Acute left ventricular (LV) failure has been reported after surgical closure of atrial septal defect (ASD) in adult patients. We report acute LV failure in a 56 year old gentleman following coronary artery bypass grafting (CABG) and surgical closure of ASD. Transesophageal echocardiography examination of the patient following closure of ASD and CABG showed a residual ASD and a shunt (Qp :Qs = 1.5). The residual ASD was closed after re-institution of cardiopulmonary bypass (CPB) under cardioplegic cardiac arrest. However, the patient did not tolerate closure of the residual ASD. The CPB was re-established and under cardioplegic cardiac arrest residual ASD was reopened to create a fenestration. This time patient was weaned easily from CPB. Postoperatively, 16 hours after extubation, patient became hemodynamically unstable, the patient was electively put on ventilator and intra-aortic balloon pump. Later the patient was weaned off successfully from ventilator. Retrospective analysis of pulmonary venous flow diastolic deceleration time (PVDT D ) recorded during prebypass period measured 102 msec suggestive of high left atrial pressure which indicate possibility of LV failure after ASD closure.
How to cite this article: Agrawal DR, Sayeed MR, Chakravarthy MR, Patil T A. Utility of pulmonary venous flow diastolic deceleration time in an adult patient undergoing surgical closure of atrial septal defect and coronary artery bypass grafting. Ann Card Anaesth 2013;16:44-6
How to cite this URL: Agrawal DR, Sayeed MR, Chakravarthy MR, Patil T A. Utility of pulmonary venous flow diastolic deceleration time in an adult patient undergoing surgical closure of atrial septal defect and coronary artery bypass grafting. Ann Card Anaesth [serial online] 2013 [cited 2021 Jun 13];16:44-6. Available from: https://www.annals.in/text.asp?2013/16/1/44/105369
Surgical closure of atrial septal defect (ASD) in patients of more than 40 year has higher risk than normal. ,, Closure of ASD in this age group of patients is not well tolerated, particularly, in the presence of high left ventricular (LV) end diastolic pressure (EDP). The surgical closure of ASD can be even more challenging if both coronary artery disease (CAD) and LV diastolic dysfunction exists together. Pulmonary venous flow diastolic deceleration time (PVDT D ) can reliably predict left atrial (LA) pressure. We report difficulty in separating a 56 year old patient from CPB following coronary artery bypass grafting (CABG) and surgical closure of ASD. The patient had shown decreased PVDT D (Normal PVDT D > 175 ms) in the prebypass period.
A 56 year old male patient presented with complaints of chest pain on exertion for the past six months and chest pain at rest for the past three days. Transthoracic echocardiogram revealed normal LV systolic function, no regional wall motion abnormalities, dilated right atrium, right ventricle (RV) and 35 mm large ostium secundum ASD with left to right shunt. Coronary angiogram revealed significant two-vessel CAD. Biochemical and hematological parameters were within normal limits. The vital parameters were stable. The patient was scheduled for CABG and surgical closure of ASD. Intraoperative monitoring apart from ASA standards included transesophageal echocardiography (TEE; multi plane, GE Vingmed Ultrasound, Horten, Norway). Anesthesia was induced with fentanyl, propofol and rocuronium. Anesthetic maintenance included gas mixture (O2: air 50:50 with sevoflurane 1%) with intermittent boluses of vecuronium and propofol infusion. Pre-bypass TEE showed dilated right atrium (50 mm), 30 mm ostium secundum ASD [Figure 1], normal LV systolic function and grade III LV diastolic dysfunction (E wave deceleration time (DT) 106 msec, LV internal diastolic dimension 28 mm, and LV length 56 mm) [Figure 2]. The PVDT D was 102 msec [Figure 3]. After the conduits were ready, the patient was heparinized with 25000 units of heparin. Activated clotting time was used to monitor the adequacy of anticoagulation. On CPB, and on beating heart, left internal mammary artery was grafted to left anterior descending artery, and reversed saphenous vein graft was anastomosed to first obtuse marginal artery. Direct surgical closure of ASD was done under cardioplegic cardiac arrest. After completion of the surgery, CPB was terminated with infusion of 5 μg/kg/min dopamine. TEE imaging after termination of CPB revealed a 5 mm residual ASD [Figure 4] with Qp: Qs ratio of 1.5:1 (measured by Doppler volumetric method). CPB was re-established and the residual ASD was closed under cardioplegic cardiac arrest. CPB was terminated successfully yet again. Thirty minutes after termination of CPB the pulmonary artery (PA) pressure started increasing and subsequently equalized with systemic arterial pressure. Despite increased inotropic support (dopamine 10 μg/kg/min and adrenaline 0.1 μg/kg/min), hemodynamic stability could not be achieved; therefore, we decided to reopen the residual ASD with an intention to create a fenestration [Video 1]. After creation of fenestration, weaning from the CPB was achieved without much difficulty and only 5 μg/kg/min dopamine was used. Patient was extubated after 12 hours with stable hemodynamics. Sixteen hours after extubation, systemic arterial pressure decreased to 77/35 mmHg and PA pressure increased to 60/38 mmHg. In view of unstable hemodynamics, the patient was electively put on mechanical ventilation and intra-aortic balloon pump to support the compromised circulation. At this time, the patient was receiving infusions of adrenaline 0.06 μg/kg/min and milrinone 0.42 μg/kg/min. Patient did well from here on and was gradually weaned from ventilatory and circulatory support and discharged in a hemodynamically stable condition.
Figure 1: Size of atrial septal defect in midesohpageal view
Surgical closure of ASD in adult patient is a debatable issue.  In a long term follow-up, Murphy, et al. reported 40% less survival in patients of age group >41 years than controls after surgical closure of ASD.  Two large studies have examined morbidity and mortality in surgical ASD closure in contrast to medical management in patients with age over 40 years, and neither showed a clear survival benefit with the surgical strategy. The first study showed a survival benefit in favor of surgery but this was with exclusion of patients of CAD and mitral valve disease.  Second prospective study at The National Institute of Cardiology in Mexico showed no clear survival benefit with surgical closure of ASD.  However, Humenberger et al., showed that ASD closure at any age is followed by symptomatic improvement and regression of RV size and PA pressure.  When ASD is associated with CAD, its closure becomes more challenging because the presence of an ASD can mask LV failure. There are reported cases where fenestrated device were used for ASD closure from the beginning to avoid acute LV failure.  In elderly patients, the presence of an ASD can mask the LV restrictive physiology.  The presence of LV diastolic dysfunction also can be missed in presence of an ASD; but presence of LV diastolic dysfunction in presence of an ASD strongly indicate possibility of LV decompensation following closure of an ASD. Perhaps, direct closure of ASD in such a situation can immediately precipitate LV failure. The LV diastolic function can be evaluated by measuring E-wave deceleration time during Doppler flow assessment across the mitral valve, by the PVDT D; and by PA occlusion pressure. In our patient, prebypass PVDT D measured 102 msec which indicated high LA pressure. A PVDT D of less than 175 ms had 100% sensitivity and 94% specificity for predicting a high LA pressure of more than 17 mmHg.  In the present patient, the residual ASD was only 5 mm but the Qp: Qs was 1.5 which also indicated a high LA pressure. Arguably, because of LV diastolic dysfunction and high LA pressure, the patient did not tolerate ASD closure and developed LV failure.
The pulmonary venous Doppler waveform is comprised of four waves. Early systolic wave (PVS1) is produced by LA relaxation. The continuing LA relaxation and downward displacement of mitral annulus during systole enhances pulmonary venous return and creates another positive wave (PVS2) in the late systole. The pulmonary venous diastolic wave (PVD) is produced by blood flow from pulmonary veins to LV via LA during early diastole. This wave is followed by a retrograde flow velocity (PVa) which coincides with LA contraction in late diastole. Deceleration slope of diastolic pulmonary venous flow is often bimodal, with two different slopes. The first slope starts at peak velocity and generally steeper than the second, which reaches the zero line; the first component mainly depend on the initial driving pressure of the pulmonary venous flow and specific compliance of the receiving chamber that is LA. The second component is affected by the duration of the LV relaxation, compliance and heart rate. The pulmonary venous flow pattern is affected by various factors like mitral valve disease, change in preload, rhythm, cardiac output etc. However, PVDT D can be effectively used to predict LA pressure regardless of rhythm and heart function.
To summarize, a PVDT D of < 175 ms in a patient with combined ASD and CAD predict risk of acute LV de-compensation following ASD closure and may indicate necessity of creating a fenestration in the ASD. The routine use of Doppler indices to assess the ability of the LV to sustain ASD closure in adult patients with associated CAD may prevent avoidable morbidity.
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