Pulmonary embolism (PE) is a common and potentially lethal condition. Most clients who succumb to PE do so within the first few hours of the event. Despite diagnostic advances, delays in pulmonary embolism diagnosis are common and represent an important issue. As a cause of sudden death, massive pulmonary embolism is second only to sudden cardiac death
A pulmonary embolism occurs when a blood clot (thrombus) becomes lodged in an artery in the lung and blocks blood flow to the lung. PE usually arises from a thrombus that originates in the deep venous system of the lower extremities; however, it rarely also originates in the pelvic, renal, upper extremity veins, or right heart chambers. 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
Three primary influences predispose the client to blood clot formation; these form the Virchow triad, which consists of the following:
- Endothelial injury. Thrombosis usually originates as a platelet nidus on valves in the veins of the lower extremities. Further growth occurs by accretion of platelets and fibrin and progression to red fibrin thrombus, which may either break off and embolize or result in total occlusion of the vein
- Stasis or turbulence of blood flow. Venous stasis leads to the accumulation of platelets and thrombin in veins. Increased viscosity may occur due to polycythemia and dehydration, immobility, raised venous pressure in cardiac failure, or compression of a vein by a tumor.
- Blood hypercoagulability. Concomitant hypercoagulability may be present in disease states where prolonged venous stasis or injury to veins occurs.
Risk factors can be classified as genetic and acquired. Genetic risk factors include:
- Thrombophilia. Hereditary factors associated with the development of pulmonary embolism include antithrombin III deficiency, protein C deficiency, protein S deficiency, factor V Leiden (most common genetic risk factor for thrombophilia), plasminogen abnormality, plasminogen activator abnormality, fibrinogen abnormality, and resistance to activated protein C.
Acquired risk factors include:
- Prolonged immobilization. Immobilization leads to local venous stasis by the accumulation of clotting factors and fibrin, resulting in blood clot formation. The risk of PE increases with prolonged bed rest or immobilization of a limb in a cast.
- Surgery and trauma. Surgical and accidental traumas predispose clients to venous thromboembolism by activating clotting factors and causing immobility. PE may account for 15% of all postoperative deaths.
- Obesity. It has been shown that the risk of venous thromboembolism (VTE) increases with increasing BMI. The risk is higher when obesity interacts with other thrombotic risk factors.
- Pregnancy. The incidence of thromboembolic disease in pregnancy has been reported to range from one case to 1400 deliveries. Fatal events are rare, with one to two cases occurring per 100,000 pregnancies.
- Oral contraceptive use. Estrogen-containing birth control pills have increased the occurrence of venous thromboembolism in healthy women. The risk is proportional to the estrogen content and is increased in post-menopausal women on hormonal replacement therapy.
- Malignancy. Malignancy has been identified in 17% of clients with VTE. Pulmonary emboli have been reported to occur in association with solid tumors, leukemias, and lymphomas.
- Cigarette smoking. Current smoking is associated with a 50% increased risk of VTE in clients diagnosed with active cancer. In cancer, the risk of VTE among current smokers remains unchanged after adjustments for cancer site and metastasis, suggesting that the effect was not explained by more advanced cancers in smokers than non-smokers.
The most common symptoms of PE include:
- Dyspnea. Dyspnea may be acute and severe in central PE, whereas it is often mild and transient in small peripheral PE. In clients with preexisting heart failure or pulmonary disease, worsening dyspnea may be the only symptom.
- Pleuritic chest pain. Chest pain is a frequent symptom and is usually caused by pleural irritation due to distal emboli causing pulmonary infarction. In central PE, chest pain may be from underlying right ventricular ischemia and needs to be differentiated from an acute coronary syndrome or aortic dissection.
- Cough and hemoptysis. Cough is present in approximately 50% of children with pulmonary emboli; tachypnea occurs with the same frequency, Hemoptysis is a feature in a minority of children with PE, occurring in about 30% of cases.
- Presyncope or syncope. Syncope may occur and may be associated with a higher prevalence of hemodynamic instability and RV dysfunction.
Pulmonary Embolism
PE reduces the cross-sectional area of the pulmonary vascular bed, resulting in an increment in pulmonary vascular resistance, which, in turn, increases the right ventricular afterload. If the afterload is increased severely, right ventricular failure may ensue. Additionally, the humoral and reflex mechanisms contribute to pulmonary arterial constriction. Chronic pulmonary hypertension may occur with failure of the initial embolus to undergo lyses or in the setting of recurrent thromboembolism.
Nursing interventions for a client diagnosed with pulmonary embolism initially focus on supportive measures. The following are nursing diagnoses associated with pulmonary embolism.
- Ineffective Tissue Perfusion
- Impaired Gas Exchange
- Acute Pain
Pulmonary Embolism (PE) Nursing Care Plan
Below are sample nursing care plans for the problems identified above.
Ineffective Tissue Perfusion
In PE, pulmonary vascular resistance (PVR) increases due to mechanical obstruction of the vascular bed with thrombus and hypoxic vasoconstriction. Pulmonary artery pressure (PAP) increases if the thromboemboli occludes greater than 30 to 50% of the total cross-sectional area of the pulmonary arterial bed. Increased PVR increases the right ventricular afterload, which impedes right ventricular outflow, which, in turn, causes right ventricular dilation and flattening or bowing of the intraventricular septum.
Nursing Diagnosis
- Ineffective Tissue Perfusion
Related Factors
- Decreased blood flow
- Venous stasis
- Partial or complete venous obstruction
Evidenced by
- Tissue edema
- Pain
- Diminished peripheral pulses
- Slow or diminished capillary refill
- Pallor or erythema
Desired Outcomes
After the implementation of nursing interventions, the client is expected to:
- Demonstrate improved perfusion as evidenced by present peripheral pulses, equal skin color distribution, and normal temperature and absence of edema.
- Engage in behaviors or actions to enhance tissue perfusion.
- Display increasing tolerance to activities.
Nursing Interventions
| Assessment | Rationale |
| Inspect the lower extremities for skin color and temperature changes as well as edema. | Symptoms help distinguish between thrombophlebitis and DVT. Redness, heat, tenderness, and localized edema are characteristic of superficial involvement. Unilateral edema is one of the most reliable physical findings in DVT. |
| Note symmetry calves; measure and record calf circumference. | Calf vein involvement is associated with the absence of edema; femoral vein involvement is associated with mild to moderate edema, and iliofemoral vein thrombosis is characterized by severe edema. |
| Assess capillary refill and cyanosis. | A diminished capillary refill is usually present in DVT and PE. If cyanosis and hypoxemia are present, it may suggest a massive embolism leading to a marked ventilation-perfusion (V/Q) mismatch and systemic hypoxemia. |
| Palpate gently for local tissue tension, stretched skin, and knots and bumps along the course of the vein. | Distention of superficial veins can occur in DVT, which predisposes to PE because of backflow through communicating veins. Thrombophlebitis in superficial veins may be visible or palpable. |
| Independent | |
| Promote early ambulation. | Short, frequent walks are better for extremities and prevent pulmonary complications than one long walk. If the client is confined to the bed, ensure range-of-motion exercises. Activity is recommended as tolerated. |
| Elevate the client’s legs when in bed or chair, as indicated. | This reduces tissue swelling and rapidly empties superficial and tibial veins, preventing overdistention and thereby increasing venous return. |
| Assist in active or passive exercises while in bed. | Assist the client in performing exercises such as flexing, extending, and rotating the feet periodically. These measures are designed to increase the venous return from the lower extremities and reduce venous stasis as well as improve general muscle tone and strength. They also promote normal organ function and enhance general well-being. |
| Instruct the client to avoid crossing the legs or hyperflexing the knee. | Physical restriction of the circulation impairs blood flow and increases venous stasis in pelvic, popliteal, and leg vessels, thus increasing swelling and discomfort. |
| Instruct the client to avoid rubbing or massaging the affected area. | This activity potentiates the risk of fragmenting and dislodging thrombus, causing embolization, and increasing the risk of complications. |
| Encourage the client to perform deep-breathing exercises. | Deep breathing exercises increase negative pressure in the thorax, which assists in emptying the large veins. |
| Dependent/Collaborative | |
| Administer thrombolytic therapy as prescribed. | All clients diagnosed with PE require rapid risk stratification. Thrombolytic therapy should be used in clients with acute PE associated with hypotension who do not have a high bleeding risk. Do not delay thrombolysis in this population because irreversible cardiogenic shock can develop. |
| Administer anticoagulants as prescribed. | In clients diagnosed with acute PE, anticoagulation with IV unfractionated heparin (UFH), low molecular-weight heparin (LMWH), or fondaparinux is preferred over no anticoagulation. UFH is the recommended form of initial anticoagulation, especially when medical or surgical procedures are likely to be performed. |
| Assist in embolectomy as appropriate. | Either catheter embolectomy and fragmentation or surgical embolectomy is reasonable for clients with massive PE who have contraindications to fibrinolysis. These interventions are not recommended for clients with low-risk or submissive acute pulmonary embolism who have a minor RV dysfunction and no clinical worsening. |
| Assist and instruct the client in wearing compression stockings. | For clients with proximal DVT, the use of elastic compression stockings provides a safe and effective adjunctive treatment that can limit postphlebitic syndrome. Stockings with a pressure of 30 to 40 mm Hg at the ankle, worn for two years following diagnosis, are recommended to reduce the risk of postphlebitic syndrome. |
| Monitor laboratory studies as indicated. | This monitors anticoagulant therapy and the presence of risk factors such as hemoconcentration and dehydration, which potentiate clot formation. |
Impaired Gas Exchange
PE leads to impaired gas exchange due to obstruction of the pulmonary vascular bed leading to a mismatch in the ventilation-to-perfusion ratio because alveolar ventilation remains the same, but pulmonary capillary blood flow decreases, effectively leading to dead space ventilation and hypoxemia.
Nursing Diagnosis
- Impaired Gas Exchange
Related Factors
- Altered blood flow to alveoli or to major portions of the lung
- Alveolar-capillary membrane changes
- Airway or alveolar collapse
- Pulmonary edema or effusion
- Excessive secretions
Evidenced by
- Profound dyspnea
- Restlessness
- Apprehension or somnolence
- Cyanosis
- Changes in ABG levels or pulse oximetry
Desired Outcomes
After the implementation of nursing interventions, the client is expected to:
- Demonstrate adequate ventilation and oxygenation by ABGs within the normal range.
- Report or display resolution or absence of symptoms of respiratory distress.
Nursing Interventions
| Assessment | Rationale |
| Assess respiratory rate and depth. | Tachypnea and dyspnea accompany pulmonary obstruction. Dyspnea and increased work of breathing may be the first or the only sign of subacute PE. Severe respiratory distress and failure accompany moderate to severe loss of functional lung units. |
| Auscultate the lungs for areas of decreased and absent breath sounds and the presence of adventitious sounds. | Nonventilated areas may be identified by the absence of breath sounds. Crackles occur in fluid-filled tissues and airways or may reflect cardiac decompensation. |
| Observe for generalized duskiness and cyanosis in “warm tissues”, such as the earlobes, lips, tongue, and buccal membranes. | These signs are indicative of hypoxemia. Cyanosis suggests a massive embolism leading to a marked V/Q perfusion mismatch and systemic hypoxemia (Ouellette & Mosenifar, 2020). |
| Monitor vital signs and note changes in cardiac rhythm. | Tachycardia, tachypnea, and changes in BP are associated with advancing hypoxemia and acidosis. Rhythm alterations and extra heart sounds may reflect increased cardiac workload related to worsening ventilation imbalance. |
| Assess the level of consciousness and mentation changes. | Systemic hypoxemia may be demonstrated initially by restlessness and irritability, then by progressively decreasing mentation. |
| Assess activity intolerance, such as reports of weakness and fatigue or increased dyspnea upon exertion. | These parameters assist in determining the client’s response to resumed activities and ability to participate in self-care. |
| Independent | |
| Institute measures to restore or maintain patent airways, such as deep breathing exercises, coughing, and suctioning. | Plugged or collapsed airways reduce the number of functional alveoli, negatively affecting gas exchange. |
| Elevate the head of the bed as tolerated. | Head elevation promotes maximal chest expansion, making it easier to breathe and enhancing psychological and physiological comfort. |
| Assist with frequent changes of position, and encourage the client to ambulate early. | Turning and ambulation enhance the aeration of different lung segments, thereby improving oxygen diffusion. |
| Encourage the client to express their feelings. Provide information about the current situation. | Feelings of fear and severe anxiety are associated with the inability to breathe and may actually increase oxygen consumption and demand. Information may allay anxiety related to the unknown and may help reduce fear concerning personal safety. |
| Dependent/Collaborative | |
| Administer supplemental oxygen as appropriate. | This maximizes available oxygen for gas exchange, reducing the work of breathing. If the obstruction is large or hypoxemia does not respond to supplemental oxygenation, it may be necessary to move the client to a critical care area for intubation and mechanical ventilation. |
| Provide supplemental humidification, such as ultrasonic nebulizers. | Ultrasonic nebulizers deliver moisture to mucous membranes and help liquefy the secretions to facilitate airway clearance. |
| Assist with chest physiotherapy as indicated. | Chest physiotherapy, such as postural drainage and percussion of nonaffected areas may facilitate deeper respiratory effort and promotes drainage of secretions from lung segments into the bronchi, where they may more readily be removed by coughing or suctioning. |
| Monitor ABG levels or pulse oximetry. | Hypoxemia is present in varying degrees, depending on the amount of airway obstruction, usual cardiopulmonary function, and the presence or degree of shock. Respiratory alkalosis and metabolic acidosis may also be present. |
| Prepare for or assist in a bronchoscopy or a lung scan. | Bronchoscopy may be done to remove blood clots and clear airways. A lung scan may reveal the pattern of abnormal perfusion in areas of ventilation, reflecting ventilation and perfusion mismatch, confirming the diagnosis of PE and degree of obstruction. |
| Prepare for surgical intervention, as indicated. | In clients with submassive acute PE, either catheter embolectomy or surgical embolectomy may be considered if they have clinical evidence of an adverse prognosis. These interventions are not recommended for clients with low-risk or submissive acute PE who have minor right ventricular dysfunction, minor myocardial necrosis, and no clinical worsening. |
Acute Pain
Acute onset chest pain is one of the most common presentations in the emergency department and could be seen as the sentinel symptom of life-threatening diseases, including acute coronary syndrome, aortic dissection, tension pneumothorax, pulmonary embolism, and esophagus rupture. Pleuritic chest pain without other symptoms or risk factors may be a presentation of PE. Pleuritic or respirophasic chest pain is a particularly worrisome symptom. Pleuritic chest pain is reported to occur in as many as 84% of clients with PE Its presence suggests that the embolus is located more peripherally and thus may be smaller.
Nursing Diagnosis
- Acute Pain
Related Factors
- Diminished arterial circulation and oxygenation of tissues
- Accumulation of lactic acid in tissues
- Inflammatory process
Evidenced by
- Reports of chest pain
- Guarding of affected area
- Restlessness, distraction behaviors
Desired Outcomes
After the implementation of nursing interventions, the client is expected to:
- Report that pain or discomfort is alleviated or controlled.
- Verbalize methods that provide relief.
- Display a relaxed manner; be able to sleep or rest and engaged in desired activities.
Nursing Interventions
| Assessment | Rationale |
| Assess the degree and characteristics of pain. | The degree of pain is directly related to the extent of circulatory deficit, inflammatory process, degree of tissue ischemia, and extent of edema associated with thrombus development. Changes in the characteristics of pain may indicate the development of complications. |
| Monitor vital signs, especially temperature. | Elevations in the heart rate may indicate increased discomfort that may occur in response to fever and inflammatory processes. Fever can also increase the client’s discomfort. |
| Determine reports of sudden or sharp chest pain, accompanied by dyspnea, tachycardia, apprehension, or development of new pain. | These signs and symptoms suggest the presence of PE as a complication of DVT or peripheral arterial occlusion. Both conditions require prompt medical evaluation and treatment. |
| Independent | |
| Instruct the client to remain on bed rest during the acute phase. Wearing compression stockings is advised. | This may reduce discomfort associated with muscle contraction and movement. Regular ROM exercises, leg elevation, and wearing compression stockings may aid in preventing pulmonary embolism. |
| Elevate the affected extremity. | Elevation of the lower extremities encourages venous return to facilitate circulation, reducing stasis and edema formation. |
| Provide and promote the use of a foot cradle. | A foot cradle keeps the pressure of bedclothes off the affected leg, thereby reducing pressure discomfort. |
| Encourage the client to change positions frequently. | Changing positions frequently reduces muscle fatigue, helps minimize muscle spasms, and maximizes circulation to the tissues. |
| Dependent/Collaborative | |
| Administer analgesics and antipyretics as indicated. | Analgesics relieve the pain and decrease muscle tension. Antipyretics reduce fever and inflammation. However, the risk of bleeding may be increased by the concurrent use of drugs that affect platelet function, such as aspirin and NSAIDs. |
| Apply moist heat to the affected extremity as appropriate. | Moist heat causes vasodilation, which increases circulation, relaxes the muscles, and may stimulate the release of natural endorphins. |
References
- Hotoleanu, C. (2020). Association between obesity and venous thromboembolism – PMC. NCBI. Retrieved November 29, 2022, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7243888/
- Lu, Y.-W., Tsai, Y.-L., Chang, C.-C., & Huang, P.-H. (2018, March). A potential diagnostic pitfall in acute chest pain: Massive pulmonary embolism mimicking acute ST elevation myocardial infarction. American Journal of Emergency Medicine, 36(3). https://doi.org/10.1016/j.ajem.2017.11.046
- Moorhouse, M. F., Doenges, M. E., & Murr, A. C. (2010). Nursing Care Plans: Guidelines for Individualizing Client Care Across the Life Span. F.A. Davis Company.
- Ouellette, D. R., & Mosenifar, Z. (2020, September 18). Pulmonary Embolism (PE): Practice Essentials, Background, Anatomy. Medscape Reference. Retrieved November 29, 2022, from https://emedicine.medscape.com/article/300901-overview
- Paulsen, B., Gran, O. V., Severinsen, M. T., Hammerstrom, J., Kristensen, S. R., Cannegieter, S. C., Skille, H., Tjonneland, A., Rosendaal, F. R., Overvad, K., Naess, I. A., Hansen, J.-B., & Braekken, S. K. (2019, January 17). Association of smoking and cancer with the risk of venous thromboembolism: the Scandinavian Thrombosis and Cancer cohort. Scientific Reports. Retrieved November 29, 2022, from https://www.nature.com/articles/s41598-021-98062-0
- Vyas, V., & Goyal, A. (2022, August 8). Acute Pulmonary Embolism – StatPearls. NCBI. Retrieved November 29, 2022, from https://www.ncbi.nlm.nih.gov/books/NBK560551/
