**Table 1.**

*Risk factors for DVT/PE.*

expectoration, 2) Shortness of breath only, 3) Hemodynamic instability, 4) Subclinical clot, 5) Chronic non-resolving clot [1, 17]. The fourth and fifth clinical syndrome may be identified incidentally on the imaging studies while working for dyspnea of unknown origin or as a study to rule out other clinical conditions.

## **4. Non-imaging modalities**

A complete blood cell count can disclose leukocytosis, while a peripheral smear and a differential count can reveal leukemia, myeloproliferative disorders, or other hematological conditions. NLR (Neutrophil to lymphocyte ratio) and PLR (platelet to lymphocyte ratio) if elevated at PE diagnosis signify an elevated short-term risk and overall mortality; however, the exact cutoff for NLR and PLR is yet to be decided. Both NLR and PLR can serve as cheap prognostic indicators in acute PE [18]. Acute PE causes myocardial distension and stretching, leading to an increase in BNP (Brain Natriuretic Peptide) and NT-proBNP (N-terminal pro-brain Natriuretic Peptide). The right ventricle (RV) undergoes significant strain during an acute massive PE, resulting in RV ischemia that can be small and cause elevated troponin and H-FABP (heart-type fatty acid-binding protein levels). Elevated above-mentioned cardiac biomarkers and troponin in nonmassive PE signify higher short-term mortality and PE-related adverse events [19, 20]. Also, in nonmassive PE, RV dysfunction correlated appropriately with short-term mortality [20]. Arterial blood gases (ABG) reveal hypoxemia in acute PE, which can worsen with increased PE size. PE leads to increased dead space ventilation and hypercapnia; however, this is seen in patients with limited ventilatory reserve or mechanically

ventilated patients [1]. In an earlier study, a 100% NPV (negative predictive value) for PE correlated with respiratory rate < 20 per minute, normal D-dimer level, and partial pressure of oxygen ≥80 mmHg [21]. This was later found to have an NPV of 95% in a more extensive study where multiple ABG prediction rules were assessed and were found to lack adequate NPV, likelihood ratios, or specificity [22]. Thus ABG has minimal conclusive value in suspected PE patients and is inadequate to diagnose or exclude PE.

D-dimer presence in blood indicates intrinsic fibrinolysis by plasmin. In DVT, D-dimer elevation is lesser than that seen in PE due to the smaller size of the thrombus. Thus D-dimer sensitivity is higher in PE (> 95%) than in DVT (>80%) [13]. The D-dimer elevation is observed in infection, inflammation, ischemia, cancer, trauma, and postoperatively making it a nonspecific test. Thus its predictive role in hospitalized patients is minimal. D-dimer is outstanding in patients <65 years of age plus lower pretest PE probability. D-dimer had a diminishing value in the patient subset >65 years of age due to more false positives [23]. Another study suggested using age-adjusted D-dimer testing alongside Well's score as it improved efficiency with no effect on safety in all subgroups studied. The efficiency was notably observed in elderly patients, patients with cancer, obstructive lung disease, prior venous thromboembolism, or a late presentation [24]. A standardized hypersensitive negative test result safely rules out PE among mild or moderate-risk patients [1].

In a small proportion(10–25%) of PE patients an ECG (electrocardiogram) is normal [25]. ECG can reveal multiple findings that lack sensitivity and specificity individually to diagnose PE. The commonest ECG finding is acute sinus tachycardia [26]. Other significant ECG findings are mentioned in **Table 2** below [27].

In an established extensive PE, a frequent earlier finding is precordial T wave inversions [28]. The observation of S1Q3T3, RBBB, and inverted T waves (V1-V4 leads) in a PE patient's ECG indicated RV dysfunction [28, 29]. V1 to V3 precordial lead T wave inversions had a higher true positive rate and diagnostic accuracy than S1Q3T3 and RBBB findings in RV dysfunction detection in acute PE [30]. If ECG reveals an RV strain pattern, the patient is at a higher mortality risk and adverse outcomes, despite being hemodynamically stable [31]. RBBB, Lead V1 ST-segment elevation, and low voltage QRS complexes are observed in PE patients with cardiogenic shock [32]. The following findings were frequently seen in patients who had a fatal outcome after a PE, including complete RBBB, atrial arrhythmias, Q wave (leads III & aVF), Peripheral small amplitudes, and left precordial ST changes. In a study, 29% of patients with these ECG findings did not make it out of the hospital on discharge [33]. A concurrent occurrence of inverted T waves in leads II, III, aVF, and V1 to V4 is highly distinct for PE (99%) than ACS but uncommon [34]. Acute PE accurately


distinguishes from ACS by the presence of lead III and V1 T wave inversions on ECG [35]. An essential role of performing an EKG in acute PE is its help in ruling out other differential diagnoses, such as ACS, myocarditis, or acute pericarditis.
