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Cardiovascular Anesthesiology: Echo Didactics & Rounds

McConnell’s Sign in Acute Pulmonary Embolism

Lau, Gary, MBChB, FRCA*; Ther, Gabor, MD, DESA*; Swanevelder, Justiaan, MBChB, FRCA, FCA (SA), MMED (Anes)

Author Information
doi: 10.1213/ANE.0b013e31828a4b38

A 52-year-old woman presented with right calf swelling, chest pain, and shortness of breath. A computed tomography pulmonary angiography was performed, which demonstrated a massive pulmonary saddle embolus. She was transferred to our institution for an emergency surgical pulmonary embolectomy. After induction of anesthesia, a transesophageal echocardiography probe was inserted. The midesophageal ascending aorta short-axis view demonstrated a mass in the right pulmonary artery (PA) that occupied approximately two thirds of the vessel (Video 1, see Supplemental Digital Content 1,, and demonstrated a filling defect on color-flow Doppler (Fig. 1). There was no obvious mass in the main PA, and the left PA was not clearly visible. These findings suggested that the embolus had migrated distally. There were no further emboli identified in the inferior vena cava, the right atrium, or the right ventricle (RV).

Figure 1
Figure 1:
Color-flow Doppler of the midesophageal short-axis view of the ascending aorta demonstrating a filling defect in the right pulmonary artery. TEE = transesophageal echocardiography.

The right atrium was severely enlarged, with the interatrial septum bulging into the left atrium throughout the entire cardiac cycle (Fig. 2). The RV systolic function was severely depressed. McConnell’s sign, with a hypokinetic midpapillary free wall and preserved apical contractility, was observed (Video 2, see Supplemental Digital Content 2, The tricuspid annulus was dilated with moderate–severe tricuspid regurgitation. There was severe PA hypertension with an estimated RV systolic pressure of 64 mm Hg (maximum pressure gradient of the tricuspid regurgitation jet 50 mm Hg + central venous pressure 14 mm Hg). The left ventricle was underfilled with good systolic function. It had a “D-shaped” appearance with a flattened interventricular septum during the entire cardiac cycle, with paradoxical septal motion during late systole.

Figure 2
Figure 2:
Echocardiographic image demonstrating indirect signs of pulmonary embolism: right atrial (RA) and ventricular (RV) enlargement, and bowing of the interatrial septum into the left atrium. TEE = transesophageal echocardiography.

After sternotomy, the surgeon performed a longitudinal arteriotomy on the main PA and removed 2 large emboli from each of the right and left PAs. The patient was discharged from intensive care on the third postoperative day.


Diagnosis of acute pulmonary embolism (PE) can be difficult because the clinical presentation can mimic other pulmonary or cardiac disorders. The first-line diagnostic imaging test is the computed tomography pulmonary angiography. Although echocardiography may visualize the pulmonary thrombus,1,2 its use is not recommended as a primary diagnostic modality for patients with suspected PE who are hemodynamically unstable.3 It has been demonstrated that the thrombus detection rate with transesophageal echocardiography is >50% in patients with suspected PE.4 In many clinical cases, only indirect signs of PE are present (Table 1).

Table 1
Table 1:
Indirect Echocardiography Signs Associated with Acute Pulmonary Embolism

Echocardiography is a useful adjunct in patients with hemodynamic instability to exclude other potential cardiac diseases such as RV infarction, valvular disease, and tamponade (Table 2). In addition, in patients with a suspected PE, echocardiography can assess its hemodynamic consequences and may be used to indicate the need for aggressive thrombolytic or surgical therapy.

Table 2
Table 2:
Echocardiographic Findings in Other Potential Causes of Hemodynamic Instability

The sudden occlusion of large portions of the pulmonary vascular bed results in an acute pressure overload on the RV. A distinct regional pattern of RV dysfunction may be noted, with akinesia of the midfree wall, and apparent normal motion at the apex. This characteristic echocardiographic finding has been described as “McConnell’s sign,” and 3 mechanisms have been proposed to explain these findings.5

First, in acute PE, apical sparing may be an illusion. Longitudinal velocity vector imaging demonstrated that there is a significant decrease in RV strain and RV apical deformation,6 and the appearance of preserved wall motion at the RV apex may occur due to the tethering of the dilated RV apex to a hypercontractile left ventricle. Second, the RV may assume a more spherical shape to equalize regional wall stress when subjected to an abrupt increase in afterload.5 Finally, there may be localized ischemia of the RV free wall as a result of increased wall stress.5 However, McConnell’s sign requires a significant degree of pulmonary perfusion obstruction before these echocardiographic findings become apparent. In addition, this pattern of RV dysfunction can be observed in cases of RV infarction and thus, cannot be considered a specific marker for the diagnosis of acute PE.

Another indirect sign of acute PE is the “60/60 sign,” which may appear with smaller perfusion defects. The 60/60 sign is the finding of a PA acceleration time (AT) of <60 milliseconds with a maximal tricuspid regurgitant pressure gradient of <60 mm Hg. The maximum tricuspid regurgitant pressure gradient should not exceed 60 mm Hg, as this is the maximum output of a nonhypertrophied RV. The PA AT is defined as the interval between the onset of systolic PA flow and peak flow velocity (Fig. 3). It can be measured by pulsed-wave Doppler interrogation of the PA in the midesophageal ascending aorta short axis, the upper esophageal aortic arch long axis, or the transgastric RV inflow–outflow views, with the sample volume in the main PA. The AT decreases in PE because of increased PA impedance from proximal thrombi with only moderately increased PA pressures. This may be a more sensitive variable for diagnosing acute PE than McConnell’s sign in patients without underlying cardiorespiratory disease.7

Figure 3
Figure 3:
PA AT can be measured by PWD interrogation of the PA. The PA AT is defined as the interval between the onset of systolic pulmonary artery flow and peak flow velocity. A, Normal pulmonary vascular resistance demonstrating a normal domed appearance of the PA PWD trace and a normal AT of 134 ± 24 ms. B, Increased pulmonary vascular resistance resulting in a triangular ejection curve and AT shortening. In pulmonary embolism the AT is usually <60 to 90 ms. PA = pulmonary artery; AT = acceleration time; PWD = pulsed-wave Doppler.

Recognition of these echocardiographic findings associated with massive PE could help critical care physicians in early management decisions regarding thrombolysis or embolectomy.


Name: Gary Lau, MBChB, FRCA.

Contribution: This author helped prepare the manuscript.

Name: Gabor Ther, MD, DESA.

Contribution: This author helped prepare the manuscript.

Name: Justiaan Swanevelder, MBChB, FRCA, FCA (SA), MMED (Anes).

Contribution: This author helped prepare the manuscript.

Attestation: Justiaan Swanevelder approved the final manuscript.

This manuscript was handled by: Martin J. London, MD.


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2. Brzezinski M, Corkey WB, Grichnik KP, Swaminathan M. Transesophageal echocardiography of pulmonary thrombus causing complete left pulmonary artery occlusion. Anesth Analg. 2005;101:639–40
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Clinician’s Key Teaching Points

By Martin J. London, MD, Nikolaos J. Skubas, MD, and Roman M. Sniecinski, MD

  • An acute pulmonary embolism (PE) can often lead to significant hemodynamic instability, which is typically the result of right heart strain. Although computed tomography pulmonary angiography is the preferred diagnostic method for PE, transesophageal echocardiography can often be used to first exclude other causes of right-sided hypotension, including right ventricular (RV) infarction, cardiac tamponade, and hypovolemia.
  • In this case of acute PE, the nonspecific signs of RV pressure overload (right atrial and RV enlargement, tricuspid regurgitation, and bowing of interatrial and interventricular septa to the left) were imaged together with McConnell’s sign, a hypokinetic RV free wall with normal contraction of the RV apex. Additionally, the authors were able to actually view the PE in the right main pulmonary artery, which, unlike the left main pulmonary artery, can usually be reliably imaged.
  • Although it is rare to actually visualize a PE with transesophageal echocardiography, indirect findings such as McConnell’s sign and the “60/60 sign” (pulmonary artery acceleration time <60 milliseconds with tricuspid regurgitation gradient <60 mm Hg) can help clinicians make a presumptive diagnosis and institute timely treatment.
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