions, pericardi al effusion, and to exclude intracardiac thrombus prior to version to SR. LA size is an imp ortant predictor of likely future maintenance of SR. thyroid function : thyrotoxicosis may present as AF only. \200 CXR: cardiomegaly, pulmona ry oedema, intrathoracic precipitant, valve calci \201 cation (mitral stenosis (MS)). urea and electrolytes (U&Es) : hypokalaemia, renal impairment. \200 troponin or cardiac e nzymes: ?MI. Expect small rise after DC shock. Troponin may be elevated with any prolonged tachycardia without an acute coronary syndrome. drug levels : especially if taking digoxin. \200 arterial blood gasses (ABGs) : if hypoxi c, shocked or ?acidotic. \200 other investigations depend on suspected precipitant. Other investigations when the patient is stable 24-hour ambulatory monitor to assess heart- rate control and look for episodes of symptomatic bradycardia, exercise test (or other isch aemia stress test), coronary angiography, cardiac magnetic resonance. 1 Wyse DG , Waldo AL , DiMarco JP et al. ( 2002 ). A comparison of rate control and rhythm control in patients with atrial \201 brillation . N Engl J Med 347 : 1825 \200\223 33 . This page intentionally left blank 504 CHAPTER 10 Arrhythmias Atrial \201 brillation: management (see Fig 10.10) The most important aspects of AF manag ement are preventing stroke and controlling patients \200\231 symptoms, not restoration of SR. Limiting the ven- tricular rate by pharmacologically blocking the atrioventricular (AV) node ( rate control ) is safe and often effective. Currently available antiarrhythmic drug s (AADs) that maintain SR ( rhythm control ) are limited by their toxicity and ef \201 cac y, which explains why a strategy of rhythm control (electrical cardioversion and AADs) may be worse than rate control alone. 1 Non- pharmacological strategies (ablation) and new effe ctive, safer AADs for rhythm control may change this paradigm in the future. Fig. 10.10 sum marizes contemporary AF management.