Year : 2009 | Volume
: 20 | Issue : 6 | Page : 1061--1064
Supraventricular tachycardia following insertion of a central venous catheter
Onder Yavascan, Sevgi Mir, Hakan Tekguc
Ege University, Faculty of Medicine, Department of Pediatric Nephrology, Izmir, Turkey
9105/14 Sokak, No. 9/5, Serdar Apartmani Akevler 35370, Yesilyurt-Izmir
Placement of central venous catheters (CVCs) in patients is associated with several risks including endocardial injury and dysrhythmias. In addition, CVC extending into intracardiac chambers can provoke premature atrial and ventricular complexes, which have been reported to initiate supraventricular tachycardia (SVT). A 15-year-old boy with end-stage renal failure developed SVT after insertion of a CVC.
|How to cite this article:|
Yavascan O, Mir S, Tekguc H. Supraventricular tachycardia following insertion of a central venous catheter.Saudi J Kidney Dis Transpl 2009;20:1061-1064
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Yavascan O, Mir S, Tekguc H. Supraventricular tachycardia following insertion of a central venous catheter. Saudi J Kidney Dis Transpl [serial online] 2009 [cited 2020 Aug 4 ];20:1061-1064
Available from: http://www.sjkdt.org/text.asp?2009/20/6/1061/57264
Central venous catheters (CVCs) are widely used for hemodialysis (HD) either as permanent dialysis accesses in patients with severe peripheral vascular disease or transiently during the maturation period of an arteriovenous fistula (AVF). Placement of percutaneous CVCs has become a common procedure in adult intensive care units , and pediatric patients. ,,,
Despite their advantages, CVCs can manifest a number of complications such as pneumothorax, chylothorax, hemothorax, air embolisms, infections, vessel injuries, thrombosis, malposition, clavicle osteomyelitis, brachial plexus palsy, phrenic nerve injuries and cardiac dysrhythmias. ,,,,,
To our knowledge there is a few reports of supra ventricular tachycardia (SVT) in children associated with CVCs.  Here we report a pediatric case with SVT after placement of a percutaneous CVC.
A 15-year-old boy (height 165 cm, weight 55 kg) who had been on chronic peritoneal dialysis (CPD) for 3 months due to reflux nephropathy presented with acute peritonitis which was intractable to therapy and mechanical obstruction that rendered peritoneal dialysis treatment impossible. Therefore, the decision was made to insert a CVC under local anesthesia and transfer the patient temporarily to HD. The insertion was performed by a pediatric nephrologist skilled in this procedure under continuous monitoring of the patient's electrocardiogram (ECG), heart rate, and oxygen saturation. Before the procedure, his blood pressure, pulse and respiratory rates were 118/74 mmHg, 88 beats per minute and 18 breaths per minute, respectively. The complete blood count, liver profile and serum chemistry except for urea (244 mg/dL), creatinine (7.8 mg/ dL), K (5.7 mmol/L) were within normal limits. Room air oxygen saturation (SatO 2 ) was 98%. Sedation was achieved with midazolam (0.05 mg/kg, i.v.). For local anesthesia 1% lidocain was used. The CVC was inserted by the Seldinger technique as described previously. , Briefly, a 12F, double lumen CVC line was inserted without difficulty via the right subclavian vein to a length of 15 cm; however, there was no blood flow. After the line was advanced 1 cm further to a final length of 16 cm, the blood flow was satisfactory. At this point the patient reported a "strange" feeling in the chest; his SatO 2 was 99%. At that time, the ECG showed an SVT at a rate of 180 bpm. The line was immediately withdrawn by 1 cm but the sinus rhythm could not be achieved. The ECG showed a persistent SVT at a rate of 180-200 bpm [Figure 1]A. A chest roentgenogram revealed that the distal fragment of the catheter touched on the base on the right atrium [Figure 2]. We assumed that the SVT was induced by the irritation caused by the catheter to the atrial wall. The catheter was withdrawn by 1 cm again but the patient did not return to sinus rhythm even by vagal maneuvers. We administered adenosin (Adenocard IV; , 0.1 mg/kg rapid i.v. push), and he recovered after a few moments [Figure 1]B and the SVT did not recur. After the rapid improvement, the patient was hemodialyzed uneventfully. The PD catheter was removed on day 20 because of persistence of a high dialysate WBC count and malposition. The patient was continued on HD via the CVC. As living renal transplantation is under consideration, an AVF was not performed. There was no recurrence of SVT during the following 3 months of follow-up.
Optimal positioning of the tip of a CVC is a controversial subject. The United States Food and Drug Administration (FDA) strongly disagrees with the practice of positioning the tip of a CVC into the right atrium because of the potential cardiac-related complications.  National Kidney Foundation: Dialysis Outcomes Quality Initiative (NKF=DOQI) recommends positioning the catheter tip at the superior vena cavaright atrial (SVC-RA) junction or in the SVC.  Central venous catheters extending into cardiac chambers can provoke premature atrial and ventricular complexes, which have been reported to initiate SVT.  After blind placement of a CVC, an intracardial position is found in up to 50% of the cases. ,
Symptomatic dysrhythmia induced by a guide wire or a malposition of a catheter represents an acute complication of the central venous access devices.  A brief dysrhythmia induced during an insertion of a catheter or a guide wire is usually an indicator of a direct irritation to the right endocardium, which can be deleterious in patients with impaired cardiac output or aortic valvular stenosis. 
Arhythmias occur commonly during CVC insertion. In a recent study, atrial arhythmias and ventricular ectopy occurred with a frequency of 41 and 25%, respectively.  This is in contrast to the data of McDowell et al  who described symptomatic ventricular tachycardia in 1% of the hemodialysis patients. It has been reported that patients with acute renal failure are at increased risk for cardiac arhythmias during the insertion of the CVCs. An important risk factor is the guide wire over-insertion, a technical error that should be avoided.  In our patient, both uremia and catheter over-insertion could have provoked the SVT. In the setting of symptomatic dysrhythmia, immediate retraction of the guide wire or the catheter should be the first interaction.
The vagal maneuvers should be attempted, and if the SVT cannot be terminated, then intravenous adenosine or calcium channel blockers should be administered. Adenosine is a short acting drug that blocks AV node conduction; it terminates 90% of tachycardias. Synchronized cardioversion can also be used immediately in patients who develop hypotension, pulmonaryedema, or ischemic chest pain.  In our patient, the SVT responded to the administration of adenosine. Also, such dysrhythmias can easily be avoided by using the intravascular ECG monitoring during the advancement of the catheter even with catheters that are too short to reach the atrium. ,
In conclusion, CVCs placement procedure can induce dysrhythmias. In the setting of SVT, the guide wire or catheter should be immediately retracted. Intravascular ECG monitoring can be helpful during the insertion of the CVCs.
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