Friday, May 10, 2013



Feroze Mahmood, MD Madhav Swaminathan, MD
Section Editors

Major Surgery, Hemodynamic Instability, and a Left Atrial Appendage Clot: What to Do?

Remco Bergman, MD, Omair Shakil, MD, Bilal Mahmood, BA, and Robina Matyal, MD

A 77-YEAR-OLD PATIENT was scheduled for emergency spinal surgery for multiple cervical vertebral fractures. He had sustained bilateral fractures of the C5 and C6 pedicles after falling from his bed. Of note, the injury was associated with neurologic deficits (motor and sensory) in the upper and lower extremities and the patient’s cervical spine was deemed unstable. His medical history was significant for coronary artery disease, congestive heart failure, and transient ischemic attacks and he had an automatic internal cardiac defibrillator placed recently for recurrent ventricular tachycardia.

After obtaining intravenous access by 2 peripheral catheters and 1 arterial catheter, the patient was brought to the operating room. The induction of general anesthesia was uneventful and the airway was secured with modified rapid-sequence induction using a glidescope while maintaining inline traction. Immediately after the start of the surgery, the patient went into atrial fibrillation (AF), with a heart rate of 120-130 beats/min, accompanied by a decrease in blood pressure from 110/80 to 80/50 mmHg. There were no accompanying ST-segment changes on the electrocardiogram. The position of his endotracheal tube was confirmed, the depth of anesthesia was ensured, and he was administered a rapid fluid bolus of lactated Ringer’s solution, 500 mL. Intermittent boluses of intravenous phenylephrine (500 [H9262]g) and esmolol (total 50 mg) also were administered to support his systolic blood pressure and control his heart rate, respectively. With these measures, the patient’s heart rate decreased to 90 beats/min and his blood pressure improved to 90/50 mmHg. Given his medical history of coronary artery disease and persistent hemodynamic instability, transesophageal echocardiography (TEE) was performed to assess his volume status and cardiac function. The TEE demonstrated mild symmetric left ventricular hypertrophy with cavity dilation, global moderate-to-severe systolic dysfunction, an ejection fraction of 30%, and severe diastolic dysfunction (decreased compliance) with an E/e= of 15. There also was moderate aortic stenosis (AS) with an aortic valve area of 1.0 cm2. Although the degree of myocardial dysfunction was known from the patient’s history, the moderate AS was a new finding. In addition, the left atrium was dilated moderately, with a sluggish flow and significant spontaneous echocardio-graphic contrast in the left atrial appendage (LAA). Interestingly, an echodensity measuring 2 cm [H11003] 1.5 cm also was visualized in the LAA; the appearance of which was consistent with a thrombus (Fig 1).

Fig 1. Midesophageal 2-chamber view showing the left atrial appendage with an echodensity most consistent with a thrombus.


1. The presence of a significant compliance abnormality of the left ventricle, given the patient’s history of congestive heart failure, necessitated a judicious approach to fluid administration.

2. The occurrence of AF with moderate AS, leading to a loss of an atrial contribution to left ventricular filling, required fluid administration.

3. The moderate AS and LAA thrombus were unexpected findings.

From the Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA

Address reprint requests to Omair Shakil, MD, Research Fellow, Department of Anesthesia, Critical Care, and Pain Medicine, Beth Israel Deaconess Medical Center, One Deaconess Road, CC-470, Boston, MA 02215. E-mail:

© 2013 Elsevier Inc. All rights reserved. 1053-0770/2703-0001$36.00/0

Journal of Cardiothoracic and Vascular Anesthesia, Vol 27, No 3 (June), 2013: pp 625-626



1. To achieve optimal fluid management, despite the contradictory demands of the patient’s clinical situation; ie, AF and AS requiring fluid administration versus the conservative approach demanded by the decreased left ventricular compliance.

2. Optimal management of the AF and LAA thrombus; ie anticoagulation (risk of persistent hemodynamic instability) versus cardioversion (risk of thrombus dislodgement).


1. The patient’s blood pressure was supported with pre-load augmentation and [H9251]-adrenergic drugs (phenylephrine).
2. Heart rate control was achieved with [H9252]-adrenergic blocking drugs (esmolol).

3. A mutual decision was reached with the surgical team to withhold cardioversion to decrease the risk of possible LAA thrombus dislodgement.

4. A cardiology consultation was scheduled in the immediate postoperative period to manage the anticoagulation and AF.


Afterwards, the patient was extubated uneventfully and transferred to the coronary care unit. On the second postoperative day, intravenous heparin infusion was started, which was bridged to oral anticoagulation with coumadin. The patient was discharged a few days later in stable condition.


Anesthesiologists and Transesophageal Echocardiography: Echocardiographers or Echocardiologists?

DURING HEMODYNAMIC INSTABILITY, clinicians choose to use monitors which they are most accustomed to.1 The time-limited nature of decision-making in the perioperative arena necessitates an approach that quickly can establish a diagnosis and dictate treatment. The use of TEE under such circumstances has been established as an essential monitor.2 The therapeutic impact of intraoperative TEE traditionally has been defined as a change in the surgical/anesthetic management or the addition of postoperative follow-up.3 Life-threatening hypoxia and intractable hypotension are considered category I indications for intraoperative TEE3 and there is unequivocal evidence of the impact of TEE for these indications. However, the use of intraoperative TEE to confirm a clinical suspicion with no change in therapy generally is not considered a major therapeutic intervention. Although arguably equally valuable, such an impact is difficult to quantify and therefore not considered, possibly leading to an underestimation of the true therapeutic effect.

The case presented in this issue of the Journal highlights many of these very important and debatable issues.4 The presented patient undergoing emergency cervical spine surgery suddenly developed significant hemodynamic instability shortly after the start of surgery. At this point, the anesthesia team did not have adequate access to the patient to place invasive monitoring lines, and the traumatic nature of the case made it a rather urgent situation. The team quickly had to establish or exclude a diagnosis for the sudden hemodynamic instability. Under the circumstances, a rapid TEE examination was the most obvious and logical choice. However, although the TEE examination provided the necessary answers, it raised certain questions. A thrombus was visualized unexpectedly in the left atrial appendage during TEE. Although atrial fibrillation and hemodynamic instability are indications for an emergency cardioversion, the presence of a left atrial appendage

thrombus was a complicating factor. The risk of possible dislodgment of the thrombus with cardioversion had to be weighed against the risk of further hemodynamic deterioration. Although a discussion of the pros and cons of cardioversion under these circumstances is beyond the scope of this editorial, this intraoperative situation represented a decision-making dilemma. The multiple complicating factors (history of trauma, nature of the injury/surgery, atrial fibrillation, and the unexpected finding of a left atrial appendage thrombus) necessitated a patient-specific approach in a multidisciplinary fashion.

Although the patient did not have “life-threatening” hemodynamic instability, the circumstances were such that a diagnosis had to be established or excluded rapidly. Although TEE provided the desired information, ironically it created a clinical challenge, with no absolutely correct answers. Not only did TEE assist in resuscitation and the exclusion of diagnoses, it also had an enormous therapeutic impact in the conventional sense, in that it changed the anesthetic management and eventual disposition of the patient.5

With the increasing use of intraoperative TEE, anesthesiologists are finding themselves in unchartered territories and increasingly are involved in the decision-making that was once considered outside the scope of their traditional practice and expertise. There seems to have been a gradual transformation of anesthesiologists’ role from perioperative “echocardiographer” to “echocardiologist.” This changes the anesthesiologists’ role from a service provider to an active decision-maker with the ability to affect outcome.5

Remco Bergman, MD Feroze Mahmood, MD
Department of Anesthesia, Critical Care, and Pain Medicine
Beth Israel Deaconess Medical Center
Harvard Medical School
Boston, MA

1. Jacka MJ, Cohen MM, To T, et al: The use of and preferences for the transesophageal echocardiogram and pulmonary artery catheter among cardiovascular anesthesiologists. Anesth Analg 94:1065-1071, 2002

2. Mahmood F, Christie A, Matyal R: Transesophageal echocardiography and noncardiac surgery. Semin Cardiothorac Vasc Anesth 12:265-289, 2008

3. American Society of Anesthesiologists and Society of Cardiovascular Anesthesiologists Task Force on Transesophageal Echocardiography: Practice guidelines for perioperative transesophageal echocardiography. An updated report by the American Society of Anesthesiologists and the Society of Cardiovascular Anesthesiologists Task Force on Transesophageal Echocardiography. Anesthesiology, 112:1084-1096, 2010
4. Bergman R, Shakil O, Mahmood B, et al: Major surgery, hemo-dynamic instability, and left atrial appendage clot: What to do? J Cardiothorac Vasc Anesth 2012 (in press)

5. Suriani RJ, Neustein S, Shore-Lesserson L, et al: Intraoperative transesophageal echocardiography during noncardiac surgery. J Cardiothorac Vasc Anesth 12:274-280, 1998

© 2013 Elsevier Inc. All rights reserved. 1053-0770/2703-0001$36.00/0

Friday, March 22, 2013


Feroze Mahmood, MD Madhav Swaminathan, MD
Section Editors

Percutaneous Closure of an Atrial Septal Defect and 3-Dimensional Echocardiography

Faraz Mahmood, BA,*† Omair Shakil, MD,*† Jeniffer R. Gerstle, MD,*† and Robina Matyal, MD*†

AN OTHERWISE HEALTHY 50-year-old man was scheduled for percutaneous atrial septal defect (ASD) closure with an Amplatzer Septal Occluder (AGA Medical Corp, Plymouth, MN). The patient initially had presented to an outside hospital 1 year earlier with an episode of chest pain at rest. A chest x-ray performed during that admission showed a widened mediastinum. A subsequent computed tomography scan and transthoracic echocardiogram (TTE) revealed a 2.1-cm wide secundum ASD (Fig 1) with a dilated right ventricle and moderately dilated right and left atria. The patient did not follow through with recommendations for a TEE and possible ASD closure and was lost to follow-up. A year later, he returned to the authors’ institution with a 6-month long history of dyspnea and episodic chest pain with moderate exertion that was relieved by rest. He underwent cardiac catheterization to assess for the presence of coronary artery disease, but which was negative for any flow-limiting lesions. Resting hemodynamics revealed normal right-sided pressures, and oxygen saturation measurements that were consistent with a left-to-right shunt (Qp/Qs [H11005] 2.4). He subsequently was referred for ASD closure under TEE guidance. After an uneventful induction of general anesthesia, a TEE examination was performed using an IE-33 Ultrasound System X7-2E Probe (Philips Medical Systems, Andover, MA) capable of real-time 3-dimensional (3D) imaging.

The preliminary TEE examination revealed a 2.1-cm (edge-to-edge) wide secundum ASD (Fig 1). A left-to-right shunt with a large flow across the interatrial septum was detected, and the right atrium was also dilated; the left atrium was normal in size. Although the right ventricular cavity was dilated, the overall left ventricular systolic function was normal (left ventricular ejection fraction [H11022]55%). Mild mitral regurgitation ([H11001]1) was noted, but the aortic and mitral leaflets appeared structurally normal. No spontaneous echocardiographic
 contrast or thrombi were seen in the left atrium, the right atrium, or the left and right atrial appendages. There was also a small patent foramen ovale along the inferior edge of the interatrial septum with a left-to-right shunt. The edge of the secundum ASD were seen to consist of a thin mobile filamentous tissue (Video 1 supplementary videos are available online]).

Video 1

Although the procedure itself was relatively uncomplicated, the clinical team faced considerable difficulty in the deployment of the Amplatzer device and its seating. Initially, a size 22 Amplatzer device was percutaneously deployed across the ASD, but TEE imaging showed significant residual left-to-right shunting, and the device was assessed to be mechanically insecure in that it was not well seated on the relatively large ASD. As a result, this device was removed (Video 2). Next, a larger, 24-mm Amplatzer device was deployed with some reduction in residual shunting, but the mechanical seating of the device was again evaluated to be insecure with a likelihood of dislodgement (Video 2).

Video 2

The clinical challenges encountered during the case were as follows: (1) Has the ASD size been measured accurately? (2) Should the thin and mobile portion of the ASD be excluded from ascertaining the ASD diameter? and (3) Would a larger device be suitable for this ASD?

From the *Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, Boston, MA; and †Harvard Medical School, Boston, MA.
Address reprint requests to Omair Shakil, MD, Department of Anesthesia, Critical Care and Pain Medicine, Beth Israel Deaconess Medical Center, One Deaconess Road, CC-470, Boston, MA 02215. E-mail:
© 2013 Elsevier Inc. All rights reserved. 1053-0770/2702-0001$36.00/0
Key words: atrial septal defect, 3-dimensional transesophageal echocardiography, Amplatzer device

Fig 1. The ASD had a diameter of 2.1 cm on 2-dimensional transesophageal echocardiography. RA, right atrium; LA, left atrium. (Color version of figure is available online.)

400 Journal of Cardiothoracic and Vascular Anesthesia, Vol 27, No 2 (April), 2013: pp 400-401

Fig 2. MPRF of volumetric data acquired during transesophageal echocardiography confirmed the diameter of the ASD to be 3.4 cm. (Color version of figure is available online.)


At this point, the size of the ASD was measured again using the multiplanar reformatting (MPRF) of the volumetric 3D data acquired during the TEE examination. Using the 3D quantification function of the Q-Lab software (Philips Medical Systems), the filamentous tissue of the ASD was excluded from the measurement of the diameter (Fig 2). The diameter obtained with the MPRF method was 3.4 cm (Fig 2). Based on this new reading, the team decided to deploy a size 34 Amplatzer occluding device. The device was deployed uneventfully and was seated securely across the rim of the ASD. The absence of any residual shunt on fluoroscopy and 3D transesophageal echocardiography confirmed the optimal positioning of the device. The rest of the case proceeded uneventfully, and the patient was discharged a few days later.

For further information and follow-up discussion of the E-Challenge, please go to:
(1) JCVA online web page for the video images at
(2) JCVA blog site for adding your comments or for viewing the other responses:


Friday, July 13, 2012


Feroze Mahmood, MD
Madhav Swaminathan, MD
Section Editors

Dynamic Mitral Regurgitation Without Regional Wall Motion Abnormality
 Greg Balfanz, MD,* Harendra Srora, MD,* Brett C. Sheridan, MD,† Jason N. Katz, MD, MHS, ‡ & Priya A. Kumar, MD*

*Department of Anesthesiology, University of North Carolina, Chapel Hill, NC     Department of Surgery, University of North Carolina, Chapel Hill, NC
Department of Medicine, University of North Carolina, Chapel Hill, NC
Address reprint requests to Priya A. Kumar, MD, Department of Anesthesiology, N2201 University of North Carolina Hospitals, Campus Box 7010, Chapel Hill, NC  27599-7010.  E-mail:

Key words:  dynamic mitral regurgitation

A 55-YEAR-OLD white man was transferred from an outside hospital with complaints of chest tightness and pain radiating to his jaw and left arm. These symptoms were associated with shortness of breath and diaphoresis. A cardiac catheterization revealed triple-vessel coronary artery disease (75% stenosis in the left anterior descending artery, 80% stenosis in the left circumflex artery near the takeoff of the obtuse marginal artery, and 80% stenosis in the right coronary artery). A transthoracic echocardiogram showed normal left ventricular (LV) function and mitral valve leaflets that were mildly thickened with normal mobility and trivial-to-mild mitral regurgitation (MR) (Video 1). The patient consented to coronary artery bypass graft (CABG) surgery.

The patient underwent uneventful anesthetic induction. The initial intraoperative transesophageal echocardiogram (TEE) showed normal LV systolic function with impaired relaxation by mitral inflow pulse-wave and tissue Doppler studies. Two-dimensional echocardiographic examination revealed the mitral valve leaflets as mildly thickened, with normal coaptation in the midesophageal 4-chamber, 2-chamber, and long-axis views. Annular dimensions in the midesophageal commissural and long-axis views were measured at 3.6 and 3.3 cm, respectively. Color-flow Doppler interrogation of the mitral valve in the midesophageal views showed a trivial centrally directed MR jet. The right ventricular function was normal with a mild central tricuspid regurgitation jet.

Approximately 1 hour after the induction of anesthesia, before the sternotomy incision, an abrupt increase in the mean pulmonary arterial pressures (PAPs) (mmHg) from the mid-20s to the mid-60s occurred. At about the same time, the heart rate (beats/min) changed from the 50s to the 70s, without any associated ST-T wave changes on the electrocardiogram. The mean arterial pressures (mmHg) ranged from the 60s to the 90s. On the TEE, this corresponded with the appearance of a severe centrally directed MR jet along with a systolic reversal of the pulmonary venous flow (Video 2 and Figs 1 and 2).The mechanism of the MR involved symmetric tethering of both the anterior and posterior leaflets, with a complete lack of coaptation and restricted leaflet motion. Although there was no obvious regional wall motion abnormality (RWMA), there were subtle decreases in the global left and right ventricular contractility. The decreased right ventricular contractility was associated with a worsening of the central tricuspid regurgitant jet.

Fig 1.  A transesophageal 2-dimensional echocardiographic image showing the midesophageal 4-chamber view along with color-flow Doppler across the mitral valve showing the lack of leaflet coaptation during systole and severe mitral regurgitation.

Fig 2.  A pulse-wave Doppler signal in the left upper pulmonary vein showing systolic reversal of flow.  (Color version of figure is available online.)

Challenge 1: What Was the Cause for the Abrupt Pulmonary Hypertension?

The differential diagnosis for pulmonary hypertension included the following: (1) pulmonary arterial causes (eg, idiopathic vasospasm, hypoxia, hypercarbia, increased cardiac output, pulmonary embolus, and unmasking of congenital left-right shunts), (2) pulmonary parenchymal dysfunction (eg, parenchymal disease, pneumothorax, light anesthesia, and bucking), and (3) pulmonary venous obstruction (thrombus, mitral stenosis, and mitral regurgitation).


To rule out these causes, the anesthetic depth, bilateral breath sounds, oxygenation, ventilation, and muscle relaxation were reconfirmed. A comprehensive TEE examination was repeated to rule out a pulmonary thromboembolic etiology or any unmasking of congenital shunts. Milrinone and nitric oxide were instituted briefly to rule out a reversible component of pulmonary arterial vasospasm, with no benefit. Small doses of phenylephrine and nitroglycerin were used to maintain the coronary perfusion.
The PAPs remained persistently elevated for a total of 105 minutes, followed by acute normalization. At this time, the heart rate (beats/min) reverted to the 50s, whereas other hemodynamic parameters were remarkably unchanged from baseline. The TEE once again showed trivial-to-mild central MR with normal leaflet coaptation, normal ventricular contractility, and disappearance of the systolic flow reversal pattern on pulse-wave Doppler of the pulmonary venous flow (Video 3 and Figs 3 and 4).

Fig 3.  A transesophageal 2-dimensional echocardiographic image showing the midesophageal 4-chamber view along with color-flow Doppler across the mitral valve showing trivial MR and normal leaflet coaptation.  (Color version of figure is available online.)

Fig 4.  A pulse-wave Doppler signal in the left upper pulmonary vein showing the disappearance of the systolic reversal of flow.

Challenge 2: What is the Cause for the Wide Range of Variability in the Degree of MR?

Dynamic MR that is ischemic in origin is the result of incomplete closure of the mitral leaflets from geometric distortion of the mitral apparatus.1 This occurs in the setting of normal mitral leaflets, and the causes may include annular dilatation, LV dilatation, or distortion resulting in papillary muscle displacement and tethered chordae, all leading to restricted leaflet closure. Left ventricular contraction provides the closing force to oppose the tethering force of the subvalvular apparatus. The presence of LV dysfunction results in an imbalance in favor of this tethering force, thereby aggravating ischemic MR. Transient ischemia of the papillary muscle also can lead to papillary muscle dysfunction, thereby resulting in dynamic MR.

Acute changes in the loading conditions can alter the degree of MR dynamically, which may decrease in severity in a reduced afterload state, such as under general anesthesia. By contrast, acute volume overload and congestive heart failure may worsen MR, whereas a reduced preload of the LV may improve it.2 Lancellotti et al1 and Lebrun et al3 showed that patients with mild MR at rest may have severe MR when provoked by exercise accompanied by an increase in PAPs. The tenting area (the area enclosed between the annular plane and mitral leaflets) and coaptation height (the distance between the annular plane and the mitral leaflet coaptation plane) were the major determinants of exercise-induced increases in MR although their population comprised patients with some degree of LV dysfunction at rest.1

Other causes of dynamic MR may include LV dyssynchrony, which is observed in patients with systolic heart failure.4,5 Its magnitude may be altered significantly by various conditions, such as inducible ischemia, tachycardia, exercise, and pharmacologic agents. This dynamic phenomenon can be unmasked with exercise or dobutamine stress echocardiography even in the absence of detectable ischemia. Because dyssynchronous contraction is inefficient at ejecting the ventricular volume, it can result in delayed mitral valve opening and distorted mitral annulus, hence worsening MR.6 Emerging echocardiographic techniques combining speckle-tracking analysis and 3-D echocardiography are useful in screening patients for LV dyssynchrony. Cardiac resynchronization therapy can result in reverse ventricular remodeling and thereby improve MR because of papillary muscle dyssynchrony. Diastolic dysfunction can also cause functional MR because of the variation in loading conditions.7

Challenge 3: Would CABG Surgery Alone Be Sufficient to Correct Dynamic MR?

Considerable controversy exists regarding the appropriate therapy in patients with MR undergoing CABG surgery.8,9 Surgical correction of ischemic MR is associated with poor long-term survival. It is difficult to decide whether valve replacement or repair would be the most appropriate surgical treatment because of the lack of randomized trials and long-term survival data. Gillinov et al,10 in a retrospective review of 482 patients with ischemic MR, concluded that although late survival in this surgical population is poor, patients may benefit from repair. However, in the more complex high-risk population, there was no survival advantage after repair as compared with replacement.

After an extensive discussion with the surgical team, the therapeutic options considered were the following:

1. CABG surgery alone: a reasonable option with the hope that resolution of the subclinical myocardial ischemia would cure the dynamic severe MR. Reverse remodeling of the myocardium with a final resolution of MR could take months to occur. Also, the target vessels for CABG surgery in this case were believed to be acceptable but not ideal, which left a risk for potentially persistent residual MR. The challenges of a redo sternotomy to address persistent MR at a later time, in light of a left internal mammary artery-to-left anterior descendingartery graft, certainly could increase the risk to the patient.

2. Mitral valve repair: there was no apparent annular dilatation, and the mechanism appeared to be dynamic tethering of mitral leaflets. An undersized annuloplasty ring could result in better coaptation of the leaflets to relieve the dynamic severe MR. However, undersizing could also add the risk of possible iatrogenic mitral stenosis or a dynamic outflow tract obstruction with the occurrence of systolic anterior motion.
3. Mitral valve replacement: with a somewhat nebulous understanding of the true mechanism of the symptomatic dynamic severe MR in this patient, normal annular dimensions, less-than-ideal target vessels, a lack of obvious RWMAs, a relatively young age, and mildly thickened mitral leaflets and chordae, a surgical decision was made to replace the mitral valve with a St Jude's mitral prosthesis.

A post-cardiopulmonary bypass TEE showed an appropriately seated mechanical valve with no paravalvular leak. The patient had an uncomplicated hospital course and subsequently was discharged home.

The acute shortness of breath and symptomatology that this patient experienced likely were caused by the intermittent severe MR that he might have suffered in his daily life. The strikingly dynamic nature of MR in this case, along with the subtle changes in the global right and left ventricular contractility, were suspected to be ischemic in origin (Video 4). However, the impressive change in the grade of MR from trivial to severe likely would have been associated with some RWMA. However, this was conspicuously absent. A 30% increase in heart rate from baseline was possibly a cause for coronary demand-supply mismatch. It probably resulted in ventricular distortion and leaflet tethering, resulting in severe MR and an associated acute increase in PAPs, which resolved when the heart rate returned to baseline.

Mitral valve dysfunction can be elusive in CABG surgery patients if evaluated exclusively at rest. Successful mitral valve repair must target the mechanism of dysfunction. An intraoperative TEE evaluation of the mitral valve with a hemodynamic challenge, such as varying loading conditions, heart rate, and perfusion pressure, can unmask a dynamic condition for which a repair or replacement may be indicated. In this patient, the preoperative echocardiogram showed trivial MR; hence, the patient was scheduled for CABG surgery alone. The incidentally observed intraoperative dynamic changes in MR, which increased from a trivial to a severe grade, changed the surgical approach. The subtle change in the geometry of the LV possibly resulted in symmetric mitral valve leaflet tethering, a type IIIB mechanism. This, in turn, led to a severe and clinically significant change in the degree of MR, warranting a mitral valve replacement in addition to CABG surgery.


1. P. Lancellotti, F. Lebrun, L.A. Pierard. Determinants of exercise induced changes in mitral regurgitation in patients with coronary artery disease and left ventricular dysfunction J Am Coll Cardiol 42:1921-1928, 2003

2. L.B. Rosario, L.W. Stevenson, S.D. Solomon, et al. The mechanism of decrease in dynamic mitral regurgitation during heart failure treatment: Importance of reduction in the regurgitant orifice size J Am Coll Cardiol 32:1819-1824, 1998

3. F. Lebrun, P. Lancellotti, L.A. Pierard. Quantitation of functional mitral regurgitation during bicycle exercise in patients with heart failure J Am Coll Cardiol 38:1685-1692, 2001

4. P. Lancleotti, M. Moonen. Left ventricular dyssynchrony: A dynamic condition Heart Fail Rev 2011 Jul 29 [Epub ahead of print]

5. P. Lancellotti, P.Y. Stainier, F. Lebois, et al. Effect of dynamic left ventricular dyssynchrony on dynamic mitral regurgitation in patients with heart failure due to coronary artery disease Am J Cardiol 96:1304-1307, 2005

6. J.K. Ho, A. Mahajan. Cardiac resynchronization therapy for treatment of heart failure Anesth Alalg 111:1353-1361, 2010

7. T. Karaahmet, K. Tigen, C. Dundar, et al. Papillary muscle dyssynchrony as a cause of functional mitral regurgitation in non-ischemic dilated cardiomyopathy patients with narrow QRS complexes Anadolu Kardiyol Derg 9:196-203, 2009

8. L. Aklog, F. Filsoufi, K.Q. Flores, et al. Does coronary artery bypass grafting alone correct moderate ischemic mitral valve regurgitation? Circulation 104:168-175, 2001

9. I.G. Duarte, Y. Shen, M.J. MacDonald, et al. Treatment of moderate mitral regurgitation and coronary disease by coronary bypass alone: Late results Ann Thorac Surg 68: 426-430, 1999

10. A.M. Gillinov, P.N. Wierup, E.H. Blackstone, et al. Is repair preferable to replacement for ischemic mitral regurgitation? J Thorac Cardiovasc Surg 122: 1125-1114, 2001

Fig 1 A transesophageal 2-dimensional echocardiographic image showing the midesophageal 4-chamber view along with color-flow Doppler across the mitral valve showing the lack of leaflet coaptation during systole and severe mitral regurgitation.

Fig 2 A pulse-wave Doppler signal in the left upper pulmonary vein showing systolic reversal of flow.

Fig 3 A transesophageal 2-dimensional echocardiographic image showing the midesophageal 4-chamber view along with color-flow Doppler across the mitral valve showing trivial MR and normal leaflet coaptation.

Fig 4 A pulse-wave Doppler signal in the left upper pulmonary vein showing the disappearance of the systolic reversal of flow.

Thursday, May 17, 2012


Feroze Mahmood, MD
Madhav Swaminathan, MD

Section Editors

Severe Tricuspid Valve Regurgitation:  
A Case for Laminar Flow

Frederick C Cobey, MD, * Maria Fritock, MD, Frederick W. Lombard, MD, Donald D.Glower, MD, § Madhav Swaminathan, MD, FAHA, FASE‡

 * Georgetown University, the Washington Hospital Center, Washington, DC
†Department of Anesthesiology, Mayo Clinic, Rochester, MN
§Department of Surgery, Division of Thoracic Surgery, Duke University Health System, Durham, NC
 ‡Department of Anesthesiology, Division of Cardiothoracic, Anesthesiology and Critical Care Medicine, Duke University Health System, Durham, NC

Address reprint requests to Madhav Swaminathan, MD, FAHA, FASE, Department of Anesthesiology, Division of Cardiothoracic, Anesthesiology and Critical Care Medicine, Box  3094/5691F HAFS Building, Duke University Health System, Durham, NC  27710.  Email:

Key Words:  tricuspid regurgitation, Doppler, laminar flow

A 67-YEAR-OLD WOMAN presented with progressive dyspnea limiting her ability to perform daily activities. Her past medical history was significant for hyperlipidemia and Hashimoto thyroiditis. Upon further workup, a transthoracic echocardiogram (TTE) was performed, which revealed severe mitral regurgitation (MR) with mild tricuspid regurgitation (TR). Subsequently, she was scheduled for mitral valve repair. After an uneventful induction of anesthesia, an intraoperative transesophageal echocardiogram (TEE) was performed using a matrix array transducer and images acquired on an IE33 ultrasound system (Philips Healthcare, Andover, MA). The examination showed biatrial enlargement and prolapse of both the mitral and tricuspid valves. The tricuspid annulus in diastole measured 4 cm in the midesophageal 4-chamber view. The diagnosis of severe MR and mild TR was confirmed. The surgeon proceeded as planned with a mitral valve repair via a minimally invasive port-access approach. After cardiopulmonary bypass (CPB), the TEE showed a satisfactory mitral repair. However, there was hemodynamic evidence of TR with right ventricular dysfunction and an underfilled left ventricle. The central venous pressure was elevated; there were large "v" waves on the pressure waveform. Although the echocardiographic examination clearly showed TR, there was no clearly defined turbulent jet, and, therefore, the TR could not be quantified simply using the vena contracta, the proximal isovelocity surface area, or the jet area. The systolic flow across the tricuspid valve was laminar (Fig 1)and had a low peak velocity of 0.9 m/s. Both hepatic venous systolic flow reversal and a dense triangular-shaped spectral Doppler tricuspid regurgitant flow pattern also were noted. 

Fig 1 The midesophageal right ventricle inflow-outflow view showing laminar regurgitant flow into the right atrium after the discontinuation of CPB after mitral valve repair.


How Should the Severity of TR Be Evaluated and Graded When a Regurgitant Jet Is Laminar?

In typical cases of TR with a turbulent flow regurgitation jet, the simplest, initial, and most common approach is to use color-flow Doppler to visualize the jet. The severity of TR may be graded by mapping the area of the color jet in the right atrium.1-3 Other established approaches include measurement of the vena contracta and proximal isovelocity surface area.2,4,5 However, TR jets are often ellipsoid, often eccentrically directed, and are difficult to accurately capture in a 3-dimensional space with 2-dimensional echocardiographic planes.6 These factors likely contribute to the significant overlap seen in TR severity grades and the underestimation of TR in 20% to 30% of severe cases evaluated with color-flow Doppler.2,7 When flow is laminar, the borders of a color jet can be so difficult to appreciate that even a large jet can be missed entirely.8 Regurgitant laminar flow in contrast to flow that is turbulent allows a much greater regurgitant volume for a given transvalvular pressure gradient. The lower energy loss of laminar flow likely results in a smaller pressure drop and sustained flow. The American Society of Echocardiography (ASE) guidelines for evaluating regurgitant valve lesions suggest integrating different parameters when evaluating TR severity to avoid such errors.7 Right-sided anatomic changes consistent with severe TR include enlarged cardiac chambers with a dilated tricuspid annulus, a lack of leaflet coaptation, paradoxic septal motion, and a distended venous system.7 The morphology of the spectral tracing also may be used, with a dense triangular pattern suggestive of severe TR. A high-velocity jet does not indicate severe TR, and, indeed, laminar jets generally are associated with velocities <2 m/s.7,9,10 Antegrade and retrograde spectral patterns may almost mirror each other relating to the "to-and-fro" flow across the valve.7,10 Hepatic venous systolic flow reversal is a sensitive indicator of severe TR and also should be present.7 If most of the ASE parameters suggest moderate-to-severe TR, even in the absence of a clearly visible turbulent jet, then the presence of a significantly incompetent valve needs to be considered.

How Should Unexpected Moderate-to-Severe TR in the Operating Room Be Managed?

Recently, there has been a paradigm shift in how TR is viewed and when it should be repaired, especially in the context of left-sided valve disease. Although there is general agreement that severe TR should be repaired, guidelines are less clear regarding moderate TR.11,12 The development of late significant TR after left-sided surgery is associated with a higher rate of cardiovascular death, repeat cardiac surgery, and congestive heart failure requiring hospital admission.13 Given such findings, a large meta-analysis concluded that tricuspid dilation may be the most important risk factor for late TR and that the valve should be repaired regardless of the regurgitant severity if significant dilation is present.12 New TR that is present immediately after CPB presents a different management dilemma because this may be related to myocardial stunning or coronary air embolization and may be recoverable.


In the case presented, the decision was made not to repair the tricuspid valve given the lack of a firm preoperative diagnosis and the absence of a conventional turbulent jet that was difficult to quantify. The patient required significant inotropic support, and on the 3rd postoperative day a TTE confirmed the presence of a laminar tricuspid jet and worsening right ventricular function (Fig 2).The patient was taken back to the operating room for possible tricuspid valve repair. The intraoperative TEE confirmed the presence of laminar TR (Fig 3)with hepatic vein systolic flow reversal (Fig 4)that resolved after the tricuspid ring annuloplasty (Fig 5).Subsequently, the patient had an uneventful postoperative recovery and was discharged in a routine fashion. A summary of echocardiographic video clips and spectral Doppler images is provided in Video 1. Upon retrospective review of the echocardiographic images, certainly repairing both valves initially could have been considered given the dilated tricuspid annulus with a prolapsing valve. The TR jet seen on both the initial TTE and prebypass TEE was also laminar and arguably misinterpreted by 2 different echocardiographers. An early case series suggested that up to a quarter of severe tricuspid jets are laminar.9 Although this number seems high, it certainly is possible that laminar TR may be an under appreciated entity. 

Fig 2 The transthoracic apical 4-chamber view showing severe TR with a laminar jet in the right atrium on the 2nd postoperative day after mitral valve repair.

Fig 3 The midesophageal 4-chamber view confirming a large laminar jet of TR before tricuspid valve repair.

Fig 4 The pulsed-wave Doppler of hepatic vein flow showing systolic flow reversal (arrow).

Fig 5 The midesophageal 4-chamber view showing a satisfactory repair of the tricuspid valve without evidence of TR on color-flow Doppler.


The case presented highlights the difficulty in quantifying a TR jet that shows laminar flow. When this occurs immediately after CPB intraoperatively in the setting of mitral valve surgery, the issues become even more complex. Surgical decision making is also complicated after decannulation, especially in the minimally invasive approach. Given the growing body of evidence that early intervention may be indicated in cases of TR, especially in the setting of left-sided valve surgery and the possibility of laminar flow, vigilance for identifying such cases of "silent" regurgitation is warranted.9,12 


1. Y. Shapira, A. Porter, M. Wurzel, et al. Evaluation of tricuspid regurgitation severity: Echocardiographic and clinical correlation J Am Soc Echocardiogr 11:652-659, 1998
2. G. Grossmann, M. Stein, M. Kochs, et al. Comparison of the proximal flow convergence method and the jet area method for the assessment of the severity of tricuspid regurgitation Eur Heart J 19:652-659, 1998
3. F. Gonzalez-Vilchez, J. Zarauza, J.A. Vazquez de Prada, et al. Assessment of tricuspid regurgitation by Doppler color flow imaging: Angiographic correlation Int J Cardiol 44:275-283, 1994
4. S. Yamachika, C.L. Reid, D. Savani, et al. Usefulness of color Doppler proximal isovelocity surface area method in quantitating valvular regurgitation J Am Soc Echocardiogr 10:159-168, 1997
5. W.I. Yang, C.Y. Shim, M.K. Kang, et al. Vena contracta width as a predictor of adverse outcomes in patients with severe isolated tricuspid regurgitation J Am Soc Echocardiogr 24:1013-1019, 2011
6. J.M. Song, M.K. Jang, Y.S. Choi, et al. The vena contracta in functional tricuspid regurgitation: A real-time three-dimensional color Doppler echocardiography study J Am Soc Echocardiogr 24:663-670, 2011
7. W.A. Zoghbi, M. Enriquez-Sarano, E. Foster, et al. Recommendations for evaluation of the severity of native valvular regurgitation with two-dimensional and Doppler echocardiography J Am Soc Echocardiogr 16:777-802, 2003
8. S. Akamatsu, N. Ueda, E. Terazawa, et al. Mitral prosthetic dehiscence with laminar regurgitant flow signals assessed by transesophageal echocardiography Chest 104: 1911-1913, 1993
9. K. Yoshida, J. Yoshikawa, T. Akasaka, et al. Silent severe tricuspid regurgitation: A study by Doppler echocardiography J Cardiol 19:187-194, 1989
10. S. Minagoe, S.H. Rahimtoola, P.A. Chandraratna. Significance of laminar systolic regurgitant flow in patients with tricuspid regurgitation: A combined pulsed-wave, continuous-wave Doppler and two-dimensional echocardiographic study Am Heart J 119:627-635, 1990
11. R.O. Bonow, B.A. Carabello, K. Chatterjee, et al. Focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing committee to revise the 1998 guidelines for the management of patients with valvular heart disease): Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons Circulation 2008:e523-e661, 2008
12. G. Bianchi, M. Solinas, S. Bevilacqua, et al. Which patient undergoing mitral valve surgery should also have the tricuspid repair? Interact Cardiovasc Thorac Surg 9:1009-1020, 2009
13. H. Song, M.J. Kim, C.H. Chung, et al. Factors associated with development of late significant tricuspid regurgitation after successful left-sided valve surgery Heart 95:931-936, 2009

Fig 1 The midesophageal right ventricle inflow-outflow view showing laminar regurgitant flow into the right atrium after the discontinuation of CPB after mitral valve repair. 

Fig 2 The transthoracic apical 4-chamber view showing severe TR with a laminar jet in the right atrium on the 2nd postoperative day after mitral valve repair.

Fig 3 The midesophageal 4-chamber view confirming a large laminar jet of TR before tricuspid valve repair.

Fig 4 The pulsed-wave Doppler of hepatic vein flow showing systolic flow reversal (arrow).

Fig 5 The midesophageal 4-chamber view showing a satisfactory repair of the tricuspid valve without evidence of TR on color-flow Doppler.