 \200 \200 Box 9.1 External cardiac pacing In emergencies, external cardiac pacing may be used but is often painful for the patient (i f conscious) and should be viewed as a temporary meas- ure until transvenous pacing can be initiated. External cardiac pacing is useful in patients who have received thrombolysis for an acute m yocardial infarction (MI) when the risks of perforation and bleeding from transvenous pacin g are high. Hemodynamically stable patients with anterior MI and bifasicular block may be managed simpl y by application of the external pacing electrodes and having the pulse generator ready if necessary. Familiarize yourself with the machine in your hospital as soon as possible \200\224a cardiac arrest is not the time to read the manual. CHAPTER 9 Arrhythmias 358 Sinus bradycardia The sinoatrial node discharges <60/min. P waves are normal in appear- anc e. It is often normal in sleep and in athletes and healthy young adults. Causes \200 \200 \200 \200 Hypothyroidism Hypothermia Ischemia or infarction of the sinus node Chronic degeneration of sinus or AV nodes or atria Cholestatic jaundice Raised intracranial pressure Cervical and mediastinal tumors Young athletic individual B-blockers, calcium Drugs ( channel blockers, digoxin, morphine, amiodarone, lithium, propafenone, clonidine) Increased vagal tone \200 \200 \200 \200 \200 \200 \200 Vasovagal syncope Nausea or vomiting Carotid sinus hypersensitivity Acute MI (especially in ferior) Nasal or endotracheal suctioning Management If hypotensive or presyncopal \200 \200 \200 \200 \200 \200 Atropine 0.5 mg IV bolus repeating as necessary. Isoproterenol infusion 2 \200\22310 g/mi n. Theophylline infusion 0.2 \200\2230.7 mg/kg/hr. Temporary pacing. Avoid and correct prec ipitants. Stop drugs that may suppress the sinus or AV nodes. Long-term treatment \200 If all possible underlying causes have been removed and symptomatic bradycardia remains, re fer for permanent pacing. Consider Holter monitoring in patients with possible episodic bra dycardia. R-R intervals >2.5 seconds may require permanent pacing, especially if associated with symptoms. SICK SINUS SYNDROME 359 Sinus pause The SAN fails to generate impulses (sinus arrest) or the impulses are not condu cted to the atria (SA exit block). The PP interval with sinus pause does not equal a multip le of the basic sinus interval (PP). A single dropped P wave with a PP interval that is a m ultiple of the basic PP interval suggests exit block. A period of absent P waves suggests s inus arrest. Causes include excess vagal tone, acute myocarditis, MI, aging ( \201 brosis), stroke, digoxin toxicity, and antiarrhythmic drugs. Sick sinus syndrome This syndrome encompasses a number of sinus node problems: 1) persist- ent, inappropriate sinus bradycardia not caused by drugs; 2) sinus arrest or exit block; 3) SAN and AV conduction disturbances; 3) paroxysms of atrial, supraventricular, or junctiona l tachyarrythmias alternating with slow atrial or ventricular rates. It is usually diagnose d by ambulatory cardiac monitoring. CHAPTER 9 Arrhythmias 360 Atrioventricular block AV block occurs when an impulse from the atria is conducted with del ay or not conducted at all to the ventricle. This can occur at the level of the AVN (nodal) or His \200\223Purkinje system (infranodal). Common causes are ischemic heart disease, conduction system \201 brosis (aging), calci \201 c aortic stenosis, congenital, cardiomyopathy, hypothermia, hypothyroidism, trauma, ra diotherapy, infection, connective tissue disease, sarcoidosis, tick-born diseases, and anti -arrhythmic drugs (see Box 9.2). AV block is classi \201 ed as follows. 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 inter- val (>200 ms). If the QRS width is normal on ECG, then the delay is usually in the AV node. If the QRS sho ws aberration (RBBB or LBBB), then the delay may be in the AV node or His \200\223Purkinje system. Second-degree AV block Some, but not all, atrial impulses are conducted to the ventricle. Mobitz type 1 (Wenckebach) ECG shows a regularly irregular rhythm with grouped beating and progres- sive prolongation of the PR interval until the P wave is not conducted. The PR int erval following the dropped P wave is the shortest in the sequence. The RR interval is ther efore irregular. This block is characteristic of normal AVN physiology and generally is a stable rhythm that does not progress to advanced AVN block. Mobitz type 2 ECG shows a stable PR interval with periodic block of the atrial impulse at a ratio of 2:1, 3:1, or 4:1. Block is predominantly below the AVN at the His bundle and ther e is often an aberrant pattern to the QRS complex. Type 2 block is an unstable rhythm that often predates the development of complete AV block. Third-degree AV block (complete heart block) There is no conduction of atrial impulses to t he ventricle. The ECG shows no relationship between P and QRS complexes (dissociation). Generally, a ventricular pacemaker originating just below the site of the block takes over. A narrow QRS usually indicates block in the AVN and the His bundle is the pacemaker, which is faster and more stable than more distal sites. A wide QRS indicates infranodal block an d a distal, slower ventricular pacemaker. Distal block carries a worse prognosis and a greater risk of sudden asystole. ATRIOVENTRICULAR BLOCK 361 Box 9.2 Causes of atrioventricular block \200 Valvular disease (aortic stenosis, incompetence, endocarditis) Myocarditis (diphtheria, rhe umatic fever, viral, Chagas \200\231 disease, tick-borne) Associated with neuromuscular dis ease, i.e., myotonic dystrophy. Collagen vascular disease (SLE, rheumatoid arthritis, scler oderma) Cardiomyopathies (hemochromotosis, amyloidosis) Granulomatous disease (sarcoid) Con genital heart block Congenital heart disease (ASD, Ebstein \200\231s, PDA, L-transposition) Acute myocardial infraction or ischemia Drugs ( Ca2+-blockers) Conduction system \201 bro sis (Lev and Lenegre syndromes) Increased vagal tone Trauma or following cardiac surgery Hy pothyroidism (rarely thyrotoxicosis) Hypothermia Hyperkalemia and other electrolyte abnorma lities Hypoxia In \201 ltrative diseases (amyloidosis) B-blockers, digitalis, \200 \200 \200 \200 \200 CHAPTER 9 Arrhythmias 362 Bundle branch block Bundle branch block (BBB) is due to disease in the His \200\223Purkinje system resulting in conduction delay that manifests as a prolonged QRS on sur- face ECG (Q RS >120 ms). Common causes are conduction system \201 brosis (aging), ischemic heart dise ase, hypertension, cardiomyopathies, cardiac surgery, and in \201 ltrative diseases (see B ox 9.3). LBBB: left ventricular depolarization is delayed, giving large notched R waves in leads I a nd V6 and an inverted-M pattern in V1. Block con \201 ned to the anterior or posterior fas cicles of the left bundle gives left-axis or right-axis deviation, respectively, on the ECG . BBB leads to asynchronous contraction of the left and right ventricles, which worsens fun ction. RBBB: right ventricular depolarization is delayed, giving an RSR pattern in V1 and a promin ent S wave in I and V6. This can be a normal variant but more commonly is due to causes lis ted in Box 9.3 as well as atrial septal- defect (ASD), pulmonary embolism (PE), and cor pul monale. Bifascicular block = RBBB + left anterior hemiblock (left-axis deviation on ECG), RBBB + le ft posterior hemiblock (right-axis deviation on ECG) or LBBB. All of these may progress to complete AV block. Trifascicular block = bifascicular block + \201 rst-degree AV block. Management Interventricular conduction disturbances alone do not require temporary pacing. However, when associated with hemodynamic disturbance or pro- gression to higher levels of block (even if intermittent), a transvenous pacing wire must be considered. The need for longer term pacing is dependent on the persistence of symptoms and underlying cause. Consult a cardiologist. Box 9.3 Common causes of bundle branch block \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 Ischemic heart disease Hypertensive heart disease Valve disease (especially aortic stenosis ) Conduction system \201 brosis (Lev and Lenegre syndromes) Myocarditis or endocarditis C ardiomyopathies In \201 ltrative diseases (amyloidosis, sarcoidosis) Cor pulmonale (RBBB) (acute or chronic) Trauma or postcardiac surgery Neuromuscular disorders (myotonic dystroph y) Polymyositis TACHYARRHYTHMIAS: GENERAL APPROACH 363 Tachyarrhythmias: general approach Tachyarrhythmias may present with signi \201 cant sympt oms, syncope, and hemodynamic compromise. The approach to patients depends on 1. The effect of the rhythm on the patient 2. The diagnosis from the ECG and rhythm strips 3 Any underly ing cardiac abnormality or identi \201 able precipitant (Box 9.4) Effect of tachyarrhythmi a on the patient Patients with signs of severe hemodynamic compromise \200 Impending card iac arrest with an unstable rhythm \200 Shock \200\224systolic BP <90 mmHg \200 Severe pulmonary edema \200 Altered mental status Treat immediately with synchronized external c ardioversion for SVT, VT or unsynchronized external de \201 brillation for VF. Patients with mild to moderate hemodynamic compromise \200 \200 \200 Try to record an ECG and long rhythm strip before giving pharmacologi- cal agents and/or de \201 brillatio n or intervention. This will be invaluable for long-term management. If the patient deterio rates, treat as above. Diagnosing the arrhythmia The main distinctions to make are the foll owing (see also Box 9.5): \200 \200 \200 Mild pulmonary edema Low cardiac output with cool extremities and oliguria Angina at rest d uring tachycardia Tachy- (>100/min) vs. brady- (<60/min) arrhythmia Narrow ( Regular vs. irregular rhythm (cid:100)120 ms or 3 small sq.) vs. broad QRS complex (Box 9.6) Box 9.4 Common precipitating factors Underlying cardiac disease \200 Ischemic heart disea se \200 Acute or recent MI \200 Angina \200 Mitral valve disease \200 LV aneurysm \200 Congenital heart disease \200 Conduction system disease \200 Pre excitation (shor t PR interval) \200 Long QT (congenital or acquired). Metabolic abnormalities i \200 i \200 d \200 d \200 i \200 \200 or d K+ or d Ca2+ Mg2+ PaO2 PaCO2 Acidosis Endocrine abnormalities \200 \200 Thyrotoxicosis Pheochromocytoma Drugs \200 \200 Miscellaneous \200 \200 \200 \200 Antiarrhythmics Sympathomimetics ( cocaine) Antidepressants (tricyclic) Adenylate cyclase i nhibitors (aminophylline, caffeine) Alcohol Febrile illness Emotional stress Smoking Fatigue B 2 agonists, \200 CHAPTER 9 Arrhythmias 364 Box 9.5 Investigations for patients with tachyarrhythmias \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 \200 12 Lead ECG and rhythm strip Regular vs. irregular rhythm Narrow vs. broad QRS complex Relation of P waves to QRS CBC, c hemistries including Cr, glucose (urgently) 2+, Mg2+ (especially if on diuretics) Ca Bioche mical markers of myocardial injury Blood cultures, CRP, ESR Thyroid function tests Drug lev els/toxicology screen Arterial blood gasses Heart size Evidence of pulmonary edema Other pa thology (e.g., COPD, cancer, AF, pericardial effusion, sinus tachycardia, hypotension AF ) Blood tests Where appropriate Chest X-ray Box 9.6 Narrow vs. wide complex tachyarrhythmia \200 Narrow complex tachycardias originate in the atria or AV node (i.e., supraventricular tachy cardias [SVT]). Irregular, narrow complex tachycardia is most commonly AF or atrial \202 utter with varying AV block. Wide complex tachyarrhythmias may originate from either the ve ntricles (VT) or from the atria or AV node (SVT) with aberrant conduction to the ventricles (RBBB or LBBB con \201 guration or preexictation). If the patient has previous documented arrhythmias, compare the morphology of the current arrhythmia to old ECGs. The diagnosis o f VT vs. SVT and thus the appropriate therapy may be evident from review of the prior ECG o r history. TACHYARRHYTHMIAS: CLASSIFICATION 365 Tachyarrhythmias: classi \201 cation Tachyarrhythmias are generally classi \201 ed via an anatomical approach that can then be subdivided on the basis of arrhythmia mechanism (see also Box 9.7). This provides a simple foundation for understanding the ECG morphology and t he tachycardia mechanism. Atrial tachyarrhythmias originate in the atria (or SAN). \200 \200 \200 \200 Sinus tachycardia Sinus node reentrant tachycardia Atrial \201 brillation Atrial tachycar dia \200 \200 Focal atrial tachycardia Macro-reentrant atrial tachycardia (aka atrial \202 utter) Atrioventricular tachyarrhythmias are dependent on activation in or conduction via the AV n ode for maintenance of the arrhythmia. \200 \200 \200 Atrioventricular reentry tachycardia (AVRT) Atrioventricular nodal reentry tachycardia (AVN RT) Junctional tachycardia Ventricular tachyarrhythmias originate in the ventricle(s). \200 Ventricular tachycardia (VT) \200 \200 Ventricular \201 brillation Monomorphic VT Polymorphic VT (e.g., torsades de pointes) Features of wide complex tachycardia suggesting a ventricular origin \200 AV dissociation or lack of 1:1 AV relationship (although, VA conduction may be present duri ng VT) \200 \200 QRS width >140 ms (if RBBB appearance) >160 ms (if LBBB appearance) QR S axis < \210\22230 or > +90 Concordance of QRS complexes in precordial leads (all positiv e or all negative) Delayed/slurred initial forces (>100 ms) P waves with no clear association to the QRS Capture and fusion beats or \200 Supraventricular causes of a wide complex tachycardia \200 \200 SVT with aberrancy (bundle branch block) SVT with pre-excitation (activation of the ventric le via antegrade conduction over an accessory pathway other than the AV node) e.g., antidro mic AVRT SVT + class Ic drug ( \202 ecainide) CHAPTER 9 Arrhythmias 366 Box 9.7 Supraventricular tachycardias Regular tachycardia \200 Sinus tachycardia \200 Sinus node reentrant tachycardia (SNRT) \200 Atrial tachycardia \200 \200 Irregular tachycardia \200 \200 Atrial \201 brillation (AF) Atrial \202 utter with variable block Multifocal atrial tac hycardia Focal atrial tachycardia Macro-reentrant atrial tachycardia (atrial \202 utter) Atrioventricular reentry tachycardia (AVRT) (i.e., with accessory path, e.g., WPW) AV nodal reentry tachycardia (AVNRT) ECG DIAGNOSIS OF TACHYARRHYTHMIAS 367 ECG diagnosis of tachyarrhythmias By following simple rules when interpreting the ECG, any tachycardia can be classi \201 ed into the categories described earlier; however, the ECG should always be considered in the clinical context. A wide complex tach- ycardia (WCT) sho uld always be diagnosed as VT in the acute setting, as treating such patients incorrectly m ay be fatal. Review the ECG in both tachycardia and the patient \200\231s usual rhythm to a id in diagnosis (e.g., may see features of Wolff \200\223Parkinson \200\223White [WPW]) (se e also Fig. 9.3). For narrow complex tachycardias (NCTs) use carotid sinus massage, vagal maneuvers or IV ade nosine to facilitate identi \201 cation of the underly- ing atrial rhythm. A simple approach follows. 1. Is the tachycardia regular? Grossly irregular RR intervals generally indicate AF or \202 utter with variable block (or VF, but expect the patient to be unconscious!). A slight vari- ability in rate can occur in other tachycardias, particularly at their onset. Altern atively, multiple atrial and/or ventricular ectopic beats or atrial tachycardia with variab le AV block can give irregularity. 2. Is the QRS complex wide (>120 ms)? Yes \200\224ventricular or SVT with aberrancy; no \200\224supraventricular. SVT should only be considered for a wide complex tachycardia in the appropriate clinical se tting (e.g., young patient, no previous cardiac history, normal RV and LV function, no acco mpanying cardiovascular compromise) and after review with senior colleagues. Note: Look at the baseline, sinus ECG (if available) for pre-existing bun- dle branch block or pre-excitation (suggesting an accessory pathway). 3. Identify P waves, their morphology, and P:QRS ratio \200 1:1 P:QRS, normal P-wave morphology: atrial tachycardia originating from close to the SA no de (high crista terminalis or right superior pulmonary vein), or, rarely, sinus node reentr y tachycardia. 1:1 P:QRS, abnormal P-wave morphology: AVRT or AVNRT (if slow ventricular to atrial conduction = long RP tachycardia). P waves not visible: conduction). Compare QRS mo rphology in tachycardia with that in NSR, as a slight de \202 ection in the tachycardia QR S complex not seen in NSR may represent a retrograde P wave. P:QRS 2:1, 3:1, or greater: wi th AV nodal block and varying AV conduction. P wave rate >250 bpm: tachycardia). Usually th ere will be a 2 or 3:1 P:QRS ratio. In typical atrial \202 utter, a characteristic saw to oth baseline is seen in the inferior leads with upright P waves (dart-and-dome) in leads V1 and V2. sinus tachycardia, focal focal atrial tachycardia. AVRT or AVNRT (with rapid ventricular to atrial focal or macro-reentrant atrial tachycardia atrial \202 utter (macro-reentrant atrial CHAPTER 9 Arrhythmias 368 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 -reentrant or focal atrial tachycardia or SNRT. If tachycardia is terminated by AV nodal block, it is dependent on the AVN (either AVRT or AVNRT, rarely junctional tachycardia). Focal atrial tachycardia and sinus node reentry may also be terminated by adenosine, not through AV nodal block but because they are adenosine sensitive. Tachycardia Yes No Irregular RR intervals? 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? Yes No P:R 1:1 ratio? AVNRT \200 AVRT Focal atrial tachycardia \200 Atrial flutter Yes No P wave morphology normal? (upright in I, II, III, aVF) 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 acces- sory pathway AVRT \200 AVNRT Figure 9.3 ECG diagnosis of tachycardia. TACHYCARDIA: EMERGENCY MANAGEMENT 369 Tachycardia: emergency management History This includes previous cardiac disease, palpitati ons, dizziness, chest pain, symptoms of heart failure, and medication. Ask speci \201 call y about con- ditions known to be associated with certain cardiac arrhythmias (e.g., AF \200 \224alcohol, thyrotoxicosis, mitral valve disease, CAD, pericarditis; VT \200\224previous M I, LV aneurysm, cardiomyopathy). Examination Check BP and assess for heart sounds and murmurs that are signs of heart failur e and carotid bruits. Management (see Fig. 9.4) Hemodynamically unstable patients Tachyarrhythmias causing severe hemodynamic compromise (cardiac arrest, systolic BP <90 mmHg, severe pulmonary edema, evid ence of cerebral hypoperfusion) require urgent treatment, usually with external de \201 br illation/cardioversion. Drug therapy needs time to take effect and hemodynamic stability bu t may be considered for some awake patients. \200 Sedate awake patients with midazolam (2 .5 \200\22310 mg IV) fentanyl (25 \200\22350 g/IV) for analgesia. Monitor for respirat ory depression and have \202 umazenil and naloxone readily available. General anesthesia with propofol is preferred, but remember the patient may not have an empty stomach and prec autions should be taken to prevent aspiration (e.g., cricoid pressure, ET intubation). For a monophasic de \201 brillator use 360 J synchronized shock and for biphasic de \201 bril lators use 200 J or the maximum available. synchronized shock. If tachyarrhythmia recurs or is unresponsive, try to correct iPaCO2, acidosis or dK+. Give Mg2+ (2 g IV) and shock agai n. Amiodarone 150 \200\223300 mg bolus IV may also be used, but be aware that it may increa se de \201 brillation thresholds. Give speci \201 c antiarrhythmic therapy (see p. 614). If there is ongoing VT in the context of cardiac arrest or recurrent VT episodes, causing h emodynamic compromise and requiring repeated DC cardioversions, then give IV amiodarone (15 0 mg IV over 10 minutes bolus x 1 with a repeat x 1, followed by 1 mg/min IV x 6 hour follo wed by 0.5 mg/min IV x 18 hour). Alternately, IV lidocaine may be administered (1 to 1.5 mg /kg bolus over 3 \200\2235 minutes with repeat dose in 2 minutes) (max dose 300 mg in 1 hou r) followed by 2 \200\2234 mg/min. Follow ACLS guidelines for treatment of unstable tachyar rhythmias. dPaO2, \200 Hemodynamically stable patients \200 \200 Admit patient to telemetry and obtain a 12 lead ECG. Try vagal maneuvers (e.g., Valsalva/ca rotid sinus massage) after ensuring that the patient has no carotid bruits. If type of arrh ythmia is apparent, then initiate appropriate treatment. If there is a question regarding t he diagnosis, give adenosine 6 mg rapid IVP followed immediately by 5 mL saline \202 ush. If there is no response, try 6 and then 12 mg in succession with continuous ECG rhythm str ip. \200 CHAPTER 9 Arrhythmias 370 De \201 nitive treatment should start as soon as the diagnosis is known. First episodes of AVNRT, AVRT, and focal atrial tachycardia may need no further treatment. Patients with all other diagnoses and WPW should undergo further investigation and management in conjunction with a cardiologist or electrophysiologist as necessary. Patient with tachycardia No Yes Is patient in shock? 12 lead ECG, UEs, TFTs Emergency DC cardioversion No Yes QRS >120 ms Is rhythm regular? No Treat as VT. Ignore possibility of SVT. Try lignocaine 50 \200\223100 mg. If fails arrange. DC CV Refer to cardiology. Yes Treat as AF. Control rate with -blocker or Verapamil. Start anticoagulation with heparin. If < 48 hours since onset consider 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 Yes No 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. Figure 9.4 Guidelines to the safe management of arrhythmias in the emergency department. Ad apted from Barts and the London A+E guidelines. DRUG TREATMENT OF TACHYARRHYTHMIAS 371 Drug treatment of tachyarrhythmias Table 9.1 Drug treatment of tachyarrhythmias Sinus tachycardia Identify and treat underlying cause Conversion to SR \200 Amiodarone \200 Ibutilide \200 Dofetilide \200 Sotalol \200 Flecainide \200 Disopyramide \200 Synchronized DC shock Propafenone Dronedarone \200 \200 \200 \200 \200 \200 Prevention \200 \200 \200 \200 \200 \200 \200 \200 Rate control (AV node) B \200 \200 Atrial \201 brillation Atrial \202 utter SVT Amiodarone Sotalol Flecainide Dofetilide Quinidine Disopyramide Propafenone Dronedarone Blockade Calcium blocker (e.g., diltiazem) Digoxin \200 B \200 \200 \200 \200 \200 \200 Adenosine -Blockade AV nodal reentrant tachycardia (AVNRT) Amiodarone Digoxin Flecainide Synchronized DC shock Dronedarone Propafenone Verapamil Vagal stimulation Flecainide Dronedarone Propafenone At AV node \200 B \200 Accessory pathway tachycardias (i.e., AVRT) Termination only \200 Synchronized shock At accessory pathway I \200 butilide \200 Sotalol \200 Flecainide \200 Disopyramide \200 Quinidine \200 Amiodarone \200 Propafenone \200 Dronedarone Adenosine Blockade Termination and prevention \200 \200 \200 Ventricular tachycardia \200 \200 B \200 \200 \200 \200 \200 Lidocaine Amiodarone Magnesium if Torsades (TdP) DC shock Flecainide Disopyramide Propafenone -Blockade Procainamide Dronedarone Mexiletine Amiodaron e CHAPTER 9 Arrhythmias 372 Supraventricular tachycardia This section deals with the diagnosis and pharmacological mana gement of individual supraventricular tachycardias (SVTs) (see Fig. 9.5). Their mecha- nism s and ablation are discussed in detail in Chapter 13. Atrial tachycardia (ectopic focus re-entry) Atrioventricular re-entry tachycardia (AVRT) Sinus node AV node re-entry tachycardia (AVNRT) AV node Figure 9.5 Types of supraventricular tachycardia. Reproduced with permission from Ramrakha P, Moore K (2004). Oxford Handbook of Acute Medicine, 2nd ed. Oxford, UK: Oxford University Press. SINUS NODAL REENTRANT TACHYCARDIA 373 Sinus tachycardia De \201 ned as a sinus rate >100 for an adult, this may be physiological (e.g., exercise or emotion) or pathological. Look for and treat underlying caus- es \200 \224anemia, drugs (e.g., caffeine, cocaine, etc.), hyperthyroidism, pain, hyp- oxia, fever and infection, hypovolemia, and cardiac tamponade. If no underlying cause is found and the rate is stable without normal variation, consider s inus node reentrant tachycardia (SNRT) or focal atrial tachycardia as alternative diagnoses . These will be paroxysmal in nature, have sudden onset or offset, and are often terminated by IV adenosine. If, after a thorough search, no underlying cause is found it may be terme d inappropriate sinus tachycardia. B-Blockers are useful for symptomatic persistent inappropriate sinus tachycardia and are vi tal in controlling the sinus rate in hyperthyroidism and post-MI in the absence of overt he art failure. Sinus nodal reentrant tachycardia This is a rare cause of narrow complex tachycardia due to a micro- reentrant circuit within the SAN. The P wave on the ECG is identical to sinus tac hycardia, making diagnosis dif \201 cult. B-Blockers or calcium channel blockers are the \201 rst-line treatment. Modi \201 cation of the SA node by radiofrequency ablation (RFA) is reserved for drug-refractory cases or t hose not wishing to take drugs. CHAPTER 9 Arrhythmias 374 Atrial tachycardia The term atrial tachycardia (AT) describes all regular atrial rhythms wi th a P rate >100 regardless of the mechanism, and this should be pre \201 xed by either fo cal or macro-reentrant unless the mechanism is unknown. Focal atrial tachycardias These are due to an automatic focus of atrial cells \201 ring f aster than the SA node. The P wave morphology and axis during tachycardia can be used to pr edict the location of the source. They are characteristically paroxysmal with short bursts at a rate of 150 \200\223200 bpm, but they may be incessant, increasing the risk of tachyca rdia-induced cardiomyopathy. They occur in normal hearts but are also associated with many forms of cardiac disease as w ell as metabolic disarray, digitalis toxicity, and pulmo- nary disease. They are generally long-RP/short-PR tachycardias. Treatment is needed only for symptomatic patients or incessant tachy- cardia. B-Blockers an d calcium channel blockers can be used to slow the atrial rate and the ventricular response by AV nodal blockade. Class 1c ( \202 ecainide and propafenone) or class III drugs (amiod arone and sotalol) may suppress the tachycardia. RFA can be curative. Some ATs may be termi nated with IV adenosine. Macro-reentrant atrial tachycardia (atrial \202 utter) Atrial \202 utter (AFL) is an EC G de \201 nition of a P wave rate >240 bpm and an absence of an isoelectric baseline betwe en de \202 ections. It is caused by a reentry circuit over large areas of the right or lef t atrium. The circuit is not in \202 uenced by adenosine, and block of the AVN reveals the underlying rhythm seen as a \200\234saw-tooth \200\235 pattern to the P waves on ECG. It may be associated with underlying heart disease or seen in patients with structurally no rmal hearts. AFL with rapid ventricular rates can exac- erbate heart failure symptoms and, if incessant, worsen LV function. Synchronized DC cardioversion effectively restores sinus rhythm (SR), but AFL often recurs. Drug therapy is not very effective. AVN blockade is dif \201 cult to achieve and the high doses of B-blockers, calcium channel blockers, and digoxin required may have unwanted side effects. Class Ic and III drugs as well as amiodarone can be used to maintain SR; however, propafenone and \202 ecainide can paradoxically accelerate the ventricular rate in AFL b y slowing the tachycardia rate suf \201 ciently to allow the AVN to conduct 1:1. They shou ld always be used in combination with an AVN blocking agent. Amiodarone is an alternative a gent, particularly if LV func- tion is impaired. RFA is the most effective way of maintaining SR and is frequently cura- tive. If curative a blation is not possible and effective rate control is not achieved with drugs, then ablatio n of the AV node and implantation of a permanent pacemaker is a palliative solution. Antico agulation recommen- dations for patients with AFL are identical to those with AF.1 1 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 \2231531. ATRIOVENTRICULAR NODAL REENTRANT TACHYCARDIA 375 Atrioventricular nodal reentrant tachycardia (AVNRT) This is the most common cause of a nar row complex tachycardia in patients with normal hearts, typically in young adults, occurrin g more often in women than men. AVNRT characteristically causes paroxysms of severe palpita tions, with a pounding in the neck (due to re \202 ux of blood into the jugular veins caus ed by simultanous atrial and ventricular con- traction). It has a benign prognosis and may require no treatment. The ECG in SR is usually normal (see Fig. 9.6). The tachycardia is terminated by IV adenosine or vagal maneuvers. The underlying reentrant circuit is entirely within the AV node and therefore can be controlled long term with B-blo ckers, verapamil, or diltiazem. Alternative second-line agents are \202 ecainide, propafe none, or sotalol. The \201 rst-line treatment for recurrent symptomatic episodes, however , is RFA, which can be curative. When symptoms are very infrequent a \200\234pill in the pocket \200\235 approach is someti mes helpful, i.e., a large oral dose of, e.g., verapamil is taken to terminate the event. aVR V4 V1 I aVL V2 V5 II avF V3 V6 III II Figure 9.6 Typical presenting ECG of AVNRT or AVRT, showing a narrow complex tachycardia wi thout visible P waves. CHAPTER 9 Arrhythmias 376 Atrioventricular reentrant tachycardia (AVRT) This is due to an AV reentrant circuit involv ing a connection between the atria and the ventricles other than the AV node (Fig. 9.7). As these acces- sory pathways (AP) are present at birth, arrhythmias usually present much you nger than AVNRT (infancy or childhood). Rapid paroxysmal palpitations are the usual symptom. It is usually nar- row complex as the ventricle is activated by antegrade conduction via the AVN (orthodromic). However a WCT is also possible if the antegrade conduction to the ventricle is via the accessory pathway (an tidromic). The presence of symptomatic AP-mediated SVT is associated with an increased risk of sudden death and referral to a specialist is mandatory. RFA of the AP is the treatment of choice. The most useful drugs are \202 e- cainide and p ropafenone, which slow conduction in the accessory pathway and the AV node. Verapamil, dilt iazem, and B-blockers should be used only when there is no history of atrial \201 brillat ion, there is no antegrade conduction during tachycardia, or the AP is known to have a long ante- grade refractory period. FP AVN SP Left side AP Figure 9.7 Mechanism of AVNRT and AVRT. Both AVNRT and AVRT have reentrant mechanisms. Orth odromic AVRT via a left-sided accessory pathway (AP) (above). Activation from A to V is dow n the atrioventricular node (AVN), then across the ventricular myocardium and back from V t o A up the AP, thus completing the circuit. The ventricle therefore is an essential part of the circuit. Antidromic AVRT (not shown) would activate in the opposite direction. Typical AVNRT (below) activates from the atrium to the AVN via the slow pathway (SP) and from the AVN 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. ATRIAL FIBRILLATION 377 Junctional tachycardia This term should only be used for focal tachycardias that originate from the AV nodal tissue directly. They are rare in adult cardiology. Distinction from othe r forms of narrow complex tachycardia is only possible at the EP study. RFA is high risk as the AV node may be damaged. B-Blockers and \202 ecai- nide, and propafenone are effective. 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 grea ter in those aged over 65. It is an atrial arrhythmia where uniform activation is replaced by chaos, such that coordinated contractile function is lost and the atria dilate. It is ch aracterized by an ECG lacking consistent P waves and a rapid, often irregular ventricular r ate. Classi \201 cation Previously, many terms were used to classify AF. However, now an inter- national consensus on nomenclature has been reached,1 allowing the cor- rect selection of management options for patients. All episodes of AF lasting >30 seconds should be described as follows: \200 or a recurrent episode \200 \200 \200 \200 First detected Self terminating Symptomatic Paroxysmal Persistent regardless of how it term inates) Permanent cardioversion) Lone idiopathic (in the absence of any disease) or not self terminating or asymptomatic (if self-terminating within 7 days) (if cardioverted to SR by any means or lasts >7 days (if it does not terminate or relapses within 24 hours of (in the absence of underlying structural heart disease) or Causes (see Table 9.2) AF is a common end point for many forms of cardiac disease where atr ial myocytes are damaged or subject to adverse stress generated by ischemia, cyanosis, elev ated intracavity, or pericardial pressures. These changes are hypothesized to alter the con duction properties of the myocardium facili- tating \201 brillation. 1 Levy S, Camm AJ, Saksena S, et al. (2003). International consensus on nomenclature and cl assi \201 ca- tion of atrial \201 brillation. J Cardiovasc Electrophysiol 14:443 \200 \223445. CHAPTER 9 Arrhythmias 378 Table 9.2 Causes of atrial \201 brillation Common \200 \200 Potentially reversible \200 \200 \200 \200 \200 \200 Rare \200 Congenital heart disease Autonomic \200\234vagal \200\235 overactivity Pericardial effusio n Cardiac metastases Myocardial in \201 ltrative diseases (e.g., amyloid) Atrial myxoma Alcohol binge Hyperthyroidism Acute MI Acute pericarditis Myocarditis Exacerbation of pulmo nary disease Pulmonary embolism Cardiac surgery Hypertension Left ventricular failure (any cause) Coronary artery disease Mitral or tricusp id valve disease HCM COPD \200 \200 \200 \200 Symptoms and signs Palpitations, dyspnea, fatigue, presyncope, syncope, and chest pains are common. However, 30% of patients present with AF as an incidental \201 nd- ing only. Amb ulatory monitoring reveals that even patients with sympto- matic paroxysmal AF have many as ymptomatic episodes. Physical \201 ndings are an irregular pulse (which, if rapid, will be faster at the apex than wrist), variable intensity of the \201 rst heart sound, and absent a-waves in the JV P. ATRIAL FIBRILLATION: EVALUATION 379 Atrial \201 brillation: evaluation A reversible cause should be sought early to allow app ropriate treatment. The most important investigations are the following: \200 ECG: on intact AV nodal function. In the presence of complete AV nodal block a slow regular junctional or ventricular escape rhythm is present. The QRS will be broad if there is aber rant conduction; ST-T wave changes may be due to rapid rate, digoxin, or underlying cardiac disease. CXR: calci \201 cation (MS) Chemistries: Cardiac enzymes: Thyroid function: Live r function tests Drug levels: Arterial blood gas (ABG): Echocardiogram (TTE TEE): perica rdial effusion, and to exclude intracardiac thrombus prior to conversion to SR. LA size is an important predictor of likely future maintenance of SR. Other investigations irregular ventricular rate and absence of P waves. V rate depends cardiomegaly, pulmonary edema, intrathoracic precipitant, valve \200 \200 \200 \200 \200 \200 hypokalemia, renal impairment; check Mg2+, Ca2+ ?MI. Small rise after DC shock thyrotoxicosis may present as AF only. especially if patient is taking digoxin if hypoxic, in shock or ?acidotic for LV function, valve lesions, and depend on suspected precipitant. Other investigations when patient is stable Use a 24-hour ambulatory monitor to assess hear t rate control and look for intermittent AF or bradycardia. CXR, exercise testing (or other ischemia stress test), and coronary angiography can also be used. Management There is some controversy regarding the ideal strategy for management of atrial \201 brillation. However, depending on the clinical situation and the patient \200\231s l evel of symptoms, a rate or rhythm control strategy may be preferable. Currently available antiarrhythmic drugs (AADs) are limited by their toxicity, including pr oarrhythmia, and if a rhythm control strategy is cho- sen, AAD administration should be und ertaken in concert with a specialist. Patients should remain on anticoagulation with warfar in to decrease the incidence of thromboembolic complications regardless of whether a rate o r rhythm control strategy is chosen. Emergency management If the patient is hemodynamically compromised, then urgent external sy nchronized DC cardioversion under general anesthesia or sedation is needed. This is rarely necessary; usually rate control is suf \201 cient to acutely control symptoms. CHAPTER 9 Arrhythmias 380 If symptoms persist despite rate control, cardioversion can be attempted pharmacologically with ibutilide 1 mg over 10 minutes repeated x1, \202 ecai- nide (2 mg/kg, max 150 mg, in fused via a peripheral line over 30 minutes) or if LV dysfunction is suspected, amiodarone (5 mg/kg, max 300 mg; gen- erally, 150 mg IV over 10 minutes repeated x 1). Patients must be monitored throughout for possible ventricular arrhyth- mia, bradycardia, a nd hypotension. If AF has been present for >48 hours, cardioversion should be preceded by a TEE to exclude atrial thrombus. All patients should be anticoagulated with Coumadin for at least 4 weeks post-cardioversion . Decisions regarding long-term anticoagulation should be made on the basis of the patient \200\231s risk pro \201 le.