PARKINSONS TREMOR MIMICKING MULTIPLE ARRYTHMIAS. M.F. Jhandir 1 , D. Brotman 1 ; 1 Cleveland Clinic Foundation, Clevland, OH LEARNING OBJECTIVES: 1. Rule out Parkinson's tremor first when pateints with Parkinson's disease present with symptoms or electrocardiogram changes suggestive of tachyarrythmia. 2. Appreciate that holding anti-Parkinon's medications can be a simple provocative manuever to determine whether the electrocardiogram abnormalitites are of noncardiac origin in such patients. CASE INFORMATION: A 75 year old nursing home resident with a history of coronary artery disease and Parkinson's disease presented to the emergency department for evaluation of pre-syncopal episodes and hypotension. He had a three day history of feeling lightheaded and unsteady while standing but had no true syncope. He denied chest pain, dyspnea and palpitations. There was no prior history of documented arrhythmia. His medications included aspirin, donepezil, levodopa/carbidopa, and lisinopril. On physical examination, he was not in acute distress. Heart rate was 68 with occasional premature beats. Blood pressure was 65/45 bilaterally with orthostatic changes. Cardiac exam was without murmurs or gallops. Neck veins were flat, lungs were clear and there was no peripheral edema. He had cogwheel rigidity but no tremor. The admission ECG showed sinus rhythm with occasional premature ventricular contractions. After intravenous crystalloids were given, the blood pressure normalized, and he was admitted to a monitored hospital bed for further observation. The following morning, the intern was called to the patient's bedside because of an apparent supraventricular tachycardia (SVT)(figure 2). Despite his abnormal ECG, the patient was asymptomatic, with a pulse of 64, and a blood pressure of 160/90. He had developed a pronounced bilateral upper extremity resting tremor at about 5 Hz, but otherwise his examination was unchanged. After the patient received his morning anti-Parkinson medications, the tremor resolved and his ECG returned to baseline. In order to prove that the tremor was responsible for the ECG changes, the next dose of levodopa/carbidopa was held; his tremor returned as did his pseudo-atrial flutter. DISCUSSION: Because the classic Parkinson's tremor has a frequency of 4±5 Hz (260±300 cycles/min), it is not surprising that its electrical potentials on ECG can mimic atrial flutter, as in our case. Furthermore, Parkinson's disease is commonly associated with orthostatic hypotension and syncope, which may in turn prompt cardiac evaluations. Although there are previously documented cases of Parkinson's tremor leading to ECG artifacts resembling wide complex tachyarrhythmias such as ventricular tachycardia, we know of no other reports of Parkinson's tremor mimicking atrial flutter or SVT. Careful review of our patient's rhythm strip reveals that there are buried QRS complexes within the pseudo-SVT complexes (figure 2). The importance of correlating the ECG with the clinical exam cannot be overemphasized in this case, as the heart rate during the pseudo-SVT was normal, and the ECG artifacts were present only when the patient was tremulous. Finally, our case illustrates that if a patient with Parkinson's disease has transient ECG abnormalities suggestive of tremor-induced artifact, holding medicines can be a simple provocative maneuver to determine whether the ECG abnormalities are of non-cardiac origin. We conclude that Parkinson's tremor should be thoroughly ruled out when a patient with Parkinson's disease presents with symptoms and ECG changes suggestive of a tachyarrhythmia.