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Pulmonary Embolism (PE)

Obstruction of the pulmonary arterial bed by a dislodged thrombus, which may be fatal. Complication of venous thromboembolism.

Aetiology DVT and all associated risk factors. Untreated acute proximal DVT causes clinical PE in 33-50% of
patients. Atrial fibrillation Valvular heart disease

Pathophysiology A thrombus arising from DVT dislodges, travels through the bloodstream (large veins & vena cava)

and through the right atrium into the lungs, lodging in the arterial bed of the lungs. After traveling to the lung, large thrombi can lodge at the bifurcation of the main pulmonary artery or the lobar branches and cause hemodynamic compromise. Smaller thrombi typically travel more distally, occluding smaller vessels in the lung periphery. Mechanical obstruction of the pulmonary circulation leads to reflex vasoconstriction due to release of vasoactive agents (ie, serotonin) by platelets. The arterial obstruction increases alveolar dead space and leads to redistribution of blood flow, thus impairing gas exchange due to the creation of low ventilation-perfusion areas within the lung. Obstruction of pulmonary blood flow by an embolus causes reflex bronchoconstriction in the affected area of the lung, augmenting airway resistance and leading to impaired gas exchange and loss of alveolar surfactant. The increased pulmonary vascular resistance causes an increase in right ventricular afterload, and tension rises in the right ventricular wall, which may lead to dilatation, dysfunction, and ischemia of the right ventricle. The result is right heart failure, cardiogenic shock and even death.

Clinical Manifestations
Diagnosis of PE can be difficult because classic signs and symptoms are often absent in patients and it can mimic other diseases, such as pneumonia. The "classic" presentation with abrupt onset of pleuritic chest pain, shortness of breath, and hypoxia is rarely seen. A thorough history and physical examination often provide the first clue for early diagnosis of PE. History: acute onset of shortness of breath; sometimes able to pinpoint the moment of distress. May have signs of deep venous thrombosis, lower extremity swelling and warmth to touch or tenderness. Tachypnea (respiratory rate _ 20 breaths/min) Dyspnea Tachypnea (more than 18 breaths per minute) Tachycardia (heart rate >100 bpm) Pleuritic or central chest pain Cyanosis Hemoptysis Sudden collapse Cough Sweating Pyrexia may be present Patients with massive pulmonary embolism are in shock. They have systemic hypotension, poor perfusion of the extremities, tachycardia, and tachypnea. In addition, patients appear weak, pale, sweaty, and oliguric and develop impaired mentation. Very high fatality rate (About 1/3 of PE cases are fatal) most people dying from PE do so in the first 30 minutes. If a patient is thought to have PE or has documented PE, the absence of tenderness, erythema, edema, or a palpable cord upon examination of the lower extremities does not rule out

thrombophlebitis, nor does it imply a source other than a leg vein. More than two thirds of patients with proven PE lack any clinically evident phlebitis. Nearly one third of patients with proven PE have no identifiable source of DVT, despite a thorough investigation. DVTs can lie undetected within the deep venous system of the lower extremity and pelvis in 90% of cases.

Diagnosis
Imaging studies: Chest radiograph: findings most often are normal. Doppler ultrasonography: can evidence the presence of thrombus within a vein Pulmonary angiography: diagnostic criterion standard, which allows for the visualization of the pulmonary vasculature using contrast material. Evidences a cutoff of a vein and lack of flow to the affected area. Ventilation-perfusion scanning: most common screening technique. Helical (spiral) CT scanning Contrast venography: invasive technique that can provide direct proof of thrombus by demonstrating a filling defect with the aide of contrast medium through the deep venous system Echocardiography can demonstrate signs of right heart strain and can be used to identify signs of impending heart failure. Electrocardiography is of greatest value in ruling out myocardial infarction. Chest computed tomography Laboratory studies: D-dimer test: D-dimers are degradation products of cross-linked fibrin by plasmin and levels may be elevated in any medical condition where clots form (trauma, recent surgery, hemorrhage, cancer, and sepsis). D-dimer test can be used as a rapid screening measure in cases where leg swelling exists in the face of equivocal or negative clinical or radiologic findings. Additional blood work: coagulation studies to evaluate for a hypercoagulable state. ABGs: hypoxemia, hypocapnia, and respiratory alkalosis WBC count: may be normal or elevated (as high as 20,000) Serum troponin levels can be elevated due to acute right ventricular myocardial stretch Patients suspected of having pulmonary embolismbecause of unexplained dyspnea, tachypnea, or chest pain or the presence of risk factors for pulmonary embolismmust undergo diagnostic tests until the diagnosis is ascertained or eliminated or an alternative diagnosis is confirmed.

Nursing Intervention
ABC O2 therapy via cannula or mask; patient may need ventilation if lungs are severely compromised Monitor ABG levels Monitor coagulation studies and monitor for bleeding when on anti coagulants Analgesia See DVT nursing care for other considerations and patient education

Pharmacology
Immediate full anticoagulation is mandatory for all patients suspected to have DVT. Anticoagulant therapy Heparin is the first line of therapy. It is administered by bolus dosing, followed by a continuous infusion. A short course of heparin is followed by a longer course of oral anticoagulant, warfarin sodium. It should be started only after effective anticoagulation has been achieved, as there can be an increase in coagulability and thrombogenesis during the first few days of oral anticoagulant administration. The goal is to achieve an international normalized ratio (INR) of 2.0-3.0. Thrombolytic therapy Thrombolytic therapy dissolves recent clots promptly by activating a plasma proenzyme, plasminogen, to its active form, plasmin. Plasmin degrades fibrin to soluble peptides. Thrombolytic therapy speeds pulmonary tissue reperfusion and rapidly reverses the right heart failure. It

improves pulmonary capillary blood flow and more rapidly improves hemodynamic parameters. contraindications to thrombolysis include gastrointestinal bleeding within the last 6 months, active or recent internal bleeding, a history of hemorrhagic stroke, intracranial or intraspinal disease, recent cranial surgery or head trauma, and pregnancy. Other: The vena caval filter is designed to trap potentially lethal emboli while maintaining vena caval patency. It is indicated in cases where there is a contraindication to anticoagulation, when there has been a complication of anticoagulation, in the event of failure of anticoagulation, and in the case of pulmonary embolectomy. References: De Palo, V. A. (2010). Thromboembolism. Retrieved from http://emedicine.medscape.com/article/1267714-overview Gaspard, K. J. (2009). Disorders of hemostasis. In C. M. Porth & G. Matfin (Eds.), Pathophysiology: Concepts of altered health states (8th ed., pp. 262-277). Philadelphia, PA: Wolters Kluwer Health, Lippincott Williams & Wilkins. Matfin, G. (2009). Disorders of blood flow in the systemic circulation. In C. M. Porth & G. Matfin (Eds.), Pathophysiology: Concepts of altered health states (8th ed., pp. 477-504). Philadelphia, PA: Wolters Kluwer Health, Lippincott Williams & Wilkins. Morrison, R. (2006). Venous thromboembolism: Scope of the problem and the nurses role in risk assessment and prevention. Journal of Vascular Nursing 24(3), 82-90. doi:10.1016/j.jvn.2006.05.002 Ouelette, D. R. (2011). Pulmonary embolism. Retrieved from http://emedicine.medscape.com/article/300901-overview Patel, K. (2011). Deep venous thrombosis. Retrieved from http://emedicine.medscape.com/article/1911303-overview Pooler, C. (2009). Disorders of ventilation and gas exchange. In C. M. Porth & G. Matfin (Eds.), Pathophysiology: Concepts of altered health states (8th ed., pp. 701-738). Philadelphia, PA: Wolters Kluwer Health, Lippincott Williams & Wilkins.