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LETTER TO EDITOR Table of Contents   
Year : 2010  |  Volume : 13  |  Issue : 2  |  Page : 176-178
Dynamic RVOT obstruction after transatrial/transpulmonary repair of valvular and infundibular pulmonary stenosis and VSD closure: Role of dobutamine/epinephrine infusion

Department of Anaesthesiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram - 695011, Kerala, India

Click here for correspondence address and email

Date of Web Publication3-May-2010

How to cite this article:
Neema PK, Sethuraman M, Singha S, Rathod RC. Dynamic RVOT obstruction after transatrial/transpulmonary repair of valvular and infundibular pulmonary stenosis and VSD closure: Role of dobutamine/epinephrine infusion. Ann Card Anaesth 2010;13:176-8

How to cite this URL:
Neema PK, Sethuraman M, Singha S, Rathod RC. Dynamic RVOT obstruction after transatrial/transpulmonary repair of valvular and infundibular pulmonary stenosis and VSD closure: Role of dobutamine/epinephrine infusion. Ann Card Anaesth [serial online] 2010 [cited 2022 Dec 3];13:176-8. Available from:

The Editor,

Dobutamine is frequently used to augment myocardial contractility during separation of patients from cardiopulmonary bypass (CPB). Its use in the presence of hypertrophic nonobstructive cardiomyopathy is reported to cause dynamic obstruction of left ventricular (LV) outflow tract. [1] We report hemodynamic instability, arrhythmias, and dynamic right ventricular outflow tract (RVOT) obstruction with dobutamine infusion and its resolution after changeover to epinephrine infusion in a patient undergoing intracardiac repair (ICR) of ventricular septal defect (VSD) and pulmonary valvular and infundibular stenosis.

A 22-year-old woman weighing 52 kg presented for ICR of pulmonary valvular and infundibular stenosis and VSD. The preoperative transthoracic echocardiography examination (TTE) showed LV diastolic and systolic dimensions of 18, and nine mm respectively and RV internal dimension of 17 mm along with severe infundibular and valvular pulmonary stenosis.

The RV was severely hypertrophied and estimated RV pressure was 120 mmHg. peak gradient across the pulmonary valve was 98 mmHg, LV function was normal. She underwent RV angiogram to delineate pulmonary artery (PA) anatomy that showed normal PA anatomy and a small three mm subaortic VSD. The body surface area (BSA) of the patient was 1.4 m2 and required PA annulus was about 18 mm.

Anesthesia induction and maintenance included thiopentone 200 mg, pancuronium 10 mg, fentanyl 300 μg, midazolam five mg, isoflurane (zero to three per cent), and morphine infusion 60- μg/kg/hour. A triple-lumen catheter (TLC) was inserted in the right internal jugular vein. The patient was monitored with ECG, heart-rate, pulse-oximetry, arterial blood pressure (ABP), and central venous pressure (CVP). Transesophageal echocardiography (TEE) was not available. After anticoagulation with heparin and ensuring an ACT of more than 400 seconds, CPB was established by aortic and bicaval cannulation. Under hypothermic (28°C) CPB and cold blood cardioplegic arrest, transatrial/transpulmonary ICR was performed; the pulmonary annulus was spared. After ICR, the RVOT easily allowed an 18 size Hegar. After re warming to 35°C and ensuring normal serum electrolytes, dobutamine five μg/kg/min was started and the patient was separated from CPB at a CVP of six to seven mmHg, the monitored systolic ABP showed 65-75 mmHg. Preload was increased by transfusing about 100 ml blood from extracorporeal circuit and dobutamine infusion was increased to 10 μg/kg/min. Spontaneously, the TLC migrated into RV; at this moment, the monitored ABP and the RVP ranged 78/38 (50) to 89/47 (60) mmHg and 85/6 to 95/5 mmHg, the heart rate ranged 136-140 min -1 [Figure 1] and the PA felt soft. The ECG showed supraventricular tachycardia with multiple atrial ectopic; the 'ST' segment was erratic and did not allow interpretation. In view of tachyarrhythmias, dobutamine was discontinued and epinephrine infusion 0.1 μg/kg/min was started. Within moments the heart-rate decreased to 93 min -1 , the ABP and the RVP increased to 150/73 (97) and 131/6 mmHg, respectively, [Figure 1]. Epinephrine infusion was decreased to 0.05 μg/kg/min. The ABP and the RVP decreased and settled at 104/58 and 89/6 mmHg, sinus rhythm returned and the heart-rate stabilized at about 100- min 1 [Figure 2]. The TLC was pulled in the right atrium.

The patient was weaned from ventilatory support and extubated after overnight ventilation, epinephrine was tapered off. A repeat TTE on day three showed no significant RVOT gradient (less than 20 mmHg), the RV internal dimension was 25 mm, and the RV and LV functions were normal.

The objectives of the combined transatrial/transpulmonary repair techniques are the avoidance of a ventriculotomy and preservation of pulmonary valve/annulus integrity with the aim of maintaining a normal RV function in long term. [2] Several previous reports, [3] and recently Boni et al.[4] Showed significant reduction in RV/LV pressure ratio in pediatric patients after ICR for tetralogy of Fallot (TOF) with pulmonary valve sparing procedure even in patients who had a high RV/LV pressure ratio (0.70 to 0.90) measured after surgical repair in the operating room. However, the postoperative course of patients operated on with a pulmonary annulus sparing procedure could be a complicated one, since the RV still faces a high afterload at annulus level. Our patient suffered hemodynamic instability, tachyarrhythmias, and suprasystemic RVP at the time of separation from CPB with dobutamine infusion 10 μg/kg/min. On its discontinuation and changeover to epinephrine, the RVP immediately decreased to sub-systemic levels and sinus rhythm established. Apparently, the arrhythmias were due to dobutamine and/or myocardial ischemia because of unfavorable O2 demand-supply determinants (suprasystemic RVP, severe tachycardia, significant RV hypertrophy and low mean arterial pressure (MAP) and decreased diastolic time). After changeover to epinephrine infusion, the O2 demand-supply determinants became favorable (sub systemic RVP, increased MAP, mild tachycardia, and improved diastolic period) and the hemodynamics stabilized and sinus rhythm returned.

The causes of high RV/LV pressure ratio include hypovolemia, hyper-contractility due to inotropes and residual RVOT obstruction. Denault et al.[3] reported hemodynamic instability in 10 of 11 patients of dynamic RVOT obstruction after analyzing 670 surgical patients. Although pressures in PA and RVOT were not measured for our patient, the presence of soft PA, hemodynamic instability, suprasystemic RVP, and tachycardia, strongly indicates dynamic RVOT obstruction. Unfortunately, RVOT obstruction could not be demonstrated as TEE was not available.

Mason et al.[5] demonstrated dynamic RVOT obstruction in 16 patients with hypertrophic sub-pulmonary stenosis with an intact ventricular septum by isoprenaline. Kroshus et al. described dynamic RVOT obstruction confirmed by TEE in two patients with Eisenmenger syndrome, in one after single-lung transplantation and VSD repair, and in other after bilateral lung transplantation; [6] the authors believe that a severely hypertrophied RV infundibulum may be stented open by marked elevation in PA pressures and acute reduction in the RV afterload accompanying lung transplantation can lead to a state of dynamic RVOT obstruction after transplantation. Apparently, the patients with infundibular hypertrophy (PS, VSD with severe PAH, TOF, and hypertrophic subpulmonary stenosis with an intact ventricular septum) can develop dynamic RVOT obstruction in situations of hypovolemia, tachycardia, decreased PA pressure and enhanced myocardial contractility [Figure 3]. All these hemodynamic changes tend to result in a reduced RV volume. Conceivably, in such situations preservation of preload and afterload, normal heart-rate, and a mild suppression of myocardial contractility are likely to reduce RVOT obstruction. This is why several reports emphasize adequate preloading (CVP 10-12 mmHg) before starting inotropes. Apparently the pathway for dynamic RVOT obstruction is same as for LVOT obstruction - a reduction in RV volume. [7] Since dobutamine increases myocardial contractility and heart rate, causes systemic vasodilatation and decreases PA pressure; its infusion is likely to result in a smaller RV volume and dynamic RVOT obstruction whereas. epinephrine because of venoconstriction and less tachycardia, is expected to result in improved RV filling; Therefore, epinephrine is unlikely to result in dynamic RVOT obstruction despite enhanced myocardial contractility. Increases in mean and diastolic ABP and diastolic period will also improve myocardial perfusion. Klima et al. [8] reported improved RV performance with improved myocardial perfusion. Evidently, the choice of inotrope can influence the severity of RVOT obstruction.

Intraoperative TEE helps identify residual RVOT obstruction as well as hypovolemia but does not predict RV/LV pressure ratio postoperatively or at follow-up. It is noteworthy that despite adequate infundibular resection dynamic RVOT obstruction can develop. It is important to be aware of this complication; else, the operating team might contemplate return to CPB for further resection of infundibulum that may not be necessary.

   References Top

1.Bolca O, Ozer N, Eren M, Daπdeviren B, Norgaz T, Akdemir O, et al . Dobutamine induced dynamic left ventricular outflow tract obstruction in patients with hypertrophic non-obstructive cardiomyopathy. Tohoku J Exp Med 2002;198:79-87.  Back to cited text no. 1      
2.Helbing WA, Niezen RA, Le Cessie S, van der Geest RJ, Ottenkamp J, de Roos A. Right ventricular diastolic function in children with pulmonary regurgitation after repair of tetralogy of Fallot: Volumetric evaluation by magnetic resonance velocity mapping. J Am Coll Cardiol 1996;28:1827-35.  Back to cited text no. 2  [PUBMED]    
3.Denault AY, Chaput M, Couture P, Hιbert Y, Haddad F, Tardif JC. Dynamic right ventricular outflow tract obstruction in cardiac surgery. J Thorac Cardiovasc Surg 2006;132:43-9.  Back to cited text no. 3      
4.Boni L, Garcνa E, Galletti L, Pιrez A, Herrera D, Ramos V, Marianeschi SM, et al. Current strategies in tetralogy of Fallot repair: pulmonary valve sparing and evolution of right ventricle/left ventricle pressures ratio. Eur J Cardiothorac Surg 2009;3:885-90.  Back to cited text no. 4      
5.Mason DT, Braunwald E, Ross J Jr. Hemodynamic alterations induced by isoprenaline in patients with obstruction to right ventricular outflow. Br Heart J 1965;27:884-91.   Back to cited text no. 5      
6.Kroshus TJ, Kshettry VR, Hertz MI, Everett JE, Bolman RM 3rd. Suicide Right Ventricle after Lung Transplantation for Eisenmenger Syndrome. Ann Thorac Surg 1995;59:995-7.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]  
7.Jackson JM, Thomas SJ: Valvular heart diseases, in Kaplan JA (Ed): Cardiac Anesthesia. Philadelphia, PA, Saunders; 1993. pp. 629-80.  Back to cited text no. 7      
8.Klima UP, Guerrero JL, Vlahakes GJ: Myocardial perfusion and right ventricular function. Ann Thorac Cardiovasc Surg 1999;5:74-80.  Back to cited text no. 8      

Correspondence Address:
Praveen Kumar Neema
Additional Professor Anaesthesiology, B-9, NFH, Sree Chitra Residential Quarters, Poonthi Road, Kumarpuram, Thiruvananthapuram -695011, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-9784.62943

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