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Table of Contents
Year : 2012  |  Volume : 15  |  Issue : 4  |  Page : 320-321
Iatrogenic superior vena cava syndrome during off pump CABG

Department of Anaesthesia and Critical Care,Heart Hospital, Patna, India

Click here for correspondence address and email

Date of Web Publication1-Oct-2012

How to cite this article:
Kumar R. Iatrogenic superior vena cava syndrome during off pump CABG. Ann Card Anaesth 2012;15:320-1

How to cite this URL:
Kumar R. Iatrogenic superior vena cava syndrome during off pump CABG. Ann Card Anaesth [serial online] 2012 [cited 2022 Dec 2];15:320-1. Available from:

The Editor,

A 51-years-old obese male patient presented with a history of chest pain on exertion. He was diagnosed with triple vessel coronary artery disease (CAD); the left main coronary artery was 70% stenosed. All the laboratory investigations were within normal limits. Transthoracic echocardiography showed left ventricular ejection fraction 60% with no regional wall motion abnormality. Pulmonary function test was not conducted because of left main coronary artery stenosis. His past medical history was insignificant for any abnormality, including chronic obstructive pulmonary disease. He had no history of smoking. He was scheduled for coronary artery bypass grafting (CABG).

A peripheral venous cannula was inserted in the right hand and a cannula was inserted in the right femoral artery for arterial blood pressure (ABP) monitoring and arterial blood gas (ABG) analysis. A pulmonary artery catheter (PAC) was inserted in the right internal jugular vein. PAC was used to continuously monitor pulmonary artery pressure (PAP) and intermittently measure central venous pressure (CVP), cardiac output (CO), cardiac index (CI) and other hemodynamic data. All the invasive venous lines were inserted without any difficulty and were checked and found flowing freely.

Anaesthesia was induced with midazolam, fentanyl, thiopentone and vecuronium; anesthesia was maintained with isoflurane in oxygen-air mixture with inspired oxygen fraction (FiO 2 ) of 0.5, and intermittent boluses of fentanyl, vecuronium and midazolam. Baseline monitored parameters were-ABP 130/70 mmHg, PAP 24/13 mmHg, CVP 6 mmHg, CO 6.8 L/min, CI 3.1 L/min/m 2 and peripheral saturation (SpO 2 ) was 100%. ABG was within normal limits except hypokalemia. To correct hypokalemia, potassium drip was started using a burette set connected to a lumen of PAC; the maintenance fluid, Ringer lactate, was started in the peripheral venous line. After sternotomy, the surgeon placed an internal mammary artery (IMA) sternal retractor (SISCO, CMR-100) to facilitate left IMA dissection. On request of the operating surgeon, the tidal volume was reduced; however, to obtain an end tidal carbon dioxide (EtCO 2 ) of 35-40 mmHg, the minute ventilation was maintained by increasing the respiratory rate. Few minutes after placement of the retractor, the potassium drip stopped flowing, the burette and its connections were checked, patency of the venous line was rechecked by aspirating blood and by flushing it with 5 ml of normal saline (NS); however, in spite of the patent venous line, the potassium drip failed to start. Five minutes later, the peripheral venous line also stopped flowing and flow reversal was noticed in both the venous lines. The monitored CVP was 70 mmHg; at the same time, the monitor showed a decrease in ABP and a decrease in SpO 2 from baseline. The ABG showed severe acidosis, hypoxia and hypercarbia. The FiO 2 was increased from 0.6 to 1 and a search was made to find the cause of these changes. On inspection, both the lungs were expanding normally during inspiration. Examination of the face showed gross edema of the face, neck, lips, eyelids and cyanosis of the face. On close inspection of the surgical field, it was noticed that the sternal retractor was malpositioned and it was compressing the right atrium (RA) and superior vena cava (SVC); the RA and SVC compression was relieved by readjusting the retractor. Gradually, the hemodynamics and the respiratory parameters improved. The rest of the perioperative course was uneventful.

In case of acute occlusion of a normally flowing SVC, the clinical features in an anesthetized patient may include a sudden decrease in ABP and SpO 2 , acute and progressively increasing edema of the face, neck, tongue and upper extremities and bulged eyeballs that may become uncovered by the swollen eyelids. [1] CVP measured above occlusion show higher than normal reading. The peripheral and central venous infusions may flow poorly or stop, or even reverse flow may occur because of high CVP. [2] In the present case, the offending mechanism was malpositioned retractor, which caused acute SVC obstruction. The anesthesiologist must observe the clinical and hemodynamic findings, interpret them and act on those findings to conduct the operative procedure in a safe and effective manner.

   References Top

1.Onwere JL, Spackman TN, Click RL. Intraoperative hypoxemia from compression of the right pulmonary artery caused by a sternal retractor. Anesth Analg 2008;106:415-6.  Back to cited text no. 1
2.Galatoudis Z, Soumpasis I, Vretzakis G. Anesthetic considerations for surgery involving clamping of superior vena cava. The Greek E-Journal of Perioperative Medicine 2005;3:49-59.  Back to cited text no. 2

Correspondence Address:
Rajnish Kumar
House No.- 28-I/1, West-Anandpuri, Boring Canal Road, Patna- 800 001
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0971-9784.101856

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Amundson, A.W., Pulido, J.N., Hayward, G.L.
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