A pulmonary embolus (PE) usually results after a deep vein thrombus partially or totally dislodges from the pelvis, thigh, or calf. The clot then lodges in one or more of the pulmonary arteries and obstructs forward blood flow and oxygen supply to the lung parenchyma.
Pressure is backed up and results in increased pulmonary artery pressures and vascular resistance, right ventricular failure, tachycardia, and shock. Alveolar dead space is increased


which results in ventilation/perfusion mismatching and decreased PaO2,. The embolus releases chemicals that decrease surfactant and increase bronchoconstriction. Hyperventilation due to carbon dioxide retention results in decreased PaCO2,. Fat embolism, septic embolism, or amniotic fluid embolism are rarely causes of PE and when they are, usually occlude smaller arterioles or capillaries. A pulmonary embolus is classified as being massive when more than half the pulmonary artery circulation is occluded.
Infarction of the pulmonary circulation occurs less than 10 per cent of the time and usually results when the patient has an underlying chronic cardiac or pulmonary disease. Pulmonary infarcts may be reabsorbed and fibrosis may cause scar tissue formation. Usually collateral pulmonary circulation maintains lung tissue viability.


The main risk factors that may predispose pulmonary embolism formation are bedrest, immobility, cardiac disease, venous disease, pregnancy, malignancy, fractures, estrogen contraceptives, obesity, burns, blood dyscrasias, surgery, and trauma. Thrombus formation occurs with blood flow stasis, coagulopathy alterations, and damage to the endothelium of the vessel walls, and these three factors are known as Virchow’s triad.
The most common signs/symptoms are dyspnea, chest pain, and cough with hemoptysis. Other symptoms may be present, such as lightheadedness, diaphoresis, cyanosis, pleural friction rubs, S, split, tachypnea, tachycardia, anxiety, mental changes, gallops, dysrhythmias, rales, and hypotension, but are dependent on the size of the embolus and presence of infarction or complications.
Laboratory: PTTs done daily to monitor heparin therapy; LDH may be elevated in pulmonary embolus, but other diagnoses must be ruled out; fibrin split products usually increase consistently with PE; CBC may show increased hematocrit due to hemoconcentration, and increased RBCs
Chest x-ray: used to rule out other pulmonary diseases; shows atelectasis, elevated diaphragm and pleural effusions, prominence of pulmonary artery, and occasionally, a wedge-shaped infiltrate commonly seen in pulmonary embolism
Nuclear radiographic testing: lung scans are used to show perfusion defects beyond occluded vasculature; xenon ventilation scans are used to differentiate between pulmonary embolism and COPD, and together with perfusion scans, will reveal ventilation/perfusion mismatch.
Pulmonary angiography: used as a definitive test when other tests do not ensure the diagnosis in high-risk patients; identifies intra-arterial filling defects and obstruction of pulmonary artery branches
Electrocardiography: used to reveal right axis deviation, right-sided heart strain, right bundle branch block, tall peaked P waves, ST segment depression and T wave inversion, as well as supraventricular tachydysrhythmias
Phlebography: used to identify deep vein thrombosis in legs
Oxygen: to provide supplemental oxygen to maintain oxygenation
Pulmonary artery catheterization: used to place catheter to enable hemodynamic monitoring and to assess response to therapies
Arterial blood gases: used to assess for hypoxemia and acid-base imbalances
Thoracentesis: may be used to rule out empyema if pleural effusion is noted on chest x-ray
Beta-blockers: used in pulmonary hypertension to dilate the pulmonary vasculature to increase tissue per fusion
Cardiac glycosides: used only if absolutely mandatory during the acute hypoxemia phase due to the potential for lethal dysrhythmias or cardiac failure
Analgesics: used to alleviate pain and discomfort
Anticoagulants: heparin is used initially in the treatment of PE, with change to coumadin/warfarin PO for 3-6 months
Thrombolytics: streptokinase or urokinase enhances conversion of plasminogen to plasmin to prevent venous thrombus Antiplatelet drugs: aspirin and dipyridamole used to prevent venous thromboembolism
Surgery: embolectomy may be performed to remove the clot; umbrella filter may be placed or surgical interruption of the inferior vena cava may be performed to prevent migration of clots into the pulmonary vasculature
Ineffective breathing pattern
Related to: increase in alveolar dead space, physio- logic lung changes due to embolism, bleeding, increased secretions, decreased lung expansion, inflammation
Defining characteristics: dyspnea, use of accessory muscles, shallow respirations, tachypnea, increased work of breathing, decreased chest expansion on involved side, cough with or without productivity) adventitious breath sounds
Outcome Criteria
Patient will be eupneic with clear lung fields and arterial blood gases within normal limits.
Monitor respiratory status for changes in rate and depth, use of accessory muscles, increased work of breathing, nasal flaring, and symmetrical chest expansion.
In PE, respiratory rate is usually increased. The effort of breathing is increased and dyspnea is often the first sign of PE. Depending on the severity and location of the PE, depth of respirations may vary. Chest expansion may be decreased on the affected side due to atelectasis or pain.
Provide supplemental oxygen via nasal cannula or mask.
Provides oxygen and may decrease work of breathing.
Monitor for presence of cough and character of sputum.
Bloody secretions may result from pulmonary infarction or abnormal anticoagulation. A dry cough may result with alveolar congestion.
Auscultate lung fields for adventitious breath sounds and/or rubs.
Breath sounds may be diminished or absent if airway is obstructed due to bleeding, clotting, or collapse. Rhonchi or wheezing may result in conjunction with obstruction.
Auscultate heart sounds.
Splitting of S, may occur with pulmonary embolus.
Encourage deep breathing and effective coughing exercises.
Improves lung expansion and helps to remove secretions which may be increased with PE.

Information, Instruction, Demonstration
Prepare patient/family for placement on mechanical ventilation.
May be required if respiratory distress is severe.
Instruct on avoiding shallow respirations and splinting.
Eupnea decreases potential for atelectasis and improves venous return.
Prepare patient/family for bronchoscopy as warranted.
May be required to remove mucous plugs and/or clots in order to clear airways.

Discharge or Maintenance Evaluation
·       Patient will be able to maintain his own respirations without mechanical assistance.
·       Patient will be eupneic, with no adventitious lung or heart sounds.
·       Patient will be able to recall all information accurately.
Impaired gas exchange
[See Mechanical Ventilation]
Related to: atelectasis, airway obstruction, alveolar collapse, pulmonary edema, increased secretions, active bleeding, altered blood flow to lung, shunting
Defining characteristics: dyspnea, restlessness, anxiety, apprehension, cyanosis, arterial blood gas changes, hypoxemia, hypoxia, hypercapnia, decreased oxygen saturation
Risk for decreased cardiac output
[See Heart Failure]
Related to: dysrhythmias, cardiogenic shock, heart failure
Defining characteristics: elevated blood pressure, elevated mean arterial blood pressure, elevated systemic vascular resistance, cardiac output less than 4 L/min or cardiac index less than 2.7 L/min/m2, cold, pale extremities, EKG changes, hypotension, S, split sounds, S3 or S4 gallops, dyspnea, crackles (rales), chest pain
Risk for altered tissue perfusion: cardiopulmonary, peripheral, cerebral
Related to: impaired blood flow, alveolar perfusion and gas exchange impairment, occlusion of the pulmonary artery, migration of embolus, hypoxemia, increased cardiac workload
Defining characteristics: dyspnea, chest pain, tachycardia, dysrhythmias, productive cough, hemoptysis, edema, cyanosis, syncope, jugular vein distention, weak pulses, hypotension, convulsions, loss of consciousness, restlessness, hemiplegia, coma
Outcome Criteria
Patient will be hemodynamically stable, eupneic, with no alterations in perfusion to any body system.
Monitor vital signs and notify MD for significant changes.
Hypoxemia will result in increased heart rate as the body tries to compensate for the decrease in perfusion.
Monitor EKG for rhythm disturbances and treat as indicated.
Hypoxemia, right-sided heart strain, and electrolyte imbalances may induce dysrhythmias.
Auscultate for S, or S4 heart sounds.
Increases in heart workload may result in heart strain and failure as perfusion decreases, and may result in gallop rhythm.
Monitor for presence of peripheral pulses and notify MD for significant changes.
Presence of deep vein thrombus may occlude the circulation and result in diminished or absent pulses.
Assess for Homan's and Pratt's signs.
Presence of these signs may or may not be related to PE.
Assess skin color, temperature and capillary refill.
Impairment of blood flow may induce pallor or cyanosis to the skin or mucous membranes. Cool clammy skin or mottling may indicate peripheral vasoconstriction/shock.
Monitor for restlessness or changes in mental status or level of consciousness.
May indicate occlusion, impaired cerebral blood flow, hypoxia, or development of stroke.
Information, Instruction, Demonstration
Prepare patient for insertion of pulmonary artery catheter.
May be required to monitor hemodynamic status and assess response to therapy.
Prepare patient for surgery as warranted.
Surgical intervention may be required if patient develops recurrent emboli in spite of treatment, or if anticoagulant therapy cannot be given. Ligation of the vena cava or insertion of an umbrella filter may be necessary.
Instruct on thrombolytic agents as warranted.
Streptokinase, urokinase, or alteplase (t-PA) may be required if the pulmonary embolus is massive and compromises hemodynamic stability.

Discharge or Maintenance Evaluation
·       Patient will have adequate tissue perfusion to all body systems.
·       Patient will have stable hemodynamic parameters and vital signs will be within normal limits.
·       Oxygenation will be optimal as evidenced by pulse oximetry greater than 90% and adequate ABGs.