Electrocardiographic Changes in Submassive Pulmonary Embolism

Surface electrocardiograms (ECG) of 37 documented cases of submassive pulmonary embolism were evaluted after excluding various confounding factors like pulmonary disease, intraventricular conduction defects, old myocardial infarction, left ventricular systolic dysfunction and electrolyte imbalance. Twenty-seven patients had evidence of pulmonary embolism on computed tomography (CT) of thorax and 10 patients had ventilationperfusion scan suggestive of pulmonary embolism. A 19-lead ECG (including leads I to V9 and V3R to V6R) was recorded in all cases at the time of admission and subsequently daily for next 4 to 6 days of hospitalization. Sinus tachycardia was the commonest finding (67.6%). Other findings with decreasing frequency were S wave of any magnitude in lead I (56.7%), S wave of > 1.5 mm in leads I and aVL (54%). ECG findings, conventionally considered suggestive of right ventricular overload, had very low sensitivity [S1Q3T3: 40%, right axis deviation (RAD): 18.9%, p-pulmonale 18.9%, R/S> 1 in V1:21.6%]. T wave inversion (8.1%) and ST segment elevation (5.4%) in leads V1 to V3 was the commonest new change observed in sequential ECG recorded during 48 hours following admission. Twenty-one (56.7%) patients had ST segment depression in leads V1 and V6; 18.9% of patients had ST segment depression in leads V1-V6. S wave of > 20 mm in either of leads V1, V2 or V3 was present in 16.2% cases. Left axis deviation (LAD) and ECG evidence of left atrial overload was present in 13.5% and 8% cases, respectively.

S wave of any magnitude was present in lead I in 56.7% of our cases on day 1 and another 5.4% cases manifested this finding during hospitalization. S wave of > 1.5 mm was observed less frequently (54%) and S>R in lead I (RAD) was still less frequent (18.9%). Therefore, even small S wave in lead I is important, more so if it is a new transient change. Clear RAD (R/S < 1 in lead I) was seen in only in 18.9% of our cases on day 1 and one more patient developed it on subsequent ECG. Petrov1 observed RAD without right bundle branch block (RBBB) in only 20% cases of massive pulmonary embolism. Ciurzynski et al.2 also reported it in less than one-third cases of hemodynamically significant pulmonary embolism. This ECG finding, therefore, has very low sensitivity. S1Q3T3 was observed in 40% of our cases on day 1. Another 3 (5.4%) cases developed it on subsequent day. Prevalence of this finding has ranged from 3% to 60% in previous studies of massive pulmonary embolism.1 Its incidence is still lower in non-severe pulmonary embolism.3 Thus, this electrocardiographic finding has low sensitivity in diagnosing both massive and submassive pulmonary embolism. In our study, S1Q3 (without T3) or S1T3 (without Q3) alone were present only in 2.7% and 8.1% cases, respectively. Cutforth and Oram3 also reported similar incidence (4%) of isolated S1T3. Ppulmonale was present only in 18.9% cases in our study. Previous studies have reported an incidence of 0-1% in small emboli4,5 and 7-26% in patients of massive pulmonary embolism.4-6 P-pulmonale, therefore, has low sensitivity even in patients with massive pulmonary embolism. Ciurzynski et al.2 observed p-pulmonale only in patients with symptom duration of > 14 days. In the study of Cutforth and Oram,3 5 out of 6 patients with ppulmonale showed this finding only after 1 to 9 days. Any increase in P-wave height over an ECG recorded before embolism or in subsequent ECG recorded during hospitalization can be a useful diagnostic clue for pulmonary embolism.

ST segment elevation and T wave inversion in leads V1-V3 was the commonest sequential ECG change. Cutforth and Oram3 also observed that depth of T wave inversion in leads V1-V4 may increase sequentally over next 2-3 days without any fresh embolism. Ferrari et al.7 also observed that there is always some time delay between onset of symptoms and appearance of this electrocardiographic finding. Mechanism of this ECG change and reason for delay after onset of symptoms is not clear. Progressive right ventricular dilation with secondary right ventricular ischemia could be held responsible for it. Ciurzynski et al.2 described a direct correlation between end-diastolic right ventricular diameter and sum of negative T waves in V1-V4. Small subendocardial right ventricular infarct can also produce similar ECG finding. ST segment elevation with Q wave in any one of the right precordial leads (V3R to V6R) was observed in 37.8% cases at admission. Other workers8,9 have also observed that this is a very early but transient sign of moderate to severe pulmonary embolism. Prominent R wave and ST segment elevation in lead aVR are considered signs of pulmonary embolism10,11 but detailed information regarding changes in this lead are not available. We found R wave of > 2 mm and ST elevation of > 1 mm in 18.9% and 32.4% cases, respectively on day 1. Thus, changes in lead aVR alone have low sensitivity in  diagnosing pulmonary embolism.

ECG evidence of left atrial (LA) overload i.e. p-mitrale or prominent negative terminal deflection of P wave in lead V1 was seen in 8% cases in our study. Significant right atrial (RA) enlargement is also known to produce prominent negative deflection of P wave in lead V1.12 Acute RV dilation shifts interventricular septum (IVS) to left resulting in increased left ventricular end-diastolic pressure (LVEDP). This could also strain LA. We are, however, not sure if pulmonary embolism resulted in this finding or this ECG abnormality was present in these patients prior to embolism. We observed LAD in 13.5% cases. Presence of LAD prior to embolism could not be excluded in these patients. Other have also reported this finding5,6 However, Lynch et al.13 observed that leftward shift of frontal plane QRS axis was common in pulmonary embolism and an axis <30 at the time of onset of symptom was twice as frequent as RAD. No satisfactory explanation for such occurrence is available.

We observed deep S wave (>20 mm) in leads V1-V3 in 16.2% of our cases. Dilated right ventricle occupying whole of anterior aspect of heart and displacing left ventricle posteriorly could explain this finding in some of our cases. ST segment depression in leads V1-V6 or in leads I, II, V5-V6 was seen in 18.9% and 56.7% cases, respectively in our study. Watanabe et al.14 described ST segment depression in leads V2-V6 with T wave inversion in III, aVF, V1 to V3 in patients of pulmonary embolism during episodes of pulmonary embolism. Ahonen15 noted ST segment depression in leads I, V5 and V6 in 74% cases of fatal massive pulmonary embolism. ST segment depression in precordial leads could be due to RV dilation, clockwise rotation and shift of transition zone to left. Hypoxia or concomitant coronary artery disease could also contribute to this ECG finding.

References

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SR Mittal, Monika Maheshwari
Department of Cardiology
JLN Medical College, Ajmer