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Table of Contents
Year : 2012  |  Volume : 15  |  Issue : 1  |  Page : 64-66
ST segment depression following pulmonary artery banding

1 Department of Cardiac Anaesthesia, Amrita Institute of Medical Sciences, Edappaly, Cochin, Kerala, India
2 Pediatric Cardiothoracic Surgeon, Amrita Institute of Medical Sciences, Edappaly, Cochin, Kerala, India

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Date of Web Publication5-Jan-2012

How to cite this article:
Retnamma RK, Nair SG, Sunil G S, Benedict R. ST segment depression following pulmonary artery banding. Ann Card Anaesth 2012;15:64-6

How to cite this URL:
Retnamma RK, Nair SG, Sunil G S, Benedict R. ST segment depression following pulmonary artery banding. Ann Card Anaesth [serial online] 2012 [cited 2022 Nov 28];15:64-6. Available from:

Pulmonary artery banding (PAB) is a useful palliative procedure for a diverse group of patients with congenital cardiac anomalies and unrestricted pulmonary blood flow. With improved results following primary repair of intracardiac anomalies in neonates and infants, PAB is reserved for severely ill patients with complex lesions not amenable to early definitive correction. Currently, PAB is indicated in patients with excessive pulmonary blood flow (PBF) associated with single ventricle (SV) or biventricular physiology. [1] Children undergoing PAB have a stormy postoperative period secondary to sudden alterations in their existing physiology. We noted two neonates who had ST segment changes in the perioperative period, for which we did not have an explanation.

The first case is of a month-old baby weighing 2.5 kg diagnosed to have hypoplastic left ventricle (LV), atretic mitral valve, transposed, side by side great arteries, and the SV of right ventricle morphology. There was torrential PBF through an unrestrictive bulboventricular foramen. The baby was taken up for elective atrial septectomy and PAB. The prebanding saturation was 96%. Banding perimeter was 25 mm with a band gradient of 20 mmHg at inspired oxygen fraction of 0.5. Pulmonary artery (PA) pressures were 40/20 mmHg with the systemic pressures of 60/20 mmHg. The patient maintained a saturation of 85% postbanding. Soon after the PA band was tightened, we noticed the appearance of ST depression in the all electrocardiograph leads, more so in the chest leads [Figure 1]. This persisted despite elevating the systemic pressures to 80 mmHg with inotropes (epinephrine 0.04 mg/kg/min to 0.08 mg/kg/min) and adequate filling. The coronary arteries were inspected by the surgeon to rule out any pressure by the band. Such an occurrence was possible because the great vessels were lying side by side. The ST Segment changes persisted into the postoperative period despite nitroglycerine infusion at 0.5 mg/kg/min and relatively normal arterial oxygen saturations [Table 1]. After 48 hours, the ST changes subsided without any further intervention.
Table 1: Hemodynamics pre and post PA banding

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Figure 1: Image showing ST depression of −3 mm in the chest leads (see arrows)

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The second case was also a month old baby weighing 2.9 kg, with multiple muscular and inlet VSD with an outlet extension. There was mild hypoplasia of the left atrium and LV. A small Patent Foramen Ovale (PFO) was present. The prebanding saturation was 100%. The banding perimeter was 22 mm at a 0.5 FiO 2 . The PA pressure was 40/17 mmHg with systemic pressures of 80/34 mmHg and systemic oxygen saturations of 82% in the period immediate after banding.

In this case too, ST depression of −3 mm was noted without any hemodynamic instability. However, after 10 minutes, tachycardia and worsening of ST depression to −7 mm warranted a loosening of the band to 23 mm. The ST depression reduced to −3 mm in the leads II, III, and AVF but remained at that level despite our attempts to increase the aortic diastolic pressures with blood transfusion and increasing the ionotropic support (epinephrine from 0.02 mg/kg/min to 0.04 m/kg/min). Similar to the previous case, coronary artery compression by the band was ruled out. The ST depression in this case persisted till the second postoperative day without any hemodynamic compromise and despite relatively normal arterial oxygen saturations [Table 1].

Both these cases had an intensive care unit (ICU) stay of 14 to 16 days with 5 to 7 days of mechanical ventilation. The prolonged ventilation was due to respiratory insufficiency during the weaning period unassociated with any further ST changes.

   Discussion Top

PAB is usually done while ventilating the child with an FiO 2 of 0.5. Banding is done keeping in mind the final corrective surgery required. Trusler's rule is often followed in such patients. [2] According to Trusler, the PA band circumference in patients with noncyanotic nonmixing lesions (e.g., ventricular septal defects [VSD]) is 20 mm+1 mm/kg body weight. For patients with mixing lesions (e.g., transposition of great arteries with VSD), the formula is 24 mm+1 mm/kg body weight. In patients with SV in whom a Fontan procedure is anticipated, an intermediate circumference of 22 mm+1 mm/kg body weight is preferred. Lower systemic arterial oxygen saturation (80 to 85%) is accepted in children in whom a SV repair is subsequently planned. Note that these estimates of band circumference are used simply as guidelines and the final circumference is determined by a combination of PA pressures attained, systemic arterial oxygen saturations, and the fact that the band will become tighter and arterial saturations lower over a period of time.

In the two infants discussed above, we noticed ST depression immediately after the bands were in place. The coronaries were inspected to see if there was any mechanical compression on the vessels. There was no response to Nitroglycerine infusion as we thought that this may be related to ischemia. A review of literature on PAB did not bring up any mention of ST changes among the hemodynamic events mentioned. Transient ST elevations noted in ASD device closures have been attributed to air and particulate emboli as well as the distortion of the AV groove during manipulation of the Amplatzer device during placement that could temporarily affect the flow through the right coronary artery. [3] However, in our case, we detected ST depression rather than ST elevation, and hence we believe it to be a ventricular strain pattern.

We hypothesize that the ST depression seen in the chest leads could be the reflection of a "strain pattern." In patients with SV physiology as well as those with two ventricles with large VSD (or multiple VSDs), where both the ventricles behave as a single unit, the output from the ventricles is determined by the relative resistance of the systemic and pulmonary vascular resistance. This results in torrential PBF with only a fraction of the ventricular output going into the systemic circulation as the pulmonary vascular resistance is only a fraction of the systemic resistance. Following a PAB, there is a sudden increase in the after load to the ventricles. The low resistance in the pulmonary circulation is eliminated. The ventricle/ventricles now have to eject blood into the high resistance systemic circulation as well as the resistance offered by the banded PA. This can result in increased left ventricular wall stress and strain. Compensation occurs in the form of increased coronary blood flow from the elevated aortic diastolic blood pressure. In the immediate postband period, this could result in an imbalance between myocardial oxygen demand (increased wall stress) and supply (coronary flow) and manifest as ST changes in the electrocardiogram.

In the preband period, systemic arterial oxygen saturations are high due to the excessive PBF. Once the PA band is in place, there is a dramatic drop in PBF and consequently systemic arterial oxygen saturations will decrease. This coincides with the increased oxygen demand immediately after banding. Thus, an element of oxygen deficiency could contribute to the changes in ST segment after banding. However, this cannot be the sole reason for the ST changes, as in the postoperative period, although the arterial oxygen saturations returned to normal limits in the ICU, the ST changes persisted [Table 1].

Adaptive changes occur within a few days. [4] In the immediate postband period, when the afterload is suddenly increased, there is an increase in ventricular end systolic volume (VESV) and ventricular end diastolic volume (VEDV). This results in elevated wall stress. Adaptive changes take place in the next few days. The ventricle responds to the altered situation by hypertrophy and subsequently the VESV and VEDV returns to normal. This would reduce the wall stress. This physiology has already been described for rapid two-stage arterial switch procedures. A similar physiology could also occur in children undergoing PAB.

In conclusion, we have proposed a hypothesis for the changes in ST segment seen at the time of PAB. Myocardial stretch following PAB might result in myocardial stress. The question whether this could be used as a guide to determine the banding perimeter should also be evaluated. We are planning a larger prospective study of the hemodynamics associated with PAB to identify the incidence and risk factors associated with this finding.

   References Top

1.Albus RA, Trusler GA, Izukawa T, Williams WG. Pulmonary artery banding. J Thorac Cardiovasc Surg 1984;88:645-53.  Back to cited text no. 1
2.Miura T, Kishimoto H, Kawata H, Hata M, Hoashi T, Nakajima T. Management of univentricular heart with systemic ventricular obstruction by pulmonary artery banding and Damus-Kaye-Stansel operation. Ann Thorac Surg 2004;77:23-8.  Back to cited text no. 2 La Torre Hernández JM, Fernández-Valls M, Vázquez De Prada JA, Figueroa A, Zueco J, Colman T. Transient ST Elevation: A finding that may be frequent in Percutaneous Atrial Septal Defect Closure in adults. Rev Esp Cardiol 2002;55:686-8.  Back to cited text no. 3
4.Jonas RA, Giglia TM, Sanders SP, Wernovsky G, Nadal-Ginard B, Mayer JE Jr, et al. Rapid two-stage arterial switch for transposition of the great arteries and intact ventricular septum beyond the neonatal period. Circulation1989;80:1203-8.  Back to cited text no. 4

Correspondence Address:
Rakhi K Retnamma
Anaesthesia Office, Amrita Institute of Medical Sciences, Edappaly, Cochin, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-9784.91486

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  [Figure 1]

  [Table 1]