The objective of this work was to review current data about the pathophysiology, clinical features, and treatment of pulmonary thromboembolism. Venous thromboembolism (VTE) remains a major challenge in hospitalised especially the care of critically ill patients. Pulmonary embolism (PE) is the major complication of VTE. By occluding the pulmonary arterial bed it may lead to acute life-threatening but potentially reversible right ventricular failure. The outcome of patients with PE is quite variable depending primarily on the cardio-respiratory status and the embolus size. PE is a difficult diagnosis that may be missed because of non-specific clinical presentation. Clinical signs include hypoxia, tachypnea, and tachycardia. Severe cases of untreated PE can lead to circulatory instability, and sudden death. However, in ICU, most of patients require sedation and mechanical ventilation. The clinical manifestations usually observed in this condition (PE) cannot be exhibited by these patients and clinical presentation is usually atypical. For these reasons, the diagnosis of PE is usually suspected when un-explicated hypoxemia and/or shock and arterial hypotension were observed. Positive diagnosis is based on these clinical findings in combination with laboratory tests and imaging studies. D-dimer testing is of clinical use when there is a suspicion of DVT or pulmonary embolism PE. In Emergency department, a negative D-dimer test will virtually rule out thromboembolism with a negative predictive value at 95 to 98%. In massive and submassive PE, dysfunction of the right side of the heart can be seen on echocardiography. While the gold standard for diagnosis is the finding of a clot on pulmonary angiography, CT pulmonary angiography is the most commonly used imaging modality today. When the diagnosis is confirmed, anticoagulant therapy is the mainstay of treatment. Acutely, supportive treatments a pivotal role in the management of patients with PE. Severe cases may require thrombolysis with drugs such as tissue plasminogen activator (tPA) or may require surgical intervention via pulmonary thrombectomy. Prevention is highly warranted.