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CASE REPORT Table of Contents   
Year : 2009  |  Volume : 12  |  Issue : 2  |  Page : 140-145
Intra-operative assessment of biventricular function using trans-esophageal echocardiography pre/post-pulmonary thromboembolectomy in patient with chronic thromboembolic pulmonary hypertension


1 Department of Anesthesia, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala - 695 011, India
2 Department of Cardiothoracic and Vascular Surgery, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala - 695 011, India

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Date of Web Publication21-Jul-2009
 

   Abstract 

Postoperative studies in patients with chronic thromboembolic pulmonary hypertension (CTPH) have shown that pulmonary thromboembolectomy (PTE) results in a rapid decrease of right ventricular (RV) size, improvement in the RV systolic function and left ventricular (LV) diastolic function. However, the extent to which the biventricular function recovers immediately after embolectomy in post-cardiopulmonary bypass period is not clear. A 45-year-old male patient was operated for retrieval of thrombus from pulmonary trunk and right pulmonary artery. Intraoperative transesophageal echocardiography (TOE) before surgery revealed signs of RV dysfunction and enlargement. The interventricular septum was seen moving paradoxically during end-systole and early-diastole. E/A ratio on transmitral Doppler flow velocity profile was about 0.63 and S/D ratio on pulmonary venous Doppler profile was 2.25, indicative of LV diastolic dysfunction. After weaning the patient from bypass, navigation on TOE showed marginal recovery of the RV systolic function and abatement of septal paradox to some extent. However, significant improvement was observed in the LV diastolic parameter (normal E/A ratio, S/D ratio of 1.08). We conclude that the geometrically altered LV recovers more than the hypertrophied and hypokinetic RV in a patient with CTPH in the post-bypass period

Keywords: Cardiopulmonary bypass, transesophageal echocardiography, thromboembolism

How to cite this article:
Gadhinglajkar S, Sreedhar R, Jayakumar K, Misra M, Ganesh S, Panicker V. Intra-operative assessment of biventricular function using trans-esophageal echocardiography pre/post-pulmonary thromboembolectomy in patient with chronic thromboembolic pulmonary hypertension. Ann Card Anaesth 2009;12:140-5

How to cite this URL:
Gadhinglajkar S, Sreedhar R, Jayakumar K, Misra M, Ganesh S, Panicker V. Intra-operative assessment of biventricular function using trans-esophageal echocardiography pre/post-pulmonary thromboembolectomy in patient with chronic thromboembolic pulmonary hypertension. Ann Card Anaesth [serial online] 2009 [cited 2020 Mar 30];12:140-5. Available from: http://www.annals.in/text.asp?2009/12/2/140/53449



   Introduction Top


Post-operative studies in patients with chronic thromboembolic pulmonary hypertension (CTPH) have shown that pulmonary thromboembolectomy (PTE) results in a rapid decrease of right ventricular (RV) size, improvement in the RV systolic function and left ventricular (LV) diastolic function. However, the extent to which the biventricular function recovers, immediately after embolectomy in post-cardiopulmonary bypass (CPB) period, is not clear. We assessed functions of both ventricles using trans- esophageal echocardiography (TEE) before PTE and compared it with biventricular function after termination of the CPB.


   Case Report Top


A 45-year-old male, a chronic smoker, was diagnosed to have chronic pulmonary thromboembolism (PE) originating in the right femoro-popleteal venous system. He had features suggestive of CTPH on transthoracic echocardiography (TTE), which included RV free wall hypertrophy; RV systolic pressure (RVSP) of 62 mmHg [measured by tricuspid regurgitation (TR) jet method]; paradoxical motion of interventricular septum (IVS) and normal left ventricular ejection fraction (LVEF). A filter was inserted in the lower portion of inferior vena cava under fluoroscopic guidance a month earlier because he complained of dyspnea, chest pain and one episode of hemoptysis. He was re-admitted a week prior to the surgery with exacerbation of dyspnea and chest pain; and was detected to have a thrombus of 1.8 cm × 1.5 cm situated at the main pulmonary artery (MPA) bifurcation on TTE, CT chest and contrast angiography. Coronary angiography ruled out the presence of coronary artery disease. He was scheduled for surgical PTE electively as he could maintain a stable hemodynamic condition and satisfactory arterial blood gases. Oral warfarin 6 mg that he was receiving pre-operatively was omitted two days before the surgery and instead, 5000 IU of subcutaneous heparin was started eight-hourly. He also received oral aspirin 75 mg once a day, and salbutamol inhalation, 100 mcg, eight-hourly. Pre-operative TTE revealed presence of thrombus in the MPA; dilated right atrium (RA) and RV; RVSP of 74 mmHg; and LVEF 62%. The RV end-diastolic diameter (RVEDD) in apical four-chamber view was 37 mm. Biochemical investigations were within normal limits.

On the day of surgery, he was pre-medicated with oral diazepam, 10 mg, and omeprazole, 20 mg, one hour before surgery. Anesthesia induction was performed in the 65 kg weighing patient with fentanyl 500 mcg, midazolam 5 mg, and propofol 70 mg. Pancuronium 10 mg was injected before endotracheal intubation. Anesthesia was maintained with oxygen plus air (FiO 2 33%) and isoflurane, about one MAC, supplemented with additional fentanyl 500 mcg and midazolam five mg. Routine parameters were monitored in addition to the central venous pressure (CVP) via right internal jugular vein and invasive arterial pressure (ABP). The hemodynamic condition remained stable before establishment of CPB; the mean ABP and CVP were maintained in the range of 70-90 mmHg and 10-14 mmHg respectively.

The heart was inspected after anesthesia induction on TEE (Philips Envisor ultrasound, USA), which showed a thrombus in MPA bifurcation on modified RV inflow-outflow view and ascending aortic short axis view [Video 1]-[Multimedia file 1], [Figure 1]a, extending to right pulmonary artery (RPA). No floating thrombus was observed in right heart or great veins. Presence of patent foramen ovale (PFO) and atrial septal defect (ASD) was ruled out after injecting agitated saline in the RA. The RA, RV and MPA were enlarged. RV function was assessed in midesophageal (ME) four-chamber view and transgastic mid-short axis (TG MIDSAX) view. The free wall of RV was hypokinetic and hypertrophic [Video 2]-[Multimedia file 2]. Indices of RV systolic function including fractional area change (FAC) and tricuspid annular plane systolic excursion (TAPSE) revealed severe RV dysfunction. RVEDD in TG MIDSAX view and RV end-diastolic area/ left ventricular end-diastolic area (RVEDA/LVEDA) ratio in ME four-chamber view were greater than 30 mm and greater than 0.9 respectively, suggesting dilatation of RV. Other signs of chronic RV pressure overload detected were paradoxical motion of the IVS [Video 3]-[Multimedia file 3], leftward bowing of the interatrial septum (IAS), and elevated RVSP to 60 mmHg. The IAS was bowing to left both in systole and diastole. The IVS paradox was characteristically marked by leftward movement in end-systole and early-diastole [Video 4]-[Multimedia file 4], [Figure 2]a. On transgastric MIDSAX view, the systolic shortening of LV cavity was more apparent along the axis of septum to posterior wall rather than that of anterior to inferior wall [Video 5]-[Multimedia file 5]. Transmitral mitral Doppler flow (TMDF) demonstrated impaired LV relaxation pattern (E/A ratio 0.63; E velocity: 0.48 m/ sec; A velocity: 0.76 m/sec). The important pre-operative and post-operative observations are summarized in [Table 1]. Doppler interrogation of the left upper pulmonary vein revealed maximum velocities for S, D and A reversed waves of 0.45 m, 0.2 m and 0.16 m respectively. The S/D ratio was 2.25 [Figure 3]a, b.

Heparin 260 mg was injected to achieve anticoagulation and to maintain activated clotting time greater than 480 seconds. After cross-clamping the aorta on CPB and arresting the heart with cardioplegia, the thrombus was removed via pulmonary arteriotomy using scoop, dissector and suction. Open pulmonary vessels were allowed to bleed in the retrograde direction. The patient was weaned from bypass with infusions of dobutamine 10 mcg/kg/minute and norepinephrine 0.05 mcg/kg/ minute. The left atrial pressure (LAP) (monitored by inserting a cannula in the LA and connecting it to a transducer) and the CVP were maintained in the range of seven-10 mmHg with mean ABP about 80-100 mmHg.

On TEE navigation, after CPB, the pulmonary vessels were found free of thrombus [Figure 1]b and forward flow was present in RPA. The size of MPA and the degree of systolic paradox of IVS [Video 6]-[Multimedia file 6], [Figure 2]b were reduced. Features on TMDF included raised E/A ratio (1.14) and increased amplitude of E and A wave to 0.96 m/sec and 0.84m/sec respectively [Figure 3]c. Unlike before surgery, the IAS was becoming flat during early-diastole. RV-FAC and TAPSE had improved marginally. The patient maintained stable hemodynamic parameters in the post-operative period. Tracheal extubation was carried post-operatively after 12 hours of elective ventilation. The patient had an uneventful post-operative course.


   Discussion Top


TEE has been recommended as a technique for rapidly confirming the diagnosis of PE. It is easily available in the operating room, safe and does not interfere with resuscitation efforts. Although intra-operative TEE was only 46% sensitive in identifying embolus during emergency PTE, [1] it was reported to be 84% sensitive in intensive care unit (ICU) under non-emergent circumstances. [2] We could inspect the thrombus as a mobile mass in the MPA, projecting into the RPA in our patient. Sometimes delineation of the thrombus may not be satisfactory on two-D imaging and echo-contrast studies [3] may be required for its better appreciation. TEE visualization of the thrombus may be difficult if the thrombus is located in peripheral portion of pulmonary arteries or in the segment of left pulmonary artery, which overlies left main bronchus. In those cases, the diagnosis may be supported by indirect evidence of MPA obstruction such as RV dysfunction, severe TR or leftward bowing of the IAS.

CTPH is a severe disease caused by obstruction of the pulmonary arteries by recurrent pulmonary thromboemboli which do not undergo complete resolution. These lesions lead to endothelialized residua that obliterate or significantly narrow segmental and subsegmental branches of pulmonary arteries. The embolic material gets transformed over a period of months to years into fibrous tissue that is incorporated into the intima and media of the arterial wall. [4] The RV in these patients is subjected to chronic pressure overload that eventually decreases its systolic and diastolic function. Acute RV dysfunction may be precipitated in a patient with CTPH due to acute or sub-acute event of embolism. If the embolus obstructs less than 50% cross-sectional area of pulmonary arterial tree, the hemodynamic condition may remain stable (defined as [5] systolic BP greater than 90 mmHg, without requirement for vasopressors) and patient may be considered for PTE electively. Our patient had thrombus in the MPA extending into the RPA. It was an indication for the surgery. However, urgent surgery was not required as patient was hemodynamically stable.

The RV function may improve after thrombolytic therapy within 12 hours. [6] Meneveau et al ., [7] showed that initial RV dysfunction was reversible within 48 hours following thrombolytic therapy in 80% of patients with recent PE (less than 15 days). However, these reports were applicable to patients who were free from CTPH. Follow-up studies in patients with CTPH have shown that PTE lowers the RV after-load significantly within a few days, which results in a rapid decrease of RV size, improvement in the RV systolic function and LV diastolic function. [8] However, the extent to which the RV function recovers in post-CPB period after PTE is not clear. The RV systolic function improved marginally in our patient, although the LV diastolic function ameliorated significantly.

Echocardiographic features of RV dysfunction are defined by various authors in different ways. Important among them are [9],[10] include: RV hypokinesia; dilation of the RV cavity (transesophageal four-chamber view); TR velocity greater than 2.8 m/s; RVEDD greater than 30 mm or RV to LV end-diastolic diameter ratio greater than one in four-chamber view; paradoxical septal systolic movements; and leftward bowing of IAS. Most of these features were described for patients with acute or recent onset PE. As patients with CTPH are likely to have biventricular involvement, pulmonary hypertension (TR jet velocity greater than 3.7 m/sec) and RV free wall hypertrophy (enddiastolic RV free wall thickness greater than seven mm) the echocardiographic observations in these patients after acute or subacute event of PE must be correlated with baseline echocardiographic parameters. Our patient had undergone serial TTE before surgery and the baseline data had indicated the presence of CTPH. Follow-up studies in CTPH patients have considered RV-FAC as a parameter for evaluation of the RV function. Systolic RV function assessment using RV-FAC correlates well with that assessed on TAPSE. [11] As the RV lies in a far field on the TEE sector, and also being extensively trabeculated, a cautious approach is needed during the measurement of the RV-FAC, as inaccuracies may occur while tracing the RV endocardial border at the end systole. [12]

RV systolic overload results in leftward ventricular septal shift that is most marked at end-systole and early diastole and decreases substantially by end-diastole. [13] The IVS moves towards the center of the LV and occupies LV cavity partly at the end-systole and early-diastole. The early diastolic distortion of left ventricular geometry results in decreased LV transmitral filling, which is the most important cause of left heart failure in patients with CTPH. [8] It is reflected as E/A ratio less than one on TMDF, as observed in our patient. However, in patients with chronic pulmonary hypertension, the resting LVEF is preserved due to active augmentation of short-axis systolic shortening in the ventricular septal-to-posterolateral free wall dimension. [14] This increase in systolic fractional shortening is confined only to the septum-to-posterolateral free wall axis and not to the orthogonal short axis (anterior wall-to-inferior wall) and the long axis of the left ventricle.

The PTE results in normalization of E/A ratio in the postoperative period, [14],[15],[16] which indicates that the LV diastolic function improves as time rolls on. We noticed this change in the E/A ratio during intraoperative period. It may be attributed to the increase in the LA pressure and decrease in the IVS paradox. The atrial septum was bowing leftwards both during systole and diastole before surgery because the RAP exceeded the LAP. It attended a flat position during early-diastole after embolectomy, implies that the RAP had equalized with the LAP, which we verified on direct pressure measurements. This change in the atrial pressure could be the result of augmented forward flow across the pulmonary circulation after PTE or improved loading conditions in the post-CPB period. The E/A ratio consistently remained greater than 1.4 in our patient during post-CPB period. Comparison of the end-systolic frames (just before opening of the mitral valve) before and after bypass period clearly demonstrated partial recovery from the end-systolic septal paradox in the later period. It probably had restituted the LV geometry and accelerated the transmitral filling in early-diastole. Kasper et al . [17] have reported that a correlation exists between the paradoxical motion of IVS and the pulmonary hypertension. They found that motion of the IVS was normal in all patients without pulmonary hypertension, while those with pulmonary hypertension had paradoxical septal wall motion. Decrease in the pulmonary hypertension after PTE could have been responsible for reducing the IVS paradox in our patient. An inverse correlation also has been reported between the E/A ratio on the TMDF and postoperative mPAP. [16] Following PTE, the E/A ratio greater than 1.5 signifies absence of severe pulmonary hypertension (mPAP greater than 35 mm Hg), which also was evident in our case.

Preoperative observations on TMDF and pulmonary venous Doppler flow are indicative of type I diastolic dysfunction in our patient. These changes in transmitral E and A waves and pulmonary venous waves should be regarded as true normalization of the LV filling pattern, and not pseudonormalization. There were no preoperative clinical findings suggestive of a left ventricular disease that would have affected its diastolic function. Preoperative investigations and intraoperative TEE did not reveal evidence of any structural changes in the left ventricular myocardium like concentric hypertrophy, myocardial ischemia, or fibrosis, which are the common factors associated with the left ventricular diastolic dysfunction. We did not expect the left ventricular diastolic dysfunction to advance to class II in our patient. The loading conditions may affect transmitral E/A ratio before and after CPB. However, the transmitral flow velocity followed a consistent pattern throughout the pre-CPB period and post-CPB period. The improved E/A ratio remained constant in the post-bypass period till the patient was transferred to ICU. LAP never increased >7-10 mmHg in the post-bypass period, suggesting that raised LAP was not the reason that altered the E/A ratio. Pseudonormalization should be suspected when a normal transmitral waveform is seen with an elevated LA pressure; echocardiographic evidence of LV hypertrophy; [18] the transmitral E/A ratio >1.8; and pulmonary S/D ratio <1 with pulmonary reversed A wave >0.35 m. Although, the E/A ratio remained above 1.4 after surgery, it never exceeded 1.8. Post-bypass pulmonary venous Doppler revealed near normal S/D ratio and a normal A wave reversal. All these observations rule out the possibility of class II LV diastolic dysfunction after surgery. We believe that the preoperative transmitral filling pattern consistent with type I diastolic dysfunction (impaired relaxation) could be attributed to the paradoxical movement of the ventricular septum that occupied space within the LV cavity and altered the LV geometry during diastolic filling. Pulmonary thromboembolectomy reduced the degree of paradox that eventually created more space within the LV cavity during early diastole, and attenuated the early-diastolic pressure in the LV. Our conclusion could have been further strengthened by the tissue Doppler studies or by measuring propagation velocity on color M mode. Although, the PTE could make the LV diastolic function better, it failed to bring about similar changes in the RV diastolic (based upon changes in RVEDD and RVEDA/LVEDA ratio) and systolic function. Reducing the pulmonary obstruction and lowering the RV afterload could decrease the size of PA and TR jet velocity, but could not increase the RV contractility significantly. This suggests that despite afterload reduction, the hypertrophied and hypokinetic RV in a patient with CTPH is resistant to improve immediately in the post-bypass period and requires a longer postoperative time to recover. However, large studies are required to support our observation as evidence.

In summary, our patient with CTPH had baseline RV systolic and LV diastolic dysfunction that had worsened after subacute embolic event. The RV systolic function recovered marginally and the septal paradox abated to some extent after PTE. However, significant improvement was observed in the LV diastolic parameters (normal E/A ratio). The LV diastolic function had improved toward normalization and we could exclude the presence of pseudonormal pattern of transmitral diastolic filling on TEE examination. We conclude that the geometrically altered LV recovers more than the hypertrophied and hypokinetic RV in a patient with CTPH in the post-bypass period.

 
   References Top

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2.Vieillard-Baron A, Qanadli SD, Antakly Y, Fourme T, Loubiθres Y, Jardin F, et al . Transesophageal echocardiography for the diagnosis of pulmonary embolism with acute cor pulmonale: A comparison with radiological procedures. Intensive Care Med 1998;24:429-33.  Back to cited text no. 2    
3.Izrailtyan I, Clark J, Swaminathan M, Podgoreanu MV, Mackensen B, Davis RD, et al . Case report: Optimizing intraoperative detection of pulmonary embolism using contrast-enhanced echocardiography. Can J Anaesth 2006;53:711-5.  Back to cited text no. 3  [PUBMED]  
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5.Miller RL, Das S, Anandarangam T, Leibowitz DW, Alderson PO, Thomashow B, et al . Association between right ventricular function and perfusion abnormalities in hemodynamically stable patients with acute pulmonary embolism. Chest 1998;113:665-70.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]
6.Hartmannsgruber MW, Trent FL, Stolzfus DP. Thrombolytic therapy for treatment of pulmonary embolism in the postoperative period: Case report and review of the literature. J Clin Anesth 1996;8:669-74.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]
7.Meneveau N, Ming LP, Sιronde MF, Mersin N, Schiele F, Caulfield F, et al . In-hospital and long-term outcome after sub-massive and massive pulmonary embolism submitted to thrombolytic therapy. Eur Heart J 2003;24:1447-54.  Back to cited text no. 7    
8.Menzel T, Wagner S, Kramm T, Mohr-Kahaly S, Mayer E, Braeuninger S, et al . Pathophysiology of impaired right and left ventricular function in chronic embolic pulmonary hypertension: Changes after pulmonary thromboendarterectomy. Chest 2000;118:897-903.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]
9.Ten Wolde M, Sφhne M, Quak E, Mac Gillavry MR, Büller HR. Prognostic value of echocardiographically assessed right ventricular dysfunction in patients with pulmonary embolism. Arch Intern Med 2004;164:1685-9.  Back to cited text no. 9    
10.Kasper W, Konstantinides S, Geibel A, Tiede N, Krause T, Just H. Prognostic significance of right ventricular afterload stress detected by echocardiography in patients with clinically suspected pulmonary embolism. Heart 1997;77:346-9.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]
11.Ghio S, Raineri C, Scelsi L, Recusani F, D'armini AM, Piovella F, et al . Usefulness and limits of transthoracic echocardiography in the evaluation of patients with primary and chronic thromboembolic pulmonary hypertension. J Am Soc Echocardiogr 2002;15:1374-80.  Back to cited text no. 11  [PUBMED]  [FULLTEXT]
12.Wong S. The right ventricle, tricuspid valve and pulmonary valve. In: David Sidebotham, Alan Merry, Malcolm Legget (ed): Practical perioperative transesophageal echocardiography. London: Butterworth Heinemann; 2003. p. 201-14.  Back to cited text no. 12    
13.Louie EK, Rich S, Levitsky S, Brundage BH. Doppler echocardiographic demonstration of the differential effects of right ventricular pressure and volume overload on left ventricular geometry and filling. J Am Coll Cardiol 1992;19:84-90  Back to cited text no. 13  [PUBMED]  
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15.Menzel T, Wagner S, Mohr-Kahaly S, Mayer E, Kramm T, Fischer TA, et al . Reversibility of changes in left and right ventricular geometry and hemodynamics in pulmonary hypertension. Echocardiographic characteristics before and after pulmonary thromboendarterectomy. Z Kardiol 1997;86:928-35.  Back to cited text no. 15    
16.Mahmud E, Raisinghani A, Hassankhani A, Sadeghi HM, Strachan GM, Auger W, et al . Correlation of left ventricular diastolic filling characteristics with right ventricular overload and pulmonary artery pressure in chronic thromboembolic pulmonary hypertension. J Am Coll Cardiol 2002;40:318-24.  Back to cited text no. 16  [PUBMED]  [FULLTEXT]
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18.Sidebotham D, Hussey M. Left ventricular diastolic dysfunction. In Sidebotham D, Merry A, Legget M, editors. Practical perioperative transesophageal echocardiography. London: Butterworth Heinemann; 2003. P. 117-129.  Back to cited text no. 18    

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Correspondence Address:
Shrinivas Gadhinglajkar
Department of Anaesthesia, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, Kerala - 695 011
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9784.53449

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