Management of Perioperative Conduction Disorders

Educational Objectives

The goal of this program is to improve management of perioperative conduction disorders. After hearing and assimilating this program, the clinician will be better able to:

1. Optimize management of atrial fibrillation.
2. Administer phenylephrine in patients with unstable arrhythmia.

Summary

Stable arrhythmia: older patients (≈70 yr of age) are at a high risk of developing an arrhythmia, particularly after lung or cardiac surgery; for those experiencing atrial fibrillation (AF) with rapid ventricular rate but are stable with normal blood pressure (BP), reduce heart rate (HR) to allow characterization of the arrhythmia on electrocardiography and thereby determine whether anticoagulation is needed; β-blockers are effective unless the patient is on an inotrope; other options include adenosine, which is both diagnostic and therapeutic; digoxin is an atrioventricular AV nodal blocking agent that does not affect β-1 receptors, making it useful for patients on inotropes; if slowing the HR reveals a sinus rhythm with premature atrial contractions, anticoagulation is unnecessary

Management of stable arrhythmia: in AF electrolyte correction is a priority for speaker; a potassium level of ≥4 mmol/L and a magnesium level of ≥2 mg/dL should be maintained; a basic metabolic panel with magnesium levels should be obtained and corrected as needed; HR control is then pursued using medications (eg, metoprolol and diltiazem), with calcium channel blockers showing some benefit in patients undergoing lung surgery; amiodarone is another option frequently used in cardiothoracic intensive care unit and cardiac anesthesia; caution is necessary as amiodarone can also convert AF to normal sinus rhythm, which may lead to embolization if an atrial clot is present

Cardioversion: an option even for stable patients; although often performed on unstable patients, stable patients with rapid HR may eventually require rhythm correction; if medications fail, elective cardioversion should be considered; if AF has been present for <48 hr, cardioversion can be performed without ruling out an atrial clot

Unstable arrhythmia: another patient scenario involves severe aortic stenosis with a wide complex rhythm; despite the appearance, this is also caused by AF with rapid ventricular response, which is complicated by a bundle branch block; not all AF presents as a narrow complex rhythm; patients with severe aortic stenosis can rapidly become unstable because of reduced ventricular compliance and reliance on atrial contraction for adequate preload and BP maintenance; loss of atrial contraction severely affects hemodynamics

Management of unstable arrhythmia: treatment involves increasing BP while addressing the rhythm; fluids are a first-line intervention to increase preload, followed by vasopressor support; phenylephrine, an α-1 agonist, is speaker’s first-line choice because it raises BP without exacerbating the arrhythmia; norepinephrine, with β-1 activity, risks worsening the rhythm; amiodarone is another useful option; when treating AF in unstable patients, electrical cardioversion is often necessary; the first step in cardioversion is applying the defibrillator pads correctly to create an optimal energy vector through the heart; improper pad placement, ie, placing both pads on the chest without a clear energy pathway, can render cardioversion ineffective; pads should be placed anterolaterally or anteroposteriorly, with some evidence suggesting better chances of success with anterior-posterior placement

Defibrillation: defibrillators deliver energy in monophasic or biphasic forms; most modern machines use biphasic energy, which is more effective and requires lower energy levels; most common brands use biphasic energy; once the patient is connected to the defibrillator, the device must be turned on, set to defibrillation mode, and synchronized; synchronization ensures energy delivery occurs at the correct time in the cardiac cycle; the defibrillator detects R waves and places markers above them; if energy is delivered at the wrong time (eg, on the T wave), it can induce ventricular fibrillation (VF) or ventricular tachycardia (VT); if cardioversion is performed incorrectly and induces VF, immediate defibrillation is necessary; the defibrillator should be charged to 200 J and the shock delivered without synchronization; if unsuccessful, standard Advanced Cardiac Life Support protocols should be followed, including chest compressions, medications, and repeated defibrillation attempts; alternative strategies include adjusting pad placement to anterior-lateral or anterior-posterior positions or using dual sequential defibrillation with 2 machines, if needed; the goal is to persist with different strategies until a successful rhythm conversion is achieved

Diagnosis of VT: often characterized by a tombstone-like appearance on electrocardiography; in monomorphic VT, each QRS complex looks the same; it can also present in a polymorphic form (eg, torsades de pointes); the same treatment can be used for both; it is important to differentiate VT from conditions like hyperkalemia, which can produce large T waves resembling VT; misidentifying hyperkalemia could lead to inappropriate treatment; always confirm with electrocardiography before making treatment decisions; the large T waves may also mislead automated readings, so be mindful of the true QRS before delivering energy

Management of VT: if the patient is stable, medications are the first choice, with amiodarone recommended by speaker, typically administered as a bolus followed by an infusion; sodium channel blockers (eg, lidocaine, procainamide) are also effective; if the patient is unstable, the treatment approach remains largely the same, but additional interventions may be needed; for regular VT, synchronized cardioversion is the method of choice, similar to treating atrial arrhythmias; regular VT is not treated with defibrillation; an advanced technique involves using a transvenous pacemaker; by placing the pacemaker in the right ventricle and setting the HR higher than the intrinsic VT, the external pacemaker can take over; once control is established, the HR is gradually reduced to restore normal rhythm; if the VT is irregular, defibrillation is required; pads should be applied, the device charged, and energy delivered without synchronization; torsades de pointes, a unique arrhythmia, requires magnesium bolus in addition to standard antiarrhythmic drugs (eg, amiodarone, lidocaine, procainamide)

Stellate ganglion block: an another emerging treatment for refractory VT and VF; the stellate ganglion consists of sympathetic neurons that dictate catecholamine release and heart tone; bilateral blocking has been shown to significantly reduce VT and VF episodes, as well as the frequency of shocks from an automatic implantable cardioverter defibrillator (AICD); this intervention improves patient outcomes and reduces the distress caused by repeated AICD shocks; while primarily diagnostic, a successful block may lead to a permanent sympathectomy to prevent persistent arrhythmias

Complications: as noted above, one major complication of synchronized cardioversion is induction of VF, which must be promptly treated; heart block — the same defibrillation devices can be used for pacing; when drugs fail to improve AV node conduction, transcutaneous pacing is the next step; the pacing function on defibrillators is activated by selecting the “pace” mode and adjusting the amplitude until complete electrical capture is achieved (ie, each pacing spike is followed by a QRS complex); mechanical capture must also be verified by checking for a pulse or arterial waveform; some devices offer asynchronous pacing (VOO mode), which delivers pacing regardless of intrinsic rhythm; while useful in some cases, lethal arrhythmias can be induced if pacing coincides with a T wave, potentially triggering VF; therefore, asynchronous pacing should be used with caution

Readings

Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society [published correction appears in J Am Coll Cardiol. 2018 Oct 2;72(14):1756-1759. doi: 10.1016/j.jacc.2018.08.2131]. J Am Coll Cardiol. 2018;72(14):1677-1749. doi:10.1016/j.jacc.2017.10.053; Cohn SL. Update in perioperative cardiac medicine 2021 [published correction appears in Cleve Clin J Med. 2021 May 3;88(5):294.]. Cleve Clin J Med. 2021;88(4):216-220. Published 2021 Apr 1. doi:10.3949/ccjm.88a.21014; Gupta A, Lokhandwala Y, Rai N, et al. Adenosine-A drug with myriad utility in the diagnosis and treatment of arrhythmias. J Arrhythm. 2020;37(1):103-112. doi:10.1002/joa3.12453; Harmon DM, Heinrich CK, Dillon JJ, et al. Mortality risk stratification utilizing artificial intelligence electrocardiogram for hyperkalemia in cardiac intensive care unit patients. JACC Adv. 2024;3(9):101169. doi:10.1016/j.jacadv.2024.101169; Kim M, Kwon CH. Perioperative management of patients with cardiac implantable electronic devices. Korean J Anesthesiol. 2024;77(3):306-315. doi:10.4097/kja.23826; Lambiase PD, Maclean E. Review of the National Institute for Health and Care Excellence guidelines on the management of atrial and ventricular arrhythmias. Heart. 2024;110(5):313-322. doi:10.1136/heartjnl-2022-322122; Law AC, Bosch NA, Peterson D, et al. Comparison of heart rate after phenylephrine vs norepinephrine initiation in patients with septic shock and atrial fibrillation. Chest. 2022;162(4):796-803. doi:10.1016/j.chest.2022.04.147; Niimi N, Yuki K, Zaleski K. Long QT syndrome and perioperative torsades de pointes: What the anesthesiologist should know. J Cardiothorac Vasc Anesth. 2022;36(1):286-302. doi:10.1053/j.jvca.2020.12.011; O’Glasser AY, Manjarrez EC. Perioperative care of heart failure, arrhythmias, and valvular heart disease. Med Clin North Am. 2024;108(6):1053-1064. doi:10.1016/j.mcna.2024.05.001; Pecha S, Kirchhof P, Reissmann B. Perioperative arrhythmias. Dtsch Arztebl Int. 2023;120(33-34):564-574. doi:10.3238/arztebl.m2023.0052.

Disclosures

For this program, members of the faculty and the planning committee reported nothing relevant to disclose.

Acknowledgements

Dr. Rosenkrans was recorded at Carolina Refresher Course 2024: 35th Annual Update in Anesthesiology, Pain, and Critical Care Medicine, held June 19-20, 2024, on Kiawah Island, SC, and presented by University of North Carolina at Chapel Hill, School of Medicine. For information about upcoming CME activities from this presenter, please visit https://www.med.unc.edu/cpd/. Audio Digest thanks the speakers and University of North Carolina at Chapel Hill, School of Medicine, for their cooperation in the production of this program.

CME/CE INFO

Accreditation:

Lecture ID:

AN671201

Qualifies for:

ABA MOCA, Geriatrics

Expiration:

This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.

Instructions:

To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.

Estimated time to complete this CME/CE course:

Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.