Stable patient and PERC not met or intermediate probability of PE: Obtain D-dimer.Stable patient and low probability of PE: Assess whether patient meets pulmonary embolism rule-out criteria ( PERC).Obtain other laboratory studies or imaging as needed.Low: modified Wells score for PE ≤ 4, Wells score for PE 4, Wells score for PE > 6, or revised Geneva score > 10.Unstable patients: systolic BP 15 minutes, evidence of shock, or BP drop > 40 mm Hg for > 15 minutes.Stable patients: systolic BP > 90 mm Hg.Pretest probability of pulmonary embolism Drop in partial pressure of end-tidal CO 2 (PetCO 2) in capnography.Ĭonsider PE as a differential diagnosis in recurring or progressive dyspnea of uncertain etiology.Features of PE under anesthesia during surgery.Features of massive PE: syncope and obstructive shock with circulatory collapse (e.g., due to a saddle thrombus).Features of DVT : unilaterally painful leg swelling.Jugular venous distension and Kussmaul sign (in the event of a massive pulmonary embolism).Tachycardia ( ∼ 25% of cases), hypotension.Possibly decreased breath sounds, dullness on percussion, split second heart sound audible in some cases.Sudden pleuritic chest pain ( ∼ 50% of cases), worse with inspiration.

Dyspnea and tachypnea ( > 50% of cases).Acute onset of symptoms, often triggered by a specific event (e.g., on rising in the morning, sudden physical strain/exercise).Pulmonary vasoconstriction: thromboxane A 2, prostaglandins, adenosine, thrombin, and serotonin secreted by activated platelet and the thrombus → pulmonary vasoconstriction and bronchospasm.Elevated pulmonary artery pressure ( PAP) due to blockage → right ventricular pressure overload → forward failure with decreased cardiac output → hypotension and tachycardia.Mechanical vessel obstruction → vent ilation- perfusion mismatch → arterial hypoxemia ( ↓ PaO 2 ) and elevated A-a gradient (See “Diagnostics” below.).Triggers respiratory drive → hyperventilation and tachypnea → respiratory alkalosis with hypocapnia ( ↓ PaCO 2).Leads to surfactant dysfunction → atelectasis → ↓ PaO 2.Causes pleuritic chest pain and hemoptysis.Infarction and inflammation of the lungs and pleura.Pathophysiologic response of the lung to arterial obstruction.

” ) → deep vein thrombosis in the legs or pelvis (most commonly iliac vein ) → embolization to pulmonary arteries via inferior vena cava → partial or complete obstruction of pulmonary arteries

Mechanism: thrombus formation (see “ Virchow's triad.

In massive PE with obstructive shock, the thrombus is resolved with thrombolytic agents or embolectomy. Anticoagulation with heparin is initiated to prevent further thromboembolisms as well as to promote the gradual dissolution of the embolism and the underlying thrombosis. Another commonly performed test is the measurement of D-dimer levels, which can rule out PE if negative. Arterial blood gas analysis typically shows evidence of respiratory alkalosis with low partial oxygen pressure, low partial carbon dioxide pressure, and elevated pH. The diagnosis of PE is based primarily on the clinical findings and is confirmed by the detection of an embolism in CT pulmonary angiography ( CTPA). Symptoms are often nonspecific, including chest pain, coughing, dyspnea, and tachycardia. The clinical presentation is variable and, depending on the extent of vessel obstruction, can range from asymptomatic to obstructive shock. Risk factors include immobility, inherited hypercoagulability disorders, pregnancy, puerperium, and recent surgery. In most cases, the embolism is caused by blood thrombi, which arise from the deep vein system in the legs or pelvis ( deep vein thrombosis) and embolize to the lungs via the inferior vena cava. Pulmonary embolism ( PE) is the obstruction of one or more pulmonary arteries by solid, liquid, or gaseous masses.

Pe ecg findings