ECG of the Month Presentation is on p 176.
Table 1: Some risk factors for pulmonary embolism Prior venous thromboembolism Hypercoaguability Acute trauma Hip or knee replacement Other major operation Paralysis Hospitalization Other prolonged immobilization Malignancy Autoimmune disease Venous endothelial injury Indwelling venous catheter or pacemaker lead Heart failure Atrial fibrillation
DIAGNOSIS: Atrial fibrillation with a rapid ventricular response (150 beats/minute) and right bundle branch block. The list of causes of systemic arterial hypotension is long and in this patient, should take into account his prior good health, the absence of legal or illegal drugs, the recent discovery of what appears to be a widespread malignancy, the profound nature of the hypotension, and the changes on ECG. Although the first manifestation of coronary arterial disease can be a large myocardial infarct with profound hypotension, there is nothing in this ECG to indicate a large acute infarct. Pericardial metastases can produce atrial fibril- lation, cardiac tamponade, and profound hypotension; but no pericardial effusion was noted on CT 10 days earlier, and the ECGdoes not suggest pericarditis. Malignancy is amajor risk factor for pulmonary emboli (Table 1), 1-7 and pulse- less electrical activity, atrial fibrillation, and right bundle branch block are among the ECG changes seen in patients with pulmonary embolism (Table 2). Although pulmonary emboli may not affect the ECG, the number and severity of the abnormalities listed in Table 2 roughly correlate with the degree of right ventricular dysfunction, which in turn is related to the extent of the pulmonary arterial obstruc- tion. 1,7-14 Sinus tachycardia, non-specific ST-segment change, and anterior T-wave inversion are the changes found most frequently in patients with hemodynamically significant pulmonary emboli. 1,2,8
Myocardial infarction Estrogenic medications Pregnancy Cigarette smoking Obesity Advanced age
As is often the case, the echocardiogram provided crucial information: right ventricular pressure overload and a severely dilated and hypokinetic right ventricle with preserved right ventricular apical contraction, i.e., McCon- nell’s sign, characteristic of extensive pulmonary emboli. 15 The left ventricle was hyperdynamic and underfilled, consistent with obstructive shock. CT revealed multiple bilateral pulmonary emboli as the cause of the obstructive
Table 2: Electrocardiographic abnormalities in pulmonary embolism Rhythm Sinus tachycardia
Atrial flutter, fibrillation, or premature complexes Right ventricular (RV) premature complexes Ventricular fibrillation Pulseless electrical activity Sinus bradycardia or asystole (rarely)
Rightward axis (>75 o ) Tall (>2.5 mm) in leads II, III, or a VF
P waves
QRS complex
Right axis deviation or rightward axis shift Clockwise rotation RV conduction delay or R bundle branch block Right ventricular hypertrophy Inferior, anterior, and/or RV pseudoinfarction S 1 Q 3 T 3 pattern of McGinn and White 1 Left axis deviation (rarely)
ST segment
Elevation inferiorly and/or anteriorly Depression
T wave
Inversion inferiorly Inversion anteriorly QT prolongation
Modified from references 8, 14
J La State Med Soc VOL 166 July/August 2014 177
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