EDITORIALS

Diagnostic Considerations in Electromechanical HOWARD

S. FRIEDMAN,

MD,

Dissociation

FACC

Bronx and New York, New York

Cardiac electromechanical dissociation in the intact animal refers to a phenomenon in which adequate electrocardiographic complexes are recorded when effective cardiac output has ceased. Such findings in man are almost invariably associated with a fatal outcome although one can observe this phenomenon in potentially treatable disorders. Recognition of these disorders on the basis of certain clinical and electrocardiographic findings may be of clinical importance. Three kinds of hemodynamic alterations can produce electromechanical dissociation: inadequate preload, excessive (obstructive) afterload and depressed cardiac muscle or “pump” performance. A precipitous decrease in preload leading to electromechanical dissociation can occur in exsanguinating hemorrhage, an inflow-obstructing atria1 myxoma or acute cardiac tamponade; severe outflow obstruction producing electromechanical dissociation can occur in pulmonary or aortic stenosis and massive pulmonary embolism; and cardiac “pump” dysfunction with electromechanical dissociation can occur as a result of a diffuse myocardial process, extensive ventricular asynergy or disruption of the integrity of the heart itself, for example, in rupture of a panillary muscle or the interventricular septum. The clinical and electrocardiographic features that distinguish the common causes of electromechanical dissociation are shown in Table I. When electromechanical dissociation is associated with tachycardia, pump failure is not the only explanation; hemorrhage and massive pulmonary embolism are alternative possibilities. These two disorders can be distinguished by recording a venous pressure. When an acute massive hemorrhage produces electromechanical dissociation, venous pressure will be decreased, whereas in massive pulmonary embolism it will generally be increased.

From the Veterans Administration Hospital, Bronx, N. y. and the Department of Medicine, the Mount Sinai School of Medicine, New York, N. Y. Address for reprints: Howard S. Friedman, MD, Cardiac Section, Veterans Administration Hospital, 130 W. Kingsbridge Rd.. Bronx, N. Y. 10468.

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Another clue during a cardiac arrest that might suggest an occult exsanguinating hemorrhage is the apparent response to vasopressors only when these agents are administered as a “wide-open” infusion. When the rate of fluid administration is reduced, blood pressure abruptly disappears. In this situation, it is probably the acute volume expansion rather than the vasopressor that is maintaining blood pressure. When the triad of electromechanical dissociation, tachycardia and abdominal distension is present, a ruptured abdominal aneurysm should be considered. In three cardiac arrests I observed, this triad was present and autopsy confirmed the diagnosis of ruptured abdominal aneurysm. When electromechanical dissociation is associated with bradycardia, activation of a vagally mediated depressor reflex is a likely possibility.’ In fact, the occurrence of sinus bradycardia with hypotension should suggest either a primary vagal effect or an inappropriate heart rate response to a decrease in blood pressure. Such blunted heart rate responses are observed in the “sick sinus syndrome,” or after treatment with beta- or ganglionic blocking agents. The sudden occurrence of electromechanical dissociation and bradycardia, especially in a clinical setting that might be associated with acute cardiac compression-for example, after cardiac surgery, chest injury or myocardial infarction-should suggest acute cardiac tamponade.2 Although the occurrence of electromechanical dissociation and bradycardia was originally described in the setting of cardiac studies3 have demonrupture,2 recent experimental strated that the bradycardia of cardiac rupture is a characteristic finding in the late phase of acute cardiac tamponade in dogs. Vagotomy3 or administration of atropine’ reverses the bradycardia, and in the vagotomized dog acute cardiac tamponade does not produce bradycardia until anoxic slowing ensues.3 These findings appear to be more than a physiologic curiosity associated with experimental cardiac tamponade. Administration of atropine at the time of the bradycardic effect increased left ventricular systolic pressure, improved various indexes of left ventricular performance and permitted a greater pericardial volume before the

Volume 36

EDITORIALS

TABLE

I

Clinical

and Electrocardiographic

Hemodynamic Alteration

Findings

of the Common

Disorders

Causes of Electromechanical Venous Pressure

Heart Rate

Dissociation

Associated

Electrocardiographic

Findings

Exsanguinating hemorrhage

Tachycardia

Low

Acute cardiac tamponade

Bradycardia

High

Low QRS voltage; prominent P waves; QRS axis shift; S-T and T changes; electrical alternans

Acute outflow obstruction

Pulmonary

Tachycardia

High

Findings of right-sided

Pump failure

Acute myocardial infarction

Tachycardia or Bradycardia

High

Frequently associated with atrioventri cular block or intraventricular conduction abnormality, or both

Reduced

preload

embolism

Cardiomyopathy

t

occurrence of electromechanical dissociation.l Such changes were not produced by atria1 pacing at a rate comparable with that produced by administration of atr0pine.l These experiments also demonstrated other electrocardiographic features that might assist in the diagnosis of cardiac tamponade4: (1) QRS complex voltage recorded on surface leads decreased when intracardiac voltages increased; (2) P wave voltage did not change until the late phases of tamponade; (3) left axis deviation occurred in 6 of the 12 dogs studied and electrical alternans in 3; (4) striking T wave inversions and S-T junction elevations occurred, especially with rapid rates of infusion;,and (5) S-T segment elevations developed when tamponade was prolonged. Except for alteration of the QRS axis and the dissimilar effect of cardiac tamponade on the QRS complex and P wave, these findings have previously been observed in clinical

t

overload

acute cardiac tamponade.2 Thus, when these electrocardiographic findings are observed with electromechanical dissociation and bradycardia the diagnosis of acute cardiac tamponade is a possibility. Clinical implications: It should be clear from this discussion that the finding of electromechanical dissociation during a cardiac arrest is not necessarily a hopeless clinical situation. Its occurrence with tachycardia might indicate an exsanguinating hemorrhage or a massive pulmonary embolism, whereas its occurrence with bradycardia might indicate cardiac tamponade, especially when accompanied by the electrocardiographic findings presented here. Thus, although electromechanical dissociation is frequently associated with extensive, irreversible cardiac injury and a grave prognosis, such findings can also be produced by conditions whose recognition and prompt treatment can result in a favorable outcome.

References 1. Friedman HS, Lajam F, Games JA, et al: Experimental acute cardiac

tamponade. II. Hemodynamic effects (abstr). Clin Res 23:184A, 1975 2. Friedman HS, Kuhn LA, Katz AM: Clinical and electrocardiographic features of cardiac rupture following acute myocardial infarction. Am J Med 50:709-720, 1971

3. Friedman HS, Games JA, Tardlo AR, et al: The electrocardiographic features of acute cardiac tarnponade. Circulation 50~260-265, 1974 4. Friedman HS, Lajam F, Calderon J, et al: Experimental acute cardiac tamponade. I. Electrocardiographic features (abstr). Clin Res 23:183A. 1975

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