PE is a condition that is often difficult to recognize due to its varied clinical presentation, ranging from unclear symptoms to severe conditions that quickly leading the patient to shock and death.1
It is the third most common cardiovascular disease worldwide, of high mortality and morbidity, with an estimated incidence of 100-200 per 100,000 inhabitants, according to the Guidelines of the European Society of Cardiology.2
There is a variety of related risk factors, including major orthopedic surgeries, traumas, prolonged immobilization, malignant neoplasia, spastic and flaccid paralysis, hormonal contraception, congestive heart failure, thrombophilia, obesity and pregnancy.3,4
However, PE can occur even in the absence of known risk factors.2
About 10% of all PE patients die within three months after the diagnosis, which is established by right ventricular failure caused by massive occlusion of pulmonary circulation.2
Acute cor pulmonale in PE is an important determinant of the severity and early clinical outcome. Therefore, rapid recognition of serious medical conditions is of the essence.
Diagnosis should be suspected in patients with suggestive clinical symptoms in the presence of risk factors. The most common symptoms are non-specific, such as dyspnea, pleuritic pain and hemoptysis.1-3
Syncope is not a common symptom and may occur even in the absence of hemodynamic instability, where brief and self-limited hypotension may occur due to vasovagal reflection.5,6
The Wells and Geneva probability scores include clinical criteria for the diagnosis of PE,7 simply obtained and validated on three levels (high, intermediate and low probability) or two levels (probable or improbable PE), as shown in Table 1.2
The investigation continues with complementary tests to confirm or rule out the diagnosis. For patients with improbable PE, a D-dimer test is run. D-dimer is a fibrin degradation product with high negative predictive value for the diagnosis of PE. A low D-dimer value in this context can virtually rule out such diagnosis.2,3
The method of choice for diagnosing patients with probable PE and D-dimer greater than 1. 600 is the computed tomography angiography of the chest, which shows thrombi in the pulmonary tree.8
Despite the applicability of probability scores, diagnosis only considers clinical parameters, leaving out an essential tool for the evaluation of most cardiac disorders: ECG. PE may present abnormalities on electrocardiogram, such as T-wave inversion on leads V1 to V4, QR complex on V1, S1Q3T3 pattern and right bundle branch block, suggesting RV overload.1,2,9
These signs point to a more serious condition associated with pulmonary hypertension and acute cor pulmonale in cases of suspected PE, confirmed with relative ease by transthoracic echocardiogram (TTE).2,3
We describe a clinical case in which, despite the low pretest probability found by the scores of Wells and Geneva, and no high-risk of death detected by PESI and simplified PESI, ECG drew attention to the presence of pulmonary hypertension, serving as useful tool not only for the diagnosis but also for the prognosis of this disease with well-established severity.
Keywords: Pulmonary Embolism; Thromboembolism; Ventricular Dysfunction,Right; Hypertension, Pulmonary; Indicators of Morbidity and Mortality.