A woman in her 50's complained of dyspnea on exertion for two days. Her lungs were clear on exam. Her first troponin I returned at 0.1 ng/mL (elevated, upper limit of normal = 0.30 ng/mL). Here is her ECG:
Sinus tachycardia. The QRS duration is 103 ms and there is some left axis deviation. What is the likely diagnosis (before I give more clinical information)? -- See below
More data on this patient:
She only had a h/o well controlled AIDS and hypertension. She had no fever or cough. Her oxygen saturations were 92% on room air. On exam, she had clear lungs, normal heart sounds, and no peripheral edema. A chest x-ray was normal. A bedside echo showed "grossly normal function, good global contractility, no obvious wall motion abnormalities, no pericardial effusion and no B lines present in her lungs." They did not comment on the right ventricle.
The BNP was significantly elevated. Hemoglobin and electrolytes normal.
After admission, a D Dimer was ordered and returned at 6x the upper limit of normal. A CT pulmonary angiogram showed multiple bilateral superior and inferior segmental pulmonary arteries with central filling defects (extensive pulmonary emboli.) There was leftward bowing of the interventricular septum consistent with right heart strain.
The clinicians were cognitively steered down the ACS pathway because of the elevated troponin, and also down the heart failure pathway due to the elevated BNP.
However: This is a classic case of PE until proven otherwise: 1. When there is hypoxia with a normal chest x-ray, put PE near the top of the differential. Also consider: hypoventilation (including low respiratory drive), vasodilators and sepsis (both of which cause shunting, with V-Q mismatch), and, most commonly, asthma.
2.ACS infrequently is associated with sinus tachycardia (usually when it is severe ischemia with cardiogenic shock and pulmonary edema)
3.Positive troponins in unselected ED patients, especially at a low level, are more commonly due to demand ischemia than to ACS. Think CHF, hypertension, sepsis, PE, etc.
4.BNP is elevated in PE as well as in heart failure, from right ventricular strain.
5.This ECG is classic for PE: 1) sinus tach 2) right ventricular conduction delay (R' in V1) 3) T-wave inversions in BOTH precordial leads and in lead III. 4) S1Q3T3 (a tiny R-wave in III is equivalent to a Q-wave). (see the primer on the ECG in PE below)
I was sent this ECG without clinical information and asked what it was. My first thought was "pulmonary embolism." All because of the above ECG findings.
Kosuge et al. showed that , when T-waves are inverted in precordial leads, if they are also inverted in lead III and V1, then pulmonary embolism is far more likely than ACS. In this study, (quote) "negative T waves in leads III and V1 were observed in only 1% of patients with ACS compared with 88% of patients with Acute PE (p less than 0.001). The sensitivity, specificity, positive predictive value, and negative predictive value of this finding for the diagnosis of PE were 88%, 99%, 97%, and 95%, respectively. In conclusion, the presence of negative T waves in both leads III and V1 allows PE to be differentiated simply but accurately from ACS in patients with negative T waves in the precordial leads." Witting et al.looked at consecutive patients with PE, ACS, or neither. They found that only 11% of PE had 1 mm T-wave inversions in both lead III and lead V1, vs. 4.6% of controls. This does not contradict the conclusions of Kosuge et al. that when T-wave inversions in the right precordial leads and in lead III are indeed present, then PE may indeed by more common. In my experience, this is true, but needs validation in a study of similar methodology. Supporting Kosuge, Ferrarifound that anterior T-wave inversions were the most common ECG finding in massive PE.