, Benjamin Hohlfelder2 and Samuel Z. Goldhaber3
(1)
Cardiovascular Division, Harvard Medical School Brigham and Women’s Hospital, Boston, Massachusetts, USA
(2)
Department of Pharmacy Services, Brigham and Women’s Hospital, Boston, Massachusetts, USA
(3)
Thrombosis Research Group, Harvard Medical School Brigham and Women’s Hospital, Boston, Massachusetts, USA
Abstract
A subset of initially normotensive patients with pulmonary embolism (PE) may clinically deteriorate and develop systemic arterial hypotension, cardiogenic shock, and sudden death, despite prompt therapeutic-level anticoagulation. Elevated cardiac biomarkers and right ventricular (RV) enlargement on imaging studies identify such vulnerable PE patients who may benefit from more advanced therapies. Clinical examination, electrocardiography, cardiac biomarker determination, chest computed tomogram (CT), and echocardiography are key instruments in the detection of RV dysfunction and risk stratification of patients with acute PE.
Keywords
Cardiac biomarkersPulmonary embolismRight ventricular dysfunctionRisk stratificationSelf-Assessment Questions
1.
All of the following predict increased risk of adverse outcomes in the setting of acute PE except?
(a)
A PE Severity Index (PESI) score of 55
(b)
Cardiac troponin elevation
(c)
Chest CT-measured RV diameter-to-LV diameter ratio greater than 0.9
(d)
RV dilation and hypokinesis detected by transthoracic echocardiography
2.
Which of the following clinical parameters in the PESI is associated with the greatest incremental increase in risk?
(a)
Cancer
(b)
Systolic blood pressure <100 mmHg
(c)
Oxygen saturation <90 %
(d)
Abnormal mental status
3.
Based on the 2014 European Society of Cardiology (ESC) Guidelines on the Diagnosis and Management of Acute Pulmonary Embolism, for which of the following patients would advanced therapy in addition to immediate anticoagulation be considered?
(a)
A 23-year-old woman with acute PE, normal blood pressure and heart rate, hypoxemia with an oxygen saturation of 88 % on room air, normal cardiac troponin level, and chest CT-measured RV diameter-to-LV diameter ratio of 0.8.
(b)
A 74-year-old man with acute PE, atrial fibrillation with a heart rate of 136 beats per minute, hypotension with a blood pressure of 82/58 mmHg, hypoxemia with an oxygen saturation of 84 % on room air, increased cardiac troponin, and a chest CT-measured RV diameter-to-LV diameter ratio of 1.2.
(c)
A 66-year-old woman with acute PE, normal blood pressure, heart rate of 111 beats per minute, hypoxemia with an oxygen saturation of 89 % on room air, normal cardiac troponin level, and a transthoracic echocardiogram showing RV dilation and hypokinesis.
(d)
A 70-year-old woman with acute PE, normal blood pressure, heart rate of 106 beats per minute, hypoxemia with an oxygen saturation of 87 % on room air, abnormal cardiac troponin level, and a transthoracic echocardiogram showing normal RV size and function.
Acute PE presents as a broad spectrum of clinical syndromes. Some patients complain of pleuritic pain, which usually results from small pulmonary emboli that affect nerve fibers in the periphery of the lung. In contrast, others may suffer massive PE resulting in syncope, systemic arterial hypotension, cardiogenic shock, or cardiac arrest. The majority of patients with acute PE presents with normal blood pressure. However, a subset of these initially normotensive patients may abruptly deteriorate and manifest systemic arterial hypotension, cardiogenic shock, and sudden death, despite prompt therapeutic-level anticoagulation. Accurate and rapid risk stratification to identify such vulnerable patients who may benefit from more advanced therapies has become a critical part of acute PE management. Clinical examination, electrocardiography, cardiac biomarker determination, chest CT, and echocardiography are key instruments in the detection of RV dysfunction and risk stratification of patients with acute PE.
Clinical Vignette
A 63-year-old man with hypertension, diabetes mellitus, and a recent rheumatoid arthritis exacerbation associated with relative immobility presented to the Emergency Department with sudden onset pleuritic pain, dyspnea at rest, and palpitations. Two days prior, he noted right lower extremity edema and pain upon ambulation which he attributed to rheumatoid arthritis. Upon physical examination, he was noted to have a heart rate of 112 beats per minute, blood pressure of 102/72 mmHg, respiratory rate of 24 breaths per minute, and room air oxygen saturation of 88 %. He has moderate pitting edema up to his right knee associated with erythema and tenderness to palpation along the calf. His electrocardiogram was remarkable for sinus tachycardia to 114 beats per minute. Given that a diagnosis of PE was “likely” (based on a Wells score of 9 points), he underwent a contrast-enhanced chest CT which demonstrated large bilateral PE (Fig. 6.1). The chest CT also documented RV enlargement as defined by an RV diameter-to-LV diameter ratio of 1.0 (Fig. 6.2). His initial laboratory evaluation was remarkable for a cardiac troponin of 0.4 ng/mL (normal range <0.01 ng/mL). Because of the elevated cardiac troponin, a bedside transthoracic echocardiogram was performed and demonstrated severe RV dilation and moderate pulmonary hypertension (Figs. 6.3 and 6.4).
Fig. 6.1
Contrast-enhanced chest computed tomogram (CT) demonstrating large bilateral pulmonary embolism (PE) (arrows) in a 63-year-old man with recent rheumatoid arthritis exacerbation associated with relative immobility and sudden onset pleuritic pain and dyspnea
Fig. 6.2
Contrast-enhanced chest computed tomogram (CT) demonstrating right ventricular (RV) enlargement as defined by an increased RV diameter-to-left ventricular (LV) diameter ratio (3.82 cm/3.67 cm = 1.0; normal ≤ 0.9) in a 63-year-old man with acute pulmonary embolism (PE)
Fig. 6.3
Transthoracic echocardiogram, apical four-chamber view, demonstrating severe right ventricular (RV) dilatation relative to the left ventricle (LV) in a 63-year-old man with acute pulmonary embolism (PE)
Fig. 6.4
Transthoracic echocardiogram, apical four-chamber view, demonstrating moderate pulmonary hypertension as defined by a peak tricuspid regurgitant jet velocity (X) of 300 cm/s in a 63-year-old man with acute pulmonary embolism (PE). Using the modified Bernoulli equation (4× [peak tricuspid regurgitant jet velocity]2 + the estimate of right atrial pressure), the estimated pulmonary artery systolic pressure was 51 mmHg
Clinical Clues
The history and physical examination can provide important clues for risk stratification. The Pulmonary Embolism Severity Index (PESI) assigns 1 score point for the patient’s age in years, 10 points for male sex, history of heart failure, and history of chronic lung disease, 20 points for a heart rate greater than or equal to 110 beats per minute, respiratory rate greater than or equal to 30 per minute, temperature less than 36 °C, and oxygen saturation less than 90 %, 30 points for history of cancer, and systolic blood pressure less than 100 mmHg, and 60 points for altered mental status (Table 6.1) [1, 2]. Patients with a score of 65 or less are classified as class I, or very low risk; 66–85 as class II, or low risk; 86–105 as class III, or intermediate risk; 106–125 as class IV, or high risk; and greater than 125 as class V, or very high risk. Class V corresponds with a class of patients at highest risk for 30-day mortality (25 %). In general, patients are not considered candidates for outpatient treatment of PE if their PESI score exceeds 85 points. A simplified PESI (sPESI) has also been evaluated and offers similar prognostic accuracy with greater ease of use [3]. The patient in the Clinical Vignette would be classified as high risk (Class IV) with a PESI point score of 113 (63 points for age + 10 points for male gender + 20 points for heart rate ≥100 beats per minute + 20 points for oxygen saturation <90 %).
Table 6.1
A generally accepted clinical decision rule for risk stratification of patients with acute pulmonary embolism (PE)
Variable | Points |
|---|---|
Demographics | |
Age, per year | Age, in years |
Male sex | 10 |
Comorbid illnesses
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