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Tricuspid Regurgitation Jet Velocity Suggestive of Severe Pulmonary Hypertension
DIAGNOSTIC DILEMMA
Tricuspid Regurgitation Jet Velocity Suggestive of Severe Pulmonary Hypertension Bryan G. Maxwell, MD, MPH, Daryl A. Oakes, MD, Robert L. Lobato, MD, MS, and Charles C. Hill, MD
A
73-YEAR-OLD WOMAN suffered a cardiac arrest in the emergency department waiting room. After prompt resuscitation and admission to the coronary care unit, coronary angiography showed critical stenosis of the left main and left circumflex arteries. An intra-aortic balloon pump was placed, a heparin infusion was initiated, and the patient was brought for urgent coronary artery bypass grafting. Transesophageal echocardiography revealed the unexpected finding of near-systemic right ventricular systolic pressure by tricuspid regurgitation jet
Fig 3. Continuous wave Doppler examination of the tricuspid regurgitation jet shows a maximum velocity of 4.88 m/sec, which predicts a right ventricular systolic pressure of at least 95 mmHg above right atrial pressure by the modified Bernoulli equation.
Fig 1. Modified midesophageal four-chamber view showing the tricuspid regurgitation jet in relation to the coronary sinus (CS). RA, right atrium; RV, right ventricle.
Fig 2. Modified transgastric right ventricular inflow view confirming the tricuspid regurgitation jet. LV, left ventricle; RA, right atrium; RV, right ventricle.
velocity on continuous wave Doppler. Midesophageal 4-chamber (Fig 1), midesophageal right ventricular inflowoutflow, and transgastric right ventricular inflow (Fig 2) views revealed a moderate tricuspid regurgitation jet with maximum velocity of 4.88 m/sec, which predicts a right ventricular systolic pressure of at least 95 mmHg above right atrial pressure (Fig 3). There was no evidence of pulmonary stenosis, right ventricular outflow tract obstruction, or atrial or ventricular septal defects. Central venous pressure was measured (by right internal jugular vein catheter) at 10 mmHg. Right atrial size, systolic hepatic vein flow, right ventricular size and function, septal position, and septal motion appeared normal. Direct measurement of pulmonary artery systolic pressure (44 mmHg) did not correlate with the TEE estimate. With the catheter withdrawn into the right ventricle, right ventricular systolic pressure was measured at 42 mmHg. What is the diagnosis?
From the Department of Anesthesia, Stanford University School of Medicine, Stanford, CA. Address reprint requests to Bryan G. Maxwell, MD, MPH, Stanford University Medical Center, Department of Anesthesia, 300 Pasteur Drive H3586, Stanford, CA 94305-5640. E-mail: bryanmaxwell@ gmail.com © 2013 Elsevier Inc. All rights reserved. 1053-0770/2602-0033$36.00/0 http://dx.doi.org/10.1053/j.jvca.2013.03.032
Journal of Cardiothoracic and Vascular Anesthesia, Vol ], No ] (Month), 2013: pp ]]]–]]]
1
2
MAXWELL ET AL
DIAGNOSIS: ACQUIRED INDIRECT GERBODE DEFECT WITH TRICUSPID REGURGITATION
The intraoperative finding of tricuspid regurgitation velocity that predicts severe pulmonary hypertension is concerning from the perspective of perioperative risk. Direct measurement of pulmonary artery pressures revealed the TEE to have overestimated pulmonary artery pressure. Because of the crossing angle theta, Doppler velocity can underestimate true velocity. Overestimation of pressure gradients by Doppler examination has been reported to result in a discrepancy between Doppler-estimated and directly measured pressures in a phenomenon called pressure recovery. This has been observed in relation to the gradients across stenotic1 and prosthetic valves,2,3 but not in the current setting. Except for these instances of pressure recovery, overestimation of true velocity is not thought to routinely occur.4 A jet originating from a higher pressure chamber, ie, the left ventricle, is an alternative explanation for a tricuspid regurgitation jet of higher velocity than a true right ventricular systolic pressure would produce. A direct left ventricle to right atrium shunt (Gerbode defect) would not be expected to mimic high velocity flow crossing the tricuspid valve itself; however, an indirect Gerbode defect (left ventricle to right atrium flow via a small perimembranous ventricular septal defect and passing through the tricuspid valve) would mimic high velocity tricuspid regurgitation from high right ventricular systolic pressure. This diagnosis might be expected to produce a tricuspid regurgitation jet that is directed at the coronary sinus (see arrows, Fig 4). Based on these factors, we made a presumptive diagnosis of an indirect Gerbode defect although direct TEE evidence to visualize the pathway at the septum could not be found. If small and restrictive, this defect may not have produced pressure equalization throughout the right atrium or the expected signs of right-sided overload. While Gerbode defects are often congenital, acquired defects have been associated with endocarditis5 and blunt chest trauma.6 Gerbode defects have previously resulted in an erroneous diagnosis of severe pulmonary hypertension.7 Post-infarction ventricular septal defects resulting from acute myocardial necrosis are well-known complications of acute coronary syndromes but typically develop in the anterior muscular interventricular septum, not near the tricuspid valve. In this case, we suspect that blunt chest trauma (from chest compressions) or direct ventricular septal trauma from the retrograde placement of a guidewire during balloon pump insertion may have been the cause of the small defect. To assess the magnitude of the left-to-right shunt, a comparative oximetry shunt study was performed by obtaining
Fig 4. Depiction of the location of direct (D) and indirect (I) Gerbode defects. The resulting regurgitation jet will be directed at the coronary sinus (CS). Ao, aorta; IVC, inferior vena cava; PA, pulmonary artery; RA, right atrium; SVC, superior vena cava; TV, tricuspid valve; VSD, ventricular septal defect. Image copyright 2012, used with permission from CTSNet (www.ctsnet.org). All rights reserved.
oxygen tension and saturation measurements on superior vena cava, right atrium, and pulmonary artery samples, which did not demonstrate abnormalities. Prior studies have identified a 9% absolute step-up from right atrium to pulmonary artery oxygen saturation as a threshold that confirms an intracardiac shunt with high sensitivity and specificity, but note that this finding is less likely to be present in patients with a Qp/Qs smaller than 1.9 to 1.8 Because of the absence of elevated right sided pressures, substantially increased right atrial volume, or clinically evident shunt by comparative oximetry, the decision was made along with the surgical team to manage the suspected defect expectantly. Coronary artery bypass grafting proceeded uneventfully. The atria were not opened; therefore, surgical inspection could not confirm our presumptive diagnosis. Post-procedure transesophageal echocardiography after protamine reversal of heparin showed no further evidence of high-velocity tricuspid regurgitation. Postoperative transthoracic echocardiography also estimated normal right ventricular systolic pressure by tricuspid regurgitation jet velocity. The patient had an uneventful recovery without evidence of right ventricular dysfunction, pulmonary hypertension, or heart failure symptoms.
REFERENCES 1. Baumgartner H, Schima H, Tulzer G, et al: Effect of stenosis geometry on the Doppler-catheter gradient relation in vitro: A manifestation of pressure recovery. J Am Coll Cardiol 21:1018-1025, 1993 2. Dohmen G, Schmitz C, Langebartels G, et al: Impact of pressure recovery in the evaluation of the Omnicarbon tilting disc valve. Thorac Cardiovasc Surg 54:173-177, 2006 3. Rehfeldt KH, Click RL: Prosthetic valve malfunction masked by intraoperative pressure measurements. Anesth Analg 94:857-858, 2002 4. Yock PG, Popp RL: Noninvasive estimation of right ventricular systolic pressure by Doppler ultrasound in patients with tricuspid regurgitation. Circulation 70:657-662, 1984
5. Matt P, Winkler B, Gutmann M, et al: Acquired Gerbode defect after endocarditis. Eur J Cardiothorac Surg 36:402, 2009 6. Hezzell MJ, Dennis S, Lewis DH, et al: Gerbode defect associated with blunt trauma in a dog. J Vet Cardiol 13:141-146, 2011 7. Xhabija N, Prifti E, Allajbeu I, et al: Gerbode defect following endocarditis and misinterpreted as severe pulmonary arterial hypertension. Cardiovasc Ultrasound 8:44, 2010 8. Hillis LD, Firth BG, Winniford MD: Variability of right-sided cardiac oxygen saturations in adults with and without left-to-right intracardiac shunt. Am J Cardiol 58:129-132, 1986
Tricuspid Regurgitation Jet Velocity Suggestive of Severe Pulmonary Hypertension Bryan G. Maxwell, MD, MPH, Daryl A. Oakes, MD, Robert L. Lobato, MD, MS, and Charles C. Hill, MD
A
73-YEAR-OLD WOMAN suffered a cardiac arrest in the emergency department waiting room. After prompt resuscitation and admission to the coronary care unit, coronary angiography showed critical stenosis of the left main and left circumflex arteries. An intra-aortic balloon pump was placed, a heparin infusion was initiated, and the patient was brought for urgent coronary artery bypass grafting. Transesophageal echocardiography revealed the unexpected finding of near-systemic right ventricular systolic pressure by tricuspid regurgitation jet
Fig 3. Continuous wave Doppler examination of the tricuspid regurgitation jet shows a maximum velocity of 4.88 m/sec, which predicts a right ventricular systolic pressure of at least 95 mmHg above right atrial pressure by the modified Bernoulli equation.
Fig 1. Modified midesophageal four-chamber view showing the tricuspid regurgitation jet in relation to the coronary sinus (CS). RA, right atrium; RV, right ventricle.
Fig 2. Modified transgastric right ventricular inflow view confirming the tricuspid regurgitation jet. LV, left ventricle; RA, right atrium; RV, right ventricle.
velocity on continuous wave Doppler. Midesophageal 4-chamber (Fig 1), midesophageal right ventricular inflowoutflow, and transgastric right ventricular inflow (Fig 2) views revealed a moderate tricuspid regurgitation jet with maximum velocity of 4.88 m/sec, which predicts a right ventricular systolic pressure of at least 95 mmHg above right atrial pressure (Fig 3). There was no evidence of pulmonary stenosis, right ventricular outflow tract obstruction, or atrial or ventricular septal defects. Central venous pressure was measured (by right internal jugular vein catheter) at 10 mmHg. Right atrial size, systolic hepatic vein flow, right ventricular size and function, septal position, and septal motion appeared normal. Direct measurement of pulmonary artery systolic pressure (44 mmHg) did not correlate with the TEE estimate. With the catheter withdrawn into the right ventricle, right ventricular systolic pressure was measured at 42 mmHg. What is the diagnosis?
From the Department of Anesthesia, Stanford University School of Medicine, Stanford, CA. Address reprint requests to Bryan G. Maxwell, MD, MPH, Stanford University Medical Center, Department of Anesthesia, 300 Pasteur Drive H3586, Stanford, CA 94305-5640. E-mail: bryanmaxwell@ gmail.com © 2013 Elsevier Inc. All rights reserved. 1053-0770/2602-0033$36.00/0 http://dx.doi.org/10.1053/j.jvca.2013.03.032
Journal of Cardiothoracic and Vascular Anesthesia, Vol ], No ] (Month), 2013: pp ]]]–]]]
1
2
MAXWELL ET AL
DIAGNOSIS: ACQUIRED INDIRECT GERBODE DEFECT WITH TRICUSPID REGURGITATION
The intraoperative finding of tricuspid regurgitation velocity that predicts severe pulmonary hypertension is concerning from the perspective of perioperative risk. Direct measurement of pulmonary artery pressures revealed the TEE to have overestimated pulmonary artery pressure. Because of the crossing angle theta, Doppler velocity can underestimate true velocity. Overestimation of pressure gradients by Doppler examination has been reported to result in a discrepancy between Doppler-estimated and directly measured pressures in a phenomenon called pressure recovery. This has been observed in relation to the gradients across stenotic1 and prosthetic valves,2,3 but not in the current setting. Except for these instances of pressure recovery, overestimation of true velocity is not thought to routinely occur.4 A jet originating from a higher pressure chamber, ie, the left ventricle, is an alternative explanation for a tricuspid regurgitation jet of higher velocity than a true right ventricular systolic pressure would produce. A direct left ventricle to right atrium shunt (Gerbode defect) would not be expected to mimic high velocity flow crossing the tricuspid valve itself; however, an indirect Gerbode defect (left ventricle to right atrium flow via a small perimembranous ventricular septal defect and passing through the tricuspid valve) would mimic high velocity tricuspid regurgitation from high right ventricular systolic pressure. This diagnosis might be expected to produce a tricuspid regurgitation jet that is directed at the coronary sinus (see arrows, Fig 4). Based on these factors, we made a presumptive diagnosis of an indirect Gerbode defect although direct TEE evidence to visualize the pathway at the septum could not be found. If small and restrictive, this defect may not have produced pressure equalization throughout the right atrium or the expected signs of right-sided overload. While Gerbode defects are often congenital, acquired defects have been associated with endocarditis5 and blunt chest trauma.6 Gerbode defects have previously resulted in an erroneous diagnosis of severe pulmonary hypertension.7 Post-infarction ventricular septal defects resulting from acute myocardial necrosis are well-known complications of acute coronary syndromes but typically develop in the anterior muscular interventricular septum, not near the tricuspid valve. In this case, we suspect that blunt chest trauma (from chest compressions) or direct ventricular septal trauma from the retrograde placement of a guidewire during balloon pump insertion may have been the cause of the small defect. To assess the magnitude of the left-to-right shunt, a comparative oximetry shunt study was performed by obtaining
Fig 4. Depiction of the location of direct (D) and indirect (I) Gerbode defects. The resulting regurgitation jet will be directed at the coronary sinus (CS). Ao, aorta; IVC, inferior vena cava; PA, pulmonary artery; RA, right atrium; SVC, superior vena cava; TV, tricuspid valve; VSD, ventricular septal defect. Image copyright 2012, used with permission from CTSNet (www.ctsnet.org). All rights reserved.
oxygen tension and saturation measurements on superior vena cava, right atrium, and pulmonary artery samples, which did not demonstrate abnormalities. Prior studies have identified a 9% absolute step-up from right atrium to pulmonary artery oxygen saturation as a threshold that confirms an intracardiac shunt with high sensitivity and specificity, but note that this finding is less likely to be present in patients with a Qp/Qs smaller than 1.9 to 1.8 Because of the absence of elevated right sided pressures, substantially increased right atrial volume, or clinically evident shunt by comparative oximetry, the decision was made along with the surgical team to manage the suspected defect expectantly. Coronary artery bypass grafting proceeded uneventfully. The atria were not opened; therefore, surgical inspection could not confirm our presumptive diagnosis. Post-procedure transesophageal echocardiography after protamine reversal of heparin showed no further evidence of high-velocity tricuspid regurgitation. Postoperative transthoracic echocardiography also estimated normal right ventricular systolic pressure by tricuspid regurgitation jet velocity. The patient had an uneventful recovery without evidence of right ventricular dysfunction, pulmonary hypertension, or heart failure symptoms.
REFERENCES 1. Baumgartner H, Schima H, Tulzer G, et al: Effect of stenosis geometry on the Doppler-catheter gradient relation in vitro: A manifestation of pressure recovery. J Am Coll Cardiol 21:1018-1025, 1993 2. Dohmen G, Schmitz C, Langebartels G, et al: Impact of pressure recovery in the evaluation of the Omnicarbon tilting disc valve. Thorac Cardiovasc Surg 54:173-177, 2006 3. Rehfeldt KH, Click RL: Prosthetic valve malfunction masked by intraoperative pressure measurements. Anesth Analg 94:857-858, 2002 4. Yock PG, Popp RL: Noninvasive estimation of right ventricular systolic pressure by Doppler ultrasound in patients with tricuspid regurgitation. Circulation 70:657-662, 1984
5. Matt P, Winkler B, Gutmann M, et al: Acquired Gerbode defect after endocarditis. Eur J Cardiothorac Surg 36:402, 2009 6. Hezzell MJ, Dennis S, Lewis DH, et al: Gerbode defect associated with blunt trauma in a dog. J Vet Cardiol 13:141-146, 2011 7. Xhabija N, Prifti E, Allajbeu I, et al: Gerbode defect following endocarditis and misinterpreted as severe pulmonary arterial hypertension. Cardiovasc Ultrasound 8:44, 2010 8. Hillis LD, Firth BG, Winniford MD: Variability of right-sided cardiac oxygen saturations in adults with and without left-to-right intracardiac shunt. Am J Cardiol 58:129-132, 1986