Echocardiography in the Management of Pulmonary Embolism

Patients with acute pulmonary embolism are undergoing echocardiography with increasing frequency (1). Because the use of echocardiography in these patients is burgeoning, I provide my perspective on the utility of this test in bedside management. I do not recommend echocardiography as a routine imaging test to diagnose suspected pulmonary embolism because most patients with pulmonary embolism have normal echocardiograms. Nevertheless, among patients who undergo echocardiography for suspected left-heart failure, the imaging of a normal left ventricle and dilated, hypokinetic right ventricle may serendipitously suggest the diagnosis of pulmonary embolism. In addition, echocardiography is useful for diagnosis in hemodynamically unstable patients with unexplained dyspnea, syncope, or right-heart failure. Transesophageal echocardiography is best reserved for critically ill patients in whom the cause of cardiovascular instability remains uncertain. Qualitative Abnormalities on Transthoracic Echocardiography Among patients with large pulmonary embolism, abnormalities are often apparent on the transthoracic echocardiogram (Table). These include right ventricular dilatation and hypokinesis, abnormal motion of the interventricular septum, tricuspid regurgitation, and lack of collapse of the inferior vena cava during inspiration (2). These abnormalities on echocardiography have clinical correlates, such as jugular venous distention, tricuspid regurgitation, and an accentuated pulmonic heart sound. Electrocardiographic features of right ventricular strain include a new right bundle-branch block, a finding of an S wave in lead I, a Q wave in lead III or an inverted T wave in lead III, and new T-wave inversion in leads V1 through V4 (3). Table. Abnormal Echocardiographic Findings in Patients with Pulmonary Embolism Among patients with hemodynamic impairment, there is a small difference in left ventricular area during diastole and during systole; this difference indicates low cardiac output (Figure 1) (4). Typically, this represents cardiogenic shock due to right ventricular failure (the usual cause of death from pulmonary embolism) despite the presence of an intrinsically normal left ventricle. Rarely, pulmonary embolism may be visualized directly on transthoracic echocardiography, but only if it is large and located in the central vasculature (Figure 2). Figure 1. Typical findings on transthoracic echocardiography in patients with massive pulmonary embolism. RV LV left right arrows PE Figure 2. Right main pulmonary artery embolism visualized on transthoracic echocardiography. RPA Pulmonary Hypertension An abrupt increase in pulmonary artery pressure causes the right ventricular dysfunction observed in some patients with acute pulmonary embolism. The hemodynamic response to pulmonary embolism depends on the size of the embolus, coexistent cardiopulmonary disease, and neurohumoral effects. Pulmonary artery obstruction and circulating neurohumoral substances increase right ventricular afterload. As right ventricular and pulmonary artery pressures increase, the right ventricle dilates, becomes hypokinetic, and ultimately fails. Acute increases in right ventricular pressure can cause left ventricular dysfunction because of the anatomic juxtaposition of the two ventricles and ventricular interdependency. With underfilling of the left ventricle, systemic cardiac output and pressure both decrease, potentially compromising coronary perfusion and producing myocardial ischemia. The pulmonary artery systolic pressure can be estimated by measuring the peak velocity of the tricuspid regurgitant jet obtained with Doppler echocardiography. The gradient across the tricuspid valve can be estimated by using the modified Bernoulli equation, P = 4V 2; P represents the peak pressure difference between the right atrium and right ventricle, and V is the peak velocity of the regurgitant jet (5). Estimated right atrial pressure is added to the gradient to estimate pulmonary artery systolic pressure. Note, however, that acute and massive pulmonary embolism can produce right ventricular failure without causing substantial elevations in pulmonary artery pressure (6). This estimated pressure usually correlates well with invasive measurements obtained at pulmonary artery catheterization, although it is subject to error in estimating right atrial pressure. In addition, considerable technical skill is required to ensure that the complete tricuspid regurgitant envelope is visualized. If necessary, agitated saline contrast can be used to enhance the tricuspid regurgitant Doppler tracing. In the absence of tricuspid regurgitation, other techniques can be considered for estimating pulmonary artery pressure. For example, the time to peak velocity in the right ventricular outflow tract is reduced with elevated pulmonary artery pressures. However, this measurement is not nearly as precise as the modified Bernoulli equation (5). Relationship between Right Ventricular Dysfunction and Size of Pulmonary Embolism At what point does a pulmonary embolus become large enough to cause right ventricular dysfunction visible on echocardiography? This depends on the patient population. In a clinical trial of patients with moderately large pulmonary emboli but without hemodynamic instability at baseline (7), lung scans and echocardiograms were obtained on the day of enrollment. Whereas echocardiograms were assessed qualitatively as either showing right ventricular dysfunction (defined as impaired contraction of the right ventricular systolic wall or increased right ventricular end-diastolic area detected by observation alone, without planimetry) or not, the lung scans were graded according to a precise, quantitative segmental perfusion score (8). Each lung segment was graded in terms of perfusion reduction (0 = normal and 3 = absent) and size (0 = no defect and 3 = whole segment). The defect score for each segment was defined as the volume of the abnormal perfusion times the perfusion reduction in the abnormality. The defect score for each patient was the average of 18 segmental scores, 10 from the right lung and 8 from the left lung. A receiver-operating characteristic curve was then generated by plotting the quantitative segmental perfusion score in relation to the presence of right ventricular hypokinesis (9). Patients in whom less than 30% of the pulmonary vascular cross-sectional area was impaired by pulmonary embolism on lung scanning were 6.8 times more likely to have normal right ventricular function on echocardiography. In contrast, among patients with 30% or more of the lung not perfused, 92% of those with right ventricular hypokinesis were identified. Similar results were obtained in another cohort of patients with pulmonary embolism who underwent both baseline lung scanning and echocardiography (10). On the basis of these findings, I suspect right ventricular dysfunction and obtain an echocardiogram in patients with pulmonary embolism who have approximately one third or more of the lung nonperfused on lung scanning. Regional Right Ventricular Dysfunction In reviewing serial echocardiograms in patients with known, large pulmonary emboli, my colleagues and I detected a qualitative finding that typified these patients (11). Despite moderate or severe right ventricular free-wall hypokinesis, we noted relatively normal contraction and sparing of the right ventricular apex. We quantified this abnormality (11), which has become widely known as the McConnell sign. First, we designed a computer program for quantitative analysis of right ventricular free-wall motion. Then, we traced the right ventricular free-wall endocardium in the apical four-chamber view from base to apex at end-systole and end-diastole for three separate cardiac cycles (Figure 3). For pulmonary embolism, the McConnell sign had a sensitivity of 77%, specificity of 94%, positive predictive value of 71%, and negative predictive value of 96%. The McConnell sign appears to be a useful screening test to help distinguish between right ventricular dysfunction due to pulmonary embolism and dysfunction due to other conditions, such as primary pulmonary hypertension. Figure 3. Apical four-chamber view from a transthoracic two-dimensional echocardiogram. For patients with right ventricular hypokinesis due to acute pulmonary embolism, the excursion diminished markedly when measured in the middle of the right ventricular free wall. However, the excursion improved progressively when segments closer to the apex were measured. This pattern of regional right ventricular dysfunction appeared highly specific for acute pulmonary embolism; in patients with right ventricular dysfunction due to primary pulmonary hypertension, right ventricular hypokinesis was not improved upon assessment of apical segments (11) (Figure 4). However, no completely satisfying explanation accounts for this observation. Potential mechanisms include tethering of the right ventricular apex to a hyperdynamic left ventricle, lower wall stress in the right ventricular apex, and localized ischemia of the right ventricular free wall (11). Figure 4. Segmental right ventricular free-wall excursion (mean SE) by centerline analysis as a function of right ventricular free-wall segment. P P Transesophageal Echocardiography Transesophageal echocardiography holds the promise of diagnosing pulmonary embolism by direct visualization of a thrombus rather than by relying on indirect signs, such as right ventricular enlargement and hypokinesis. The examination assesses the extent of thromboembolism as well as its surgical accessibility. This technique requires far more resources and operator skill than does transthoracic echocardiography. Technically, transesophageal echocardiography is easiest to perform in the unconscious patient. Conscious patients almost always require topical anesthesia of the pharynx and often benefit from small, sedating doses of midazolam or f