Electrocardiographic Manifestations of Pulmonary Embolism

EDWARD ULLMAN, MD,* WILLIAM J. BRADY, MD,* ANDREW D. PERRON, MD,* THEODORE CHAN, MD,1- AND AMAL MA'I-I-U, MD::I:
The electrocardiogram (ECG) may be entirely normal in the patient with pulmonary embolism (PE); alternatively, any number of rhythm and/or morphologic abnormalities may be observed in such a patient. The abnormal ECG may deviate from the norm with alterations in rhythm, in conduction, in axis of the QRS complex, and in the morphology of the P wave, QRS complex, and ST segment/T wave. The electrocardiographic findings associated with PE are numerous, including arrhythmias (sinus tachycardia, atrial flutter, atrial fibrillation, atrial tachycardia, and atrial premature contractions), nonspecific ST segment/r wave changes, T wave inversions in the right precordial leads, rightward QRS complex axis shift and other axis changes, $1Q3 or S1Q3T3 pattern, right bundle branch block, and acute cor pulomnale. This review focuses on the ECG and the various abnormalities seen in the patient with PE. (Am J Emerg Med 2001;19:514-519. Copyright ~ 2001 by W.B. Saunders Company) The diagnosis of pulmonary embolism (PE) relies predominantly on the magnitude of clinical suspicion and, at that level of suspicion, the interpretation of diagnostic investigations. Reports have shown that less than 50% of pulmonary emboli are diagnosed at presentation. The rate of diagnosis is more pronounced in the elderly population-less than 30% of PE are diagnosed on the index visit. 1 Many studies have shown that acute onset of dyspnea, pleuritic pain, tachypnea, chest pain, and hemoptysis 2,3 are signs of PE. As with most classic symptom constellations, theses complaints rarely occur simultaneously. A myriad of tests may be performed including chest radiography, 12-lead electrocardiogram (ECG), and arterial blood gas to further investigate the clinical picture. The ECG is often an initial diagnostic test performed. As electrocardiographic changes have been noted in the PE patient, it is important to recognize and understand the abnormalities. An additional indication of the importance of the ECG is that the majority of electrocardiographic manifestations are transient.4, 5 The initial electrocardiographic finding of PE was first reported in 1935 by McGinn and White 6 who noted what is now the traditional S 1Q3T3 pattern in acute cor pulmonale. Subsequent reports have described many findings ranging from sinus tachycardia and minor ST segment-T wave abnormalities to right axis deviation, transient fight bundle branch block (RBBB), and inverted T waves. 7 The relatively low sensitivities of these various electrocardiographic presentations, however, limit the ability to use the test as a sole diagnostic tool. Twenty-one different electrocardiographic manifestations of PE are discussed in the medical literature; only a minority of these findings, however, are actually useful to the clinician in establishing a diagnosis of PE. Electrocardiographic changes are best seen in those patients with massive or submassive embolization. 8 Studies have shown that 15% to 27% of ECG were normal. 4 The most common abnormalities are nonspecific ST segment-T wave changes with sinus tachycardia, unfortunately, these findings are extremely nonspecific. 6.9 CASE PRESENTATIONS Case 1 A 54 year-old man with a history of recent orthopedic surgery presented to the ED complaining of sudden dyspnea. On examination, he appeared in moderate distress because of dyspnea. His vital signs included a pulse of 125 beats/min., respiratory rate 36 breaths/min, pulse oximetry 92%, and blood pressure 165/90 mmHg. His examination was unremarkable except for a lower extremity which was casted. The patient was placed on a cardiac monitor and an ECG was obtained (Fig 1), showing sinus tachycardia. The clinical suspicion for PE was very high, resulting in a ventilation/perfusion (V/Q) scan which was reported as "high probability" for pulmonary embolism. Case 2 A 64-year-old woman with a history of diabetes and hypertension presented to the ED complaining of shortness of breath. On examination, she appeared comfortable and alert. Vital signs showed a normal temperature, pulse 110 beats/min, respiratory rate 32 breaths/min, pulse oximetry 97% on 5 liters oxygen, blood pressure 163/107 mmHg. Her examination was otherwise unremarkable. An ECG was obtained (Fig 2), revealing inverted T waves in the right to mid precordial distribution (leads V1 to V4). Chest radiography was normal. A V/Q scan was obtained, revealing a "high probability" scan. Case 3 A 52-year-old woman with a history of deep venous thrombosis (DVT) presented to the ED complaining of 3 days of dyspnea and lightheadedness. On examination, she appeared comfortable and alert with vital signs as follows: pulse 105 beats/min, respiratory rate 26 breaths/min, pulse oximetry 91%, and blood pressure 110/70 mmHg. The remainder of her examination was notable only for a swol-

From the *Department of Emergency Medicine, University of Virginia, Charlottesville, VA; the 1-Department of Emergency Medicine, University of California San Diego, San Diego, CA; and the :l:Department of Emergency Medicine, University of Maryland, Baltimore, MD. Manuscript received and accepted February 28, 2001. Reprints are not available. Key Words: Electrocardiogram, pulmonary embolism. Copyright 2001 by W.B. Saunders Company 0735-6757/01/1906-0012535.00/0 doi:l 0.1053/ajem.2001.27172 514

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FIGURE 1. Case 1, Sinus tachycardia. len, tender lower extremity. An ECG was obtained, showing an sinus tachycardia with prominent S waves in lead 1 and aVl. A V/Q scan was "low probability". With the clinician's high level of suspicion for PE, a lower extremity ultrasound revealed evidence of DVT. This finding, coupled with the clinical suspicion for PE, prompted a pulmonary angiogram, confirming the diagnosis of pulmonary embolism.

FIGURE 3. Case 4, Right bundle branch block. pain. On further review of the history, it was determined that the patient was not experiencing dyspnea but felt an increase in the pain on inspiration which limited respiration. The examination revealed a middle-aged patient in considerable distress, clutching his chest; the remainder of the examination was unremarkable. A 12-lead ECG (Fig 5) showed sinus rhythm with the S1Q3T3 pattern. The chest radiograph was normal. A V/Q scan was performed with a "low probability" result prompting a pulmonary angiogram which did not reveal PE. No evidence of PE was found in this patient. He was diagnosed with a musculoskeletal source of his pain. A prior ECG was obtained which revealed similar findings, including the S1Q3T3 pattern.

Case 4
A 2Q-year-old man with a history of hypertension presented to the ED with dyspnea, pleuritic chest pain, and cough productive of blood-tinged sputum. On arrival, the patient's temperature was 100.6F, pulse 110 beats/rain, respiratory rate 30 breaths/min, pulse oximetry 91%, and blood pressure 140/90 mmHg. His examination was notable respiratory distress and a swollen lower extremity. The ECG was obtained (Fig 3) and showed sinus rhythm with new RBBB pattern. The chest radiograph was otherwise unremarkable. The V/Q scan was "high probability" for PE.

DISCUSSION
Pulmonary thromboembolism most commonly occurs as a complication of venous thrombosis, primarily from clots located in the deep veins of the lower extremities and pelvis. These clots dislodge from their origin and travel through the venous circulation to the pulmonary artery. The formation of venous thrombosis is usually caused by one or more of the following factors: endothelial injury, hypercoagulability, or stasis of blood. Common clinical situations associated with increased risk of proximal deep venous thrombosis include congestive heart failure, myocardial infarction, immobilization (postsurgical, bed rest, stroke, prolonged travel), malignancy, pregnancy, estrogen therapy, obesity, and prior DVT. The degree of obstruction secondary to the embolism is directly related to the response of the right ventricle to the PE and, therefore, the clinical manifestations, including the

Case 5
A 2Q-year-old man without past medical history presented to the ED with dyspnea, cough, and chest pain. The physical examination was normal with the exception of a rapid pulse of 140 beats/min no chest wall tenderness was found. A 12-lead ECG (Fig 4) revealed normal sinus rhythm with the S1Q3T3 pattern. A V/Q scan was performed with a "high probability" result.

Case 6 A 42-year-old man with no past medical history presented via ambulance to the ED with dyspnea and chest

FIGURE 2. Case 2, T wave reversions in leads V1 to V4.

FIGURE 4. Case 5, Sinus tachycardia with SIQ3T3 pattern.

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FIGURE 5. Case 6, Normal sinus rhythm with S1Q3T3 pattern not related to PE. electrocardiographic abnormalities. The embolism likely causes a release of vasoconstrictive factors such as serotoninS; catecholamines may also play a role in the pathophysiologic response. 8 As noted in the cases presented, the majority of findings potentially useful to the clinician result from the right-sided heart strain pattern. The increase in right-sided heart pressures creates an increased right ventricular afterload, resulting in increased rightsided myocardial wall tension. As the right ventricle is not physiologically capable to withstand such pressures, it rapidly dilates, with an increase in chamber size and eventual contractile dysfunction. The final cardiac issue in this pathophysiologic cascade is a reduction in right heart cardiac output (ie, a reduction the preload for the left ventricle) which ultimately produces a decrease in left heart cardiac output. 8 The reduced cardiac output compromises both systemic and coronary perfusion. Under normal physiologic conditions, right-sided perfusion is constant through both systole and diastole; the increase in wall tension coupled with the systemic hypotension, however, increases the possibility of right-sided myocardial ischemia and infarction. As right-sided ventricular dysfunction worsens, right ventricular infarction and circulatory collapse may occur> The ECG may be entirely normal in the patient with PE; alternatively, any number of rhythm and/or morphologic abnormalities may be observed in such a patient. The abnormal ECG may deviate from the norm with alterations in rhythm, in intra- and interventricular conduction, in axis of the QRS complex, and in the morphology of the P wave, QRS complex, and ST segment/T wave. The electrocardiographic findings associated with PE are numerous, including arrhythmias (sinus tachycardia, atrial flutter, atrial fibrillation, atrial tachycardia, and atrial premature contractions), nonspecific ST segment/T wave changes, T wave inversions in the right precordial leads, rightward QRS complex axis shift and other axis changes, S1Q3 or S1Q3T3 pattern, RBBB, mad acute cot pulomnale defined by S1Q3T3 pattern, right axis deviation, and RBBB. I,1~ Regarding the "normal" ECG, it is meant to be completely normal--sinus rhythm between 60 and 100 beats/ rain with normal conduction, axis, and P wave, QRS complex, and ST segment/T wave morphologies. An entirely normal ECG has been found in approximately 10% to 25%

of PE patients. 12,13 Interestingly, a not insignificant number of such patients will continue to manifest a normal ECG during hospitalization. 14 Sinus tachycardia is the most frequent rhythm encountered on presentation to the ED in the patient with PE. 6,9 The rate of the sinus tachycardia is usually between 100 to 125 beats/min as seen in Fig 1; alternatively, in the patient with a large clot burden (significant right ventricular obstruction and/or hypoxemia), the rate may be very rapid as seen in Fig 4. Sinus tachycardia in the face of PE is likely related to the physiologic demand to increase cardiac output. As leftsided stroke volume decreases, heart rate must increase to maintain cardiac output. Atrial arrhythmias, particularly atrial fibrillation and atrial flutter, are also seen in the acute PE patient; these disturbances likely results from atrial enlargement (Fig 6). RBBB (Figs 3, 7, and 8), either complete or incomplete, is found in patients with PE; its incidence is variable, ranging from a low of 6% to as high as 67%. 14 A more realistic figure is approximately 25% of those with PE will show this pattern on presentation. The PE-related RBBB pattern is transient, often resolving with the restoration of normal right-sided cardiac hemodynamic parameters; it may be persistent, though still ultimately resolving 3 months to 3 years after the index PE. 12 While RBBB is suggestive of PE, its presence is still nonspecific and therefore not diagnostic. 9.15 RBBB may also be associated with ST segment elevation and prominent, upright T waves in lead V1 and/or V2, potentially mimicking anterior or posterior infarct pattern. ~4 Right, left, and indeterminant QRS axis changes have been reported in acute PE patients. Although right axis deviation (RAD) is described as the classic axis change associated with PE, left axis deviation (LAD) actually occurs more often. 12.14.16.17 Pre-existing disease may also impact the axis deviation on presentation in the ED as seen in the Urokinase-Pulmonary Embolism Trial (UPET). In this trial, the investigators report that LAD occurred more frequently than RAD in the PE study population. When those individuals with pre-existing cardiopulmonary disease were excluded, the incidence of LAD and RAD was equivalent.15 Increase in the P wave amplitude greater than 2.5 mV in lead II, known as P-pulmonale, has been classically associ-

FIGURE 6. Atrial fibrillation with a rapid venlIicul~ response is seen in this ECG obtained in a middle-aged female patient with dyspnea after prolonged bed rest. V/Q scanning was high probability for PE. She had no past history of atrial fibrillation.

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FIGURE 7. Right bundle branch block, signified by an rSR pattern in lead V1 in the setting of a widened QRS complex, in a patient with documented PE. Also note the likely right ventricular hypertrophy (RVH) pattern, large R' wave in lead V1 and large S waves in the mid to left precordial leads. Lastly, the chronic pulmonary disease pattern is suggested in this particular patient, RVH and low voltage in the limb leads. ated with PE, likely resulting from right atrial hypertrophy or enlargement associated with acute obstruction from clot. P-pulmonale has been reported in 2% to 30% of PE patients. ~s,19 Figure 9 shows the development of P-pulmonale in a patient with PE--Fig 9A was obtained on presentation to the ED with sinus tachycardia and nonspecific ST segment/T wave changes; Fig 9B, obtained 6 hours later, revealed the development of P-pulmonale. The classic SIQ3T3 pattern, mistakenly considered pathognomonic for acute PE by many clinicians, is seen less frequently--15% to 25% of patients ultimately diagnosed with PE will have this pattern. 4 A more comprehensive evaluation of the PE patient and the characteristics of presentation reveal that this classic pattern is, in fact, quite rare. The UPET reveals that approximately 12% of patients with angiographically documented acute PE initially had the electrocardiographic S1Q3T3. 2o This pattern (Figs 4 and 5) is characterized by an S wave in lead I, a Q wave in lead III, and shallow T wave inversions in one or more of the inferior leads. In addition, the ST segments may be slightly elevated in the inferior leads. Although this finding is consistent with right-sided cardiac changes, it remains unclear if this finding actually predicts PE. Reports yield conflicting data regarding its usefulness; many authorities consider this abnormal-

FIGURE 9. (A) Sinus tachycardia with nonspecific changes in a patient with dyspnea, plueritic chest pain, and hypoxemia. Subsequent evaluation revealed PE. (B) After admission to a critical care unit, P-pulmonale was noted in this tracing with large P waves in lead II. ity strongly suggestive when, in fact, it shows a very poor sensitivity--approximately 50% for the diagnosis of PE. 1.8.16 Consider the example in case 6 (Fig 5) in which the S1Q3T3 pattern was noted in a patient who did not have PE. This electrocardiographic finding should not be used as the sole criterion, ie, those patients lacking the appropriate symptomology, for initiating an evaluation for pulmonary embolism. The S1Q3T3 pattern is usually short-lived, resolving within 2 weeks after PE. 15 Other S wave abnormalities, that is, separate from the classic S1Q3T3 presentation, are encountered frequently. S wave in lead I greater than 1.5 mm (Fig 10) and/or an R wave-S wave ratio greater than 1 in leads I and aVI was noted in 73% of patients diagnosed with PE. 21 A more subtle finding is a slurred S wave in leads V1 and/or V2. The ST segment may be either depressed (Fig 11) or elevated (Fig 12) in the PE patient. Minimal ST segment depression is a common finding on the ECG in such patients. More pronounced depression may also be encountered in the anterior, inferior, and lateral distributions (Fig 11); in this case, the ST segment depression likely represents myocardial ischemia resulting from the physiologic strain of the PE itself. Less marked ST segment elevation, less than 1 mm, is also frequently seen. The S1Q3T3 pattern may be associated with ST segment elevation in the inferior leads. The RBBB pattern may present with ST segment elevation in the right precordial leads (leads V1 and V2).

FIGURE 8. Another example of RBBB, RVH, and the chronic pulmonary disease pattern in a patient with PE.

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FIGURE 10. A large S wave in lead I is seen in a PE patient. Significant ST segment elevation consistent with acute myocardial infarction is quite rare. The presence of anterior subepicardial ischemia caused by PE manifests as inverted T waves (Figs 2 and 12) in the fight to mid precordial leads (leads V1 to V3). 8,16 Early studies attributed this pattern to coronary insufficiency. More recent studies, however, suggest either cathecholamine- or histamine-induced ischemia. 8 Diffuse T wave inversion rarely is diagnostic for PE. The clinician must view the ECG as a whole in the evaluation in the patient with presumed PE; combinations of various electrocardiographic abnormalities and their diagnostic value have been considered. Sinus tachycardia and nonspecific ST segment/T wave changes are frequent, though nonspecific, findings in the PE patient; when noted together, these findings represent the most frequently encountered electrocardiographic pattern in the PE patient and are noted in approximately 50% of cases at some point in their course. Unfortunately, these findings, though commonly seen in the PE patient, are extremely nonspecific and in no way indicative of pulmonary embolus. 6,9 Unless the clinical presentation, ie, the chief complaint and/or physical examination suggests PE, the physician will likely miss the diagnosis if he or she relies on the ECG as the sole screening tool. Electrocardiographic patterns indicative of acute right ventricular strain are noted frequently on the ECG of the PE patient. In one large study 15 of patients with documented PE, 82% of cases had electrocardiographic changes suggestive of acute fight ventricular strain. These findings included: FIGURE 12. ST segment elevation in leads V2 to V5 is seen in a PE patient. Additionally, T wave inversions are also seen in this distribution. Incomplete right bundle branch block; S1Q3T3 pattern; Q wave in lead III; Inverted T waves in leads III, V2 and V3; and/or Increase in the frontal QRS axis of > 2 0 degrees? 5 Another group of investigators lead by Sreeram 14 suggested that PE should be considered when 3 or more of the following electrocardiographic changes are encountered: Incomplete or complete RBBB; Large S waves in leads I and a VL; A shift in the transition zone in the precordial leads to V5; Q waves in leads III and aVF (not lead II);

Right-axis deviation;

A low voltage QRS complex in limb leads; and/or T wave inversion in inferior and anterior leads. 14 Figure 13 is an example of an ECG obtained from a patient with acute PE. Numerous findings as suggested by Sreeram et a114 are noted, including incomplete RBBB, fight axis deviation (--120 degrees), large S waves in leads I and aVI, and T wave inversions in the anterior and inferior leads. Petruzzeli and colleagues -~1 studied 21 electrocardiographic abnormalities in 245 patients with suspected P E - 60% of patients ultimately had PE. Those patients diagnosed with PE were found to manifest the following patterns more commonly: PR segment displacement; Delayed R wave (lead aVr); Slurred S wave (leads V1 or V2); S1Q3T3 pattern;

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FIGURE 11. Sinus tachycardia and ST segment depression in leads V2 to V6 in a PE patient.

T wave inversion (leads V1 or V2); and/or Diffuse T wave inversions. ~

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REFERENCES
1. Donnamaria V, Palla A, Giuntini C: Gender, age and clinical signs of patients suspected of Pulmonary Embolism. Respiration 1994:61-7 2. Stein PD, Gottschalk A, Saltzman HA, et al: Diagnosis of acute pulmonary embolism in the elderly. Am J Cardiol 1991; 18:1452-7 3. Manganelli D, Palla A, Donnamaria V, et al: Clinical features of pulmonary embolism. Chest 1995; 107:25S-32S (suppl) 4. Panos RJ, Barish RA, Depriest WW, et al: The Electrocardiographic manifestations of pulmonary embolism. J Emerg Med 1988; 6:301-7 5. Lualdi JC, Goldhaber SZ: Right ventricular dysfunction after acute pulmonary embolism: Pathophysiologic factors, detection and theraputic implications. Am Heart J 1995; 130:1276-82 6. Mcginn S, White PD: Acute cor pulmonale resulting from pulmonary embolism. J Am Med Assoc 1935; 104:1473 7. Durnat TM, Ginsberg IW, Roesler H: Transient bundle branch block and other electrocardiographic changes in pulmonary embolism. Am Heart J 1939; 17:423 8. Ferrari E, Imbert A, Chevalier T, et al: The ECG in pulmonary embolism. Chest 1997; 111:537-43 9. Petruzzelli S, Palla A, Pieraccini F, et al: Routine electrocardiography in screening for pulmonary embolism. Respiration 1986; 50:233-243 10. Senior RM: Pulmoary embolism, in Bennett JC, Plum F, Gill GN, et al (eds): Cecil Textbook of Medicine (ed 20). Philadelphia, Saunders 1996, pp 422-429 11. Chou T: Electrocardiography in Clinical Practice (ed 2). Orlando, Grune & Stratton, 1986, pp 309-317 12. Panos RJ, Barish RA, Whye DW, et al: The electrocardiographic manifestations of pulmonary embolism. J Emerg Med 1988; 6:301-7 13. Hubloue I, Schoors D, Diltoer M, et al: Early electrocardiographic signs in acute massive pulmonary embolism. Eur J Emerg Med 1996; 3:199-204 14. Sreeram N, Cheriex EC, Smeets JLRM, et al: Value of the 12-lead electrocardiogram at hospital admission in the diagnosis of pulmonary embolism. Am J Cardiol 1994; 73:298-303 15. Nielsen -Fi-, Lund O, Ronne K, et al: Changing electrocardiographic findings in pulmonary embolism in relation to vascular obstruction. Cardiol 1989;76:274-284 16. Stein PD, Dalen JE, Mclntyre KM, et al: The electrocardiogram in acute pulmonary embolism. Prog Cardiovasc Dis 1975; 14:247-57 17. Szucs MM, Brooks HL, Grossman W, et al: Diagnostic sensitivity of laboratory findings in acute pulmonary embolism. Ann Intern Med 1971;74:161 18. Weber DM, Phillips JH: A re-evaluation of electrocardiographic changes accompanying acute pulmonary embolism. Am J Med Sci 1966; 251:381 19. Rodger M, Makropoulos D, Turek M, et al: Diagnostic value of the electrocardiogram in suspected pulmonary embolism. Am J Cardiol 2000; 86:807-9 20. Sasahara AA, Hyers TM, Cole CM, et al: The urokinasepulmonary embolism trial: A national cooperative study. Circulation 1973; 47/48 (supp 2): II 60-11 65 21. Petruzzelli S, Palla A, Pieraccini F, et al: Routine electrocardiography in screening for pulmonary embolism. Resp 1986; 50: 233-43

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FIGURE 13. Numerousfindings as suggested by Sreeram et a114 consistent with PE are noted, including incomplete RBBB, right axis deviation (--120 degrees), large S waves in leads I and aVI, and T wave inversions in the anterior and inferior leads. In addition to the Sreeram et a114criteria, RVH (prominent R' wave in lead V1 with right axis deviation) with strain (ST segmentFl" wave changes) is noted.

Alternatively, Nazeyrolas et al studied 70 patients admitted for suspected PE and found only an S wave in lead I and Q wave in lead III significantly more common among those with confirmed PE. 12 Rodger et aP 9 studied the ECGs of 246 patients with suspected PE (49 with PE) comparing the frequency of 28 different electrocardiographic findings supposedly associated with the diagnosis. Of these, the investigators found only sinus tachycardia and incomplete RBBB significantly more common in PE patients. In this study population, Sreeram's guido 4 of 3 or more findings on the ECG had only a 26.7% sensitivity and 57.1% positive predictive value for PE. Moreover, the S 1Q3T3 pattern was equally prevalent among those with and without PE. 19

CONCLUSION
PE is a very elusive disease process lacking conclusive clinical findings to aid in the diagnosis. The true gold standard is pulmonary angiography. However, this cannot be done on every patient that presents with a concerning story. As an independent marker, the ECG continues to be a limited study because of its poor sensitivity. The transient nature of electrocardiographic abnormalities and the often nonspecific changes reduce the effectiveness of the test as a single agent. Serial ECGs do not improve the ability to diagnose PE. 14 Lastly, cornorbid states and their associated electrocardiographic patterns further confound the picture provided by the ECG. The electrocardiographic abnormalities described earlier coupled with the appropriate clinical picture, however, can be helpful in the decision to pursue PE as a diagnosis.