Rescue 5 arrives at the home of a 71-year-old man whose family called 9-1-1 when they found him unresponsive. On arrival, EMS finds the elderly male lying in bed with his eyes closed, unresponsive to voice or touch. He’s breathing adequately with no airway problems. The family says he’s been aphasic and unable to walk since a stroke one year ago, but was normally alert and able to say his name and interact with them. They say he fell asleep about two hours ago, and they were unable to wake him up immediately prior to calling 9-1-1.
Initial assessment reveals faint radial pulses, a carotid pulse of 48 bpm, a systolic blood pressure (BP) palpated at about 80 mmHg and a pulse oximetry reading of 94% on room air. Additional assessment reveals no evidence of trauma. His lungs are clear bilaterally, heart rate is slow and regular and gaze is disconjugate, but his pupils are equal and reactive to light bilaterally.
He keeps his eyes shut, remains nonverbal and reacts to painful stimuli with weak but appropriate withdrawal. He has occasional purposeful movements of his limbs and a mild tremor of his hands and seems to be moving his right side more than his left.
A complete Cincinnati Stroke scale can’t be assessed. ECG monitoring shows sinus bradycardia, and his finger stick glucose is 86 mg/dL. Crew members place the patient on high-flow oxygen with a non-rebreather mask and start an antecubital IV.
The family states that the patient has had residual left-sided weakness since his stroke, plus a history of atrial fibrillation, hypertension, Parkinsonism and hyperlipidemia. There’s no history of seizures or cardiac ischemic disease. He has no allergies. His daily medications (sotalol, lisinopril, omeprazole, Plavix, amlodipine and benazepril) were taken eight hours earlier. The family says they haven’t seen any seizure activity nor witnessed any recent falls or injuries.
One dose of atropine 0.5 mg IV is administered once for the sinus bradycardia with altered mental status (AMS) and hypotension. The patient responds well; his heart rate rises to 80 bpm and his BP to 135/80. He opens his eyes, his spontaneous movement increases, and he’s able to whisper his name. He denies any pain or trouble breathing.
As EMS gave a report at the emergency department (ED) 10 minutes later, the EMS cardiac monitor began to show a narrow, complex, irregular tachycardia at about 170 bpm, and the ED monitor showed the same tracing (see Figure 1).
His BP increased to 144/85 with RR 18 and temp 36.3o C. His mental status remains good, and his lungs remain clear to auscultation. Pulse oximetry reads 98% when he’s switched to a nasal cannula at 2 L/min flow.
Two monitors and the 12-lead appeared to show a rapid irregular rhythm with mild widening of the QRS duration at 112 ms (0.11 sec), which the computer read as “atrial fibrillation with premature aberrantly conducted complexes” plus diffuse ST- and T-wave abnormalities.
Although a tachyarrhythmia at this rate isn’t likely to be tolerated for long by an elderly patient, this patient’s BP and mental status were hemodynamically stable. Therefore, there was time to determine what was wrong before administering medication or electricity. Further, this patient was in trouble with symptomatic bradycardia only minutes earlier, so giving medication to slow the heart rate could have been risky.
The ED physician took the most appropriate next step—he touched the patient and checked the pulse. The radial pulse was regular and strong at 72 bpm, as was the carotid pulse and auscultation of the heart rate at the apex. The nurse placed the patient on an older model transport monitor, which clearly showed the NSR among very tiny spikes of artifact. The atropine that was administered by EMS resulted in improved heart rate, and also caused much stronger forearm tremors that changed the monitor. A repeat 12-lead ECG done a few minutes later was identical to the first, except that now the computer read, “***Suspect a lead reversal, interpretation assumes no reversal … Undetermined rhythm … Inferior-posterior infarct, possibly acute … ** ** ACUTE MI ** **”
Careful scrutiny of leads V2–V5 on the 12-lead ECG reveals the best clues to the correct interpretation of this patient’s rhythm: There appear to be two separate “rhythms” with two different “QRS” complexes. The patient’s real cardiac rhythm is a much taller “RS” complex at a regular rate of about 70 bpm with no definite P wave in front of it, while there’s also a faster, smaller amplitude spike at about 170 bpm (slightly irregular, easily mistaken for a large P wave)—these are his tremor (see Figure 2, p. 38). Occasionally, the two rhythms coincide, or are so close together that the “rate” would be too fast to be coming from the patient’s own heart.
Tracings like this are nearly impossible for a computerized interpretation program to read accurately for either cardiac rhythm or ischemia. Unfortunately, the computer may give a wrong interpretation rather than stating “undetermined rhythm” or “possible ________ but clinical correlation required.” It’s impossible to determine this patient’s real heart rate from the cardiac monitor or its computer reading. Only a hands-on approach will work—palpating the patient’s pulse is mandatory.
Although it’s appropriate to review and consider the computer’s ECG interpretation, it’s crucial to use the clinical information from the hands-on assessment of the patient to see if that reading makes sense. Here, it clearly didn’t.
EMS management of this patient was appropriate, with rapid assessment, identification and treatment of hemodynamically significant bradycardia as the most likely cause of his AMS. This was an unstable bradycardia, so treatment choices are atropine or external pacing (or both, if necessary). Important other causes of AMS (hypoxia, hypoventilation, hypoglycemia, acute stroke, head trauma, seizures, medications) were also addressed in the bedside evaluation and in history-taking.
Given the hypotension and subsequent improvement with atropine, providers didn’t need to consider further causes. The patient’s history of hypertension underscores the significance of his low BP, while the patient’s history of atrial fibrillation was actually misleading after his monitor changed to a rapid pseudodysrhythmia—begging the question, did he ever really have atrial fibrillation, or was it misinterpretation?
In fact, the final hospital record interpretation of this 12-lead ECG by the overreading cardiologist was “atrial fibrillation with rapid ventricular rate with premature ventricular or aberrantly conducted complexes”!
Potential causes of this patient’s bradycardia include his beta blocker (sotalol) and calcium channel blocker (amlodipine), hypoventilation (best checked with capnography), myocardial ischemia (checked a 12-lead ECG in the field as soon as time permits) and other diagnoses best evaluated further in the ED (e.g., cardiac conduction system disease, other cardiac pathology, hypothyroidism, endocrinopathy, infection).
Causes of False ECG Readings
Remember that “pulse rate” is not a number on a monitor—it’s measured by hands-on assessment of the patient’s actual pulse. Several sources of artifact can cause “pseudodysrhythmias.” Patient movement, whether voluntary or involuntary, is the most frequent cause. Tremors are involuntary movements, and the true pulse rate is easiest to determine at the carotid or femoral artery, because the rapid hand/arm movements make it hard to be sure of the radial pulse.
Typically, Parkinsonian “pill-rolling” tremors are worse at rest and cause very fast but tiny “blips” on the ECG that are easily separated from the patient’s real rhythm; shivering artifact looks similar. This patient’s tremor was much coarser than most Parkinsonian tremors, probably due to his prior stroke. Familial and senile tremors are also rhythmic and rapid; they get worse with purposeful movement, such as reaching for an object.
Other types of tremors (cerebellar, chorea, hemiballismus) are very coarse with sudden jerks, with a slower rate and a much taller “complex” that’s easy to mistake for isolated ventricular beats or V-tach if the tremors occur in a short burst.
Nearby equipment using AC current (60 cycle-per-second interference) or DC power may cause electrical artifacts. Interestingly, older generation monitors (CRTs) generally have 60 cycle interference but give higher fidelity waveform tracings, while current generation monitors have different types of electrical artifact, and the tracing on the screen may not be as good as the actual printed strip from that same monitor. When in doubt, print it out, and see what the rhythm strip says—and make sure to palpate the patient’s actual pulse.
Electrical artifact resembling short bursts of V-tach and even torsades des pointes may be seen, so develop a “knee-jerk” reflex of immediately checking the patient’s pulse to correlate with the screen. During external pacing with combination defib/pacing/monitoring pads, current dispersion through the pads’ gel produces artifact that looks like a big wide QRS complex, the amplitude (height) of which varies in proportion to the current—again, it’s crucial to touch the patient to check a femoral or distal pulse. The pulse must correlate with the “beat” on the monitor, or it’s not from the patient’s heart.
It’s possible for loose connections to cause a variety of non-biologic blips. Electrode problems are common in the field, and performance is best when electrodes are attached to dry, non-hairy skin away from bony prominences. Lead misplacement (of the precordial electrodes) and misconnections (limb lead reversals) are also a common cause of misdiagnosis of cardiac problems and remind us to take the time to do the 12-lead correctly.
There are many clues to pseudodysrhythmias: The best is the lack of correlation of the “QRS” complexes with the patient’s pulse when palpated at the same time. The absence of symptoms or hemodynamic instability during a serious looking “arrhythmia” should prompt immediate consideration of artifact. A patient who’s alert, calm and asymptomatic is probably not in V-tach or rapid atrial fibrillation.
Look for correlation with visible body movements, such as tremors or shivering. Print out rhythm strips in several different leads, or 12-leads, to look closely for normal-appearing QRS complexes appearing among the dysrhythmic beats or at least for visible notching superimposed on the strip consistent with an underlying true heart rhythm marching through the pseudodysrhythmia.
Double check all lead attachments to the patient and cable connections, ensure that the lead wires and cables aren’t moving; and move away from or shut off other electrical equipment and repeat the ECG.
Also, be sure to print out strips of true arrhythmias or suspected artifact to give to the receiving physician—these are the key to correct diagnosis and treatment, especially when the abnormality is gone by the time the patient arrives at the ED. JEMS
Kathleen Schrank, MD, FACEP, FACP, is a professor at the University of Miami Miller School of Medicine, chief of the University of Miami Division of Emergency Medicine and an emergency medicine physician at Jackson Memorial Hospital. She has served as the EMS medical director for City of Miami Fire Rescue since 1988 and for the Village of Key Biscayne Fire Rescue since 1994. She can be contacted at email@example.com.
1. Chase C, Brady WJ. Artifactual electrocardiographic change mimicking clinical abnormality on the ECG. Am J Emerg Med. 2000;18:312–316.
2. Harrigan RA. Electrode misconnection, misplacement, and artifact. Emerg Med Clin N Am. 2006;24:227–235.
3. Knight BP, Pelosi F, Michaud GF, et al. Clinical consequences of electrocardiographic artifact mimicking ventricular tachycardia. NEJM. 1999;341:1270–1274.
4. Llinas R, Henderson GV. Tremor as a cause of pseudo-ventricular tachycardia. NEJM. 1999;341:1275.
This article originally appeared in May 2010 JEMS as More Than a Number :
Treat the patient, not the monitor.