Misdiagnosis in Patient With Dizziness, Leg Weakness

What's the source of the unusual electrocardiogram (ECG) findings in a patient presenting with dizziness and limb weakness? That's the mystery posed in a recent case report.

The diagnostic challenge began when a patient in their early 70s showed up at the emergency department with leg weakness and dizziness, both lasting a week in duration, according to Guilan Zhai, MD, of the First Affiliated Hospital of Jinzhou Medical University in China, and colleagues in JAMA Internal Medicine.

The patient's medical history included high blood pressure for the past 7 years and diabetes for the past 10 years. They did not smoke, drink alcohol, or use illicit drugs. An initial assessment revealed a tremor in their left hand, postural instability, and bradykinesia.

At the time of admission, the patient's blood pressure was 149/76 mm Hg and heart rate was 92 beats per minute. Findings from a complete blood count and electrolyte panel, and assessments of kidney and liver function and D-dimer levels, were all within normal limits.

An ECG performed at that time was interpreted by an emergency department resident as suggestive of ventricular tachycardia.

However, clinical examination showed no evidence of heart palpitations or hemodynamic instability; the patient had normal heart sounds and pulse rate; and assessments of pulse oxygen saturation waveform and ventricular activity were normal. The senior clinician suggested performing a second ECG while restraining the patient's left upper arm to keep it from shaking.

The team explained that the ECG at admission showed a narrow QRS complex rhythm (sinus rhythm) in lead II, and a wide QRS complex tachycardia that reflected ventricular tachycardia in the other limb leads. Lead I had clear evidence of narrow QRS complexes buried in repetitive electrical activity with a large amplitude, and the precordial leads (e.g., lead V6) revealed flutter waves and regular tall and narrow QRS complexes.

Analysis of the repeat ECG showed normal sinus rhythm. Clinicians concluded that the ECG changes were due to muscle tremors in the left upper arm, a type of tremor that is often associated with Parkinson's disease; these pseudowaves are no longer evident when the shaking extremity is held still, or the electrode is moved from the affected limb to the torso.

The team diagnosed the patient with acute cerebral infarction and Parkinson's disease. After receiving conservative treatment, the patient's condition improved and they were discharged from the hospital.

Discussion

Clinicians presenting this case of correct diagnosis impeded by an ECG artifact explained that these abnormal findings -- caused by sources other than the electrical activity of the heart -- are often seen in evaluation and monitoring of patients in the emergency, intensive care, or prehospital settings.

This patient's ECG findings were due to muscle tremors that, except for lead II, appeared to be ventricular tachycardia in the limb leads and atrial flutter in the precordial leads, Zhai and team explained; they noted that "misinterpreting these artifacts can mean unnecessary or even dangerous treatment or intervention."

A study of tremor-induced artifacts in 100 outpatients with parkinsonian resting tremor found a high frequency of artifacts in Parkinson's patients, with evidence of baseline undulation in 78% of patients and atrial flutter/fibrillation or ventricular tachycardia mimics in 11% of patients. Patients with high tremor scores, as judged by a neurologist, were more prone to develop atrial flutter/fibrillation or ventricular tachycardia mimics.

ECG artifacts are generally categorized by their cause: physiological, i.e., due to muscle activity, or non-physiological. In addition to a patient's motion, ECG artifacts may be caused by tremors, shivering, and convulsions, the authors explained, since all muscle contractions are generated by the flow of electrically charged ions, which in turn "produces a signal that appears on the ECG as rapid spikes arising simultaneously with the muscle contraction."

The frequency of a typical parkinsonian tremor is 4 to 6 Hz, about 240 to 360 times per minute at rest, comparable to that associated with atrial flutter and ventricular tachycardia, Zhai and colleagues noted, producing artifacts mimicking ventricular tachycardia at a high voltage, and atrial flutter at a low voltage.

Thorough analysis of these signals can assist clinicians in identifying and eliminating the cause of the artifact, they added; the following sources of electrical differences are compared, as described by the Einthoven triangle theory:

• Lead I: right and left arms
• Lead II: right arm and left leg
• Lead III: left arm and leg

This means that when tremors originate from the muscles from the left arm, lead II between the right arm and left leg remains normal. When tremors originate from the right arm, lead III between the left arm and leg remains normal. When the tremors originate from the left leg, lead I between the left and right arms remains normal.

Muscular tremors can also cause artifacts in the precordial leads, Zhai and colleagues noted, "because the central terminal, which constitutes the negative pole of the unipolar leads, is produced by connecting the 3 limb electrodes via a simple resistive network to provide an average potential across the body." Thus, muscular tremors that originate from a single limb will leave only one limb lead (I, II, or III) unaffected.

The authors identified this as "the most important and simplest method for detecting the ECG interference caused by muscular tremors originating from a single limb." They noted that since artifacts were generated, this patient's left arm tremor, lead II, showed normal rhythm. "In addition, the rate of suspected ventricular tachycardia in this patient was approximately 300 per minute, and R waves were visible through the abnormal rhythm in lead I, which further demonstrated that the suspected ventricular tachycardia was actually pseudo-arrhythmia," they wrote.

They described several clinical characteristics that help identify cases of pseudo-ventricular tachycardia: patients with no evidence of palpitations or hemodynamic instability, those who have normal heart sounds and pulse, and those whose pulse oxygen saturation waveform is normal.

Furthermore, three ECG signs can be used to differentiate pseudo-ventricular tachycardia from ventricular tachycardia, all of which applied to the current patient, Zhai and team noted. Pseudo-ventricular tachycardia is characterized by the presence of:

• Sinus sign, with sinus rhythm evident in one lead of leads I, II, and III
• Spike sign, i.e., small regular or irregular peaks evident between wide QRS complexes
• Notch sign, i.e., overlapping notches in the artifact that coincides with the sinus cycle length

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