An 80-year-old woman presents to the emergency department (ED) with chest tightness and palpitations over the past three hours. She called her primary care provider to make an appointment, but was prompted to go directly to the ED. She was transported by her granddaughter, who remains with her. 

The patient tries to downplay her symptoms as “a case of the flu”; however, the granddaughter states that for the past two weeks, her grandmother has had increased shortness of breath, dyspnea on exertion, a six-pound weight gain, and bilateral lower extremity edema not previously present. The patient denies fevers, chills, productive cough, syncope, or near-syncope. 

Medical history is remarkable for a bioprosthetic aortic valve replacement (21-mm Carpentier-Edwards pericardial valve) in May 2008 for critical aortic stenosis, and paroxysmal atrial fibrillation requiring cardioversion on two separate occasions (the last, six months ago). 

Her most recent echocardiogram (one year ago) was remarkable for bioprosthetic aortic valve dysfunction with a peak gradient of 60 mm Hg across the valve, well preserved left ventricular systolic function without segmental contraction abnormalities, and mild diastolic dysfunction with a left ventricular ejection fraction estimated to be 55%. Associated findings included mild to moderate mitral regurgitation and left atrial enlargement. Her right heart and central venous pressures were normal.

Medical history is also remarkable for a recent (four months ago) episode of shingles involving her left chest and flank. The patient is a retired librarian, is self-sufficient, and lives alone. Her granddaughter lives across the street from her and checks on her daily. The patient has never smoked and has an occasional glass of wine.

Her current medications include furosemide, pravastatin, metoprolol XL, a multivitamin, and sublingual nitroglycerin as needed. Of note, she did not use the sublingual nitroglycerin prior to presenting to the ED, and upon inspection, the prescription is long past its expiration date.

Physical examination reveals a blood pressure of 92/66 mm Hg; pulse, 100 beats/min; and respiratory rate, 18 breaths/min. The patient is afebrile. Pertinent physical findings include jugular venous distention to the level of the jaw, lungs that are clear to auscultation, a musical grade III/VI systolic murmur best heard at the apex with radiation to the carotid arteries bilaterally, a benign abdominal exam, and 3+ pitting edema to the level of the mid-thigh bilaterally. The neurologic exam is grossly intact.

Suspecting another episode of paroxysmal atrial fibrillation, you order an ECG. The ECG technician arrives, connects the electrodes to the patient, and promptly calls for help as the patient’s chest tightness returns and she becomes lightheaded and dizzy. You arrive promptly and are handed the ECG, which shows: a ventricular rate of 156 beats/min; PR interval, 190 ms; QRS duration, 138 ms; QT/QTc, 362/583 ms; P axis, –5°; R axis, 114°; and T axis, 0°. What is your interpretation of this ECG?

ANSWER

This ECG reveals sinus tachycardia transitioning to a wide complex tachycardia. A fusion complex is present, suggesting this is ventricular tachycardia. T-wave abnormalities in the inferior leads are present and suggest inferior ischemia.

There are two items of note that one must be aware of in order to accurately interpret this ECG. Normally, the computer measurements of heart rate and intervals are correct and often more accurate than a clinician can manually measure. These are typically measured as an average of all beats taken during the 12-second analysis prior to printing. However, when the rate abruptly changes during the analysis of the heart rate and rhythm, these measurements become inaccurate.

In this ECG, the computer notes the rate to be 156 beats/min; however, careful analysis of the sinus tachycardia prior to onset of ventricular tachycardia shows the rate is 107 beats/min, and the ventricular tachycardia rate is 188 beats/min.

The second item of note is that the ECG instrument measures all leads simultaneously over a 12-second period and separates them into the appropriate leads for printing. Hence, the progression from leads I to aVR to V₁ to V₄ represents a continuous tracing, in a similar fashion to the rhythm strip in lead II at the bottom of the page. Knowing this can help determine the presence of fusion complexes, as well as atrioventricular dissociation between QRS complexes and P waves indicative of ventricular tachycardia.

This patient developed hemodynamically significant ventricular tachycardia during the 12-second interval required for a 12-lead ECG analysis, a rare occurrence.  She was treated with DC cardioversion, which resulted in a return to normal sinus rhythm.