Cardiology Intensive Board Review, 3 ed.

Arrhythmia

ANSWERS

1.a. Propafenone. Sotalol and dofetilide are primarily excreted by the renal route and should be used cautiously, if at all, in patients with significant renal insufficiency. Flecainide primarily undergoes hepatic elimination (approximately 70%) but has 25% renal elimination. The route of elimination for propafenone is 99% hepatic.

2.a. Amiodarone. Sotalol, dofetilide, and flecainide do not have significant active metabolites. Amiodarone is metabolized to the active metabolite desethylamiodarone.

3.b. The patient is taking dipyridamole. Dipyridamole potentiates the effect of adenosine by interfering with metabolism; therefore, a reduced dose of adenosine is recommended. Although not a part of this question, it is important to remember that adenosine also needs to be used with extreme caution in heart transplant patients as a markedly exaggerated response to adenosine can be seen in the denervated heart. An increased dose of adenosine is recommended in the presence of methylxanthines such as theophylline, which antagonizes the effect of adenosine (blocks receptors), and other factors such as slow circulation time, valvular regurgitation, and left-to-right shunts that reduce the effectiveness of adenosine.

4.c. Verapamil. Verapamil may increase serum levels of dofetilide because of interference with renal excretion and hepatic metabolism.

5.b. Flecainide. Flecainide is a class IC antiarrhythmic drug, and these agents exhibit “use dependence.” This refers to the property of increased drug effect at increased heart rates. Sotalol and dofetilide are class III antiarrhythmic drugs that exhibit “reverse-use dependence”—that is, greater drug effect at slower heart rates. Quinidine has effects on both sodium and potassium channels. While the effects on the sodium channels are use dependent, it is far less pronounced compared with the Ic agents such as flecainide. The potassium-blocking properties and resulting QT prolongation are more pronounced at slower heart rates— reverse-use dependent.

6.c. Antiarrhythmic drugs with reverse-use dependence have greater efficacy for arrhythmia prevention than termination and have greater risk for ventricular proarrhythmia after AFib termination (at slower sinus rates) than during AFib. Antiarrhythmic drugs with use dependence, such as sotalol and dofetilide, have greater antiarrhythmic effect at slower heart rates. Consequently, drug efficacy is enhanced at the relatively slower rates in sinus rhythm, making these drugs more effective for prevention of AFib than those drugs with use dependence. Likewise, for proarrhythmia, the antiarrhythmic drugs with reverse-use dependence are more likely to produce ventricular proarrhythmia after conversion to sinus rhythm at the relatively slower sinus rate or with a postconversion pause.

7.c. The treatment drugs effectively suppressed premature ventricular complexes (PVCs). CAST studied the concept that PVC suppression in the postinfarction period would reduce the incidence of sudden cardiac death. Patients without heart disease were, therefore, excluded from these studies. CAST I studied flecainide, encainide, and moricizine versus placebo. Demonstration of effective suppression of PVCs by one of the drugs was necessary before a patient could be randomized to drug or placebo treatment. Propafenone, another class IC antiarrhythmic drug, was not studied. CAST I was prematurely terminated by the safety committee after only a 10-month average follow-up because of significantly increased incidence of arrhythmic death and nonfatal cardiac arrests in the flecainide and encainide treatment groups. CAST II was a continuation of the study with only moricizine versus placebo, but this study was also terminated early because of an increased incidence of cardiac arrest in the moricizine treatment group.

8.a. Flecainide. All of these drugs are class I antiarrhythmic medications and have sodium channel–blocking properties to various degrees. Class IC agents, such as flecainide, have the most potent sodium channel–blocking effects, and class IB agents, such as lidocaine, have the least potent sodium channel–blocking effects.

9.c. Enhanced effect. Patients with denervated hearts are supersensitive to the effects of adenosine.

10.c. AV nodal reentrant tachycardia (AVNRT). Atrial tachycardia and PJRT are long RP tachycardias and, therefore, would not have such a short VA interval. PJRT is a special type of orthodromic AVRT that involves a posteroseptal accessory pathway with decremental (AV nodal-like) conduction properties and, hence, has a long RP (long VA) interval. Because of the time required to reach the accessory pathway for the retrograde portion of the arrhythmia circuit, orthodromic AVRT generally has a VA interval longer than 70 milliseconds. Therefore, a VA interval shorter than 70 milliseconds excludes orthodromic AVRT and makes AVNRT the most likely diagnosis. A small r' wave (pseudo r' wave) can sometimes be seen at the terminal portion of the QRS (usually best in lead V1). This deflection represents retrograde activation of the atrial (a retrograde P wave) occurring shortly after the QRS complex.

11.c. Vagal maneuvers. A sudden onset of a regular narrow complex tachycardia with a cycle length of 375 milliseconds and an RP interval of 100 milliseconds is a short RP tachycardia (the PR interval would be 375 milliseconds – 100 milliseconds = 275 milliseconds, so the RP is shorter than the PR). This patient most likely presents with orthodromic AVRT, a reciprocating tachycardia circuit that involves antegrade conduction through the AV node and retrograde conduction through the accessory pathway (however, AVNRT is also possible). As the AV node is a necessary component of the arrhythmia circuit, AV nodal blockade effectively terminates this type of tachycardia. Vagal maneuvers, such as Valsalva, coughing, or carotid sinus massage, may be quite effective and avoid the potential risks associated with administration of medications. Verapamil and other drugs that block AV conduction, such as β-blockers and adenosine, may be quite useful for termination of AVRT. This should not be confused with the management of AFib in the setting of Wolff-Parkinson-White syndrome, in which administration of AV nodal blocking drugs, such as verapamil, is contraindicated due to a concern for uninhibited and thus rapid AV conduction of the AP, which if rapid enough can induce ventricular fibrillation. When AV conduction is occurring through both the AV node and AP, retrograde, concealed conduction into the AP can limit its antegrade conduction properties. If preexcited, AFib with IV procainamide or DC cardioversion is the correct management. A precautionary note regarding the use of adenosine for regular narrow QRS tachycardia in patients with Wolff-Parkinson-White syndrome: Adenosine may precipitate AFib and result in a very rapid ventricular response (preexcited tachycardia). Atropine has no role in the treatment of these types of arrhythmia. Catheter ablation is not generally an acute treatment option for this arrhythmia, although this approach may be an excellent option for chronic treatment (cure).

12.c. Orthodromic AVRT using a left-sided accessory pathway. A regular narrow QRS tachycardia that has VA interval prolongation with the development of bundle branch block is most consistent with an orthodromic AVRT using an accessory pathway ipsilateral to the bundle branch. During AVRT, the antegrade limb of the circuit is the AV node and His-Purkinje/bundle branch system, and the retrograde limb is the accessory pathway. Block in a bundle branch ipsilateral to an accessory pathway creates a larger circuit, as the antegrade limb must now use the contralateral bundle branch, and therefore, the VA interval increases. This results in an increase in the tachycardia cycle length (a slower tachycardia). Of note, a slower tachycardia with bundle branch block itself does not necessarily have the same significance. Other types of tachycardia may slow because of a change in conduction of other components of the tachycardia circuit, such as the conduction through the AV node (A–H interval). Thus, it is important to demonstrate VA interval prolongation during bundle branch block to implicate an ipsilateral accessory pathway participating in AVRT.

13.c. ICD implantation. Cardiac arrest with VT or VF in the absence of reversible causes (e.g., MI, severe electrolyte or metabolic disorders) is a class I indication for ICD implantation. ICD implantation for such patients is superior to amiodarone drug therapy, as demonstrated in the Antiarrhythmics Versus Implantable Defibrillator (AVID) trial. The Canadian Implantable Defibrillator Study examined a similar population of patients and, although not statistically significant, showed a strong trend for the superiority of ICDs. Demonstration of inducible VT or VF in these types of patients is not necessary.

14.b. Implantation of an ICD is indicated if an EP study shows inducible VT. The Multicenter Automatic Defibrillator Implantation Trial (MADIT) evaluated patients with CAD, ischemic cardiomyopathy with an LV ejection fraction of <35%, and nonsustained VT. This study showed that for patients with inducible VT at baseline EP study and after administration of IV procainamide, treatment with an ICD was superior to treatment with antiarrhythmic drugs. A follow-up study, MADIT II, assessed the role of ICD implantation in patients with an ischemic cardiomyopathy and an ejection fraction ≤30%. Nonsustained VT was not required to undergo ICD implant, nor was an EP study. The study was terminated early after an average follow-up of 20 months because the ICD significantly reduced all-cause mortality (14.2% versus 19.8% for conventional therapy). This study helped expand ICD implant indications. This is a class I indication for ICD implantation.

15.d. Place a “donut” magnet over the ICD site. The patient is having inappropriate or spurious shocks from the ICD, most likely caused by detection of electrical noise from a malfunction of the ICD lead. It is imperative that further shocks be prevented immediately, not only for patient comfort but also to prevent induction of life-threatening ventricular arrhythmias (including ventricular arrhythmia storm) caused by the ICD shocks. The most effective action at this point is placement of a magnet over the ICD site. This prevents the ICD from delivering any therapies. It would not be optimal to delay the prevention of further shocks while waiting for an ICD programmer. Of note, unlike pacemakers, ICDs do not have an asynchronous pacing response to application of a magnet.

16.b. Early direct current (DC) shock defibrillation. The two most crucial factors that determine the value of out-of-hospital resuscitation for patients who experience sudden cardiac death are citizen-bystander cardiopulmonary resuscitation and early DC shock defibrillation.

17.a. Asystole. EMD or PEA and, in particular, asystole tend to be found in increasing proportions as the time since arrest increases. This is likely caused by degeneration of prolonged VF. When VF is the documented rhythm at the time of resuscitation, the long-term survival is approximately 25%. When EMD or PEA is the documented rhythm, the long-term survival rate drops to approximately 6%, and it drops even further, to approximately 1%, when asystole is documented.

18.d. VF. The initial rhythm documented in a patient who undergoes sudden cardiac death is dependent on the time elapsed since the arrest. Most episodes of sudden cardiac death (approximately 65% to 85%) that are documented electrocardiographically are caused by malignant ventricular arrhythmias such as VF. Monomorphic VT is uncommonly documented as a cause of out-of-hospital sudden cardiac death, perhaps caused by degeneration of unstable VT to VF. Asystole and EMD or PEA are found in greater proportions as the time since arrest increases, as these rhythms are likely the result of prolonged VF.

19.b. β-Blocker medications. Several randomized trials of the use of β-blocker medications for patients after MI have shown efficacy for the prevention of sudden cardiac death (including propranolol, timolol, metoprolol, and acebutolol). Trials of amiodarone in this setting have provided mixed results. Two large randomized trials, the European Myocardial Infarct Amiodarone Trial (EMIAT) and the Canadian Amiodarone Myocardial Infarction Arrhythmia Trial (CAMIAT), examined the use of amiodarone in patients after MI and did not show a reduction in overall mortality with the use of amiodarone. The Polish Amiodarone Trial showed that amiodarone improved survival only in patients with preserved LV function after MI. The Survival with Oral D-sotalol (SWORD) trial studied the use of the D-isomer of sotalol (D-sotalol) in patients with recent MI and LV dysfunction. This study found worse survival in the group treated with D-sotalol than in the group treated with placebo. The Danish Investigations of Arrhythmias and Mortality on Dofetilide (DIAMOND) studies showed that dofetilide had a neutral effect on total mortality compared with placebo in the treatment of post-MI patients with LV dysfunction.

20.b. CAD. CAD is the predominant disease process associated with sudden cardiac death in the United States, accounting for 64% to 90% of cases. The other cardiomyopathies, such as dilated and hypertrophic cardiomyopathies, together account for approximately 10% to 15% of cases of sudden cardiac death.

21.c. Head-upright tilt-table testing. Syncope in the absence of structural heart disease is most likely neurally mediated (vasovagal). The head-upright tilt-table test is the most appropriate test to evaluate for this condition. This test initiates the vasovagal episode by maximizing venous pooling, sympathetic activation, and circulating catecholamines. In general, the test involves at least 30 minutes of 70-degree head-up tilt angle without a saddle support. An addition of a catecholamine challenge with isoproterenol is sometimes used. Among symptomatic patients, the sensitivity of the head-upright tilt-table test is approximately 85%. The specificity of the head-upright tilt-table test is good, with the frequency of an abnormal tilt-table test in control subjects being 0% to 15%. In the absence of structural heart disease, EP study, ambulatory Holter monitoring, and the signal-averaged ECG are low yield.

22.a. AVNRT. An “r'” in lead V1 during regular narrow complex tachycardia that is not present during sinus rhythm indicates the inscription of the P wave in the terminal QRS, is consistent with a very short VA interval, and is very specific for AVNRT.

23.d. Permanent pacemaker implant. This patient has evidence of symptomatic bradycardia on Holter monitoring, which constitutes a class I indication for permanent pacemaker placement. He has AV conduction system disease with no obvious reversible causes, which is most probably caused by idiopathic fibrosis (Lev disease). Prolonged monitoring will probably show more episodes of bradycardia, which was already seen during telemetry, and which places this elderly patient at risk for syncope and injury. EP testing for ventricular arrhythmia is not indicated in view of the absence of structural heart disease. Likewise, ICD is not indicated.

24.d. Single-chamber system in the ventricle programmed to VVIR. This patient is in chronic AFib, and, therefore, physiologic pacing in the atrium cannot be achieved. Furthermore, conversion and long-term maintenance of sinus rhythm in this situation are very unlikely. Therefore, there is no indication for placement of an atrial lead. DDDR with mode switching and DDIR will behave like a VVIR system in this patient, at the expense, however, of an additional lead (atrial) and a more expensive dual-chamber pacemaker.

25.a. Symptoms usually include fatigue, dizziness, and hypotension. Pacemaker syndrome is caused by pacing the ventricle asynchronously, which results in AV dissociation or VA conduction. Symptoms consist of fatigue, dizziness, dyspnea, and weakness, with or without hypotension. The mechanism is believed to be related in part to atrial contraction against a closed AV valve and release of atrial natriuretic peptide. It occurs with ventricular pacing and therefore is worsened by increasing pacing rate and relieved by allowing intrinsic conduction (if present) by lowering the pacing rate, programming rate hysteresis, or upgrading to a dual-chamber system. Therapy with fludrocortisone and other volume-expansion modalities is not helpful.

26.d. A 73-year-old man with persistent AFib and a ventricular rate of 40 bpm during peak treadmill test. The 73-year-old man with AFib and slow ventricular rate during exercise is the classic example of SSS. This usually indicates degenerative disease of the cardiac conduction system involving the AV node as well as the sinus node. Function of the sinus node can only be assessed after AFib has been terminated, usually by DC cardioversion. In this patient’s case, it would not be uncommon to manifest a long postconversion pause, followed by either marked sinus bradycardia or complete sinus node arrest with a resulting junctional or ventricular escape rhythm (hopefully) following cardioversion. The finding of sinus arrhythmia varying by 15 bpm in an older patient, the profound nocturnal bradycardia in young athletes, and the sinus pauses in young patients are related mostly to a high vagal tone and do not indicate sinus node disease.

27.e. Induce complete heart block (CHB). Patients with true complete LBBB are at risk for developing transient CHB during catheter manipulation in the septal region of the tricuspid valve. This is caused by transient traumatic block of the right bundle branch. A similar scenario can result when placing a Swan-Ganz catheter in patients with LBBB.

28.e. IV glucagon. This patient has an overdose of diltiazem and metoprolol. These drugs slow sinoatrial and AV conduction. Calcium and magnesium have no effect in reversing these bradycardic effects. Isuprel and atropine are not likely to overcome the β-blockade of metoprolol. IV glucagon acts on a specific receptor. This results in an increase in intracellular cyclic adenosine monophosphate, which enhances both sinoatrial and AV node conduction despite the presence of β-blockade.

29.d. IV hypertonic sodium bicarbonate. Amitriptyline has sodium channel–blocking properties and induced QRS widening and VT. Increasing the extracellular sodium concentration by the administration of sodium bicarbonate decreases the association of this drug with the sodium channel.

30.d. Atrial undersensing. This rhythm shows evidence of atrial undersensing. The pacemaker is programmed to DDD. In this mode, an appropriately sensed P wave should cause inhibition of the atrial spike; a ventricular spike is then delivered after the programmed AV interval or inhibited by an intrinsic R wave. In this strip, the P wave is present in each complex. However, in complexes 2, 4, 6, and 8, an atrial spike follows the intrinsic P wave because the intrinsic P wave was not appropriately sensed by the pacemaker. The noncapture of the atrium following the atrial spike on complexes 2, 4, 6, and 8 is anticipated as the atrium would still have been refractory from the preceding P wave. Capture of the atrium on complexes 1, 3, 5, and 7 is suggested by the P wave that is different in morphology (wider) than the intrinsic P wave. Atrial undersensing occurring early after implantation may be the result of lead dislodgment. A CXR should be obtained to assess lead position. Other possibilities include inappropriate programmed sensitivity, which can be assessed on a device check. Finally, inflammation at the lead tip–endocardium interface can result in a decrease in sensing amplitude. This may improve over several weeks as the lead matures and inflammation resolves.

31.c. Verapamil IV bolus. Adenosine is commonly used to terminate SVT. However, this patient is on theophylline, which is an effective blocker of the adenosine receptor. Propafenone might be poorly tolerated by this patient because of its associated β-blocking activity, which might increase airway resistance. Digoxin shortens the refractory period of the atrium and might potentially accelerate an atrial tachycardia. Immediate cardioversion is not needed, as the patient appears hemodynamically stable, and it would be reasonable to attempt pharmacologic therapy initially with verapamil.

32.c. Pacemaker-mediated tachycardia. In this strip, there is evidence of atrial undersensing (fifth complex). As a result, the fifth ventricular-paced beat comes “late” relative to atrial activation. This allows enough time to go by for the AV node to recover its conduction properties. This allows retrograde P-wave conduction following ventricular pacing, which is sensed by the pacer (because of short programmed postventricular atrial refractory period [PVARP]), and results in ventricular triggered pacing, causing a pacemaker-mediated tachycardia or endless-loop tachycardia. Acute treatment of this condition includes the application of a magnet to inhibit atrial sensing, thereby breaking the tachycardia loop. The spontaneous termination of these episodes in this patient is most probably related to intermittent atrial undersensing, which interrupts the tachycardia loop. Further prevention of these episodes includes reprogramming the PVARP, AV delay, or atrial sensitivity. Pacemaker-mediated tachycardia is an abnormal consequence of normal pacemaker function.

33.a. The pacing mode is VVI secondary to automatic mode switch. The initial rhythm strip shows background AFib with VVI pacing, most probably related to automatic mode switch. The absence of atrial pacing suggests adequate atrial sensing (of the fibrillation), which resulted in the mode switch behavior. Atrial pacing cannot be determined in the presence of AFib. There is adequate ventricular sensing, as determined on the nonmagnet strip (fifth complex—the small intrinsic QRS is sensed by the pacemaker which results in inhibition of pacing); however, there is intermittent ventricular capture noted (ventricular pacing spike followed by a lack of ventricular depolarization).

34.a. CHB at the level of the AV node. In this tracing, there is NSR with CHB and a narrow escape rhythm that is junctional in origin. This is apparent in the HBE tracing, in which the atrial deflections are completely dissociated from the H–V deflections. Therefore, the atrial impulse entering the AV node is not conducting down to the His bundle (A is not followed by His potential), indicating that the level of block is at the level of the AV node.

35.b. CHB at the infra-Hisian (below the His bundle) level. In this tracing, there is NSR with CHB and a relatively wide escape rhythm. In the HBE tracing, each atrial deflection is followed by an initial His deflection and a third, smaller deflection, H', indicating that there is conduction delay within the His bundle itself. This is suggestive of significant His-Purkinje conduction disease. Therefore, the atrial impulse enters the AV node, conducts down to the His bundle (normal AH interval), where it encounters conduction delay (a “split” His made up of both an H and an H'), and then fails to propagate to the ventricle, indicating that the level of block is at or below the level of the bundle of His. There is obvious AV dissociation with a ventricular escape rhythm.

36.d. Second-degree AV block at an infra-Hisian level. In this tracing, the surface ECG shows NSR with 2:1 AV block. The HBE tracing shows constant AH with 2:1 block below the level of the His bundle.

37.d. Second-degree AV block at an infra-Hisian level. In this tracing, the surface ECG shows NSR with second-degree type I AV block (Wenckebach). This pattern of block is usually localized to the AV node. However, in rare circumstances the block can occur within or below the His bundle. The wide QRS seen on the surface leads are a clue in this case that the patient has conduction disease below the level of the AV node; however, the site of block can only be determined by reviewing the His bundle recordings. In this situation, the HBE tracing shows progressive prolongation in the HV interval before it blocks in a 3:2 conduction pattern. Therefore, the conduction delay is not at the level of the AV node but at or below the His bundle. As opposed to Wenckebach in the AV node, which is usually benign in nature, this type of infra-Hisian block indicates His-Purkinje conduction system disease and is an indication for pacemaker placement, as it may progress to CHB.

38.b. Obtaining a two-view (anteroposterior and lateral) CXR to evaluate lead position. The presence of an RBBB-paced QRS complex pattern suggests that the ventricular lead may be in the LV. The lead may enter the LV through an atrial septal defect or ventricular septal defect or via perforation of the interventricular septum. It may also be inadvertently introduced into an artery and passed retrogradely through the aortic valve. Another possibility is placement into one of the LV branches of the coronary sinus. Although sometimes an apical position in the RV in a rotated heart can potentially give an RBBB-paced pattern, a two-view CXR should be obtained to rule out LV positioning. A single-view portable AP will not distinguish an LV from an apical RV placement. If LV placement is confirmed on the lateral radiograph, repositioning of the lead is indicated.

39.d. Patients with evidence of infra-Hisian block during EP testing should be considered for permanent pacing. Patients with symptomatic CHB do not need EP testing because the decision for a permanent pacemaker is already made. The sensitivity and specificity of sinus node recovery time are approximately 70%, making this test less than ideal; in most cases, the decision as to whether to implant a pacemaker in cases of suspected sinus node dysfunction depends on symptoms and correlation with ambulatory monitoring rather than results of EP testing. Patients with infra-Hisian block tend to have an unpredictable course and should be considered for permanent pacing.

40.a. It is characterized by ST elevation and a pseudo-RBBB pattern in the right precordial leads with persistent ST elevation. Brugada syndrome has been described worldwide but is most common in Asian countries and is the leading cause of death in young men in part of Thailand. It is characterized by ST-segment elevation and a pseudo-RBBB pattern in the right precordial leads with persistent ST elevation. These features can be induced with sodium channel blockers such as flecainide and ajmaline. (Sotalol is a potassium channel blocker.) It is related to a mutation in the sodium channel gene. Mutations in SCN5A, which encodes the α-subunit of the cardiac sodium channel gene, have been found in up to 30% of families with Brugada syndrome. It is associated with a high incidence of sudden cardiac death resulting from VF. Risk assessment and therapy remain poorly defined at this time, but the implantation of an ICD has been advocated in patient with a Brugada pattern on their ECG and additional risk factors including a history of syncope or sudden cardiac death.

41.b. The mechanism of torsades de pointes (TdP) is believed to be related to early afterdepolarization. The pathognomonic arrhythmia associated with long-QT syndrome is TdP. The mechanism is believed to be related to early afterdepolarization and triggered activity. Sotalol causes QT prolongation and is contraindicated in patients with long QT. Hypokalemia, not hyperkalemia, is associated with an increase of TdP in this situation. EP testing is of no value and is not indicated for the risk stratification of patients with long-QT syndrome. Cardiac arrest occurs typically with vigorous activity and infrequently during sleep in LQT1 syndrome. Acute arousal events (emotion or noise) are much more likely to trigger events in LQT1 and LQT2 than LQT3. Events in LQT3 syndrome are common during sleep.

42.c. You should perform EP testing to evaluate the AV conduction system. The patient had an episode of near-syncope, which could be related to his GI bleeding, but the possibility of intermittent heart block in the setting of bifascicular block cannot be ruled out. This is a class I indication for EP testing to evaluate AV conduction. If there is evidence of abnormally prolonged HV interval, then a permanent pacemaker should be considered. If the syncopal episode was remote from the GI bleeding and based on the clinical history of the events there was a concern for intermittent high-degree AV block causing symptoms, then empiric placement of a PPM without an EP study prior would carry a class IIa indication. There is no indication for ICD placement in this setting. β-Blockers would blunt a reactive tachycardia resulting from the patient’s anemia.

43.e. There is AV dissociation. In patients presenting with wide complex tachycardia, the presence of AV dissociation is highly specific for VT. All the other listed parameters suffer from significant overlap between SVT and VT.

44.c. Procainamide, 15 mg/kg IV over 30 to 60 minutes. Wide complex tachycardia occurring after MI is most likely to be VT. Verapamil is contraindicated in this setting, as it might lead to hypotension and VF. DC cardioversion can be used if the patient does not respond to antiarrhythmic therapy or if he becomes hemodynamically unstable. Procainamide is the drug of choice because it treats ventricular as well as supraventricular arrhythmia. There is no role for digoxin and no need for urgent cardiac catheterization in this situation.

45.b. To admit the patient for IV antibiotics and pacemaker-system extraction. This presentation is consistent with pacemaker-system infection, which occurred following the recent pulse generator replacement. Antibiotics PO or IV without extraction of the pacemaker system have limited efficacy in eradicating the infection. The patient should undergo pacemaker-system extraction, followed by IV antibiotics, until negative blood cultures are obtained. A new pacemaker system can then be implanted on the right side.

46.c. Inadequate synchronization may occur with peaked T waves, low-amplitude signal, and malfunctioning pacemakers. Cardioversion is the delivery of electric energy synchronized on the R wave. A synchronized shock should be used in AFib. A nonsynchronized shock may result in VF if they fall near the middle of the T wave when there is a marked dispersion of refractoriness within the ventricle. Improper synchronization may occur in a situation in which more than one peaked signal exists, such as with pacemakers and peaked T waves. On the other hand, a low QRS signal may not synchronize at all. In patients with pacemakers, the pads are positioned at least 3 inches away from the pulse generator to minimize damage. MI and digoxin intake are not contraindications for DC cardioversion as long as digoxin toxicity is not suspected.

47.d. Procainamide. Procainamide can slow down conduction across the accessory pathway and potentially converts AFib. Diltiazem (Cardizem) and verapamil cause hypotension and a reflex increase in sympathetic activation and may result in increased ventricular response and in rare circumstances can lead to VF. Adenosine is of no use in this setting. Lidocaine has little effect on the refractory period of the accessory pathway.

48.e. Amiodarone. Amiodarone may allow maintenance of sinus rhythm in patients with AFib and cardiomyopathy. In low doses, the side effects are minimized. Flecainide and disopyramide are not used in patients with cardiomyopathy because of their potential for proarrhythmia and their negative inotropic effects. Verapamil is not effective for maintenance of sinus rhythm. Sotalol might not be tolerated in patients with heart failure and has the potential for proarrhythmia in patients on diuretics prone to hypokalemia.

49.c. Digoxin can control the ventricular rate at rest in patients with AFib, but not with exercise. It is as effective as placebo for the acute conversion of AFib and does not help in maintaining NSR.

50.a. It may contribute to an increase in the digoxin level. Flecainide (amiodarone, propafenone [Rythmol], and verapamil) can increase digoxin level. Flecainide can regularize and slow the atrial rhythm in patients with AFib and can, therefore, lead to increased ventricular response because of improved conduction of the atrial impulses through the AV node. It is, therefore, important to use an AV nodal blocking agent in patients with AFib treated with flecainide. It is used for AFib as well as flutter; however, it needs to be used with caution in atrial flutter patients, as it may slow the cycle length of the flutter circuit and result in more rapid conduction to the ventricle. There are no definite data on its safety in patients with hypertrophic cardiomyopathy. It is effective for acute conversion as well as maintenance of NSR postconversion.

51.a. Change in the atrial refractory period as a result of the surgical manipulation. The occurrence of AFib post-cardiac surgery is believed to be related to shortening of the refractory period of atrial tissue as it recovers from surgical manipulation, cardioplegia, and, potentially, ischemia. This nonuniformity of recovery results in reentry as the mechanism of AFib.

52.a. AVNRT. This tracing shows AVNRT. It is a narrow complex tachycardia using the slow pathway of the AV node in the antegrade direction (long AH) and the fast pathway of the AV node in the retrograde direction (short HA). It is unlikely to be orthodromic reentrant tachycardia in which the retrograde limb of the circuit is an accessory pathway, because the QRS-A time is very short (atrium and ventricle are activated almost spontaneously), not long enough to involve ventricular activation as part of the circuit. Because the QRS is narrow, VT is not a likely diagnosis. Idiopathic LV-VT can sometimes be narrow but has an RBBB morphology on the surface ECG.

SUGGESTED READINGS

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The Cardiac Arrhythmia Suppression Trial II Investigators. Effect of the antiarrhythmic agent moricizine on survival after myocardial infarction. N Engl J Med. 1992;327:227–233.

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