Henry Ford Hospital Medical Journal

Volume 39 Number 3 Article 15

9-1991

Diagnosis and Management of After

Charles R. Webb

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Recommended Citation Webb, Charles R. (1991) "Diagnosis and Management of Tachycardias After Myocardial Infarction," Henry Ford Hospital Medical Journal : Vol. 39 : No. 3 , 226-235. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol39/iss3/15

This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. Diagnosis and Management of Tachycardias After Myocardial Infarction

Charles R. Webb, MD*

he patient with acute myocardial infarction (MI) may pre­ for patients taking diuretics (2). Since potassium is primarily an Tsent with acute due to as well as intracellular ion, merely correcting the serum potassium may chronic arrhythmias such as chronic atrial or ventric­ not be adequate and days to weeks may be required for complete ular ectopy. The only way to distinguish acute, chronic, or par­ correction. In the interim period, specific antiarrhythmic drug oxysmal is by a careful history from the patient and therapy is not likely to be effective. Anecdotally, it seems that a review of available old records. Guidelines for the diagnosis and serum potassium level of 4.0 mEq/L or higher is necessary to determination of the significance of arrhythmia afler acute MI stabilize arrhythmias in certain patients with cardiovascular dis­ are presented herein. ease. Hypomagnesemia also predisposes to arrhythmias and lends Rationale for Therapy to make antiarrhythmic drugs less effective (3,4). Like potas­ The three purposes for treating a patient for arrhythmia are: sium, magnesium is an intracellular ion, and correction of the 1) relief of symptoms due to the arrhythmia, 2) suppression of serum level may precede total body equilibrium by several days. arrhythmia causing hemodynamic impairment, and 3) preven­ Occasionally ectopy and tachyarrhythmias, including refractory tion of related and potentially lethal arrhythmias. or incessant ventricular (VT), appear to be sup­ The management of an arrhythmia begins with determination pressed by magnesium, even when the serum level is already ofits prognosis and hemodynamic implications and detection of normal. any potential causative factors before initiation of specific anti­ Hypokalemia and hypomagnesemia should be suspected in arrhythmic pharmacologic therapy. any patient with chronic or acute diuretic therapy, particularly Antiarrhythmic therapy should be individualized regarding without ionic supplementation, or patients with poor or re­ choice of agent, dosage, and length of therapy. Some cases re­ stricted diets, malabsorption, or diarrhea. quire acule therapy for arrhythmia termination. Others require failure is associated with arrhythmia (5,6). Ventricular chronic arrhythmia prevention or suppression. For some ar­ ectopy and nonsustained or sustained VT often are improved or rhythmias, such as chronic or chronic prema­ abolished with appropriate diuresis, inotropic therapy (7) (di- ture ventricular complexes, there may be no effective means of goxin), and/or vasodilator therapy (8). In the cardiac intensive lermination. Therefore, control of arrhythmia frequency or rate care setting, the pulmonary capillary wedge pressure, pulmo­ must be accepted. nary and vascular resistances, and cardiac output can be opti­ Determination of such individualized therapeutic goals or tar­ mized by therapy guided by right heart catheterization (Swan- gets will allow u.se of minimal effective dmg dosages, thereby Ganz catheterization). minimizing side effects, toxicity, and cost. Arrhythmia preceded by chest pain or transient electrocar­ diographic ST or T-wave changes is often due to myocardial ischemia. These arrhythmias often respond to antiischemic drug Recognition of Precipitating or Exacerbating therapy (nitrates, P-adrenergic blockade, calcium channel an­ Noncardiovascular Factors tagonists), coronary angioplasty, or bypass surgery. Paradoxi­ For diagnostic and therapeutic purposes, arrhythmias may be cally, in the period immediately after angioplasty (9), throm­ called primary if due to cardiac pathology, or secondary if reac­ bolytic therapy, or relief of Prinzmetal's vasospastic tive to a systemic or myocardial process. To delermine if and (10), arrhythmias may recur or appear de novo. These are called when to treat the arrhythmia, the first question which must be reperfusion arrhythmias. They should be suppressed with lido­ answered is whether the arrhythmia is a primary illness, merely caine or procainamide intravenously and should resolve within refiects more basic cardiovascular dysfunction, or is the result of systemic or metabolic imbalance. Hypoxia can cause or exacerbate almost any atrial or ventric­ Submitted for publieation; Seplember 3, 1991, Accepled for publication; Seplember 18, 1991, ular arrhythmia (I). Arrhythmia often results from membrane *Hean and Va,scular Institute, Cardiac Electrophysiologv Laboratory, Henry Ford Hospi­ instability which reflects more generalized electrolyte imbal­ tal, Address correspondence to Dr, Webb, Director, Cardiac Electrophysiology Laboratory, ance. Hypokalemia must be appropriately corrected particularly Henry Ford Hospital, 2799 W Grand Blvd, Detroit, Ml 48202,

226 Henry Ford Hosp Med J—Vol ,39, Nos 3 & 4, 1991 Management of Tachycardias Afler MI—Webb 24 hours. When arrhythmias occur later after angioplasty, the should routinely be assessed. The only reliable antidote appears possibility of ischemia due to reocclusion of a dilated vessel to be reduction of dosage; specific antiarrhythmic therapy is un­ must be considered. likely to be useful. Ventricular arrhythmias commonly complicate acute MI. The patient's hospital and clinic charts must be reviewed for Acutely, any significant ventricular ectopy should be sup­ any "antiarrhythmic" therapy. Indeed, there is no antiarrhythmic pressed by a lidocaine bolus of 50 to 100 mg intravenously fol­ agent which uniformly decreases arrhythmic potential. Most lowed by an infusion titratedbetwee n 2 to 4 pg/min. Sustained agents are effective for suppression of ectopy in about 60% of arrhythmias such as within the first 24 patients and for prevention of sustained arrhythmia in about hours do not portend chronic arrhythmic propensity, and once 30% of patients. In general, any antiarrhythmic agent has the arrhythmia is resolved and the patient leaves the critical care propensity to worsen arrhythmias in 10% to 15% of patients unit, routine cardiac monitoring and rehabilitation guidelines (17). Obviously, for the patient who has arrhythmia while on an­ should be followed (11,12). tiarrhythmic medication, the drug is not antiarrhythmic at the (postinfarction or Dressler's syndrome) may current dosage level. When consulted because of arrhythmia in mimic, complicate, or follow acute Ml. It usually presents as a patient already receiving chronic antiarrhythmic therapy, first chest pain, classically with a pericardial friction rub and a small review the history to determine why the therapy was instituled. pleural effusion. Pericarditis is frequently associated with atrial Ifthe patient has a history of lethal arrhythmias and only ectopy arrhythmias and less commonly ventricular arrhythmias, which is noted currently, perhaps the therapeutic goal of prevention of usually respond to antiinflammatory therapy and natural resolu­ lethal arrhythmia is indeed being fulfilled and therapy should be tion of the acute process. Because of the proximity of the sinus continued. However, if a patient has potentially lethal or lethal node to the epicardium, sinus node suppression and brady- cardiac arrhythmia while on chronic antiarrhythmic therapy, arrhythmias may also occur (13). peak and trough drug levels should be evaluated. Subtherapeu­ Cardiac manifestations may be the only physical evidence of tic levels would require an increase in dosage and reassessment thyroid disease in the elderly or critically ill patient. Patients of antiarrhythmic efficacy after a new steady-state blood level is with persistent sinus tachycardias in the absence of congestive attained (after administration of the new dose for five drug half- should have thyroid disease excluded by a serum lives). On the other hand, levels above the usual therapeutic thyroid-stimulating hormone determination (14). level call for reduction of dosage and reassessment of arrhyth­ Many dmgs may cause or exacerbate cardiac arrhythmias. Di­ mia after five drug half-lives. If the drug level is within the ther­ uretics may induce hypokalemia and/or hypomagnesemia as apeutic range, it is usually advisable to discontinue the current discus.sed above. may suppress arrhythmias if cardiac agent and employ a different agent. In difficult cases, combina­ function is improved: however, an excess may exacerbate or tion drug therapy is beneficial. Success has been reported with cause almost any cardiac arrhythmia. and heart combinations of Vaughn-Williams class lA and IB agents (18). block are the most obvious of these, particularly when digoxin Combination of IA and IC agents is contraindicated as arrhyth­ is combined with ^-adrenergic blockade or calcium channel mic deaths have been reported (19). In fact, when switching be­ blocking drugs. However, ventricular ectopy, VT, or ventricular tween these subclasses of drugs, it is safest to eliminate the first fibrillation may occur. It is important to recognize that these agent entirely, before initiation of the second agent. arrhythmias are due to because the appropriate therapy is optimization of electrolytes, correction of hypoxia, cessation of digoxin therapy, and occasionally dialysis or intra­ The Supraventricular Arrhythmias venous administration of digoxin antibodies. On the other hand, The most common arrhythmia accompanying acute Ml is si­ specific antiarrhythmic drug therapy is unlikely to be effective. nus tachycardia. is recognized by P waves Cardioversion for atrial arrhythmias or VT is hazardous because which precede each QRS complex in a 1:1 ratio with an appro­ digoxin lowers the ventricular fibrillation threshold. The di­ priate PR interval. Each P wave is upright in electrocardio­ goxin therapeutic toxic dose ratio is small and variable. Al­ graphic leads II, III, and AVF, indicating a craniocaudal se­ though markedly elevated serum levels correlate well with tox­ quence of atrial depolarization. Carotid sinus pressure results in icity, there are usually obvious clinical symptoms or signs in transient, gradual slowing wilh retum to the previous rate sec­ such cases. In more subtie cases, the serum drug levels are likely onds afterrelea.se. to be borderline. This is probably due to variable cardiac sensi­ Usually sinus tachycardia is due to anxiety or is an appro­ tivity related to the underlying type and severity of cardiac dis­ priate cardiovascular response to pain or disease and seldom ease and variations in the electrolytic and metabolic milieu should be suppressed with antiarrhythmic drugs. Digoxin at (15,16). When an antiarrhythmic drug is necessary for suppres­ therapeutic levels is rarely effective in suppressing a normal sion of ventricular arrhythmia, diphenylhydantoin has the ad­ sinus node (20). However, |3-adrenergic blockers or calcium vantage of moderate efficacy as a membrane stabilizer and the channel blockers may blunt an appropriate chronotropic re­ least negative dromotropic effect on the cardiac conduction sys­ sponse and result in hemodynamic collapse. tem. It is the least likely to exacerbate . Hypovolemia is a common cause of sinus tachycardia and the Bronchodilators, particularly the methylated xanthines, com­ heart rate should diminish gradually as plasma volume is re­ monly exacerbate arrhythmias. In the critically ill patient, previ­ stored. Relative hypovolemia may be due to decreased left ven­ ously well tolerated agents tend to accumulate and serum levels tricular compliance or ventricular infarction which can be de-

Henry Ford Hosp Med J—Vol 39, Nos 3 & 4, 1991 Management of Tachycardias After Ml—Webb 227 lected by Swan-Ganz catheterization. Other causes are anxiety, waves and make the diagnosis. Carotid sinus pressure may tran­ fear, pain, anemia, fever, hyperthyroidism or thyrotoxicosis, siently increase the AV nodal block and make the P waves visi­ overdose of thyroid replacement, vagolytic drugs (atropine), ble. Rarely, insertion of an intraatrial lead is necessary to make vasopressors (isoproterenol, dobutamine, dopamine), vasodila­ the diagnosis. tors (nitrates, procardia), and antihypertensives. may be a primary arrhythmia in patients with no Some degree of sinus arrhythmia is common. Unless long other evidence of cardiac or systemic disease. More frequently, symptomatic pauses occur, it is not an indication for specific however, it is secondary to congestive heart failure, cardiomy­ therapy. opathy, pericarditis, pulmonary disease, cardiac surgery, hyper­ Atrial premature complexes (APCs) are common in any hy- tension, alcohol, smoking, or caffeinated beverages. Occasion­ peradrenergic state that is commonly associated with sinus ally patients present with heart failure secondary to a sustained tachycardia. Usually the P-wave morphology is different from episode of paroxysmal atrial flutter. sinus P waves indicafing that the focus is ectopic, not the sinus Three basic forms of therapy are available for termination of node. However, some foci are near or within the sinus perinodal sustained atrial flutter. Atrial overdrive pacing is an invasive tissue and may appear similar to sinus node-initiated P waves. procedure involving insertion of an intraatrial electrode which Generally APCs are asymptomatic and the therapy should be di­ is useful to confirm the diagnosis and for terminafion (22, rected at correction of the systemic disease process as, more of­ 23). When the is carefully entrained and pacing abrupt­ ten than not, the heart is merely an innocent bystander. Caffeine ly stopped, sinus rhythm should prevail, but there is always and methylated xanthines and vasopressors commonly are re­ the possibility of proarrhythmia, resulting in atrial fibrillation sponsible and their dosages should be minimized. Hypoxia, hy­ which often converts to sinus rhythm spontaneously within 24 povolemia, anemia, and electrolyte imbalance should be cor­ hours. The advantage of atrial overdrive pacing is that it is rapid rected. Rarely is specific antiarrhythmic therapy indicated un­ and avoids administration of dmgs which are potentially nega­ less APCs are symptomatic or perceived as harbingers to atrial tive inotropes in critically ill patients. A brachial vein approach fi utter or fibrillafion in patients with a history of such arrhyth­ is safe for patients who are on low-dose anticoagulation therapy, mia. even in outpatients whom 1 send to work after two hours of ob­ Atrial tachycardia is an arrhythmia which originates in the servation. Digoxin toxicity is not a contraindication. atria. Therefore, each ventricular complex is preceded by an When the rate of the atrium during fiutteri s greater than 210 atrial complex with an appropriate PR interval. The P-wave beats/min, entrainment of the atrium may not be possible. In morphology is uniform, usually ectopic, and different than sinus such cases, the refractory period of the atrium may be increased P waves. Carotid sinus pressure may terminate the arrhythmia by prior oral or intravenous administration of a Vaughn-Wil­ abmptly. Ectopic atrial tachycardia is rarely of hemodynamic liams type IA antiarrhythmic agent. significance and does not require specific therapy. Intravenous procainamide, 500 to 1,000 mg, by intravenous Multifocal atrial tachycardia is a common cardiac manifesta­ infusion over 20 minutes, is often effective. This dosage re­ tion of serious acute cardiac or pulmonary disease. It is an irreg- quires constant patient supervision and blood pressure monitor­ ulariy irregular arrhythmia characterized by the triad of varying ing at least every 5 minutes. Hypotension frequentiy results, oc­ P-wave morphologies, varying P to P intervals, and varying PR casionally because of negative inotropic effect, but more com­ intervals (21). Carotid sinus pressure usually has no effect on the monly because of peripheral vasodilatation which responds to arrhythmia. Its distinction from atrial flutter or fibrillation is im­ reduction of infusion rate by half and administration of 100 to portant. Digoxin is contraindicated because the factors which 200 mL of normal saline rapidly. Depending on the estimated perpetuate multifocal atrial tachycardia also predispose to di­ likelihood of early recurrence, the infusion may be either termi­ goxin toxicity and proarrhythmia. i.e., hypoxia and electrolyte nated upon restoration of normal sinus rhythm or reduced to 2 to imbalance. Some investigators report relative success with cal­ 4 mg/min until oral loading is initiated. Oral loading of digoxin cium channel blockers. However, the most effective therapy is and subsequently a quinidine preparation may also be effective, detection and correction of the underiying cause. but it takes longer (days rather than minutes). Quinidine has a Atrial flutter is characterized by uniform P waves at a rate of potent vagolytic effect on the AV node and can accelerate the 300 to 350 beats/min. It is associated with rapid mechanical ventricular rate to 200 beats/min or higher due to 1:1 AV nodal atrial activity. There is discrete electrical and mechanical systole conduction unless the AV node is first blocked with digoxin or and diastole. Usually the atrioventricular (AV) node is effective a (i-adrenergic blocker. However, the vagolytic effect of pro­ as a filter resulting in a physiologic 2:1 or higher AV nodal cainamide is nol of clinical significance and previous admini­ block and a moderated ventricular rate of about 150 to 200 stration of digoxin is not a prerequisite. beats/min. Any rhythm at a rate of 150 beats/min should result The third method of acute termination of atrial flutter is car­ in consideration of atrial flutter with examinafion of rhythm dioversion. It is often said that low energy cardioversion (10 to strips and a 12-Iead ECG for P waves. (Caution: P waves may be 25 joules) is effecfive for atrial flutter,bu t frequentiy higher en­ small and hide on the QRS complex or in the T waves. They tend ergy is necessary. Cardioversion is uncomfortable with sedation to become more visible at early morning staff rounds than at and there is hazard of respiratory suppression in the critically night.) Careful examination of the neck veins for A waves may ill patient. Brief general anesthesia with the ultrashort-acting make the diagnosis. Movement of the V leads an interspace agent, methohexital, 40 to 100 mg intravenously, titratedunde r higher or lower than usual or even to the back may detect P supervision of an anesthetist is our preferred method of car-

228 Henry Ford Hosp Med J—Vol 39, Nos 3 & 4, 1991 Management of Tachycardias Afler Ml—Webb dioversion. Cardioversion should not be attempted if there is symptomatic pauses with a lower junctional escape rhythm electrolyte imbalance or suspicion of digoxin toxicity. demonstrating that a pacemaker should be implanted. If an acute precipitating factor for atrial arrhythmia can be As a "grandfathered" standard of clinical care, the recent liter­ identified and corrected, the patient is usually followed chroni­ ature is devoid of precise statistics on the "odds" of successful cally without antiarrhythmic therapy or given digoxin to control cardioversion to normal sinus rhythm. In the individual patient, the ventricular response if atrial flutter recurs. When chronic clinical experience dictates that the acuteness of onset is a good therapy is desired, digoxin is the basis and a type IA antiarrhyth­ predictor of success, whereas cardioversion is only occasionally mic agent such as quinidine gluconate, sustained-release pro­ successful for atrial fibrillation of six months duration. Atrial cainamide, or disopyramide is given. Preliminary data suggest size by echocardiography also plays a role, but there are major that flecainide, encainide, and propaphenone are effective for limitations to accurate atrial measurements by echocardiogra­ chronic prevention and by slowing the ventricular rate if flutter phy. Treatment and reversal of a precipitating cause is a good should recur. However, according to the results of the Cardiac predictor, i.e., thyroxine excess, congestive heart failure, alco­ Arrhythmia Suppression Trial, these agents must be avoided in hol consumption, exposure, electrolyte imbalance, antiarrhyth­ the patient with recent or acute MI. Amiodarone is also highly mic dmg noncompliance. High amplitude "flutter waves" in the effective, but its delayed onset of action, long half-life, and po­ baseline imply that the atrium is electrically active and suggest tential toxicity prevents recommendation unless other agents more recent onset and easier cardioversion. have failed or are not tolerated. Once these matters have been considered, the basic alter­ Atrial fibrillation is characterized by a chaotic electrical natives for conversion are electrical and pharmacologic. The baseline on the ECG. There is no distinct electrical systole or di­ choice should be based upon informed patient preference and astole and no effective mechanical contraction of the atria. availability of personnel and facilities. Rarely, fibrillation is isolated to one atrium. Because there is no Pharmacologic therapy has the advantage of determining ef­ effective mechanical activity, there is a high propensity to fective long-term therapy and can be initiated on any telemetry- thrombus formation and cerebrovascular embolization is one of monitored hospital floor with oral or intravenous drug admin­ the most severe complications. The cardiac output may be di­ istration. minished by 10% to 25% depending on atrial size and effective­ If atrial fibrillation is of recent onset, correction of precipitat­ ness and the ventricular compliance. In ing causes and restoration of normal sinus rhythm is desirable. with a stiff left ventricle such as asymmetric septal hypertrophy, If rapid pharmacologic termination is desired, intravenous restrictive , or severe , develop­ procainamide is administered, just as described for atrial fiutter ment of atrial fibrillation may result in hemodynamic collapse. (24). Verapamil may slow the ventricular response, but seldom, Thus the assessment of atrial fibrillation should include a com­ if ever, terminates atrial fibrillafion to restore normal sinus plete cardiovascular evaluation including an echocardiogram to rhythm (25). Use of verapamil may be complicated by hypoten­ evaluate atrial size and to search for obvious intramural atrial sion and impaired cardiac output. thrombi. If an oral pharmacologic approach is preferred, digoxin is There are two potential mechanisms of atrial fibrillation. One usually administered to control the ventricular response. Oral is a rapid chaotic atrial discharge which suppresses a normal si­ quinidine sulfate, quinidine gluconate, or sustained-release pro­ nus node; the other is an escape mechanism in the presence of a cainamide is then added. 1 do not advocate high dosage therapy diseased sinus node which results in severe bradycardia or long as the likelihood of conversion to sinus rhythm is not assured, pauses. In the former instance, if the abnormal atrial fibrillation but risk of side effects or toxicity is likely. is electrically, pharmacologically, or spontaneously terminated, Cardioversion is effective for atrial fibrillation of recent onset normal sinus rhythm supervenes. In the sick sinus syndrome, after exacerbating factors are resolved (26). If atrial fibrillation however, the abnormal atrial arrhythmia may be a vital escape has persisted for two or more weeks, four to six weeks of antico­ mechanism and its termination may reveal impaired or absent agulation therapy is required to prevent microthrombi which sinus node activity. Whenever this situation is predicted by pre­ might be dislodged during cardioversion. The technique is simi­ vious ECGs demonstrating significant bradycardia, sinus pause lar to the description for atrial flutter, except that higher energy or arrest, or junctional or lower escape mechanism, electrical or levels are used, beginning with 100 joules. Our laboratory makes chemical cardioversion should be preceded by placement of a an attempt at 100,200, and 360 joules wilh sufficient time for re­ temporary or permanent transvenous pacemaker. covery and monitoring of vital signs between shocks. If precipitating faclors can be identified, chronic antiarrhyth­ Acute versus chronic arrhythmia mic therapy may not be required for the first episode (27). How­ It is essential to determine the premorbid arrhythmia to deter­ ever, if arrhythmia is recurrent, digoxin is useful to help control mine appropriate therapy and predict outcome. All old ECGs the ventricular rate. Type IA antiarrhythmic therapy is useful for should be reviewed to determine the fimeo f onset of atrial fibril­ prevention of atrial fibrillation. In the absence of recent Ml or lation, the underlying baseline rhythm, and whether atrial fibril­ ischemia, flecainide, encainide, and propaphenone alone or in lation is a lone event that is unlikely to recur for a long time after combination with digoxin have been successful in prevention or successful restoration of normal rhythm or is paroxysmal and modulation of paroxysmal atrial flbriOation. likely to be recurrent without therapy in the future. An old For atrial fibrillation of more than six months duration or Holler monitor may document significant 3-second pauses or which has failed to respond to pharmacologic or electrical car-

Henry Ford Hosp Med J—Vol 39, Nos 3 & 4. 1991 Management of Tachycardias After Ml—Webb 229 dioversion, control of the ventricular rate is accomplished with ever, in the absence of acute MI if the hemodynamics and symp­ digoxin which may be titrated safely according to ventricular tomatology permit, appropriate recording, documentation, and rate in atrial fibrillation, occasionally requiring unusually high assessment are essential because the arrhythmia is likely to re­ dosages. Addition of other AV nodal blockers may be required cur, but perhaps never again in a controlled monitored setting to modulate the ventricular rate including p-adrenergic blocking such as the cardiac intensive care unit. The initial electrocardio­ agenls, calcium channel blocking agents, or amiodarone (28). graphic recording during the acule event facilitates appropriate In patients refractory to antiarrhythmic drug therapy, catheter in-hospital evaluation and long-term outpatient management. or surgical modulation of the AV node may be required (29). If Termination without adequate documentation can result in un­ AV nodal ablation is required or results inadvertently, a perma­ certainly of diagnosis, delay hospital discharge, and confound nent ventricular pacemaker is required. This is not all bad. Im­ the chronic management plan. plantation of a newer rate-responsive pacemaker may restore a Wide complex tachycardia is defined as a cardiac dysrhyth­ degree of appropriate chronotropic responsiveness simulating a mia having a rate greater than 100 complexes per minute (or R- sinus node which the chronic atrial fibrillator has never before R cycle length less than 600 msec) and a QRS duration greater enjoyed. Guiradon and coworkers (30.31) are developing surgi­ than 120 msec in any lead on a standardized 12-lead ECG. For cal conduit techniques to restore sinovenlricular communica­ descriptive purposes, the QRS morphology during tachycardia tion. This technique can restore chronotropic function but not is assigned a pattem (left or right or nor­ atrial mechanical function. Cox et al (32) are developing a mal). A right bundle branch block pattem is assigned if the QRS "maze" procedure to disrupt the reentrant electrical pathways of complex is predominantiy positive in lead VI; prominent termi­ atrial fibrillation and restore normal sinus rhythm and transport nal negative S waves in leads I and V5 or V6 are supportive find­ function. ings. A pattem is assigned when the AV nodal leentrant tachycardia is a common tachycardia intrinsicoid deflection is delayed in the lateral electrocardio­ usually characterized by a narrow QRS complex with retrograde graphic leads (1, and V5 or V6); usually VI is predominantiy P waves which are more often than not buried within the QRS negative. The tachycardia may be further characterized by the complex or distorting the terminal portion of it. Occasionally a predominant or mean QRS axis during the tachycardia: normal rate-dependent (usually right) bundle branch QRS pattem re­ axis ifil lies between 0 and 90 degrees; if it is sults. Carotid sinus pressure may transiently slow or terminate less than 0 degrees; or if it is greater than 90 the tachycardia abruptly. Usually the atrial rate is 140 to 210 degrees. This classification scheme does not necessarily imply beats/min with the symptoms and hemodynamic consequences mechanism or origin of tachycardia but serves as a catalog to de­ dependenl on the rate. It is common in patients with no evidence termine wheiher there is recurrence of the same tachycardia or of cardiovascular disease. Intravenous digoxin or procainamide perhaps tachycardias of different types in the same patient, each are effective for acute termination, as are atrial or ventricular of which may require specific therapy. For example, a patient pacing techniques which may also be of diagnostic value. Inter­ may have a polymorphous tachycardia due to ischemia or elec­ estingly, although the reentrant arrhythmia circuit is confined to trolyte imbalance which will not require chronic therapy and an­ the AV node (animal studies have shown that resection of atria other monomorphic tachycardia due to a reentrant focus (either and ventricles does not terminate the tachycardia), type IA anti­ supraventricular or ventricular) which is likely to recur after arrhythmic agents are effective in blocking the retrograde limb hospital discharge and requires chronic therapy. of the tachycardia (33,34). A 12-lead ECG machine, cardiorespiratory resuscitative Generically, tachycardias may be classified into three groups drugs and equipment, and a defibrillator should be brought to based on duration alone: paroxysmal, persistent, or chronic. the bedside in case cardioconversion is required for emergent Arrhythmias which are paroxysmal may be of any mechanism, termination of life-threatening arrhythmia. including VT. By definition, torsade de pointes is paroxysmal. The differential diagnosis of a regular wide complex tachy­ Paroxysmal atrial tachycardia describes any atrial arrhythmia cardia includes: I) supraventricular tachycardia with a func­ which lasts only seconds to hours. It is a mistake to develop a tional bundle branch block, 2) supraventricular tachycardia with management plan for paroxysmal atrial tachycardia, because it a preexistent bundle branch block, 3) supraventricular tachycar­ is not a specific diagnosis but a syndrome which may include dia with antegrade AV conduction over an accessory AV path­ AV nodal reentrant tachycardia, sinus tachycardia, or atrial fi­ way (antidromic supraventricular tachycardia), or 4) VT. brillation. When the mechanism is determined, specific therapy Age, heart rate, blood pressure, level of consciousness, and follows logically. duration or presence or absence of heart disease are not accurate determinants of the tachycardia mechanism. VT is the most com­ mon mechanism of wide QRS tachycardia at any age, although a heart rate of 150 complexes/min suggests atrial flutter with 2:1 Wide QRS Tachycardia heart block. There is no particular heart rate which excludes VT A wide QRS tachycardia associated with hypotension during or supraventricular tachycardia. Either arrhythmia may be fast acute MI is considered to be VT and is treated as such until or relatively slow. Occasionally patients with fast tachycardia proven otherwise. are alert and conversational despite rapid VT and underlying In the setfing of acute MI or acute ischemic syndrome, wide ventricular dysfunction. Presumably this results from an opti­ complex tachycardia must be terminated immediately. How­ mal balance of a low cardiac output and adequate peripheral

230 Henry Ford Hosp Med Vol 39, Nos 3 & 4, 1991 Management of Tachycardias After MI—Webb vasoregulation to maintain cerebral perfusion. In patients with electrocardiographic monitoring while the proximal portion of an acute MI, it is prudent to assume the tachycardia is ventricu­ the lead is connected to lead VI. A quadripolar catheter allows lar until proven otherwise, but these patients also frequently simultaneous recording and pacing. have supraventricular arrhythmia. Some patients have both. In addition to passive recording, a pacing lead allows olher di­ Ventriculoatrial dissociation is diagnostic for VT, but ven­ agnostic and therapeutic interventions. Atrial pacing at rates ex­ triculoatrial association may occur in either supraventricular ceeding the tachycardia rate can artificially produce the phe­ tachycardia or VT with I: I retrograde conduction. A single-lead nomena of atrial capture beats and fusion beats with transient electrocardiographic monitoring strip is diagnostic of VT when normalization or near-normalizafion of the QRS complexes. the QRS and P-wave morphologies are distinct and ventricu­ The latter method may also allow for termination of the tachy­ loatrial dissociation is apparent. Since wide QRS complexes are cardia by pacing in the atrium. Theoretically, atropine or iso­ usually tall, as well as wide, it is often difficult to discem the proterenol, by enhancing AV nodal conduction, may facilitate smaller P waves on emergency or bedside monitoring equip­ capture and fusion beats but could cause degeneration of the menl because they are buried within the QRS complex or a tachycardia to ventricular fibrillation. Many supraventricular broad . A fortuitously timed sinus beat may capture the tachycardias can be terminated by atrial entrainment, but this is ventricle resulting in occasional ventricular capfw/ e beats which not absolutely diagnostic as relatively slow VTs may also be ter­ are narrow and look like sinus beats (because they are) during minated by impulses conducted across the AV node. If the the tachycardia. Such sinus beats which occur later in electrical tachycardia is ventricular in origin, the electrode catheter may diastole may resull in ventricular/MS/O/? beats which are a mor­ be advanced across the to the right ventricular phologic hybrid of sinus and tachycardia QRS complexes. apex to provide a stable position to attempi to entrain and termi­ Recording three or more electrocardiographic leads simulta­ nate VT neously allows comparison of barely perceptible P waves in Carotid sinus massage may slow or terminate AV nodal or several leads and may clarify presence or absence of any tempo­ AV reentrant supraventricular tachycardia. It may result in AV ral relationship to the QRS complexes. If there is a 1:1 relation­ nodal block and dissociate the ventricles from the atria during ship with normal P waves preceding each QRS complex, sinus supraventricular tachycardias which originate in the atrium or rhythm or other atrial rhythm is present. If there is AV dissocia­ high within the AV node (sinus node reentry, intraatrial reentry, tion (i.e., atrial and ventricular activity are independent), then atrial flutter or fibrillation, or automatic atrial tachycardia). P VT is diagnosed. If there is a 1:1 relationship wilh inverted P waves may become apparent. A functional (rate-dependent) waves following each QRS complex, either VT with retrograde bundle branch block may resolve. conduction or supraventricular tachycardia may be present. Careful observaiion of any change in the tachycardia rate or A standard 12-lead ECG should be recorded during tachycar­ termination by an antiarrhythmic drug can be of diagnostic and dia whenever possible. It provides 1) a better "fingerprint" of the therapeutic value. Intravenous lidocaine is uniquely effective arrhythmia (35,36), and 2) greater likelihood of detecting P for VT; it has no efficacy for atrial tachycardias nor reentry over waves, and 3) the QRS morphology may be useful to discrimi­ an accessory AV pathway. This specificity has diagnostic value. nate tachycardia of supraventricular or ventricular origin. A Intravenous propranolol, verapamil, diltiazem, or digitalis gly­ QRS width greater than 140 msec is highly suggestive of a VT. cosides slow AV nodal conduction. Hence, a tachycardia whose Leftward deviation of the mean QRS vector is also highly corre­ mechanism depends on anterograde or retrograde AV nodal con­ lated with VT. Capture beats and fusion beats, although diag­ duction will become slower and more tolerable. If intermittent nostic of VT, are relatively uncommon (37). A "concordant pat­ AV nodal block is produced, the tachycardia will terminate. tem" of precordial complexes (i.e., all leads in VI to V6 are en­ Digitalis glycosides are the least likely to exacerbate hypo­ tirely upright or entirely inverted) is highly suggestive of VT, tension and are preferred if there is evidence of heart failure. The but is not common. In the presence of antegrade conduction over disadvantage is the slow onset of action, even when admini­ an accessory AV pathway, the ventricle is activated ectopically stered intravenously, which makes them undesirable if the pa­ and such supraventricular tachycardia cannot be distinguished tient is rapidly deteriorating. from VT by surface . Furthermore, presence Calcium channel antagonists (verapamil or diltiazem) and P- of delta waves in the resting ECG by no means excludes the pos­ adrenergic blockers (propranolol) are contraindicated if the pa­ sibility of VT. tient is hypotensive or has evidence of heart failure (35,38). If the mechanism of the arrhythmia remains unclear, position­ However, if there is no evidence of fluid overload or heart fail­ ing of chest leads one interspace higher or lower or on the back ure, it is valuable to administer about 200 mL of normal saline (nearer to the left atrium) may reveal P waves. When stable, a (0.9% aqueous sodium chloride) intravenously to achieve an "pill electrode" may be swallowed into the esophagus during the adequate intravascular volume and decrease baroreceptor drive tachycardia to record at the level of the left atrium. Otherwise a for tachycardia. This often corrects hypotension, relieves anxi­ temporary pacing wire may be passed through a nasogastric ety, slows supraventricular tachycardia rate, and occasionally tube. allows spontaneous resolution of tachycardia. If the blood pres­ The most reliable method of deiection of atrial activity during sure is normal or high, calcium channel antagonists or p-adre­ tachycardia is to record the righl intraatrial electrogram by in­ nergic blockers may be safely given with negative dromo­ serting a temporary pacing wire transvenously with fluoro­ tropic effect similar to the digitalis glycosides but more rapid in scopic guidance, or a balloon-tipped electrode catheter with onset and easier to titrate.

Henry Ford Hosp Med J—Vol 39, Nos 3 & 4, 1991 Management of Tachycardias After MI—Webb 231 , when administered intravenously, blocks AV nod­ "Wide complex tachycardia" is a syndrome with many clini­ al conduction rapidly. It is metabolized rapidly in plasma and cal presentations and several potential underiying mechanisms. human tissues. Therefore, its duration of action is brief (about 5 It may or may not be associated with structural underlying car­ minutes). Advantages are rapid termination of supraventricular diovascular disease, may be relatively benign, or may result tachycardia and brief duration of hypotension or other side ef­ in sudden death (35,38). The patient must always be evaluated fects like facial flushing(39) . promptly, but critical data must also be gathered emergentiy in Esmolol, an ultrashort-acting p-adrenergic blocking agent, order to assure good long-term diagnostic and therapeutic accu­ also offers the opportunity to observe a brief effect on AV nodal racy. Wide complex tachycardia is a most challenging phenom­ conduction and termination of supraventricular tachycardia enon for the cardiologist or electrophysiologist, but alert para­ while minimizing any residual side effect. medics, nurses, house officers, and acute care physicians pro­ If the patient has a wide complex tachycardia and has a his­ vide the cmcial and irretrievable initial data base which under­ tory of the Wolf-Parkinson-White syndrome, delta waves on lies successful long-term management. the ECG in sinus rhythm, or is young without underiying cardio­ vascular disease, particularly with a left bundle branch block morphology, tachycardia mediated by conduction over an ac­ Ventricular Arrhythmia cessory AV pathway must be considered. If an AV nodal block­ Sustained VT is arbitrarily defined by most experts as a ing agent is administered and atrial fibrillation ensues, rapid tachycardia of ventricular origin which, if unintermpted, per­ conduction over the accessory pathway can be catastrophic and sists continuously for at least 30 seconds, or is intentionally ter­ even degenerate to ventricular fibrillation requiring cardiover­ minated earlier by cardioversion because of impending hemo­ sion (40-43). In such patients, intravenous procainamide is the dynamic collapse. Sustained VT may be terminated by intrave­ agent of choice because it may effectively block the accessory nous lidocaine or procainamide, but generally requires cardio­ pathway and thereby slow or terminate AV reentry or atrial fi­ version. brillation or fiutter. Procainamide is also effecfive for termina­ In the patient with acute ischemic syndromes or evolving MI, tion of VT nonsustained VT should be suppressed because it is frequently a A variety of guidelines have been published to help determine harbinger of ventricular fibrillation. the mechanism of the tachycardia based upon the QRS morphol­ Torsade de pointes, which literally means "turning around the ogy on the 12-lead ECG. It should be compared side-by-side point," is a descriptive, not a mechanistic, term for a polymor­ with the resting ECG in sinus rhythm. If the patient has aberrant phic VT which appears to tum above and below the isoelectric conduction with a wide QRS morphology in sinus rhythm, aber­ axis (46). More simply, some QRS complexes appear upright ration will be presenl during supraventricular tachycardia. Iflhe and some appear inverted. It is usually too fast, however, to ac­ QRS morphology is similar during sinus rhythm and tachycar­ curately distinguish the QRS (ventricular depolarization) from dia, the tachycardia origin is probably supraventricular. the T wave (ventricular depolarization) and hence the negative The diagnosis can be made electrophysiologically if the pa­ deflections might be T waves or vice versa. Torsade de pointes, tient is stable enough for safe transport to the laboratory during as originally described, is nonsustained or self-terminating, usu­ the arrhythmia to allow insertion of a catheter across the tricus­ ally within several seconds. This is the major electrocardio­ pid valve to record a His-bundle electrogram. Otherwise the graphic distinction from ventricular fibrillation which is rarely tachycardia may be electively induced in the laboratory at a later (some say never) self-terminafing. time. A supraventricular tachycardia is recognized electrophysi­ Torsade de pointes is a syndrome and as such requires further ologically by the presence of a His-bundle potential preceding clinical data to determine appropriate therapy (47). It is associ­ each QRS complex with an H-V interval equal to or exceeding ated with drug toxicity or proarrhythmia, electrolyte imbalance, that recorded when the patient is in sinus rhythm. In contrast, acute ischemia, coronary reperfusion, intracranial disease, or during VT, the H-V interval, if a His-bundle potential is re­ congenital long QT syndrome. It is sometimes related to clinical corded, is shorter than normal. More commonly, the His-bundle bradycardia. The therapy begins with correction of any revers­ potential is buried within the QRS complex during VT and can­ ible exacerbating factors and discontinuation of any antiarrhyth­ not be discemed even on a recording from a catheter properiy mic drugs. If rapidly recurrent, isoproterol infusion at a rate of 1 positioned to record the His-bundle electrogram. This phenome­ to 3 |ig/min, titrated upward to increase the resting sinus heart non may also be observed during antegrade conduction over an rate to a maximum of 100 beats/min, may suppress torsade de accessory AV pathway (preexcitation syndrome) during atrial pointes. When time permits, placement of a temporary trans- tachycardia or antidromic AV reentrant supraventricular tachy­ venous pacemaker allows more precise control ofthe heart rate cardia. and suppression of arrhythmia. There is some theoretic basis for Each patient with sustained monomorphic VT, in the absence this therapy ifthe arrhythmia is due to eariy afterdepolarizations of acute MI or other reversible cause, a reasonable quality of which are suppressed in cellular preparations by pacing. life, and a reasonable life expectancy of at least six months, Ventricular fibrillation is the most serious of the cardiac should undergo a diagnostic cardiac catheterization and coro­ arrhythmias and is invariably lethal if not promptly reversed or nary angiography to determine any correctable anatomic etiolo­ unless the patient is supported by effective cardiopulmonary re­ gies (44). Thereafter, electrophysiologic testing can delermine suscitation. The only effective therapy is asynchronous DC car­ the mechanism and appropriate therapy (45). dioversion with 100 to 360 joules. If ineffective, resuscitative

232 Henry Ford Hosp Med J—Vol 39. Nos 3 & 4. 1991 Managemeni of Tachycardias After Ml—Webb efforts should continue while improving oxygenation, acid-base Another criterion for complexity was the presence of multifo­ slatus, coronary blood flow, and electrolytes. Cardioversion cal PVCs which were identified by varying PVC morphologies. may then be repeated. Clinically, coarse fibrillation seems more Although there is a possibility that PVCs from a single myocar­ easy to terminate. If fine fibrillation prevails, administration of dial focus may have varying sites of exit and/or pattems of con­ epinephrine may "coarsen" the undulations on the surface ECG duction resulting in varying QRS morphologies, this would be and facilitate cardioversion. Various experts advocate intrave­ difficult to prove by surface electrocardiography alone and nous, intracardiac, or intratracheal administration. Some studies hence "multifocal" and "multiformed" are synonymous for clin­ have shown that cardiac levels may be adequate with intrave­ ical purposes. nous or intratracheal administration, avoiding the risks of car­ "Repetitive" forms include pairs of PVCs and salvos or mns diac, pericardial, or pleural laceration, but controversy prevails of nonsustained VT. Nonsustained VT is defined as a self-termi­ and it is common to administer intracardiac epinephrine for oth­ nating mn of VT consisting of three or more complexes. Some erwise refractory fine ventricular fibrillation or . Cal­ investigators considered a frequency of 30 or more PVCs per cium chloride, 5 to 8 mg intravenously, may also be useful (48). hour to be complex. Premature ventricular depolarizations are exacerbated by the There are excellent data correlating complex PVCs with mor­ same factors as any other arrhythmia. In coronary care units and tality in a number of large studies and hence the "PVC suppres­ in survivors after MI there is a certain correlation with early sion hypothesis" was developed. In other words, it was assumed mortality, usually due to sudden arrhythmic cardiac death (49- that suppression of these lethal triggers could prevent sud­ 51). Such arrhythmias during acute MI should be suppressed den death in survivors of acute MI. Antiarrhythmic drugs were with intravenous lidocaine or procainamide. Interestingly, re­ then defined clinically by their ability to suppress spontaneous lated symptomatology does not serve to distinguish benign from PVCs. Without good data, the hypothesis was generalized to malignant premature ventricular depolarizations. Although pre­ justify the suppression of ectopy in other disease states (52) and mature ventricular complex (PVC) frequency and complexity, even apparentiy normal individuals without statistical proof of particularly in the presence of left ventricular dysfunction, is risk. highly associated with risk of early mortality after hospital dis­ In the absence of clinical trials to determine the effect of PVC charge, chronic suppression of PVCs has not been shown to di­ suppression on survival, the clinical praclice prevailed. There minish the risk. were sporadic clinical data to suggest that suppression of PVCs Originally the clinical diagnosis of acute MI was almost syn­ did not prove efficacy for prevention of the more important clin­ onymous with sudden cardiac death; survivors were few. The ical goal of preventing sustained lethal tachyarrhythmias. ability to monitor cardiac arrhythmia and lo defibrillale and the Josephson and Horowitz (53) popularized the electrophysio­ development of specialized coronary care units and personnel logic technique of triggering, or supplying, PVCs in a clinical resulted in a significant population of survivors. Many of these laboratory to detect a clinical substrate which could sustain a le­ patients, however, remained at risk for sudden death over a pe­ thal tachycardia in patients with remote Ml or inducible sus­ riod of several years despite retum to a functional life-style. tained VT. Electrophysiologic studies after acute MI are not yet Studies to determine the predictors of risk were conducied by accepted in clinical centers in the United States. cardiologists and often funded by insurance firms. All studies Chronic suppression of such arrhythmias, if frequent and par­ showed that the most common cause of sudden cardiac death in ticularly if associated with runs of nonsustained VT, is probably survivors of MI was VT or ventricular fibrillation. The most re­ desirable. However, there is no proof that such chronic suppres­ liable predictor for risk stratification during periods of relative sion prolongs survival, and each oral antiarrhythmic agent is as­ health was presence of PVCs. Left ventricular dysfunction as sociated with side effects and toxicity in a large number of pa­ measured by the ejection fraction was also an independent pre­ tients. dictor. In the Cardiac Arrhythmia Suppression Trial, suppression of More delailed analysis of substrata, however, showed that the ectopy after Ml by type IC antiarrhythmic drugs was associated PVC was a somewhat nonspecific marker. Therapy directed at with increased mortalily (54,55). Therefore, neither flecainide all patients with PVCs would treat far more patients than ap­ nor encainide should be used for chronic PVC suppression after peared actually to be at risk. Several algorithms were developed MI. based upon frequency of PVCs and/or complexity. Because of the uncertainty about the indications, benefits, Complexity was defined by the presence of at least one of and risks of chronic antiarrhythmic therapy for high-risk survi­ .several criteria. One of these was the "R on T phenomenon" vors of MI, several randomized institutional trials are being con­ which describes occurrence of an early PVC on top of the T ducted: wave of the previous normal beat or in the vulnerable period The Coronary Artery Bypass Graft/Patch(CABG/Patch) trial which had been determined in animal studies. This represenled is designed to determine the efficacy of the automatic implant­ a period of time in the relatively refractory period when the cells able cardiovertor defibrillator (AICD) on all causes of mortality had repolarized enough to be captured by such an early trigger, or sustained ventricular arrhythmias in patients with low ejec­ yet the membranes had not yet achieved the normal resting po­ tion fractions and no previous episode of or sus­ tential. In these studies repetitive ventricular depolarizations, tained ventricular arrhythmia who are undergoing coronary ar­ nonsustained arrhythmia, and sustained VT or ventricular fibril­ tery bypass graft surgery. Quality of life and cost-effectiveness lation might result. substudies are being performed concurrently.

Henry Ford Hosp Med J—Vol 39, Nos 3 & 4, 1991 Management of Tachycardias After Ml—Webb 233 The Multicenter Automatic Defibrillator Implantation Trial 12, Baum RS, Alvarez H III, Cobb LA, Survival after resuscitation from out- (MADIT) is designed to determine if the survival of high-risk, of-hospital ventricular fibrillation. Circulation 1974;50:1231-5, low ejection fraction, patients with non- 13, Spodick DH, Frequency of arrhythmias in determined by Holier monitoring. Am J Cardiol 1984;53:842-5, sustained VT and electrophysiologically inducible VT who have 14, Ciaccheri M, Cecchi F, Arcangeli C, Dolara A, Zuppiroli A, Pieroni C, not yet experienced sudden cardiac death or sustained VT can be Occult thyrotoxicosis in patients with chronic and paroxysmal isolated atrial fi­ improved with AICD device therapy versus conventional medi­ brillation, Clin Cardiol 1984;7:413-6, cal management. The study will also include quality of life and 15, Smith TW, Serum and plasma cardiac glycoside concentrations: Clinical cost-effectiveness substudies. u,se and misuse. In: Smith TW, ed. Digitalis glycosides, Oriando, FL: Grune & Stratton, 1986:153-67, The Multicenter Unsustained Tachycardia Trial (MUSTT) is 16, Duhme DW, Greenblatt DJ, Koch-Weser J, Reduction of digoxin toxicity a North American study designed to determine if therapy guided associated with measurement of serum levels: A report from the Boston Collabo­ by electrophysiologic testing will reduce the risk of sudden car­ rative Drug Surveillance Program, Ann Intern Med 1974;80:516-9, diac death in patients with coronary artery disease and low ejec­ 17, Velebit V, Podrid P, Lown B, Cohen BH, Graboys TB, Aggravation and tion fraction who have nonsustained VT. The AICD device will provocation of ventricular arrhythmias by antiarrhythmic drugs. Circulation 1982:65:886-94, be used as adjunctive therapy in one limb of the study design. 18, Greenspan AM, Spielman SR. Webb CR, Sokoloff NM, Rae AP, Horo­ The AICD cost-effectiveness trial is designed to determine if witz LN, Efficacy of combination therapy with mexiletine and a type IA agent the AICD device, when used as the therapy of first choice for for inducible ventricular tachyarrhythmias secondary to coronary artery disease. both MI patients and those who have survived cardiac arrest, is Am J Cardiol 1985:56:277-84, a more effective treatment modality than conventional medical 19, Griffith L, Platia E, Ord S, Reid P, Persistent /fi­ brillation—a possible adverse interaction between flecainide and class IA anti­ evaluation and therapy. arrhythmic dmgs, J Am Coll Cardiol 1984:13:583, At Henry Ford Hospital a study is currentiy being conducted 20, Kugler JD, Garson A Jr, Gillette PC, Electrophysiologic effect of digitalis to assess psychological implications of AICD therapy as op­ on sinoatrial nodal function in children. 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