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Pulmonary embolism: Know the signs, act fast, save lives

Simko, Lynn C. PhD, RN, CCRN; Culleiton, Alicia L. DNP, RN, CNE

doi: 10.1097/01.CCN.0000433812.63351.9f

One-third of patients who develop pulmonary embolism die. Here's how to recognize the problem and intervene appropriately to save lives.

Lynn C. Simko is a clinical associate professor and Alicia L. Culleiton is an assistant clinical professor at Duquesne University, Pittsburgh, Pa.

The authors have disclosed that they have no financial relationships related to this article.

A timely diagnosis can mean the difference between life and death, so watch for these red flags.



Pulmonary embolism (PE) is estimated to occur in at least 600,000 cases annually, with PE being the cause of death in 200,000 of the patients.1 PE is not only one of the most common causes of death, it's one of the most preventable.2 The majority of preventable deaths associated with PE are attributed to missed diagnosis.3 As a result, nurses need to have updated clinical guidelines and tools to correctly evaluate patients and PE risk factors in a variety of clinical settings and situations.

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Patient with uncertain diagnosis

Ms. M, 60, is admitted to the ED after a near-syncopal episode at home. Her past medical history is significant for hypertension and her body mass index is 30. Ms. M reports she's smoked two packs of cigarettes a day for the past 22 years. Initial assessment in the ED includes heart rate, 120 beats/min; respiratory rate, 32 breaths/min; and BP 98/60. She was afebrile at 36.8° C (98.2° F). The cardiac monitor shows sinus tachycardia. SpO2 is 89% on room air; 94% on supplemental oxygen. Peripheral venous access is established and blood specimens for a complete blood cell (CBC) count, basic metabolic profile (BMP), and serum cardiac biomarkers are obtained, as well as a 12-lead ECG. The ECG demonstrates sinus tachycardia, nonspecific ST-T wave abnormalities, and an S1Q3T3 pattern. Initial serum troponin I and troponin T levels are elevated and results of the CBC count and BMP are all within normal limits.

Ms. M appears apprehensive, is dyspneic on minimal exertion, and states she feels like she's “going to pass out again.” She's diaphoretic, tachycardic, and tachypneic. The nurse also notes bilateral jugular venous distension and unilateral right lower extremity edema. Ms. M suddenly becomes unresponsive, apneic, and pulseless while the nurse is assessing her. High-quality, effective CPR is immediately begun and a code blue is called. Ms. M is found to be in pulseless electrical activity (PEA) and despite properly performed basic life support and advanced cardiovascular life support, resuscitation measures were unsuccessful. The autopsy confirms a deep vein thrombosis (DVT) in the right lower extremity and a massive PE as the cause of death.

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Understanding PE

PE refers to an obstruction of the pulmonary artery or one of its branches by material, such as thrombus, fat, air, or tumor.1 More than 90% of PEs result from thrombi originating in the veins of the legs and pelvis.4 This article focuses on thromboembolism. Other sites of origin include the right side of the heart (in patients with chronic atrial fibrillation), renal veins, and upper extremities (rare).5 When a thrombus becomes lodged (partially or completely) within a pulmonary artery or one of its branches, physiologic dead space (alveolar area not involved in gas exchange because of insufficient perfusion) is increased.6 As a result, gas exchange is impaired or nonexistent in this area. Additionally, a variety of substances, including inflammatory mediators, are released from the thrombus and surrounding area that cause local vasoconstriction and bronchoconstriction.7 This increases pulmonary vascular resistance, leads to pulmonary hypertension and increased right ventricular (RV) workload, and worsens the ventilation-perfusion (V/Q ) mismatch. When the RV workload exceeds its capacity, RV failure occurs. These series of events cause the patient's cardiac function to deteriorate, resulting in decreased left ventricular preload, reduced cardiac output, and shock.8

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Early detection is key

Classic signs and symptoms of PE (abrupt onset of pleuritic chest pain, shortness of breath, hypoxemia, tachypnea, tachycardia, and unexplained anxiety) aren't always so obvious in some patients. More commonly, signs and symptoms vary from gradual progressive dyspnea to abrupt catastrophic hemodynamic collapse.9 Atypical signs and symptoms of PE include seizures, fever, syncope, abdominal pain, wheezes, productive cough, flank pain, new-onset atrial fibrillation, decreased level of consciousness, and delirium (seen in older adults).9

Three distinct symptom complexes associated with PE have also been described: isolated dyspnea, pleuritic chest pain or hemoptysis, and circulatory collapse.3 Isolated dyspnea and circulatory collapse have an occurrence rate of 25% and 10%, respectively.10 Pleuritic chest pain and hemoptysis occur in about 60% of patients.10

Table C

Table C

The clinical presentation of PE is also determined by the patient's past cardiopulmonary status and the size of the embolus. Acute PE can be classified as small, medium-sized, or massive.5 Some sources classify acute PE that doesn't meet the definition of massive PE as submassive PE.1 (See Clinical features of pulmonary emboli.) Remember that the clinical presentation of PE can mimic that of angina, acute myocardial infarction (AMI), bronchopneumonia, heart failure, and various other cardiopulmonary disorders. Given these circumstances, and the fact that death from PE commonly occurs within 1 hour of onset of signs and symptoms, knowing all the possible clinical presentations of PE is critical.8 (See Tools of the trade.)

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Diagnostic testing

Generally, the initial diagnostic work-up for PE includes a chest X-ray, arterial blood gas (ABG), ECG, CBC count, serum troponin levels, brain natriuretic peptide (BNP), and a D-dimer. In most cases of PE, the chest X-ray is normal or nonspecific, including infiltrates, pleural effusion, atelectasis, and consolidation, which can help diagnose other conditions when PE is ruled out.8 ABG results may be normal, but abnormalities can include hypoxemia and hypocapnia and respiratory alkalosis secondary to PE-associated tachypnea.8 Research suggests that 26% of patients with PE demonstrated on pulmonary arteriography had a PaO2 greater than 80 mm Hg.10,11 Consequently, normal PaO2 levels shouldn't exclude PE diagnosis. Nonetheless, hypoxemia in the absence of cardiopulmonary disease must raise the suspicion of PE.10

ECG findings associated with PE include tachycardia and nonspecific ST-segment and T-wave abnormalities. However, the literature reports the most specific finding is the S1Q3T3 pattern (prominent S-wave in lead I, prominent Q-wave in lead III, and T-wave inversion in lead III) pattern.12 Additional ECG abnormalities include atrial dysrhythmias, right-bundle branch block, and atrial fibrillation.11,13

The CBC count, serum troponin levels, and BNP results in some instances can be used to make a differential diagnosis (infection, respiratory disorder, AMI, heart failure). Nonetheless, serum troponin levels can be elevated in patients with PE. While troponin levels aren't diagnostic of PE, they are associated with adverse outcomes, as is the case with elevated BNP levels. Moreover, elevated BNP levels in the absence of renal dysfunction can indicate RV dysfunction in patients with PE, as well as being able to predict unfavorable outcomes in patients who experience an acute PE.14

An elevated D-dimer (a breakdown product of fibrin) can raise the suspicion of a PE. Generally, patients with a PE (or DVT) will have excessive numbers of D-dimer molecules in their blood because when the clot breaks down, it forms fibrin degradation products, including D-dimer molecules. However, elevated D-dimer levels can also be seen in many other clinical disorders, including arterial thromboembolic disease, heart failure, sepsis, severe infection, renal disease, trauma, disseminated intravascular coagulation, preeclampsia, eclampsia, and severe liver disease.11 The various clinical prediction tools used by healthcare providers aid in risk-stratifying patients with a suspected PE (Geneva Score, revised Geneva Score, Wells Score, and Pisa Model) and often, based on these results/scores, a D-dimer may or may not be ordered.15

Imaging studies used to help confirm a diagnosis of PE include computed tomography pulmonary angiography (CT-PA), pulmonary angiography, V/Q scans, and magnetic resonance angiography.16

The CT-PA is the standard criterion for diagnosing PE due to its wide availability and capacity to visualize a thrombus directly.9,16 Once a negative CT-PA is confirmed, no additional imaging is necessary.16 However, if CT-PA isn't available, one or more of the previously noted studies can be performed.

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Treatment options

The best treatment for PE is prevention. Most hospitals have a venous thromboembolism (VTE) prophylaxis protocol, which can include low-dose unfractionated heparin or low-molecular-weight heparin. For patients at high risk of bleeding, mechanical prophylaxis with intermittent pneumatic compression devices or graduated compression stockings can help decrease the incidence of VTE, and as a result, PE. As a critical care nurse, assessing patients for signs and symptoms of DVT, such as unilateral extremity edema, is critical. In addition, a mobility program can help decrease venous stasis and reduce VTE occurrence.17

If the patient is unstable, the initial focus of treatment is stabilization, which may require respiratory and hemodynamic support. The patient may require endotracheal intubation, mechanical ventilation, fluid resuscitation, I.V. vasopressor therapy, and inotropic support. I.V. fluids should be administered cautiously to prevent increasing RV dysfunction and worsening RV failure.12 A nursing intervention that can be initiated is positioning the patient with the unaffected lung down, if not contraindicated. This helps to improve perfusion to the unaffected lung, thus improving PaO2 and decreasing the FiO2 requirements.17

Postresuscitation, the standard treatment for an unstable patient with a confirmed massive PE is systemic I.V. fibrinolysis.1 Fibrinolytic agents convert plasminogen to plasmin, which degrades fibrin-rich thrombin. Commonly used fibrinolytics in the setting of acute PE include streptokinase, urokinase, and tissue-type plasminogen activator.18 Catheter-directed embolectomy and fibrinolysis is being used more frequently rather than surgical embolectomy. The lower fibrinolytic doses result in decreased bleeding complications. Fibrinolysis and suction embolectomy has been found to be effective in acute massive PE with hemodynamic collapse.19

Small and medium-sized PE are usually treated with unfractionated heparin by I.V. infusion adjusted to the activated partial thromboplastin time.19 Patients who have contraindications to anticoagulation, who have developed anticoagulation-related complications, or who have developed VTE despite anticoagulation may be considered for percutaneous placement of an inferior vena cava (IVC) filter.1 IVC filters allow blood to pass through while medium-to-large emboli from the lower extremities and pelvis are fragmented or prevented from traveling to the lungs. IVC filters can be either permanent nonretrievable filters or temporary retrievable filters.

Long-term treatment in all patients with PE is required to prevent thrombus extension and recurrence. Prophylaxis with a vitamin-K antagonist (VKA), most commonly warfarin, is recommended and should be prescribed for 3 to 12 months. The international normalized ratio range recommended for PE prophylaxis is 2 to 3.20 In the future, new oral anticoagulants, such as selective factor IIa or Xa inhibitors, could potentially improve the treatment of VTE.20

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Reading the red flags can save lives

Acute PE can be misdiagnosed due to clinical presentations that vary from patient to patient. However, Ms. M did present with red flags that should have raised the suspicion of PE1:

  • Red flag #1. Ms. M had specific risk factors for PE in women, including obesity, hypertension, and heavy cigarette smoking.
  • Red flag #2. Ms. M's signs and symptoms, tachycardia, tachypnea, dyspnea on minimal exertion, hypoxemia, and jugular venous distension may be associated with PE. PE is also a common cause of PEA.
  • Red flag #3. Ms. M's 12-lead ECG demonstrated tachycardia and nonspecific ST-T wave abnormalities as well as the classic S1Q3T3 pattern, suggestive of PE.
  • Red flag #4. Ms. M presented with unilateral edema of the right lower extremity that should have raised the possibility of a DVT.

As a critical care nurse, you must have astute assessment skills in order to help make a timely diagnosis of PE and prevent a common and often fatal event.

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Tools of the trade

These predictive tools can be used by critical care nurses to help categorize a patient's risk for developing PE prior to the use of noninvasive and invasive studies.

Wells Clinical Model for PE.

Revised Geneva Scoring System for PE.

For more information, see “An evidence-based project to decrease catheter-related bloodstream infection” in the March issue of Nursing2013 Critical Care.

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