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Figure 8.11. ECG findings in acute PE. The S1Q3T3 findings represent the volume and pressure overload experienced by the obstructed RV ('right heart strain'). The S-wave in lead I represents a complete or incomplete bundle branch block. The strain on the RV leads to conduction abnormalities which account for the Q-wave, mild ST-segment elevation, and T-wave inversion seen in lead III.

Figure 8.11. ECG findings in acute PE. The S1Q3T3 findings represent the volume and pressure overload experienced by the obstructed RV ('right heart strain'). The S-wave in lead I represents a complete or incomplete bundle branch block. The strain on the RV leads to conduction abnormalities which account for the Q-wave, mild ST-segment elevation, and T-wave inversion seen in lead III.

digital reconstructions are improving diagnostic accuracy. Pulmonary angiogram is still considered the gold standard modality of assessing for PE. PE is indicated by a filling defect or a vessel cut off sign. It is a reliable study for up to a week from the onset of symptoms, even after the initiation of anticoagulation.

Treatment

Anticoagulation is the treatment for PE and should be initiated at the clinician's discretion, but ideally once the thrombo-embolic event is suspected. A heparin infusion (goal prothrombin time (PTT) 1.5-2.0 above control) or therapeutic dose subcutaneous low-molecular-weight heparin (LMWH) is recommended to prevent further embolization. Once diagnosis is confirmed, long-term anticoagulation with Warfarin (International Normalized Ratio (INR) > 2.0) or an LMWH should be organized. Thrombolytic therapy is an alternative for patients with hemodynamic instability or severe hypoxia. Surgical embolectomy may be considered in the unstable patient who has contraindications to or failure of thrombolytic therapy.

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