Cardiology Core Curriculum - part 5 doc

Sinus nodal re-entrant tachycardia This tachycardia can mimic sinus tachycardia in that the P wave is identical to that seen during sinus rhythm. Unlike sinus tachycardia, it is a re-entrant rhythm that starts and stops abruptly. The symptoms are similar to those seen with atrial tachycardia. Treatment with β-blockers and calcium channel blockers can reduce the recurrence of the rhythm, and radiofrequency catheter ablation may offer a cure. Atrioventricular nodal re-entrant tachycardia AV nodal re-entrant tachycardia (AVNRT) is responsible for approximately 60% cases of paroxysmal supraventricular tachycardia (PSVT; also referred to as “PAT” and “SVT”). These arrhythmias have a narrow QRS complex, paroxysmal onset and termination, and ventricular rates between 150 and 250 beat/min (Table 8.2). In the typical form of AVNRT, the electrical impulse travels down the “slow” pathway of the AV node and re-enters back up the “fast” pathway. This results in a tachycardia with P waves that are either buried within or occur just before or after the QRS complex. An R’ in electrocardiogram lead V 1 that is only present during tachycardia represents the superimposed P wave and is diagnostic (Figure 8.4). In the atypical form of AVNRT (<5%), the re-entry circuit is reversed (down the “fast” and back up the “slow”) and the P wave occurs substantially after the QRS (so-called “long RP tachycardia”). AVNRT occurs in structurally normal hearts with a slight preponderance in women, and increases in incidence with age. Clinically, the patient presents with palpitations, breathlessness, and neck pounding. There may be no precipitating factor. Presyncope and syncope are uncommon, but may occur early following onset. AVNRT may be terminated using vagal maneuvers such as carotid massage and Valsalva; these techniques yield transient block in the slow pathway of the AV node and terminate re-entry. Adenosine, an endogenous nucleoside, represents the best drug option for conversion to sinus rhythm, and is effective in over 90% of cases. 6 This drug causes transient AV block when administered as an intravenous bolus injection. The drug may cause transient breathlessness and anxiety, but this resolves promptly due to the very short half-life (<2 seconds). Alternatively, intravenous verapamil injection is effective but does not work as quickly. For chronic therapy, calcium channel blockers, β-blockers, and digoxin reduce the frequency of recurrence. Membrane stabilizing agents are also effective for chronic therapy but are second line agents. Finally, radiofrequency catheter ablation is effective in curing AVNRT in over Cardiology Core Curriculum 244 90% of patients; it is associated with rare side effects and is now offered as first line therapy in many centers. Atrioventricular re-entrant tachycardia and Wolff–Parkinson–White syndrome AV re-entrant tachycardia (AVRT) is the second most common paroxysmal supraventricular tachycardia, accounting for about 30% Arrhythmias 245 laVRV 1 V 4 ll aVL V 2 V 5 lll aVF V 3 V 6 V 1 Figure 8.4 Table 8.2 Differential diagnosis of narrow complex regular tachycardia Rhythm P wave Sinus tachycardia Normal Sinus nodal re-entrant tachycardia Normal Atrial tachycardia Variable Atrial flutter Sawtooth (2:1) Atrioventricular nodal re-entrant tachycardia Inverted (superimposed on QRS) Atrioventricular re-entrant tachycardia Inverted (superimposed on QRS) of supraventricular tachycardias. The mechanism involves activation of the ventricles using the normal conduction system and re-entry to the atria via an accessory AV pathway (Kent bundle). Accessory pathways are congenital, and may occur in the left or right AV ring or septum. Most commonly, AVRT occurs in patients with Wolff–Parkinson–White (WPW) syndrome. WPW syndrome is defined by a short PR interval, QRS prolongation during sinus rhythm (due to slurring of the upstroke called a δ wave), and symptoms during tachycardia (Figure 8.5). The prolonged QRS in sinus rhythm is caused by pre-excitation of the ventricle down the accessory pathway. During orthodromic tachycardia, the QRS is narrow: anterograde activation of the ventricles occurs down the AV node, whereas retrograde activation of the atria is via the accessory pathway. In some patients with AVRT, the accessory pathway functions only in the retrograde direction; this allows AVRT but gives no evidence of pre-excitation during sinus rhythm. The electrocardiogram during AVRT may appear identical to that of AVNRT, although the P wave, if visible, occurs distinctly after the QRS (instead of being fused with the QRS complex). The differential diagnosis of regular supraventricular tachycardias and the clues from the P wave are summarized in Table 8.2. The rate of AVRT tends to be slightly faster, and may show alternation in the QRS amplitude or R–R Cardiology Core Curriculum 246 laVRV 1 V 4 ll aVL V 2 V 5 lll aVF V 3 V 6 V 1 Figure 8.5 interval (QRS or cycle length alternans). The prevalence of the WPW pattern in the general population is 1–3/1000, but less than half of patients with the WPW pattern have tachycardia. WPW syndrome occurs primarily in structurally normal hearts, but there is an association with Ebstein’s anomaly and mitral valve prolapse. Patients with WPW syndrome are also at risk for wide complex tachycardia due to either AF (with conduction down the accessory pathway) or antidromic AVRT (reversal of the usual re-entrant circuit of AVRT, with anterograde activation of the ventricle down the accessory pathway and retrograde activation of the atria via the AV node; Figure 8.6). Antidromic AVRT is quite rare, but pre-excited AF is not uncommon and can cause syncope and even sudden death. Pre- excited AF is recognized by an irregularly irregular wide complex rhythm that may also have occasional narrow beats. Patients with AVRT present with symptoms of palpitations, chest discomfort, dyspnea, and light-headedness, and rarely true syncope. There is frequently a history of palpitations dating back to childhood. Rarely, a patient presents with sudden cardiac death due to pre- excited AF and subsequent ventricular fibrillation. WPW syndrome should always be considered in the differential diagnosis of a young person resuscitated from sudden death. Arrhythmias 247 l aVR V 1 V 4 ll aVL V 2 V 5 lll aVF V 3 V 1 V 6 Figure 8.6 The acute management for AVRT is similar to that for AVNRT and is aimed at AV nodal block to terminate paroxysmal supraventricular tachycardia. If vagal maneuvers are not successful, then adenosine is the drug of choice. Alternatively, intravenous verapamil may be administered. On the other hand, if the patient presents with a wide complex tachycardia (pre-excited AF), then AV nodal blocking drugs are contraindicated because they can accelerate the tachycardia by facilitating conduction down the accessory pathway. For pre-excited AF, procainamide is the drug of choice because it blocks conduction in the accessory pathway and may terminate AF. Chronic medical management for patients who have AVRT but no pre-excitation is similar to that for patients with AVNRT, and any AV nodal blocking drug may be effective. When there is a δ wave present, drugs that impair accessory pathway conduction are indicated (quinidine, procainamide, disopyramide, flecainide, propafenone, sotalol). AV nodal blocking agents are not recommended in the presence of a δ wave because of the potential for accelerating the ventricular response to AF. Alternatively, radiofrequency catheter ablation has become a first line option. In more than 90% of cases a single procedure confirms the mechanism of the paroxysmal supraventricular tachycardia and allows ablation of the accessory pathway. Ventricular arrhythmias Monomorphic ventricular tachycardia Ventricular tachycardia is defined by three or more consecutive QRS complexes of ventricular origin at a rate of over 100 beat/min; “sustained” ventricular tachycardia is defined as lasting greater than 30 seconds or causing hemodynamic compromise. Monomorphic ventricular tachycardia has a uniform morphology and cycle length; conversely, polymorphic ventricular tachycardia is variable in morphology and cycle length. Over 90% of monomorphic ventricular tachycardia is associated with ischemic heart disease, and is secondary to re-entry in the border zone of a previous myocardial infarction. Monomorphic ventricular tachycardia also occurs in the setting of dilated cardiomyopathy, hypertrophic cardiomyopathy, infiltrative diseases (sarcoid or right ventricular dysplasia), and in the patient who has undergone surgery for congenital heart disease. In addition, monomorphic ventricular tachycardia is occasionally seen in the setting of a structurally normal heart. The patient with a sustained, regular wide complex tachycardia may present with minimal symptoms, or may experience chest pain, Cardiology Core Curriculum 248 dyspnea, presyncope, syncope, or sudden death. A bedside diagnosis of monomorphic ventricular tachycardia versus supraventricular tachycardia is useful for both acute and chronic management (Box 8.1). The clinical history is critical; prior infarction, coronary disease, or coronary risk factors are all suggestive that a wide complex tachycardia is ventricular tachycardia. Likewise, a history of heart failure or severe hypertension may suggest cardiomyopathy as the etiology of ventricular tachycardia. Box 8.1 Differential diagnosis of wide complex tachycardia Ventricular tachycardia Supraventricular tachycardia: abberancy; fixed intraventricular delay/bundle branch block Pre-excited supraventricular tachycardia Patients with ventricular tachycardia are usually hypotensive, but a normal blood pressure does not exclude the diagnosis. Intermittent cannon a waves of the jugular venous waveform and variability in the first heart sound both are consistent with dissociation of atrial and ventricular contraction, and thus suggest the diagnosis of ventricular tachycardia. Although a number of diagnostic schemes have been published for evaluation of the 12-lead electrocardiogram, a few simple guidelines will help confirm the diagnosis of ventricular tachycardia (as opposed to aberrant supraventricular tachycardia; Box 8.2). AV dissociation is the only finding that is diagnostic of ventricular tachycardia. This is demonstrated by P waves during the tachycardia that march through at a slower rate, or the presence of capture or fusion beats. A capture beat is an early, narrow complex beat originating in the atrium. A fusion beat is seen when the sinus impulse causes a QRS complex that is a combination of the ventricular tachycardia complex and the narrow QRS (Figure 8.7). Box 8.2 Wide complex tachycardia: criteria for ventricular tachycardia Atrioventricular dissociation: P waves marching through tachycardia; fusion complexes; capture beats Absence of RS in all chest leads (V 1 –V 6 ) QRS morphology: left bundle branch block pattern (monophasic downward in V 1 ) – >0·16 seconds; right bundle branch block pattern (monophasic upward in V 1 ) – >0·14 seconds R/S ratio in V 6 <1 (mostly negative QRS complex in V 6 ) Arrhythmias 249 The unstable patient with a wide complex tachycardia should undergo immediate direct current cardioversion. If the patient is without hemodynamic compromise or angina, then pharmacologic management is appropriate. The first drug of choice for suspected ventricular tachycardia is lidocaine. If the patient is stable and the diagnosis is in doubt (especially if pre-excited AF is considered), then intravenous procainamide is preferred. If drug therapy is unsuccessful, then cardioversion with synchronized direct current counter-shock (as low as 50 J) is indicated. After conversion of a wide complex tachycardia has been accomplished, evaluation of the electrocardiogram during sinus rhythm can assist in diagnosis. For example, a δ wave or a bundle branch block similar in morphology to the QRS during tachycardia would suggest a supraventricular origin of the arrhythmia. Following cardioversion of ventricular tachycardia, a patient is observed in a monitored setting and myocardial infarction ruled out. Continued intravenous therapy with lidocaine or procainamide should be considered if the patient was unstable with the ventricular tachycardia. After infarction has been excluded in the patient with monomorphic ventricular tachycardia, work up for etiology is initiated. Echocardiography is used to assess for the presence of structural heart disease such as infarction, dilated or hypertrophic cardiomyopathy, congenital anomalies, or valvular abnormalities. Patients with coronary risk factors should undergo cardiac catheterization to assess coronary anatomy, and revascularization if Cardiology Core Curriculum 250 ∗∗∗∗ l aVR V 1 V 4 ll aVL V 2 V 5 lll aVF V 3 V 6 V 1 Figure 8.7 indicated. In patients with structurally normal hearts and monomorphic ventricular tachycardia with a left bundle branch block pattern, cardiac magnetic resonance imaging is useful to assess for right ventricular dysplasia. Exercise testing may demonstrate exercise-related ventricular tachycardia. A 24-hour ambulatory (Holter) monitor will quantify the amount of spontaneous ventricular arrhythmias. Clinical electrophysiology study is indicated to confirm the diagnosis and guide therapy. At electrophysiology study, about 95% of patients with sustained ventricular tachycardia and coronary disease will have their clinical ventricular tachycardia induced by programmed electrical stimulation. This is useful to confirm the diagnosis and to determine whether the patient’s ventricular tachycardia may be terminated by overdrive pacing. If the ventricular tachycardia is pace terminable, then the patient may be a candidate for an implantable cardioverter–defibrillator (ICD) with antitachycardia pacing. Traditional management of ventricular tachycardia included serial electrophysiology studies that evaluated the response to one or more antiarrhythmic drugs. The Multicenter Unsustained Tachycardia Trial tested the hypothesis whether antiarrhythmic therapy guided by electrophysiology testing could reduce the risk for arrhythmic death and cardiac arrest in patients with coronary artery disease, reduced cardiac function (left ventricular ejection fraction of 40% or less), and non-sustained ventricular tachycardia. 7 It was found that electrophysiology guided pharmacotherapy conferred no survival benefit, and ICD implantation reduced total mortality and arrhythmic death or cardiac arrest. As an alternative to invasive electrophysiology testing, Holter guided therapy can be considered. Antiarrhythmic agents used for chronic treatment of sustained ventricular tachycardia include quinidine, procainamide, disopyramide, flecainide, propafenone, moricizine, sotalol, and amiodarone. In selected cases, if the ventricular tachycardia is tolerated hemodynamically and is unifocal in origin, then radiofrequency ablation may be effective. In recent years the ICD has become a mainstay of therapy for patients with hemodynamically significant ventricular tachycardia or sudden cardiac death. 8 The Antiarrhythmics Versus Implantable Defibrillators trial randomly assigned patients resuscitated from ventricular fibrillation or sustained ventricular tachycardia to ICD implantation or antiarrhythmic drugs (mainly amiodarone). 9 It found that ICDs were more effective than antiarrhythmic therapy in reducing arrhythmic cardiac death. ICD implantation has been simplified by the introduction of improved lead systems that are placed transvenously and by reduction in the size of the generator. Newer devices offer both low output cardioversion shocks and antitachycardia pacing to terminate ventricular tachycardia. Arrhythmias 251 In patients with non-ischemic cardiomyopathy and sustained ventricular tachycardia, electrophysiology study is successful in reproducing the clinical ventricular tachycardia in only about 60% of patients. Thus, electrophysiology study may not be useful in diagnosis and guidance of therapy. On the other hand it may be useful to assess for pace terminability of the rhythm, in order to guide selection of ICD if syncope or sudden cardiac death has occurred. Additionally, about 5–10% of patients with a dilated cardiomyopathy and sustained ventricular tachycardia will have a bundle branch re-entrant ventricular tachycardia that is amenable to cure by radiofrequency ablation of the right bundle branch. There are several ventricular tachycardias that occur in structurally normal hearts. Most commonly, the ventricular tachycardia originates in the right ventricular outflow tract and has a left bundle branch morphology and inferior axis (negative QRS in lead V 1 and positive in leads II, III, and aVF). Salvos of ventricular tachycardia may be almost constant (“repetitive monomorphic ventricular tachycardia”). Episodes of ventricular tachycardia are often exercise-related and suppressed by β-blockers or calcium channel blockers. Another ventricular tachycardia that occurs in structurally normal hearts, known as idiopathic left ventricular tachycardia, originates at the base of the posterior papillary muscle; during ventricular tachycardia the electrocardiogram has a right bundle branch and left axis pattern (positive in V 1 , I, and L; negative in F). This rhythm is responsive to verapamil and most antiarrhythmic agents. In addition to being responsive to drug therapy, both right ventricular outflow tract ventricular tachycardia and idiopathic left ventricular tachycardia are amenable to radiofrequency ablation for permanent cure. Ventricular tachycardia in what appears to be a normal heart may in fact be caused by right ventricular dysplasia. Structurally, there is focal or diffuse fatty infiltration and thinning of the right ventricle. These abnormalities may not be apparent on echocardiogram or cause minor abnormalities on right ventriculogram, but are best visualized with magnetic resonance imaging. Often there may be several different ventricular tachycardia morphologies, all originating from the right ventricle. Because of the risk of sudden cardiac death and the difficulty of suppression or ablation, ICD therapy is usually recommended. Polymorphic ventricular tachycardia Polymorphic ventricular tachycardia (PMVT), like monomorphic ventricular tachycardia, may occur in the settings of ischemic and Cardiology Core Curriculum 252 non-ischemic cardiomyopathy. At times, monomorphic ventricular tachycardia will degenerate to PMVT. Likewise, PMVT may degenerate to ventricular fibrillation. The diagnosis is usually obvious, although pre-excited atrial fibrillation in the setting of two or more accessory AV pathways may resemble PMVT. The mechanism responsible for PMVT is diagnosed according to the presence or absence of QT prolongation on the electrocardiogram during sinus rhythm. In the absence of QT prolongation, PMVT is treated in a similar manner to poorly tolerated monomorphic ventricular tachycardia or ventricular fibrillation. In the presence of QT prolongation, PMVT is called “torsades de pointes”. 10 The mechanism for torsades de pointes is believed to be “after- depolarizations” that occur during the prolonged plateau phase of the cardiac action potential. It is recognized in two distinct situations: acquired and congenital. Acquired QT prolongation typically is due to medication toxicity and/or electrolyte abnormalities (such as quinidine or sotalol, and low potassium or low magnesium). Treatment is directed at correcting the precipitating factor and increasing the heart rate with isoproterenol or pacing. Congenital long QT may occur spontaneously or may be inherited in two distinct syndromes. The Jervell–Lange–Nielson syndrome is an autosomal recessive trait and is associated with deafness. The Romano–Ward syndrome is an autosomal dominant trait and is associated with normal hearing. Patients may present with syncope, sudden cardiac death, or simply a family history of sudden cardiac death. They commonly develop arrhythmias during periods of increased adrenergic tone such as fright, exertion, and stress. Management of these patients includes β-blockers, pacemaker therapy, stellate ganglion blockade or resection, and implantation of an ICD. Ventricular fibrillation and sudden cardiac death Ventricular fibrillation (VF) is recognized on the electrocardiogram as a coarse undulating baseline without other electrical activity (Figures 8.8 and 8.9). VF often occurs in the same setting as ventricular tachycardia (other than for the “normal heart” ventricular tachycardias) and can result from degeneration of ventricular tachycardia. In addition, primary VF may be a consequence of acute ischemia. The patient who experiences VF loses consciousness within seconds. If cardiopulmonary resuscitation is not initiated and the arrhythmia persists, irreversible neurologic injury will result within minutes. The first treatment is immediate direct current defibrillation. If the first three shocks do not result in conversion, then direct Arrhythmias 253 [...]... after sinus rhythm has been restored Case 8.2 A 51 -year-old man presents to the emergency room complaining of palpitations and light-headedness Examination Vital signs are as follows: blood pressure 90/60 mmHg, pulse 220 beats/min; respiratory rate 20/min Investigations Electrocardiogram: see Figure 8.7 257 Cardiology Core Curriculum l aVR V 1 V 4 ll aVL V 2 V 5 lll aVF V 3 V 6 V 1 Figure 8.10 Questions.. .Cardiology Core Curriculum 25 mm/s 1000 ms Figure 8.8 current shocks are repeated following epinephrine (adrenaline), then lidocaine, then bretylium In spite of improved life support training and paramedic availability, only one patient in three survives out-of-hospital arrest VF resulting from a reversible cause, such as ischemia,... found in 70– 85% of people suffering sudden cardiac death or resuscitated cardiac arrest.7 Upward of 50 % of persons with sudden cardiac death appear to have an unstable coronary lesion, such as plaque rupture, observed at autopsy.6 In 20– 25% of victims, sudden cardiac death is the first manifestation of coronary artery disease and at least 50 % of victims have evidence 269 Cardiology Core Curriculum of... with high coronary risk profile Patients with previous coronary event Patients with ejection fraction < 35% , congestive heart failure Patients with previous out-of-hospital cardiac arrest Patients with previous myocardial infarction, low ejection fraction, and ventricular tachycardia 0 5 10 15 20 25 Incidence of sudden death (% of group) 30 0 100 000 200 000 300 000 No of sudden deaths per year Figure... about 90– 95% of cases Serial antiarrhythmic therapy, with response to programmed stimulation as an end-point, may be attempted If adequate suppression of the arrhythmia is not achieved, then implantation of an ICD with antitachycardia pacing capabilities should be recommended In the past, the ICD leads were often placed at the time of surgery; however, with the development of 259 Cardiology Core Curriculum. .. peripheral edema Investigations Laboratory data: normal Chest x ray: mildly enlarged cardiac silhouette, but no effusions or peripheral vascular redistribution Electrocardiogram: see Figure 8.3 255 Cardiology Core Curriculum Questions 1 What is the diagnosis? 2 What questions should be addressed in order to manage this patient? 3 How would you manage this patient over the first 24 hours? 4 How would you... from pause dependent or acquired QT prolongation), or a primary event The use of prophylactic lidocaine or procainamide infusion over the first 24–48 hours is generally unnecessary if the patient is to be monitored in a coronary care unit setting where rapid cardioversion may be performed 2 65 Cardiology Core Curriculum Answer to question 2 Given the normal coronary arteries previously and the absence... propensity for sudden cardiac death.4,6 Myocardial ischemia can produce significant local drops in tissue pH as well as elevations in extracellular potassium to 10– 15 mEq/l (10– 15 mmol/l) and increased intracellular calcium 271 Cardiology Core Curriculum Table 9.1 Medications that can prolong the QT interval State/drug type Antiarrhythmics Class I Class III Class IV Antibiotic Antifungal Antiparasitic... population studies J Am Coll Cardiol 19 85; 5(suppl):141B–9B 276 Sudden cardiac death and resuscitation 4 Spooner PM, Albert C, Benjamin EJ, et al Sudden cardiac death, genes and arrhythmogenesis: consideration of new population and mechanistic approaches from a National Heart, Lung and Blood Institute workshop, parts I and II Circulation 2001;103:2361–4, 2447 52 5 Bigger JT Relation between left ventricular... syndrome and a pre-excited R–R interval of less than 250 ms are at increased risk of sudden death (presumably due to degeneration of atrial fibrillation to ventricular fibrillation) Although WPW syndrome can be treated with antiarrhythmic medications, electrophysiology study and radiofrequency catheter ablation is the best option for primary therapy Case 8.4 You are asked to see a 74-year-old woman on . amiodarone therapy may improve survival in patients with VF. Cardiology Core Curriculum 254 1000 ms 25 mm/s Figure 8.8 Case studies Case 8.1 A 60-year-old man presents with a 4 day history of palpitations, accompanied. cardiac catheterization to assess coronary anatomy, and revascularization if Cardiology Core Curriculum 250 ∗∗∗∗ l aVR V 1 V 4 ll aVL V 2 V 5 lll aVF V 3 V 6 V 1 Figure 8.7 indicated. In patients with structurally. monomorphic ventricular tachycardia, may occur in the settings of ischemic and Cardiology Core Curriculum 252 non-ischemic cardiomyopathy. At times, monomorphic ventricular tachycardia will degenerate