Diagnosis and Management of Tachycardias After Myocardial Infarction

Henry Ford Hospital Medical Journal Volume 39 Number 3 Article 15 9-1991 Diagnosis and Management of Tachycardias After Myocardial Infarction Charles R. Webb Follow this and additional works at: https://scholarlycommons.henryford.com/hfhmedjournal Part of the Life Sciences Commons, Medical Specialties Commons, and the Public Health Commons 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 arrhythmias due to ischemia as well as intracellular ion, merely correcting the serum potassium may chronic arrhythmias such as chronic atrial fibrillation 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 arrhythmia 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 tachycardia (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 Heart 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 atrial fibrillation 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 angina 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 titrated between 2 to 4 pg/min. Sustained agents are effective for suppression of ectopy in about 60% of arrhythmias such as ventricular fibrillation 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 Pericarditis (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- heart failure 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. Digoxin 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. Bradycardia and heart combinations of Vaughn-Williams class lA and IB agents (18). block

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