November 1, 1984 THE AMERICAN JOURNAL OF CARDIOLOGY Volume 54 1155

Emergency Differentiation of Vasovagal Syncope from Stokes-Adams Attack

IAN HAMILTON CRAIG, PhD, FRACP

In the U.S.A. alone, 25,000 new cases of Stokes-Adams (S-A) syncopal attacks occur per year. 1 The incidence of vasovagal syncope is likely to be far greater than that of S-A attacks, in that vasovagal syncope accounts for approximately 55% of all cases of syncope. 1 In the el- derly, emergency differentiation of S-A attacks from vasovagal syncope may be difficult because of the oc- currence of pallor, sweating, loss of consciousness and bradycardia in both disorders. Differentiation may be particularly difficult in the absence of the electrocar- diograph and the stethoscope. Herein, I describe pu- pillary constriction in vasovagal syncope and pupillary dilatation in S-A attack, and suggest that the "pupil sign" may be useful in the emergency differentiation of the 2 conditions.

Case 1: A 73-year-old man became light-headed, pale and sweaty while eating dinner. He had recovered uneventfully from a myocardial infarction 10 years previously. Several similar fainting episodes had occurred in the previous 6 months, each lasting approximately 2 minutes. At the time of the latest episode, he was taking metoprolol (50 mg/day) for systemic hypertension.

On examination, he was unresponsive to commands, pale, sweating profusely and breathing stertorously. His pupils were small and equal. The radial pulses were impalpable.

The patient was immediately laid fiat. After approxi- mately 30 seconds, a weak, thready radial pulse was pal- pated, at a rate of approximately 40 beats/min. The patient's conscious state then rapidly improved. The radial pulse rapidly increased in both rate and volume, and the pupil size increased progressively from small to moderately dilated. During the initial return to consciousness, the pupils alter- nately changed from a state of constriction to one of moder- ate dilatation. They remained equal throughout the syncopal episode and during recovery. Thirty minutes later, the pa- tient complained of left anterior chest pain of a constricting nature, with radiation to the left arm and shoulder. He was immediately admitted to a hospital, where he was found to have a blood pressure of 130/60 mm Hg and pulse rate 60 beats/min; the electrocardiogram showed evidence of an old inferior myocardial infarction. Sinus rhythm was present, with no evidence of either intraventricular conduction defect or heart block, Cardiac enzyme levels were normal, and no further electrocardiographic changes occurred. The patient was discharged on the following day with a diagnosis of vasovagal syncope for the initial episode.

Case 2: A 65-year-old man collapsed in circumstances similar to those of case 1. He had recovered from a myocardial infarction several years previously, and was taking no medication at the time of his attack. The radial pulse was unrecordable. The patient was unresponsive to commands, was cold and sweaty and the pupils were widely dilated. After the patient had been laid flat there was no improvement in his conscious state, and stertorous respirations continued. The radial and carotid pulses remained impalpable, the pupils remained widely dilated and the patient became cy- anotic. External cardiac massage and mouth-to-mouth ventilation were commenced. An ambulance was called, and

From the Department of Medicine, Royal Adelaide Hospital and the University of Adelaide, Adelaide, South Australia 5000. Manuscript received May 15, 1984, accepted July 5, 1984.

an electrocardiogram showed high-degree atrioventricular block with nonspecific ST-T-wave changes. The patient was admitted to the coronary care unit and was shown to have complete heart block for which a permanent pacemaker was inserted. A diagnosis of S-A attack was made for the initial episode.

Vasovagal syncope {also known as either vasode- pressor syncope or the common faint) is the commonest cause of transient loss of consciousness. 1 It occurs in the upright posture as a result of emotional stress, and is aggravated by hunger, fatigue, crowding and heat. Symptoms include nausea, a sensation of impending loss of consciousness, weakness, visual difficulty and impaired hearing. 1 The syndrome is caused by relative cerebral hypoperfusion, which results from a decline in cardiac output associated with peripheral vasodilata- tion. Under normal conditions, peripheral vasodilata- tion is accompanied by a compensatory increase in heart rate and cardiac output. This does not occur in vaso- vagal syncope, 1 presumably because of inhibition of sympathetic outflow or of stimulation of parasympa- thetic (vagal) outflow.

S-A attacks consist of "giddiness, fainting and tem- porary loss of consciousness, with or without convulsive seizures, during transition from partial to complete atrioventricular block. ''2 Sudden death may occur during the transition in cardiac rhythm, either because of ventricular fibrillation or asystole. 2 The syndrome may therefore be regarded as a "superimposed" ar- rhythmia at the time of loss of consciousness, rather than due to heart block as such. 1 Arrhythmia-induced syncope is an appropriate description. 1 Clinical clues to the diagnosis of S-A attacks include the following evidence of complete heart block: variation in the in- tensity of the first heart sound, a jugular venous pulse rate greater than the apical rate, an apical rate of 20 to 40 beats/min with little response to exercise and atro- pine, and independent movement of atria and ventricles on fluoroscopic examination. 1 Causes of complete heart block, and therefore of S-A attacks, include electrolyte disturbance, antiarrhythmic drugs, and structural ab- normalities of the conduction system, particularly due to coronary heart disease. 1

Little data are available regarding the emergency differentiation of cardiac causes of syncope from vaso- vagal syncope. In 1973, Burch 3 wrote that a "patient who suddenly develops unconsciousness due to cardiac arrest often develops a marked redness or blush due to vasodilatation. On the other hand, patients with the common forms of syncopal episodes, gradually or rela- tively slowly become extremely pale to ashen gray, sweaty, weak, giddy and then faint." Often, the patient's pupils are dilated in other forms of primary cardiac syncope associated with sympathetic stimulation, in- cluding cardiac arrest. The "pupil sign" may therefore be useful in the early differentiation of patients with vasovagal syncope from those with S-A attack and cardiac arrest.

References

1. Sobel BE, Roberts R. Hypotension and syncope. In: Braunwald E, ed. Heart Disease. Philadelphia: WB Saunders, 1980:982-963.

2. Belier S. Sinoa~'ial and atrioven~icular blocks. In: Luisada AA, ed. Cardiology. New York: McGraw-Hill, 1959;11,48-49.

3. Burch GE. A sign of cardiac arrest. Am Heart J 1973;86:138.