Pulmonary embolus

12 Pulmonary embolus




Overview/pathophysiology


Pulmonary embolus (PE) is an obstruction of the pulmonary artery or one of its branches by substances (i.e., blood clot, fat, air, amniotic fluid) that originated elsewhere in the body. The most common source is a dislodged blood clot from the systemic circulation, typically the deep veins of the legs or pelvis. Thrombus formation is the result of the following factors: blood stasis, alterations in clotting factors, and injury to vessel walls. PE is classified as acute or chronic. In acute PE, patients develop signs and symptoms immediately after obstruction to the pulmonary vessels. In chronic PE, patients develop slow and progressive dyspnea over years as a result of pulmonary hypertension. Massive PE causes hypotension (systolic blood pressure [SBP] less than 90 mm Hg or a 20 mm Hg decrease from baseline in a 15-min period) (Sharpley et al., 2004), with accompanying right heart failure unexplained by a cardiac cause. Early diagnosis and appropriate treatment reduce mortality to 2% to 8% compared to 30% without treatment (Roy et al., 2005). With treatment, most pulmonary emboli resolve and leave no residual deficits; however, some patients may be left with chronic pulmonary hypertension. A fat embolus is the most common nonthrombotic cause of pulmonary perfusion disorders. It is the result of release of free fatty acids causing a toxic vasculitis, followed by thrombosis and obstruction of small pulmonary arteries by fat.


Total obstruction leading to pulmonary infarction is rare because the pulmonary circulation has multiple sources of blood supply.



Health care setting


Acute care



Assessment


Signs and symptoms often are nonspecific and variable, depending on extent of obstruction and whether patient has infarction as a result of the obstruction.




Pulmonary embolus:


Sudden onset of dyspnea and sharp chest pain, restlessness, anxiety, nonproductive cough or hemoptysis, palpitations, nausea, and syncope. With a large embolism, oppressive substernal chest discomfort and signs of diastolic (right-sided) heart failure will be present. See “Heart Failure,” p. 165, for signs and symptoms.



Pulmonary infarction:


Fever, pleuritic chest pain, and hemoptysis.



Physical assessment:


Tachypnea, tachycardia, hypotension, crackles (rales), decreased chest wall excursion secondary to splinting, S3 and S4 gallop rhythms, transient pleural friction rub, jugular venous distention, diaphoresis, edema, and cyanosis. Temperature may be elevated if infarction has occurred.



Specific findings for fat embolus:


Typically, patient is asymptomatic for 12-24 hr following embolization. This period ends with sudden cardiopulmonary and neurologic deterioration: apprehension, restlessness, mental status changes, confusion, delirium, coma, and dyspnea.



Physical assessment for fat embolus:


Tachypnea, tachycardia, and hypertension; fever; petechiae, especially of conjunctivae, neck, upper torso, axillae, and proximal arms; inspiratory crowing; pulmonary edema; profuse tracheobronchial secretions; fat globules in sputum; and expiratory wheezes.



History and risk factors




Immobility:


Especially significant when it coexists with surgical or nonsurgical trauma, carcinoma, or cardiopulmonary disease. Risk increases as duration of immobility increases.



Cardiac disorders:


Atrial fibrillation, heart failure, myocardial infarction, rheumatic heart disease.



Surgical intervention:


Risk increases in prolonged surgeries of more than 30 min duration or during the postoperative period, especially for patients with orthopedic, pelvic, thoracic, or abdominal surgery and for those with extensive burns or musculoskeletal injuries of the hip or knee. This risk is present for 3 mo postoperatively.



Pregnancy:


Especially during postpartum period.



Chronic pulmonary and infectious diseases



Trauma:


Especially lower extremity fractures and burns. The degree of risk is related to severity, site, and extent of trauma.



Mechanical ventilation:


Risk increases because of immobility and inflammatory processes.



Carcinoma:


Particularly neoplasms involving the breast, lung, pancreas, and genitourinary and alimentary tracts.



Obesity:


A body mass index greater than 29 is associated with an increased incidence of PE, especially in women.



Varicose veins or prior thromboembolic disease



Age:


Risk of thromboembolism is greatest for patients older than 55 yr.



History and risk factors for fat embolus


Multiple long bone fractures, especially fractures of the femur and pelvis; trauma to adipose tissue or liver; burns; osteomyelitis; sickle cell crisis.



Diagnostic tests



General findings for pulmonary emboli



Arterial blood gas (ABG) values:


Hypoxemia (PaO2 less than 80 mm Hg), hypocarbia (PaCO2 less than 35 mm Hg), and respiratory alkalosis (pH more than 7.45) usually are present. A normal Pao2 does not rule out presence of pulmonary emboli.



Brain natriuretic peptide (BNP):


Levels are typically greater in patients with PE compared to patients without PE; however, the test is insensitive since there are multiple causes for an elevated BNP. BNP does correlate the risk of subsequent complications and prolonged hospitalization.



D-dimer:


A degradation product produced by plasmin-mediated proteolysis of cross-linked fibrin, D-dimer is measured by an enzyme-linked immunosorbent assay. The higher the result (with less than 250 ng/ml considered negative in most laboratories), the more likely it is patient has PE. This test is not sensitive or specific enough to diagnose PE, but it may be used in conjunction with other diagnostic tests.



Chest x-ray examination:


Initially findings are normal, or an elevated hemidiaphragm may be present. After 24 hr, x-ray examination may reveal small infiltrates secondary to atelectasis that result from the decrease in surfactant. If pulmonary infarction is present, infiltrates and pleural effusions may be seen within 12-36 hr.



Electrocardiogram (ECG) results:


If PE are extensive, signs of acute pulmonary hypertension may be present: right-shift QRS axes, tall and peaked P waves, ST-segment changes, and T-wave inversion in leads V1-V4.



Spiral or helical computed tomography (CT):


Enables image acquisition of pulmonary arteries during a single breath hold and with optimal contrast enhancement. Spiral CT is rapidly becoming the test of choice in diagnosing PE because of its higher specificity and sensitivity.



Pulmonary ventilation-perfusion scan:


Used to detect abnormalities of ventilation or perfusion in the pulmonary system. Radiopaque agents are inhaled and injected peripherally. Images of distribution of both agents throughout the lung are scanned. If the scan shows a mismatch of ventilation and perfusion (i.e., pattern of normal ventilation with decreased perfusion), vascular obstruction is suggested.

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Jul 18, 2016 | Posted by in NURSING | Comments Off on Pulmonary embolus

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