Temporary Epicardial Pacing Versus Atropine after Cardiac Surgery - Essay Example

Temporary Epicardial Pacing Versus Atropine after Cardiac Surgery Introduction: Under normal conditions, the pacemaker function of the heart resides in the sinoatrial (SA) node that lies at the junction of the right atrium and superior vena cava. Once the pacing impulse exits the sinus node and perinodal tissues, it traverses the atrium until it reaches the atrioventricular (AV) node. The sinus node, atrium, and AV node are significantly influenced by autonomic tone (Saxena, P., Konstantinov, I. E., and Newman, M. A., 2007, p 60). Vagal influences depress the automaticity of the sinus node, depress conduction, and prolong AV nodal conduction and refractoriness in the tissues surrounding the sinus node; inhomogeneously decreases atrial refractoriness, slows atrial conduction and prolong AV nodal conduction and refractoriness (Reade, M.C., 2007, p 265). Sympathetic influences exert the opposite effect. In this regard, automaticity is an important property of the cardiac cells that is normally observed in the sinus node, the specialized fibres of the His-Purkinje system, and in some specialized atrial fibres. Bradyarrhythmias result from abnormalities either of impulse formation, that is, automaticity or of conduction. In cardiac surgery, due to the fact that the patient would be brought in a cardiac standstill and other pharmacologic agents would be used to facilitate this would lead to low cardiac output and hence bradyarrhythmias. (Debrunner, M., Naegeli, B., Genoni, M., Turina, M., and Bertel, O., 2004, p 16). The sinus node is normally the dominant cardiac pacemaker because of its intrinsic discharge rate that is highest of all potential cardiac pacemakers. Its responsiveness to alterations in the autonomic nervous system tone is responsible for a rapid heart rate, and the reverse in slowing (Reade, M.C., 2007, p 367). Slowing of the heart rate usually happens through decrease in the sinus rate by decreased sympathetic tone acting via beta-adrenergic receptors and/or an increase in the sympathetic tone acting via muscarinic receptors. Sinus node dysfunctions leading to bradyarrhythmias are most often found in elderly individuals. Apart from other reasons, this clinical condition is associated with open heart surgeries for any cardiac condition (Flynn, M.J., McComb, J.M., and Dark, J.H., 2005, p 252). Whatever may be the reason, the manifestations happen due to abrupt, prolonged sinus pauses caused by failure of sinus impulse formation or block of conduction of sinus impulse to the surrounding atrial tissues (Bethea, B.T. et al., 2005, p 106). In some patients, sinus node dysfunction is accompanied by abnormalities in AV conduction, and thus aside from having absence of atrial activity, the lower pacemakers fail to emerge during sinus pauses (Daoud, E.G., Snow, R., Hummel, J.D., Kalbfleisch, S.J., Weiss, R., and Augostini, R., 2003, p. 129). External energy sources can be used to stimulate the heart when disorders in impulse formation and/or transmission lead to symptomatic bradyarrhythmias. Pacer stimuli can be applied to the atria and/or ventricles (Overbay, D. and Criddle, L., 2004, p. 26). Temporary pacing is usually instituted to provide pacemaker support when a bradycardia is precipitated by what is presumed to be a transient event, such as, induced cardiac standstill during an open heart surgery, induced cardioplegia in bypass surgeries, ischemia, or drug toxicity (Roschkov, S. and Jensen, L., 2004, p. 33). Temporary pacing is usually achieved by insertion of an electrode catheter with the catheter positioned in the right ventricular apex and attached to an external generator. This generator will assist the heart to generate a pacing impulse on the face of reduced excitability. Excitatory impulses generated by the temporary pacing apparatus would generate depolarization potential to cause cardiac contraction. Epicardial wires allow temporary pacing after cardiac surgery (Puskas, J.D., Sharoni, E., Williams, W.H., Petersen, R., Duke, P., and Guyton, R.A., 2003, pp. E-103). Pacing is acknowledged often to be the best and sometimes the only method of treating temporary rhythm disturbances in this context. Temporary epicardial pacing has evolved from simple one-chamber systems to dual chamber, biatrial, and even biventricular systems. In the earlier phase of such a management, sequential atrioventricular pacing demonstrated haemodynamic benefits in patients with sinus rhythm requiring pacing postcardiopulmonary bypass (Berberian, G. et al., 2005, p. 873). It had been hypothesized and demonstrated that left ventricular pacing with active lead placement on the posterolateral left ventricular wall affords haemodynamic benefits to cardiac surgical patients. However, applying it in the field demands knowledge about troubleshooting real and apparent pacemaker malfunctions and expertise in manual adjustments of parameters, such as, AV interval, post atrial refractory period and upper rate limit to avoid over and undersensing, cross-talk, and pace-maker mediated tachycardia (Fernndez, A.L., Garca-Bengochea, J.B., Snchez, D., and Alvarez, J., 2006, p 633-4). This procedure is associated with a small risk of cardiac perforation, infection, and thromboembolism. This risks of all these complications increase if the duration of temporary pacing increases. Epicardial lead placement is used mainly when the chest is already opened in the course of a cardiac operation (Archbold, R.A. and Schilling, R.J., 2004, p. 130). Atropine: This concept of modification of conduction time in cardiac tissue has raised the possibility of use and effectiveness of atropine in these situations. Contrasted to epicardial pacing, atropine has a very big advantage in an, otherwise, uncomplicated patient. Atropine has the advantage of being a simple agent very simply administered, but the biggest advantage that atropine would enjoy is absence of complications (Toprak, V., Yentur, A., and Sakarya, M., 2002, p. 656). Placement of epicardial pacing wires has legitimate complications of bleeding from cardiac lacerations, tamponade, side branch or graft avulsion, superior epigastric artery laceration, all very hazardous (Maisel, W.H., Rawn, J.D., and Stevenson, W.G., 2001, p. 1062). If the surgeon desires to avoid such complications, he may try modifying the conduction rate of atrium or ventricle by atropine. This would, of course, preclude the patients who have absolute indications for placement of an epicardial pacing lead. These patients would be diabetics; having preoperative arrhythmia, advanced age, cardiomegaly; needing preop antiarrhythmic therapy or pacing or inotropic agents (Gerstenfeld, E.P. et al., 2001, pp. 278). Other than these settings, atropine may be an alternative worth trying. Atropine, an antimuscarinic agent, affects the receptors in the cardiac muscles, and it counteracts the vagal effects, and it can be one of the best initial treatments of nodal bradycardia .Atropine is administered every 3 to 5 minutes for a total dose of 0.03 to 0.04 mg/kg (Dzemali, O., Bakhtiary, F., Dogan, S., Wittlinger, T., Moritz, A., and Kleine, P., 2006, p. 1343). Atropine can treat the high parasympathetic tone that underlies severe bradyasystolic events, but pacing should be applied immediately whenever it is considered suitable without waiting for the atropine to take effect; otherwise, depleted high-energy phosphates with not allow the cardiac contraction despite a successful electrical capture by temporary pacing (Abu-Omar, Y., Guerrieri-Wolf, L., and Taggart, D.P., 2006, 1248). Conclusion: Atropine is a parasympathetic agent that enhances atrioventricular node conduction and sinus node automaticity that is indicated for initial and first-line management of bardycardia or systolic arrest induced by cardiac surgery or anesthesia, but where there is an absolute indication in a postsurgical patient, even with high risk of complications and increased cost, epicardial pacing remains the best therapeutic measure to deal with this. References Abu-Omar, Y., Guerrieri-Wolf, L., and Taggart, D.P., (2006). Indications And Positioning Of Temporary Pacing Wires. MMCTS: pp. 1248. Archbold, R.A. and Schilling, R.J., (2004). Atrial Pacing For The Prevention Of Atrial Fibrillation After Coronary Artery Bypass Graft Surgery: A Review Of The Literature. Heart; 90: pp. 129 - 133. Berberian, G. et al., (2005). Optimized Biventricular Pacing in Atrioventricular Block After Cardiac Surgery. Annals of Thoracic Surgery; 80: pp. 870 - 875. Bethea, B.T. et al., (2005). Determining the Utility of Temporary Pacing Wires After Coronary Artery Bypass Surgery. Annals of Thoracic Surgery; 79: pp. 104 - 107. Daoud, E.G., Snow, R., Hummel, J.D., Kalbfleisch, S.J., Weiss, R., and Augostini, R., (2003). Temporary Atrial Epicardial Pacing As Prophylaxis Against Atrial Fibrillation After Heart Surgery: A Meta-Analysis. Journal of Cardiovascular Electrophysiology; 14(2): pp. 127-132. Debrunner, M., Naegeli, B., Genoni, M., Turina, M., and Bertel, O., (2004). Prevention Of Atrial Fibrillation After Cardiac Valvular Surgery By Epicardial, Biatrial Synchronous Pacing. European Journal of Cardiothoracic Surgery; 25: p. 16. Dzemali, O., Bakhtiary, F., Dogan, S., Wittlinger, T., Moritz, A., and Kleine, P., (2006). Perioperative Biventricular Pacing Leads To Improvement Of Hemodynamics In Patients With Reduced Left-Ventricular Function--Interim Results. Pacing and Clinical Electrophysiology; 29(12): pp. 1341-1345. Fernndez, A.L., Garca-Bengochea, J.B., Snchez, D., and Alvarez, J., (2006). Temporary Left Ventricular Pacing After Cardiac Surgery. European Journal of Cardiothoracic Surgery; 29: pp. 633 - 634. Flynn, M.J., McComb, J.M., and Dark, J.H., (2005). Temporary Left Ventricular Pacing Improves Haemodynamic Performance In Patients Requiring Epicardial Pacing Post Cardiac Surgery. European Journal of Cardiothoracic Surgery; 28: pp. 250 - 253. Gerstenfeld, E.P. et al., (2001). Effectiveness Of Bi-Atrial Pacing For Reducing Atrial Fibrillation After Coronary Artery Bypass Graft Surgery. Journal of Interventional Cardiac Electrophysiology; 5: pp. 275-283. Maisel, W.H., Rawn, J.D., and Stevenson, W.G., (2001). Atrial Fibrillation After Cardiac Surgery. Annals of Internal Medicine; 135:pp. 1061-1067. Overbay, D. and Criddle, L., (2004). Mastering Temporary Invasive Cardiac Pacing. Critical Care Nurse; 24: pp. 25 - 32. Puskas, J.D., Sharoni, E., Williams, W.H., Petersen, R., Duke, P., and Guyton, R.A., (2003). Is routine use of temporary epicardial pacing wires necessary after either OPCAB or conventional CABG/CPB Heart Surgery Forum; 6(6): pp. E103-E106. Reade, M.C., (2007). Temporary Epicardial Pacing After Cardiac Surgery: A Practical Review: Part 1: General Considerations In The Management Of Epicardial Pacing. Anaesthesia; 62(3): pp. 264-71. Reade, M.C., (2007). Temporary Epicardial Pacing After Cardiac Surgery: A Practical Review: Part 2: General Considerations In The Management Of Epicardial Pacing. Anaesthesia; 62(3): pp. 364-373. Roschkov, S. and Jensen, L., (2004). Coronary artery bypass graft patients' pain perception during epicardial pacing wire removal. Canadian Journal of Cardiovascular Nursing; 14(3): p. 32-38. Saxena, P., Konstantinov, I. E., and Newman, M. A., (2007). Use Of Temporary Epicardial Pacing Wires In Cardiac Surgery. Heart Lung Circulation; 16(1): p. 60. Toprak, V., Yentur, A., and Sakarya, M., (2002). Anaesthetic Management Of Severe Bradycardia During General Anaesthesia Using Temporary Cardiac Pacing. British Journal of Anaesthesiology; 89: pp. 655 - 657. Read More