IMAGES IN MEDICINE Heart, Lung and Vessels. 2015; 7(1): 86-88
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McConnell’s echocardiographic sign in acute pulmonary embolism: still a useful pearl Jorge A. Brenes-Salazar Department of Medicine, Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN
Keywords: McConnell’s sign, echocardiography, acute pulmonary embolism.
A 69 year old female with a history of gastric bypass surgery with a recent revision (12 weeks prior to presentation) was admitted from a skilled nursing facility with subacute progressive dyspnea, cough and pleuritic chest pain. On initial assessment her blood pressure was 150/80 mmHg, pulse of 130 beats per minute, with a respiratory rate of 30 per minute and oxygen saturation of 85%. She had evidence of hypoxemic respiratory failure on arterial blood gases, with a PaO2 of 46 mmHg and thus was intubated and sedated before further workup was obtained. A bedside echocardiogram showed preserved left ventricular performance, with an ejection fraction of 65%, but exhibited severe right ventricular enlargement and systolic dysfunction (Figures 1 and 2), with akinesis of the mid-ventricular segments but preserved contractility of the apex (McConnell sign, Figure 3). Right ventricular systolic pressure was estimated to be 50 mmHg by peak tricuspid regurgitant velocity. Corresponding author: Jorge A Brenes-Salazar, MD Mayo Clinic 200 First St. SW, Rochester, MN 55905 e-mail: [email protected]
Figure 1 - Tissue Doppler signal of the systolic velocity at the lateral annulus of the right ventricle, measured at 0.07 m/s (normal 0.12-0.14 m/s).
Figure 2 - M-mode of the tricuspid annular plane systolic excursion (TAPSE), measured at 11.5 mm (normal 20-22 mm). Heart, Lung and Vessels. 2015, Vol. 7
McConnell’s echocardiographic sign in acute pulmonary embolism
Figure 3 - Apical four chamber 2-D image of the left (LV) and right (RV) ventricles, displaying preserved contraction of the RV apex with akinesis of the free wall, consistent with McConnell’s sign. Compare the relative sizes of the RV and LV.
Figure 4 - Computed tomography (CT) scan of the chest, maximum intensity projection (MPI) that shows the presence of multiple abrupt filling defects of the sub-segmental right pulmonary arteries (arrow). Notice the remarkable oligemia of the right lung as compared to the left.
No thrombus in transit was identified. Given these findings, the patient was empirically started on intravenous un-fractioned heparin while she was transported to the computed tomography (CT) scanner. Chest CT angiography displayed multiple pulmonary emboli in lobar and segmental branches of the right pulmonary arteries, with associated right ventricular enlargement consistent with right ventricular strain (Figure 4). Given the patient’s respiratory and hemodynamic compromise, intravenous tissue plasminogen activator (tPA) was administered, with marked improvement of her cardiorespiratory status in a matter of hours. She was successfully extubated on day 2 and transitioned to oral warfarin therapy. The role of echocardiography in the workup of acute pulmonary embolism has not been well established formally (1), but it can provide a series of indirect clues that can guide clinicians to reach a definitive diagnosis. In cases of pulmonary embolism with cardiorespiratory compromise, such non-invasive data can crucially aid in therapeutic decisions such as thrombolysis. McConnell’s sign is a distinct echocardiographic pattern of regional wall motion abnormalities of the right ventricle, with akinesis of the mid-ventricular free wall with normal or hyperdynamic contractility of the apex (2). Potential mechanisms that may account for this phenomenon include tethering of the right apex to a compensating and hyperdynamic left apex, attempts of the right ventricle to provide acute spherical remodeling that may be hemodynamically more efficient and localized ischemia of the free wall due to increased wall stress (3). Although not pathognomonic of acute pulmonary embolism, since it can also be present in cases of right ventricular infarction
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(4), the diagnostic value of McConnell’s sign should not be underestimated in patients presenting with hypoxemia and additional signs of right ventricular pressure overload, such as increased tricuspid jet velocity and RV outflow tract acceleration times.
REFERENCES 1. Torbicki A. Echocardiographic diagnosis of pulmonary embolism: a rise and a fall of McConnell sign? Eur J Echocardiogr 2005; 6: 2-3. 2. Sosland RP, Gupta K. Images in cardiovascular medicine: McConnell’s Sign. Circulation 2008; 118: e517-8. 3. Calvin JE. Pressure segment length analysis of right ventricular function: influence of loading conditions. Am J Physiol 1991; 260: 1087-97. 4. Casazza F, Bongarzoni A, Capozi A, Agostoni O. Regional right ventricular dysfunction in acute pulmonary embolism and right ventricular infarction. Eur J Echocardiogr 2005; 6: 11-4.
Cite this article as: Jorge A. Brenes-Salazar. McConnell’s echocardiographic sign in acute pulmonary embolism: still a useful pearl. Heart, Lung and Vessels. 2015; 7(1): 86-88. Source of Support: Nil. Disclosures: None declared.
Heart, Lung and Vessels. 2015, Vol. 7
86
McConnell’s echocardiographic sign in acute pulmonary embolism: still a useful pearl Jorge A. Brenes-Salazar Department of Medicine, Division of Cardiovascular Diseases, Mayo Clinic, Rochester, MN
Keywords: McConnell’s sign, echocardiography, acute pulmonary embolism.
A 69 year old female with a history of gastric bypass surgery with a recent revision (12 weeks prior to presentation) was admitted from a skilled nursing facility with subacute progressive dyspnea, cough and pleuritic chest pain. On initial assessment her blood pressure was 150/80 mmHg, pulse of 130 beats per minute, with a respiratory rate of 30 per minute and oxygen saturation of 85%. She had evidence of hypoxemic respiratory failure on arterial blood gases, with a PaO2 of 46 mmHg and thus was intubated and sedated before further workup was obtained. A bedside echocardiogram showed preserved left ventricular performance, with an ejection fraction of 65%, but exhibited severe right ventricular enlargement and systolic dysfunction (Figures 1 and 2), with akinesis of the mid-ventricular segments but preserved contractility of the apex (McConnell sign, Figure 3). Right ventricular systolic pressure was estimated to be 50 mmHg by peak tricuspid regurgitant velocity. Corresponding author: Jorge A Brenes-Salazar, MD Mayo Clinic 200 First St. SW, Rochester, MN 55905 e-mail: [email protected]
Figure 1 - Tissue Doppler signal of the systolic velocity at the lateral annulus of the right ventricle, measured at 0.07 m/s (normal 0.12-0.14 m/s).
Figure 2 - M-mode of the tricuspid annular plane systolic excursion (TAPSE), measured at 11.5 mm (normal 20-22 mm). Heart, Lung and Vessels. 2015, Vol. 7
McConnell’s echocardiographic sign in acute pulmonary embolism
Figure 3 - Apical four chamber 2-D image of the left (LV) and right (RV) ventricles, displaying preserved contraction of the RV apex with akinesis of the free wall, consistent with McConnell’s sign. Compare the relative sizes of the RV and LV.
Figure 4 - Computed tomography (CT) scan of the chest, maximum intensity projection (MPI) that shows the presence of multiple abrupt filling defects of the sub-segmental right pulmonary arteries (arrow). Notice the remarkable oligemia of the right lung as compared to the left.
No thrombus in transit was identified. Given these findings, the patient was empirically started on intravenous un-fractioned heparin while she was transported to the computed tomography (CT) scanner. Chest CT angiography displayed multiple pulmonary emboli in lobar and segmental branches of the right pulmonary arteries, with associated right ventricular enlargement consistent with right ventricular strain (Figure 4). Given the patient’s respiratory and hemodynamic compromise, intravenous tissue plasminogen activator (tPA) was administered, with marked improvement of her cardiorespiratory status in a matter of hours. She was successfully extubated on day 2 and transitioned to oral warfarin therapy. The role of echocardiography in the workup of acute pulmonary embolism has not been well established formally (1), but it can provide a series of indirect clues that can guide clinicians to reach a definitive diagnosis. In cases of pulmonary embolism with cardiorespiratory compromise, such non-invasive data can crucially aid in therapeutic decisions such as thrombolysis. McConnell’s sign is a distinct echocardiographic pattern of regional wall motion abnormalities of the right ventricle, with akinesis of the mid-ventricular free wall with normal or hyperdynamic contractility of the apex (2). Potential mechanisms that may account for this phenomenon include tethering of the right apex to a compensating and hyperdynamic left apex, attempts of the right ventricle to provide acute spherical remodeling that may be hemodynamically more efficient and localized ischemia of the free wall due to increased wall stress (3). Although not pathognomonic of acute pulmonary embolism, since it can also be present in cases of right ventricular infarction
Heart, Lung and Vessels. 2015, Vol. 7
87
J.A. Brenes-Salazar
88
(4), the diagnostic value of McConnell’s sign should not be underestimated in patients presenting with hypoxemia and additional signs of right ventricular pressure overload, such as increased tricuspid jet velocity and RV outflow tract acceleration times.
REFERENCES 1. Torbicki A. Echocardiographic diagnosis of pulmonary embolism: a rise and a fall of McConnell sign? Eur J Echocardiogr 2005; 6: 2-3. 2. Sosland RP, Gupta K. Images in cardiovascular medicine: McConnell’s Sign. Circulation 2008; 118: e517-8. 3. Calvin JE. Pressure segment length analysis of right ventricular function: influence of loading conditions. Am J Physiol 1991; 260: 1087-97. 4. Casazza F, Bongarzoni A, Capozi A, Agostoni O. Regional right ventricular dysfunction in acute pulmonary embolism and right ventricular infarction. Eur J Echocardiogr 2005; 6: 11-4.
Cite this article as: Jorge A. Brenes-Salazar. McConnell’s echocardiographic sign in acute pulmonary embolism: still a useful pearl. Heart, Lung and Vessels. 2015; 7(1): 86-88. Source of Support: Nil. Disclosures: None declared.
Heart, Lung and Vessels. 2015, Vol. 7
