Pulmonary embolism refers to the obstruction of one or more pulmonary arteries by a thrombus (or thrombi) usually originating in the deep veins of the legs, the right side of the heart, or, rarely, an upper extremity, which becomes dislodged and is carried to the pulmonary vasculature.
Pulmonary infarction refers to necrosis of lung tissue that can result from interference with blood supply.
Pathophysiology and Causes of Pulmonary Embolism
1. Obstruction, either partial or full, of pulmonary arteries, which causes decrease or absent blood flow; therefore, there is ventilation but no perfusion (V/Q mismatch).
2. Hemodynamic consequences:
a. Increased pulmonary vascular resistance.
b. Increased pulmonary artery pressure (PAP).
c. Increased right-sided heart workload to maintain pulmonary blood flow.
d. Right-sided heart failure.
e. Decreased cardiac output.
f. Decreased BP.
3. Pulmonary emboli can vary in size and seriousness of consequences.
4. Predisposing factors include:
a. Stasis, prolonged immobilization.
b. Concurrent phlebitis.
c. Heart failure, stroke.
d. Injury to vessel wall.
e. Coagulation disorders, hypercoagulable state.
g. Advancing age, estrogen therapy, oral contraceptives
h. Fracture of long boxes.
Symptoms of Pulmonary Embolism
1. Rapid onset of dyspnea at rest, pleuritic chest pain, cough, syncope, delirium, apprehension, tachypnea, diaphoresis, hemoptysis.
2. Chest pain with apprehension and a sense of impending doom occurs when most of the pulmonary artery is obstructed.
3. Tachycardia, rales, fever, hypotension, cyanosis, heart gallop, loud pulmonic component of S2 (split S2).
4. Calf or thigh pain, oedema, erythema, tenderness or palpable cord (signs suggestive of deep vein thrombosis).
Diagnosis of Pulmonary Embolism
1. Thoracic imaging: V/Q scan (possibly using single-photon emission computed tomography) or helical contrast-enhanced computed tomography (CT).
2. Pulmonary angiography if noninvasive testing is inconclusive or not candidate for noninvasive testing. Contrast studies should be avoided in persons who are pregnant or have advanced renal failure.
3. D-Dimer assay for low to intermediate probability of pulmonary embolism.
4. ABG levels—decreased PaO2 is usually found, due to perfusion abnormality of the lung.
5. Chest x-ray—normal or possible wedge-shaped infiltrate.
Management of Pulmonary Embolism
For massive pulmonary embolism, goal is to stabilize cardiorespiratory status.
1. Oxygen is administered to relieve hypoxemia, respiratory distress, and cyanosis and to dilate pulmonary vasculature.
2. An infusion is started to open an IV route for drugs and fluids.
3. Vasopressors, inotropic agents such as dopamine, and antidysrhythmic agents may be indicated to support circulation if the patient is unstable.
4. ECG is monitored continuously for findings suggestive of right-sided heart failure, which may have a rapid onset. Changes may include sinus tachycardia, Q waves, late T-wave inversion, S wave in lead I, right bundle-branch block, right axis deviation, atrial fibrillation, and T-wave changes.
5. Small doses of IV morphine may be given to relieve anxiety, alleviate chest discomfort (which improves ventilation), and ease adaptation to mechanical ventilator, if this is necessary.
6. Pulmonary angiography, thoracic imaging, hemodynamic measurements, ABG analysis, and other studies are carried out.
Subsequent Management–Anticoagulation and Thrombolysis
1. IV heparin—stops further thrombus formation and extends the clotting time of the blood; it is an anticoagulant and antithrombotic.
a. IV loading dose usually followed by continuous pump or drip infusion or given intermittently every 4 to 6 hours.
b. Dosage adjusted to maintain the partial thromboplastin time (PTT) at 1½ to 2 times the pretreatment value (if the value was normal).
c. Protamine sulfate may be given to neutralize heparin in event of severe bleeding.
2. Oral anticoagulation with warfarin is usually used for follow up anticoagulant therapy after heparin therapy has been established; interrupts the coagulation mechanism by interfering with the vitamin K–dependent synthesis of prothrombin and factors VII, IX, and X.
a. Dosage is controlled by monitoring serial tests of prothrombin time (PT); desired PT is 2 to 3 times the control value.
b. Reported as an international normalized ratio (INR) of 2.0 to 3.0 by most laboratories.
c. Anticoagulation is used to prevent new clot formation but does not dissolve previously formed clots. Thrombolytics are used to dissolve clots
3. Thrombolytic agents, such as streptokinase, may be used in patients with massive pulmonary embolism.
a. Effective in lysing recently formed thrombi.
b. Improved circulatory and hemodynamic status.
c. Administered IV in a loading dose followed by constant infusion.
4. Newer clot-specific thrombolytics (tissue plasminogen activator, streptokinase activator complex, single-chain urokinase) are preferred.
a. Activate plasminogen only within the thrombus itself rather than systematically.
b. Minimize the occurrence of generalized fibrinolysis and subsequent bleeding.
When anticoagulation is contraindicated or the patient has recurrent embolization or develops serious complications from drug therapy.
1. Interruption of vena cava—reduces channel size to prevent lower extremity emboli from reaching the lungs. Accomplished by:
a. Ligation, plication, or clipping of the inferior vena cava.
b. Placement of transvenously inserted an intraluminal filter in inferior vena cava to prevent migration of emboli inserted through femoral or jugular vein by way of catheter.
2. Embolectomy (removal of pulmonary embolic obstruction).Complications
1. Bleeding as a result of treatment.
2. Respiratory failure.
3. Pulmonary hypertension, cor pulmonale.
Nursing Assessment of Pulmonary Embolism
1. Take nursing history with emphasis on onset and severity of dyspnea and nature of chest pain.
2. Examine the patient’s legs carefully. Assess for swelling of leg, duskiness, warmth, pain on pressure over gastrocnemius muscle, pain on dorsiflexion of the foot (positive Homans’ sign), which indicate thrombophlebitis as source.
3. Monitor respiratory rate—may be accelerated out of proportion to degree of fever and tachycardia.
a. Observe rate of inspiration to expiration.
b. Percuss for resonance or dullness.
c. Auscultate for friction rub, crackles, rhonchi, and wheezing.
4. Auscultate heart; listen for splitting of second heart sound.
5. Evaluate results of PT/PTT tests and INR for patients on anticoagulants and report results that are outside of therapeutic range promptly; anticipate a dosage change.
Nursing Diagnoses of Pulmonary Embolism
Ineffective Breathing Pattern related to acute increase in alveolar dead airspace and possible changes in lung mechanics from embolism.
Ineffective Tissue Perfusion (Pulmonary) related to decreased blood circulation.
Acute Pain (pleuritic) related to congestion, possible pleural effusion, possible lung infarction.
Anxiety-related to dyspnea, pain, and seriousness of condition.
Risk for Injury related to altered hemodynamic factors and anticoagulant therapy.
Nursing Interventions of Pulmonary Embolism
Correcting Breathing Pattern
1. Assess for hypoxia, dyspnea, headache, restlessness, apprehension, pallor, cyanosis, behavioural changes.
2. Monitor vital signs, ECG, oximetry, and ABG levels for adequacy of oxygenation.
3. Monitor patient’s response to IV fluids/vasopressors.
4. Monitor oxygen therapy—used to relieve hypoxemia.
5. Prepare patient for assisted ventilation when hypoxemia does not respond to supplemental oxygen. Hypoxemia is due to abnormalities of V/Q mismatch.
Improving Tissue Perfusion
1. Closely monitor for shock—decreasing BP, tachycardia, cool, clammy skin.
2. Monitor prescribed medications given to preserve right-sided heart filling pressure and increase BP.
3. Maintain patient on bed rest during acute phase to reduce oxygen demands and risk of bleeding.
4. Monitor urinary output hourly because there may be reduced renal perfusion and decreased glomerular filtration.
5. Antiembolism compression stockings should provide a compression of 30 to 40 mm Hg.
1. Watch patient for signs of discomfort and pain.
2. Ascertain if pain worsens with deep breathing and coughing; auscultate for friction rub.
3. Give morphine, as prescribed, and monitor for pain relief and signs of respiratory depression.
4. Position with head of bed slightly elevated (unless contraindicated by shock) and with chest splinted for deep breathing and coughing.
5. Evaluate patient thoroughly for signs of hypoxia when anxiety, restlessness, and agitation of new onset are noted, before administering as-needed sedatives. Consider calling health care provider when these signs are present, especially if accompanied by cyanotic nail beds, circumoral pallor or cyanosis, and increased respiratory rate.
1. Correct dyspnea and relieve physical discomfort.
2. Explain diagnostic procedures and the patient’s role; correct misconceptions.
3. Listen to the patient’s concerns; attentive listening relieves anxiety and reduces emotional distress.
4. Speak calmly and slowly.
5. Do everything possible to enhance the patient’s sense of control.
Intervening for Complications
1. Be alert for shock from low cardiac output secondary to resistance to right-sided heart outflow or to myocardial dysfunction due to ischemia.
a. Assess for skin color changes, particularly nail beds, lips, earlobes, and mucous membranes.
b. Monitor BP, pulse, and SpO2
. c. Measure urine output.
d. Monitor IV infusion of vasopressor or other prescribed agents.
2. Bleeding—related to anticoagulant or thrombolytic therapy.
a. Assess patient for bleeding; major bleeding may occur from GI tract, brain, lungs, nose, and genitourinary (GU) tract.
b. Perform stool guaiac test to detect occult blood loss.
c. Monitor platelet count to detect heparin-induced thrombocytopenia.
d. Minimize risk of bleeding by performing essential ABG analysis on upper extremities; apply digital compression at puncture site for 30 minutes; apply pressure dressing to previously involved sites; check site for oozing.
e. Maintain patient on strict bed rest during thrombolytic therapy; avoid unnecessary handling.
f. Discontinue infusion in the event of uncontrolled bleeding.
g. Notify health care provider on call immediately for change in LOC or sensation or ability to follow commands, move limbs, or respond to questions with clear articulation. Intracranial bleed may necessitate discontinuation of anticoagulation promptly to avert massive neurologic catastrophe.
Patient Education and Health Maintenance
1. Advise patient of the possible need to continue taking anticoagulant therapy for 6 weeks up to an indefinite period as well as safety considerations and drug and food interactions with anticoagulants.
2. Teach about signs of bleeding, especially of gums and nose, bruising, and blood in urine and stools.
3. For patients on anticoagulants, instruct to use soft toothbrush, avoid shaving with blade razor (use electric razor instead), and avoid aspirin-containing products. Notify health care provider of bleeding or increased bruising.
4. Warn against taking medications unless approved by health care provider because many drugs interact with anticoagulants.
5. Instruct patient to tell dentist about taking an anticoagulant.
6. Warn against inactivity for prolonged periods or sitting with legs crossed to prevent recurrence.
7. Warn against sports/activities that may cause trauma or injury to legs and predispose to a thrombus.
8. Encourage wearing a MedicAlert bracelet, identifying patient as anticoagulant user.
9. Instruct patient to lose weight, if applicable; obesity is a risk factor .
10. Discuss contraceptive methods with patient, if applicable; females with history of pulmonary embolus are advised against taking hormonal contraceptives.