4 Pulmonary Embolism Nursing Care Plans

Pulmonary embolism refers to the obstruction of the pulmonary artery or one of its branches by a thrombus that originates somewhere in the venous system or in the right side of the heart. The clinical symptoms depend on the size and location of the embolus. Careful analysis of risk factors aids in diagnosis; these includes hypercoagulability, damage to the walls of the veins, prolonged immobility, recent surgery, deep vein thrombosis, postpartum state, and certain medical condition such as polycythemia, heart failure, and trauma. Treatment approaches vary depending on the degree of cardiopulmonary compromise associated with the PE. They can range from thrombolytic therapy in acute situations to anticoagulant therapy and general measures to optimize respiratory and vascular status (e.g., oxygen therapy, compression stockings).

Pulmonary embolism is a frequent hospital-acquired condition and one of the most common causes of death in hospitalized clients. Preventing thrombus formation is a critical nursing role.

Nursing Care Plans

Planning and goals for a client with pulmonary embolism include the following:

  • Decreasing the risk of pulmonary embolism
  • Preventing the formation of thrombus (ambulation and passive leg exercises)
  • Assessing potential for pulmonary embolism
  • Monitoring thrombolytic therapy
  • Managing pain and relieving anxiety
  • Managing oxygen therapy
  • Preventing possible complication

Here are four (4) nursing care plans (NCP) for pulmonary embolism:

  1. Impaired Gas Exchange
  2. Ineffective Breathing Pattern
  3. Deficient Knowledge
  4. Risk for Bleeding
  5. See Also and Further Reading
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Impaired Gas Exchange: Excess or deficit in oxygenation and/or carbon dioxide elimination at the alveolar-capillary membrane.

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 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

  • 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, relaxed breathing, and baseline HR for the client.
Nursing Interventions Rationale
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.
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 the rapid respiratory rate.
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.
Auscultate lung sounds, noting areas of decreased ventilation and the presence of adventitious sounds. Crackles are common clinical findings with pulmonary embolism.
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 an ischemic necrosis or infarction of the lung area.
Assess for calf tenderness, redness, swelling, and hardened areas. Pulmonary embolism often arises from a deep vein thrombosis and may have been previously overlooked.
Monitor for any changes in the ABGs. ABG analysis can be normal or show hypoxemia and hypocapnia because of tachypnea. Later signs of respiratory failure include low PaOand elevated Paco2. Metabolic acidosis results from a lactic acid buildup from tissue hypoxia.
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.
Maintain client on bed rest. May resume activity gradually as tolerated. This will decrease the oxygen demand during an episode of acute respiratory distress.
Position the client properly to facilitate ventilation-perfusion matching. Upright and sitting position optimize diaphragmatic excursions and lung perfusion. When the client is positioned on one side, the affected area should not be dependent.
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.
Anticipate the need to start anticoagulant therapy and, if there is a 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.
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