4 Pulmonary Embolism Nursing Care Plans

Impaired Gas Exchange

Pulmonary physiology and consequent gas exchange impairment play a pivotal role in the high risk of death from PE.  The first phenomenon of acute PE is vascular occlusion. It causes a local increase in pulmonary arterial pressure resulting in pulmonary perfusion heterogeneity, with some hypoperfused areas and others presenting blood overflow. Since only minor alterations in ventilation distribution are common, there will be an imbalance between ventilation and perfusion, generating hypoxemia, tachypnea, and consequently, hypocapnia (Fernandes et al., 2019).

Nursing Diagnosis

• Impaired Gas Exchange

May be related to

• Decreased lung perfusion caused by the obstruction of pulmonary arterial blood flow by the embolus
• Decreased bronchial airflow associated with bronchoconstriction
• Increased physiological shunting caused by the collapse of alveoli resulting from surfactant loss
• Increased alveolar dead space

Possibly evidenced by

• Confusion
• Decreased PaO₂ and increased PaCO₂
• Desaturation (Oxygen saturation below 90%)
• Dyspnea
• Headache
• Hypercapnia
• Hypoxia
• Pale skin
• Restlessness/Irritability
• Tachypnea

Desired Outcomes

• The client will maintain adequate gas exchange, as evidenced by ABGs within the normal range, oxygen saturation of 90% or greater, alert response mentation or no further deterioration on the level of consciousness, and baseline HR for the client.
• The client will report or display resolution or absence of symptoms of respiratory distress.

Nursing Assessment and Rationales

1. Assess the skin color, nail beds, and mucous membranes for color changes.
Cool, pale skin occurs as a compensatory response to hypoxemia. When oxygen and perfusion become impaired, peripheral tissues become cyanotic. General “duskiness” and cyanosis in “warm tissues” such as earlobes, lips, tongue, and buccal membranes may indicate systemic hypoxemia.

2. Monitor for any changes in vital signs.
In initial hypoxia and hypercapnia, there is an increase in the respiratory rate, heart rate, and blood pressure. As the hypercapnia and hypoxia get worse, blood pressure may drop, heart rate tends to continue to be rapid and includes dysrhythmias, and respiratory failure ensues, with the client unable to maintain a rapid respiratory rate.

3. Assess for the signs and symptoms of hypoxia (such as confusion, headache, diaphoresis, restlessness, tachycardia, and pale skin).
Hypoxia results from increased dead space (ventilation without perfusion) that reduces effective gas exchange. Arterial hypoxemia is also a frequent, but not universal, finding in clients with acute embolism. The mechanisms of hypoxemia include ventilation-perfusion mismatch, intrapulmonary shunts, reduced cardiac output, and intracardiac shunt via a patent foramen ovale (Ouellette & Mosenifar, 2020).

4. Auscultate lung sounds, noting areas of decreased ventilation, and the presence of adventitious sounds.
Crackles are common clinical findings with pulmonary embolism. Crackles occur in fluid-filled tissues and airways or may reflect cardiac decompensation. Nonventilated areas may be identified by the absence of breath sounds.

5. Assess for the signs and symptoms of pulmonary infarction (such as fever, cough, bronchial breathing, hemoptysis, pleuritic pain, pleural friction rub, and consolidation).
A large pulmonary embolus or multiple small clots in a specific area of the lung can cause ischemic necrosis or infarction of the lung area. These clients present with acute onset of pleuritic chest pain, breathlessness, and hemoptysis. Although the chest pain may be clinically indistinguishable from ischemic myocardial pain, normal ECG findings and no response to nitroglycerin rule out myocardial pain (Ouellette & Mosenifar, 2020).

6. Assess for calf tenderness, redness, swelling, and hardened areas.
Pulmonary embolism often arises from a deep vein thrombosis and may have been previously overlooked. 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 (Ouellette & Mosenifar, 2020).

7. Monitor for any changes in the ABGs.
ABG analysis characteristically reveals hypoxemia, hypocapnia, and respiratory alkalosis. The PaO2 and the calculation of the alveolar-arterial oxygen gradient contribute to the diagnosis in a general population thought to have a pulmonary embolism (Ouellette & Mosenifar, 2020).

8. Monitor oxygen saturation as indicated.
Pulse oximetry is a useful tool in the clinical setting to detect changes in oxygenation. Oxygen saturation should be at 90% or greater. Hypoxemia is present in varying degrees, depending on the amount of airway obstruction, usual cardiopulmonary function, and presence and degree of shock.

9. Assess the level of consciousness and evaluate mentation changes.
Systemic hypoxemia may be demonstrated initially by restlessness and irritability, then by progressively decreasing mentation. Syncope may occur and may be associated with a higher prevalence of hemodynamic instability and right ventricular dysfunction (Vyas & Goyal, 2022).

10. Assess activity intolerance, such as reports of weakness and fatigue, vital sign changes, or increased dyspnea during exertion.
These parameters assist in determining the client’s response to resumed activities and the ability to participate in self-care.

Nursing Interventions and Rationales

1. Maintain the client on bed rest. May resume activity gradually as tolerated.
This will decrease the oxygen demand during an episode of acute respiratory distress. Activity is recommended as tolerated, with early ambulation preferred over bed rest when feasible (Ouellette & Mosenifar, 2020).

2. Position the client properly to facilitate ventilation-perfusion matching.
Upright and sitting positions optimize diaphragmatic excursions and lung perfusion. When the client is positioned on one side, the affected area should not be dependent. Elevate the head of the bed as tolerated to promote maximal chest expansion and enhance the client’s comfort.

3. Maintain patent airways.
Institute interventions to maintain a patent airway such as deep breathing exercises, coughing, and suctioning. Plugged or collapsed airways reduce the number of functional alveoli, negatively affecting gas exchange.

4. Assist the client in dealing with fear and anxiety that may be present.
Feelings of fear and severe anxiety are associated with the inability to breathe and may actually increase oxygen consumption and demand. Encourage the client to express their feelings so that the client may regain a sense of control over their emotions.

5. Monitor frequently and arrange for someone to stay with the client as appropriate. Provide information as indicated.
This provides assurance that changes in condition will be noted and that assistance is readily available. Provide brief explanations of what is happening and the expected effects of the interventions to allay the client’s anxiety.

6. Ensure appropriate application of compression stockings.
For clients who have had a proximal DVT, the use of elastic compression stockings provides a safe and effective adjunctive treatment that can limit postphlebitic syndrome. True gradient compression stockings are highly elastic. Compression stockings of this type have been proven effective in the prophylaxis of thromboembolism and are also effective in preventing the progression of a blood clot in clients who already have DVT and PE (Ouellette & Mosenifar, 2020).

7. Prepare the client for a lung scan.
This may reveal a pattern of abnormal perfusion in areas of ventilation, reflecting ventilation and perfusion mismatch, confirming the diagnosis of PE and degree of obstruction.

8. Administer IV fluids or fluids by mouth as indicated.
Increased fluids may be given to reduce hyperviscosity of the blood, which can potentiate thrombus formation. Be aware that IV fluids may help or hurt the client who is hypotensive from PE, depending on which point on the Starling curve describes the client’s condition. A cautious trial of a small fluid bolus may be attempted, with careful surveillance of the systolic and diastolic blood pressures and immediate cessation if the situation worsens after the fluid bolus (Ouellette & Mosenifar, 2020).

9. Administer oxygen as indicated.
Supplemental oxygen maintains adequate oxygenation, decreases the work of breathing, relieves dyspnea, and promotes comfort. The appropriate amount of oxygen needs to be continuously delivered so the client does not become desaturated. Mechanical ventilation may be necessary to provide respiratory support and as adjunctive therapy for a failing circulatory system (Ouellette & Mosenifar, 2020).

10. Anticipate the need to start anticoagulant therapy and, if there is massive thromboembolism, the use of thrombolytic therapy.
Heparin or enoxaparin (Lovenox) is used to prevent the recurrence of emboli. These medications do not dissolve clots that already exist. If a massive thrombus is present or the client is hemodynamically unstable, thrombolytic therapy (e.g, alteplase or reteplase [Retavase]) is used to directly lyse or dissolve the clot. The current recommendation is anticoagulation for at least three months; the need for extending the duration of anticoagulation should be reevaluated at that time (Ouellette & Mosenifar, 2020).

11. Assist with chest physiotherapy techniques, such as postural drainage and percussion of nonaffected areas, blow bottles, and incentive spirometry.
This facilitates deeper respiratory effort and promotes drainage of secretions from lung segments into bronchi, where they may be more readily removed by coughing or suctioning.

12. Assist in surgical interventions as indicated.
Vena caval ligation or insertion of an intracaval umbrella may be useful for clients with recurrent emboli despite adequate anticoagulation. Either catheter embolectomy and fragmentation or surgical embolectomy is reasonable for clients with massive PE who have contraindications to fibrinolysis or who remain unstable after receiving fibrinolysis (Ouellette & Mosenifar, 2020).