Introduction

• Central venous catheter (CVC) placement is essential in perioperative and critical care for hemodynamic monitoring, fluid therapy, and drug delivery.
• The procedure carries potential complications, notably cardiac arrhythmias arising from mechanical irritation of cardiac structures.
• Arrhythmias commonly result from contact with the coronary sinus and right heart due to the anatomical relationship of central veins to the heart.
• This chapter examines the basic science (anatomy, electrophysiology, procedural mechanics) and integrates those principles into practical anesthetic strategies to anticipate, prevent, and manage arrhythmias during CVC placement.

Anatomy — Heart’s Venous Drainage SystemOverview of cardiac venous anatomy

• Coronary sinus
• Large venous sinus in the posterior atrioventricular groove.
• Drains approximately 70% of myocardial venous blood (great, middle, small cardiac veins; posterior vein of the left ventricle).
• Empties into the right atrium via the coronary sinus ostium; may be guarded by a Thebesian valve.
• Other venous structures
• Thebesian veins: small veins draining directly into the right atrium or ventricle.
• Anterior cardiac veins: empty directly into the right atrium.
• Spatial relationships relevant to CVC placement
• Coronary sinus lies ~2–3 cm from the superior vena cava–right atrial junction.
• Proximity to typical CVC insertion paths (right internal jugular and subclavian veins) predisposes to inadvertent catheter or guidewire entry.

Clinical relevance of anatomy

• Coronary sinus contains myocardial tissue and is electrically active; mechanical contact can trigger ectopic activity.
• Right atrium and ventricle house conduction structures (SA node, AV node, Purkinje fibers) that are susceptible to mechanical disruption.
• Anatomical variants (e.g., persistent left superior vena cava [PLSVC], dilated coronary sinus) increase the risk of misplacement and arrhythmias.
• Awareness of these anatomical nuances aids in planning access site choice and insertion technique.

Electrophysiological Basis of ArrhythmiasCardiac electrophysiology overview

• Conduction system components: sinoatrial (SA) node, atrioventricular (AV) node, bundle of His, Purkinje fibers.
• SA node generates spontaneous action potentials that propagate through the atria to the AV node and ventricles.
• Myocardial cell properties: automaticity, excitability, conductivity — governed by sodium, potassium, and calcium ion channels.
• Myocardial sleeves (including those in the coronary sinus) can act as ectopic foci when irritated.

Mechanisms of arrhythmogenesis during CVC placement

• Coronary sinus irritation
• Mechanical stimulation of myocardial sleeve can produce premature atrial contractions (PACs), atrial flutter, or atrial fibrillation.
• Mechanical disturbance can trigger early afterdepolarizations (EADs) or delayed afterdepolarizations (DADs).
• Proximity to AV nodal tissue increases risk of re-entrant arrhythmias if conduction pathways are disrupted.
• Right heart stimulation
• Catheter or guidewire contact with endocardium or conduction tissue may provoke sinus tachycardia, supraventricular tachycardia (SVT), or ventricular tachycardia (VT).
• Localized mechanical stress can precipitate ischemia, altering ion channel function and excitability.
• Guidewire-induced arrhythmias
• J-tipped or straight guidewires advanced into the right heart can transiently irritate myocardium and Purkinje fibers, causing PACs or premature ventricular contractions (PVCs).
• Phase 4 depolarization in Purkinje fibers may be induced by mechanical contact, producing ventricular ectopy.
• Electrolyte and hemodynamic effects
• Rapid or maldirected infusion (e.g., into coronary sinus) can create localized electrolyte shifts (hyperkalemia, hypocalcemia) and increase irritability.
• Direct infusion of vasoactive drugs into sensitive myocardial regions can exacerbate arrhythmogenesis.

Clinical incidence

• Reported arrhythmia rates during CVC insertion are approximately 1–2%, with higher rates when imaging guidance is not used.
• Right internal jugular access carries heightened risk due to its direct trajectory toward the superior vena cava and right atrium.

Procedural Factors Contributing to ArrhythmiasCatheter insertion techniques and risks

• Seldinger technique steps: venous needle access, guidewire insertion, dilation, catheter advancement.
• Procedural risk factors
• Lack of imaging guidance (blind landmark approach) increases misplacement risk.
• Over-advancement of guidewire (beyond ~20–25 cm) increases probability of entering the right atrium or ventricle.
• Catheter tip positioned too low (within right atrium/coronary sinus) increases arrhythmia risk.

Patient-specific risk factors

• Anatomical variations
• PLSVC or inherently dilated coronary sinus elevates misplacement risk particularly with left-sided access.
• Cardiac disease
• Atrial enlargement, pulmonary hypertension, ischemic heart disease increase myocardial irritability.
• Metabolic factors
• Pre-existing electrolyte abnormalities (hypokalemia, hypomagnesemia, hyperkalemia) potentiate arrhythmogenesis.

Anesthetic Management StrategiesPreoperative assessment

• Cardiac history
• Document prior arrhythmias, heart failure, congenital variants (e.g., PLSVC).
• Electrolyte optimization
• Correct hypokalemia and hypomagnesemia before elective central access when feasible.
• Imaging review
• Inspect prior chest radiographs and echocardiography for right heart enlargement or venous anomalies.

Intraoperative monitoring and prevention

• Continuous ECG monitoring
• Use multi-lead monitoring (e.g., 5-lead) to detect PACs, PVCs, atrial fibrillation, and ischemic ST changes in real time.
• Ultrasound guidance
• Real-time ultrasound for vessel localization and needle guidance reduces complication rates compared with landmark techniques.
• Visualize guidewire within the vessel when possible prior to dilatation and catheter advancement.
• Guidewire and catheter positioning
• Limit guidewire advancement to approximately 20–25 cm to minimize right heart entry.
• ECG-guided technique: connect guidewire to an ECG lead and monitor for P-wave amplitude changes that indicate right atrial entry; withdraw if marked increase occurs.
• Advanced imaging in high-risk cases
• Use fluoroscopy or transesophageal echocardiography (TEE) to confirm tip location when anatomical variants are suspected or in cardiac surgery settings.
• TEE allows visualization of the coronary sinus ostium and catheter position in real time.

Immediate management of arrhythmias

• Initial steps
• Halt wire/catheter advancement and withdraw slightly (1–2 cm) to reduce mechanical irritation.
• Reassess ECG to classify arrhythmia (PAC, PVC, SVT, VT, atrial fibrillation).
• Pharmacologic therapy
• Supraventricular arrhythmias: consider rate control or antiarrhythmics per ACLS (e.g., esmolol for acute rate control; amiodarone for sustained or unstable SVT/AF).
• Ventricular arrhythmias: amiodarone or lidocaine for sustained VT; defibrillation if unstable.
• Electrolyte repletion: magnesium sulfate (e.g., 2 g IV) for torsades de pointes or polymorphic VT; correct potassium and calcium as indicated.
• Confirm and correct catheter position
• Obtain chest radiograph, fluoroscopy, or TEE to confirm tip location and reposition catheter into the superior vena cava if misplaced.
• Avoid large or rapid infusions until correct placement is assured.

Postoperative considerations

• Chest X-ray confirmation
• Verify that the catheter tip lies in the superior vena cava, approximately 1–2 cm above the right atrial junction.
• Continued monitoring
• Maintain ECG monitoring for 24–48 hours post-insertion when clinically appropriate due to risk of delayed arrhythmias from migration or thrombosis.
• Patient education and follow-up
• Inform patients about signs of complications (palpitations, chest pain, syncope); arrange prompt reassessment and imaging if symptoms appear.

Integration of Basic Science into Clinical PracticeAnatomical and physiological insights

• Recognizing the coronary sinus as an electrically active structure explains why direct mechanical contact induces ectopy and arrhythmias.
• Appreciating proximity of conduction tissues in the right heart supports conservative guidewire advancement and tip positioning.
• Selecting insertion sites (e.g., right internal jugular vs left-sided access) should incorporate anatomical risks such as PLSVC.

Pharmacological considerations

• Anesthetic agents influence arrhythmia risk:
• Propofol: may exhibit antiarrhythmic properties but causes hypotension that can worsen myocardial ischemia in vulnerable patients.
• Volatile anesthetics (isoflurane, sevoflurane): generally minimal direct conduction effects but require careful hemodynamic titration.
• Local anesthetic systemic toxicity: inadvertent intravascular injection of significant lidocaine doses can cause cardiac conduction disturbances and should be avoided.

Procedural optimization through basic science

• Fluid dynamics and vessel selection
• Principles such as Poiseuille’s law support choosing larger, straighter veins for central access to minimize turbulence and mechanical stress.
• Avoiding rapid infusion through malpositioned catheters
• Understanding how localized electrolyte concentration affects membrane potentials informs conservative infusion practices until placement is confirmed.

Case Example

• Clinical vignette
• A 65-year-old male with atrial fibrillation and heart failure requires CVC placement for coronary artery bypass grafting.
• During right internal jugular cannulation, new-onset PVCs appear on ECG.
• Management
• Guidewire advancement is stopped and the guidewire is withdrawn 2 cm.
• Ultrasound confirms intravascular position; transesophageal echocardiography verifies catheter tip in the superior vena cava, not the coronary sinus.
• PVCs resolve after slight withdrawal and confirmation of correct tip placement.
• Takeaway
• Real-time monitoring, imaging guidance, and prompt withdrawal of the irritant effectively manage most procedure-related arrhythmias.

Future Directions

• Imaging and device innovations
• Magnetic-tipped guidewires and real-time navigation systems may improve accuracy of catheter placement and reduce arrhythmia risk.
• AI-enhanced ultrasound could increase vein visualization quality and operator detection of misplacement.
• Biomarker research
• Investigation into biomarkers of myocardial irritation (e.g., procedural troponin release) may help stratify risk and guide monitoring strategies.
• Procedural protocols
• Further evidence may refine guidelines on monitoring duration post-insertion and standardize ECG-guided techniques across institutions.

Conclusion

• Arrhythmias during CVC placement stem from anatomical proximity and electrophysiological sensitivity of the coronary sinus and right heart structures.
• Integration of anatomy, electrophysiology, and procedural mechanics permits anticipation and prevention of most arrhythmias.
• Critical preventive measures include pre-procedural assessment and correction of electrolytes, real-time ultrasound guidance, continuous ECG monitoring, conservative guidewire advancement, and immediate withdrawal when irritation occurs.
• Persistent or unstable rhythms require pharmacologic or advanced resuscitative measures and confirmation of correct catheter position before continuing infusions.
• Advances in imaging, device design, and AI hold promise to further reduce arrhythmia incidence and improve procedural safety.