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ECG Challenge: Dyspnea is painless, but progressive; lungs are clear, heart sounds normal, peripheral pulses strong. What does the tracing show?
A 40-year-old man with a history of diabetes, hypertension, and cigarette smoking but no known coronary disease presents to your local ED with painless dyspnea on exertion, which he has had for the past 3 days. Today he couldn’t even walk the golf course with his friend and had to use a golf cart, which he has never had to do. He denies any pain, shortness of breath at rest, leg swelling, or melena. You are called to consult based on his story and an abnormal EKG (anterior leads shown in Figure).
Figure. ED EKG tracing, anterior leads. On physical exam he is alert and is in no acute distress. Vitals signs include: temperature, 98.6°C; pulse, 90 beats/min; blood pressure, 106/74 mm Hg; respiratory rate 22 breaths/min; and pulse ox, 97% on room air. He has clear lungs, normal heart sounds, no peripheral edema, and strong peripheral pulses. A chest x-ray is read out by the radiologist as normal. Laboratory study results find no anemia and a normal troponin-i.
He is admitted over night for serial troponins and a stress test is scheduled for the next morning. The stress test is performed and results are negative, but the patient was only able to complete about 6 minutes before having to stop due to dyspnea.
Question 1. What’s your EKG read?
Question 2. What should you recommend next?
For Answers and Discussion, click here.
What's your ECG read? Deep anterior T-wave inversions suspcisious for acute coronary syndrome or a large pulmonary embolism.
What should you recommend next? You should recommend expanding the differential diagnosis beyond acute coronary syndrome and initiate testing for pulmonary embolism (this was the patient's diagnosis).
Pulmonary embolism (PE) classically causes pleuritic chest pain, dyspnea, and tachycardia, but frequently, as in this patient, not all findings are present.
Large PEs may be completely painless and may present only with dyspnea, dyspnea on exertion, or syncope. This is likely because they cause significant obstruction to total pulmonary blood flow but are less likely to cause lung infarction due to collateral circulation. Large PEs also often cause ECG changes and troponin and/or brain natriuretic peptide (BNP) elevations that may mimic cardiac disease; or the patient may experience cough, tachycardia, hypotension, and leukocytosis mimicking pneumonia. When there is no chest pain it is easy for the clinician to be lead astray.
Smaller PEs, on the other hand, tend to lodge more peripherally and because there is less chance for collateral circulation, lung infarction, and therefore pain, is more likely, while dyspnea or hemodynamic effects like syncope or tachycardia are less likely. Small PEs may be missed when the clinician doubts their presence in the absence of tachycardia or hypoxia.
ECG changes associated with PE are protean. One of the first things most physicians think of is tachycardia, but this symptom typically is caused only by large PEs and was present in only about 25% of cases in the Prospective Investigation of Pulmonary Embolism Diagnosis II (PIOPED-2) study. The S1Q3T3 pattern is also often quoted, [Brady: quoted as what?] but occurs in only about 12% of cases. More common ECG findings include T-wave inversion, about 40% nonspecific ST changes. Other ECG findings that may occur with PE are listed in Table 1, below. It is important to know that just like with cardiac ischemia, ECG changes in PE may be transient.
Diffuse subendocardial ischemia due to an acute coronary syndrome and myocardial strain due to large pulmonary embolism should be the initial two considerations when there is acute chest pain and/or dyspnea associated with deep, symmetric anterior T-wave inversions on the ECG. Other causes of T-wave inversion tend to be either less dangerous or less common or both and are listed in Table 2, below.
|Findings:||Nonspecific ST changes, tachycardia: 26-44%, T-inversion: 42% Complete or incomplete right bundle branch block:10% P-pulmonale (lead II), right axis, poor R wave progression, left axis, a-fib S1Q3T3:12%, S1S2S3, QR or R>S in V1, AV block|
|Massive PE:||ST elevation in aVR & V1, wide QRS, deep flipped anterior T waves, S1Q3T3 Right bundle branch block|
|Dangerous:||Myocarditis, large PE (especially when deep in anterior leads), CNS catastrophe Ischemia: MI, Wellens (T waves may be biphasic), prior MI|
|Conduction:||WPW, bundle branch block LV hypertrophy (asymmetric/hockey-stick shaped, terminal positivity, V6 >V4)|
|Others:||Digoxin toxicity, hyperventilation, post-prandial, normal variant Limb lead reversal, pericarditis, persistent juvenile pattern (anterior), paced|