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Cardiovascular Anesthesiology: Echo Rounds

Incidental Finding of Traumatic Ventricular Septal Defect on Transesophageal Echocardiography in the Intensive Care Unit

Lau, Gary MBChB, FRCA; Leonard, Anton MBChB, FCICM, FRCA; Swanevelder, Justiaan MBChB, FRCA, FCA(SA), MMED (Anes)

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doi: 10.1213/ANE.0b013e3182622fa6

In Brief

A 23-year-old man presented to the emergency department with a laceration to the left side of his chest. He was in cardiogenic shock, and an emergency clamshell thoracotomy was performed. The on-call cardiac surgeon was called from our cardiothoracic center to the emergency department, and a laceration on the anterior surface of the right ventricle (RV) was identified and repaired.

After 12 hours of hemodynamic stability at the admitting hospital, the patient was transferred intubated and ventilated to our cardiothoracic critical care unit for ongoing postoperative intensive care. Although the patient was hemodynamically stable, a transesophageal echocardiogram was performed on admission because no cardiac imaging had been performed up to this stage. The echo transducer was inserted without any resistance. The left ventricular and RV dimensions were within normal limits and the left ventricular function was hyperdynamic without inotropic support. The mitral and aortic valves demonstrated normal anatomy with no stenosis or regurgitation. There was moderate pulmonary arterial hypertension with an estimated systolic pressure of 48 mm Hg (maximum pressure gradient of tricuspid regurgitation jet 33 mm Hg + central venous pressure 15 mm Hg).

However, a modified midesophageal (ME) 4-chamber view demonstrated a large (11-mm) apical ventricular septal defect (VSD) (Fig. 1). Using color-flow Doppler in the ME 4/5-chamber view, the interventricular septum demonstrated a left to right shunt at the apex (Video 1, see Supplemental Digital Content 1, The transgastric (TG) short-axis (SAX) view demonstrated multiple tracks through the VSD (Video 2, see Supplemental Digital Content 2, Quantitative echo measurements demonstrated a significant hemodynamic shunt with a shunt fraction (Qp:Qs) of 1.95 (Figs. 2 and 3).

Figure 1
Figure 1:
Modified midesophageal 4-chamber view demonstrating a ventricular septal defect 11 mm in diameter.
Figure 2
Figure 2:
Measurements performed to calculate flow through the right ventricular outflow tract (RVOT) (Qp). A, RVOT diameter measured in the midesophageal right ventricular inflow-outflow view using 2-dimensional echocardiography (2.33 cm). B, Velocity-time integral RVOT (VTIRVOT) measured in a modified transgastric right ventricular inflow-outflow view with transducer rotation to 134° using pulsed wave Doppler just proximal to the pulmonary valve (16.0 cm).
Figure 3
Figure 3:
Measurements performed to calculate flow through the left ventricular outflow tract (LVOT) (Qs). A, LVOT diameter measured in the midesophageal aortic valve long-axis view using 2-dimensional echocardiography (1.90 cm). B, Velocity-time integral LVOT (VTILVOT) measured in the transgastric long-axis view using pulsed wave Doppler just proximal to the aortic valve (12.8 cm).

The patient was tracheally extubated and discharged from our intensive care unit on the seventh postoperative day and had a follow-up transcatheter closure of the VSD.


Traumatic VSDs are uncommon, with an incidence of between 1% and 4% after major chest trauma.1 Echocardiography is a useful diagnostic technique, with a specificity of 99.3% and a sensitivity of 100% in identifying penetrating cardiac injuries.2 It allows evaluation of the structural and functional impact of traumatic intracardiac foreign bodies,3 as well as assessment of the size, position, and hemodynamic effects of the VSD. In this case, however, the use of perioperative echocardiography may not have detected the VSD, because posttraumatic VSDs may present late. There are several case reports of delayed VSD presentation,4 with the incidence of delayed sequelae of penetrating cardiac injury of 23%.5 Although the mechanism of this is unclear, it has been postulated that the reason for the delayed presentation is muscular spasm or thrombus formation initially sealing small defects.4 Therefore, the physician should plan to perform serial follow-up echocardiographic examinations in patients who present with penetrating cardiac trauma with or without hemodynamic instability.

Hemodynamically, in the presence of a VSD, the flow ratio between the pulmonary and systemic circulations indicates the magnitude of the shunt.6 The systemic blood flow (Qs) can be calculated from the left ventricular outflow tract (LVOT) and the pulmonary blood flow (Qp) from the RV outflow tract (RVOT).

The cross-sectional areas of both the RVOT and the LVOT are assumed to be circular and are determined from measurement of the diameter of each orifice with 2-dimensional echocardiography, where: cross-sectional area = π × (diameter/2)2. However, the limitations of this measurement technique are assumptions that the cross-sectional areas are circular, the blood flow through the outflow tract is laminar, and that the Doppler beam is properly aligned. The RVOT diameter can be measured using the ME RV inflow-outflow view or a modified TG RV inflow-outflow view with the transducer rotated to 110° to 150°. The LVOT diameter is measured from the ME aortic valve long-axis (LAX) view.

The velocity-time integral (VTI) is equal to the distance, in centimeters, that blood travels with each beat of the heart and is measured with pulsed wave Doppler. The VTIRVOT can be measured in the RVOT proximal to the pulmonary valve using the modified TG RV inflow-outflow view, the ME ascending aorta SAX view, or the upper esophageal aortic arch SAX view. The VTILVOT is measured in the LVOT proximal to the aortic valve using the TG LAX view or the deep TG LAX view.

A shunt is considered hemodynamically significant when the Qp:Qs ratio is >1.5 and severe when the ratio is >2.2, although this classification pertains to longstanding congenital heart defects.6 Any shunt that is hemodynamically significant should have a percutaneous or surgical closure of the VSD. In this case, we calculated a shunt ratio of 1.95, which is classified as a moderate-sized defect. However, in the case of a traumatic VSD, there is an acute increase in pulmonary flow and the patient's previously normal pulmonary vasculature suddenly encounters almost twice the amount of blood flow. These immediate changes make the hemodynamic effects of this shunt more severe than the classification suggests.

A VSD will have a left to right shunt until the longstanding increased pulmonary blood flow leads to vascular changes in the pulmonary bed with subsequent pulmonary hypertension and reversal of flow from right to left. In this situation, the shunt ratio will be <1 and indicates a right to left shunt with decreased blood flow through the lungs and shunting of deoxygenated blood into the systemic circulation, therefore resulting in a state of cyanosis.

In our case, transesophageal echocardiography was invaluable in diagnosing an acquired posttraumatic VSD, thus preventing future morbidity and premature mortality in this patient.


Name: Gary Lau, MBChB, FRCA.

Contribution: This author helped prepare the manuscript.

Name: Anton Leonard, MBChB, FCICM, FRCA.

Contribution: This author helped prepare the manuscript.

Name: Justiaan Swanevelder, MBChB, FRCA, FCA(SA), MMED (Anes).

Contribution: This author helped prepare the manuscript and approve the final manuscript.

This manuscript was handled by: Martin J. London, MD.


1. Olsovsky MR, DiSciascio G, Vetrovec GW. Acute traumatic ventricular septal rupture. Am Heart J 1996;131:1039–41
2. Patel AN, Brennig C, Cotner J, Lovitt MA, Foreman ML, Wood RE, Urschel HC Jr. Successful diagnosis of penetrating cardiac injury using surgeon-performed sonography. Ann Thorac Surg 2003;76:2043–6
3. Aguirre MA, Trousdale D, John A, Greilich PE. The use of transesophageal echocardiography in determining the structural and functional impact of traumatic intracardiac foreign bodies. Anesth Analg 2008;107:1155–7
4. Vecht JA, Ibrahim MF, Chukwuemeka AO, James PR, Venn GE. Delayed presentation of traumatic ventricular septal defect and mitral leaflet perforation. Emerg Med J 2005;22:521–2
5. Cha EK, Mittal V, Allaben RD. Delayed sequelae of penetrating cardiac injury. Arch Surg 1993;128:836–41
6. Warnes CA, Williams RG, Bashore TM, Child JS, Connolly HM, Dearani JA, Del Nido P, Fasules JW, Graham TP Jr, Hijazi ZM, Hunt SA, King ME, Landzberg MJ, Miner PD, Radford MJ, Walsh EP, Webb GD. ACC/AHA 2008 Guidelines for the Management of Adults with Congenital Heart Disease. Executive summary: a report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Adults with Congenital Heart Disease). Circulation 2008;118:2395–451

Clinician's Key Teaching Points By Roman M. Sniecinski, MD, and Nikolaos J. Skubas, MD

  • Traumatic ventricular septal defects (VSD) occur in any or multiple portions of the interventricular septum. Transesophageal echocardiography (TEE) allows good visualization using the midesophageal 4-chamber view and aortic valve long-axis (LAX) views, as well as the transgastric (TG) short-axis and deep TG LAX views.
  • In a VSD, the left to right shunt results in increased pulmonary (Qp) relative to systemic (Qs) blood flow. Flows are calculated as the product of the ventricular outflow tract area and the integral of the respective spectral Doppler velocity. Traumatic VSDs are addressed surgically when Qp:Qs >1.5, or, irrespective of shunt, when acute in nature.
  • In this case, TEE visualized a traumatic VSD 1 day after the initial cardiac laceration was repaired and quantified it as a moderate-sized defect (Qp:Qs of 1.95). Delayed presentation in these situations is not uncommon, illustrating the importance of serial echocardiographic examinations and a high index of suspicion.
  • As with any intracardiac shunt, the role of the intraoperative echocardiographer is to provide information on the location and severity of the lesion, no matter what the etiology.

Supplemental Digital Content

© 2012 International Anesthesia Research Society