BBB' below.) For patients who will require temporary pacing for more than 48 hours and are hemodynamically stable for transport to the electrophysiology lab, we generally place an active fixation permanent pacing lead in the RV and externalize the pin for use in an external resterilized permanent pacemaker generator or conventional temporary pacing box. This form of temporary pacing has been shown to be far more stable and better tolerated by patients than conventional temporary pacing wires [27]. Stable inferior MI patients Second degree AV block, high grade AV block, or third degree (complete) AV block Patients with inferior MI and second degree AV block, high grade AV block, or third https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 12/34 7/5/23, 10:34 AM Conduction abnormalities after myocardial infarction - UpToDate degree (complete) AV block who are hemodynamically stable generally do not require urgent therapy with atropine or temporary cardiac pacing. However, many ventricular escape rhythms are unreliable and potentially unstable, so patients should be continuously monitored with transcutaneous pacing pads in place in the event of clinical deterioration ( algorithm 1). Additionally, in the setting of an acute myocardial ischemia, patients should undergo prompt revascularization; following revascularization, most conduction abnormalities will improve or resolve and will not require permanent pacing. Following revascularization, if second degree AV block, high grade AV block, or third degree (complete) AV block persists, patients should remain on continuous ECG monitoring and should be evaluated for any additional potentially reversible causes of AV block (eg, increased vagal tone, hypothyroidism, hyperkalemia, and drugs that depress conduction). Patients with AV block felt to be medication-induced should be observed while the offending agent or agents are withdrawn; such patients may have improvement or resolution of AV block following removal of the medication with or without administration of reversal agents. Patients with AV block in the setting of hyperkalemia should receive therapy to reduce serum potassium levels. If AV block subsequently resolves, a permanent pacemaker is not usually needed. (See "Treatment and prevention of hyperkalemia in adults" and "Treatment of primary hypothyroidism in adults".) In general, a waiting period of several days should be employed to determine potential reversibility of AV block, particularly in patients with acute inferior MI [23]. If no reversible causes are present, definitive treatment of Mobitz type II second degree AV block, high grade AV block, or third degree (complete) AV block involves permanent pacemaker placement in most patients ( algorithm 1) [23,28]. Dual-chamber (ie, AV) pacing to maintain AV synchrony is preferred (rather than single chamber RV pacing) in most patients due to the favorable hemodynamic benefits of AV synchrony [23]. Some trials suggest that biventricular cardiac pacing (ie, cardiac resynchronization) is superior to standard dual chamber pacing in patients with heart block and depressed LV systolic function [29,30]. Implantable cardioverter-defibrillators, specifically cardiac resynchronization therapy devices (CRT-Ds), should be considered in patients with AV block and significant LV dysfunction that is likely to be permanent and irreversible despite medical therapy and revascularization. (See "Permanent cardiac pacing: Overview of devices and indications", section on 'Acquired AV block' and "Modes of cardiac pacing: Nomenclature and selection".) First degree AV block and Mobitz type I second degree AV block Patients with first degree AV block or Mobitz type I second degree AV block who are hemodynamically stable and https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 13/34 7/5/23, 10:34 AM Conduction abnormalities after myocardial infarction - UpToDate asymptomatic do not require any specific therapy, other than avoidance of AV nodal-blocking agents. We agree with the professional society guidelines which do not recommend a pacemaker for most cases of first degree AV block or Mobitz type I second degree AV block [23,28]. Management of patients with BBB Patients with isolated left BBB (LBBB) or right BBB (RBBB) (complete or incomplete) are generally asymptomatic related to their conduction disorder and do not require placement of a pacemaker (temporary or permanent) or any other specific therapy. The one exception to this is for patients with alternating RBBB and LBBB, or RBBB with alternating left anterior fascicular block and left posterior fascicular block, as these indicate a higher likelihood of significant conduction system disease which may progress to unstable AV block. In cases of alternating BBB in the setting of acute MI, we insert a temporary transvenous pacemaker and pursue prompt revascularization. If alternating BBB persists or progresses following revascularization, patients typically receive a permanent pacemaker. Transient second or third degree AV block associated with new persistent BBB after MI is rarely encountered in the primary percutaneous coronary intervention era. Based on small studies in the 1970s showing high mortality in these patients, older versions of pacemaker guidelines recommended routine permanent pacemaker implantation [31]. However, this recommendation has not been adopted in the most recent American or European guidelines [23,28]. Invasive electrophysiology studies looking for severe His-Purkinje conduction disease and/or follow-up event monitoring to guide therapy may be helpful in this rarely-encountered clinical scenario. PROGNOSIS High degree AV block Advanced (second or third degree) AV block is associated with an increase in mortality in patients with an inferior or anterior MI [12-17,21,32]. The increase in mortality risk is seen largely within the first 30 days; among 30-day survivors, subsequent mortality does not appear to be consistently increased in reports of various AMI cohorts [12,13,18,21]. AV block following inferior MI Although high grade AV block in patients with an inferior MI is usually transient, it is associated with increased in-hospital mortality. Following primary PCI In one large United States registry in the PCI era, complete heart block (CHB) in the setting of inferior STEMI increased in-hospital mortality twofold [16]. A similar increase in mortality with inferior STEMI was seen in other studies in the PCI era [14,15]. https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 14/34 7/5/23, 10:34 AM Conduction abnormalities after myocardial infarction - UpToDate Following thrombolysis An increase in mortality with high degree AV block of about 15 percent at 30 days is seen in patients with an inferior MI treated with a thrombolytic agent [12,21,32-36]. AV block following anterior MI High degree AV block in patients with an anterior wall MI is associated with a greater increase in in-hospital and 30-day mortality than seen with an inferior wall infarction, probably due to more extensive myocardial involvement and a higher incidence of hemodynamic complications [12,32]. Following primary PCI In the United States National Inpatient Sample registry from the PCI era, CHB in the setting of anterior STEMI increased in-hospital mortality fourfold, versus only twofold in inferior STEMI patients [16]. A similar increase in mortality with CHB and anterior STEMI was seen in other studies in the PCI era [14,15,37]. In a study of 1295 STEMI patients undergoing PCI in Japan, complete AV block occurred in 1.7 percent of patients with anterior STEMI and 10.7 percent of those with nonanterior STEMI [37]. Multivariate analysis showed that CHB was associated with all-cause mortality (hazard ratio [HR] 3.01, 95% CI 1.33-6.09) and major adverse cardiac endpoints (HR 2.23, 95% CI 1.01- 4.38) in anterior STEMI patients. In contrast, CHB was not associated with adverse outcomes in patients with nonanterior STEMI. Following thrombolysis In a review of nearly 76,000 patients from four randomized trials of fibrinolytic therapy, 3.2 percent of patients with anterior MI developed AV block and had a significant increase in mortality at 30 days (41 versus 8 percent in those without AV block; odds ratio [OR] 3.0, 95% CI 2.2-4.1) [12]. Bundle branch block The presence of fascicular or BBB during an acute MI is associated with an increase in in-hospital and long-term mortality [9-11,22,38-47]. However, interpreting the prognostic significance of BBB is complicated for several reasons: In contrast to CHB, which is almost always a new finding due to the MI, BBB often precedes the MI. This finding most commonly reflects the prevalence of BBB among patients presenting with acute MI, not the incidence of new BBB due to the infarction, which is generally very low. In the HERO-2 trial, BBB was present on 5.1 percent of initial ECGs, but new BBB developed in only 0.9 percent of patients on a second ECG taken 60 minutes later [9]. The development of a new BBB post-MI is generally felt to be associated with increased mortality [48]. Chronic and new conduction abnormalities may both predict worse outcomes, but for different reasons. The former is due to more extensive underlying cardiac disease and the latter is due to the association with larger infarctions. https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 15/34 7/5/23, 10:34 AM Conduction abnormalities after myocardial infarction - UpToDate The following observations illustrate the range of findings among patients with BBB. These studies made the assessment of the presence or absence of BBB largely based on the initial ECG. Thus, it could not be determined whether the BBB was pre-existing or associated with the infarction unless there was resolution of the BBB. Following primary PCI Among patients undergoing primary PCI, the presence of BBB on the baseline ECG is associated with increased mortality [48-50]. In a review of 3053 patients in the Primary Angioplasty in Myocardial Infarction (PAMI) trials, LBBB was present in 1.6 percent and RBBB in 3.1 percent [43]. In-hospital mortality was 14.6, 7.4, and 2.8 percent in patients with LBBB, RBBB, and no BBB, respectively. Following thrombolysis In an analysis of 26,003 North American patients entered into the GUSTO-I trial of thrombolytic therapy, the in-hospital mortality was 18 versus 11 percent with and without a BBB [42]. Patients with a BBB were more likely to experience cardiogenic shock (19 versus 11 percent), AV block or asystole (30 versus 19 percent), and to require a pacemaker (18 versus 11 percent). Mortality was higher when the BBB was persistent (20 percent versus 12 and 8 percent in the 24 percent of patients who had partial or complete resolution of the BBB, respectively). In a meta-analysis of eight studies that included 105,861 acute MI patients (STEMI and non- STEMI), new LBBB was associated with higher mortality at 30 days (OR 2.10; 95% CI 1.27- 3.48) and at one year (OR 2.81; 95% CI 1.64-4.80) [46]. In a meta-analysis of 10 studies that included 63,103 patients (STEMI and non-STEMI), RBBB (new or old) was associated with higher in-hospital (OR 1.94; 95% CI 1.60-2.37) and long-term mortality (OR 1.49; 95% CI 1.37-1.62) [47]. SOCIETY GUIDELINE LINKS Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Non-ST-elevation acute coronary syndromes (non-ST-elevation myocardial infarction)" and "Society guideline links: ST- elevation myocardial infarction (STEMI)".) SUMMARY AND RECOMMENDATIONS Bradyarrhythmias and conduction disturbances are well-recognized complications of acute myocardial infarction (MI). They are caused by either autonomic imbalance or ischemia/necrosis of the conduction system. (See 'Introduction' above.) https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 16/34 7/5/23, 10:34 AM Conduction abnormalities after myocardial infarction - UpToDate Atrioventricular (AV) block with inferior MI generally results from ischemic and autonomic effects on the AV node. It is associated with a narrow QRS complex and develops in a progressive fashion from first to second to third degree block. It often results in an asymptomatic bradycardia (40 to 60 beats per min) and is usually transient, resolving within five to seven days. (See 'Inferior MI' above.) AV block with anterior MI generally occurs abruptly in the first 24 hours. It can develop without warning or may be preceded by the development of right bundle branch block (RBBB) with either a left anterior or posterior fascicular block pattern (bifascicular or trifascicular block). The escape rhythm usually has a wide QRS complex and is unstable, and the event is associated with a high mortality from both arrhythmias and pump failure. In-hospital and 30-day mortality are higher than seen with an inferior wall infarction. (See 'Anterior MI' above.) The initial management of the patient with post-MI conduction abnormalities depends on the presence and severity of any signs and symptoms of hemodynamic instability ( algorithm 1). Mobitz type II second degree AV block, high grade AV block, or third degree (complete) AV block are often unstable rhythms and more likely to cause, or to be associated with, hemodynamic instability. Patients with newly developed BBB, or alternating BBB, are also at increased risk of developing hemodynamic instability. Patients with Mobitz type I second degree AV block, first degree AV block, or isolated BBB rarely develop hemodynamic instability related to their heart rhythm. (See 'Management of conduction abnormalities' above.) Patients with acute MI and second degree AV block, high grade AV block, or third degree (complete) AV block who are hemodynamically unstable should be urgently treated with atropine (if block is suspected to be at the AV nodal level) and generally temporary cardiac pacing should be instituted (either with transcutaneous or, if immediately available, transvenous pacing). For patients with acute inferior MI who are unresponsive to atropine, we suggest IV aminophylline (Grade 2C). Temporary transvenous pacing is generally warranted in patients with acute MI in the following circumstances (see 'Temporary pacing' above): Complete (third degree) AV block. Alternating right and left bundle branch block (LBBB). Right BBB with alternating left anterior and posterior fascicular block. https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 17/34 7/5/23, 10:34 AM Conduction abnormalities after myocardial infarction - UpToDate Asystole. Symptomatic bradycardia of any etiology, including sinus bradycardia and Mobitz type I second degree AV block, if adverse hemodynamic effects are present and the bradyarrhythmia is not responsive to atropine. Mobitz type II second degree AV block. Bradycardia-induced tachyarrhythmias, such as torsades de pointes. In general, a waiting period of several days should be employed to determine potential reversibility of AV block, particularly in patients with acute inferior MI. If no reversible causes are present, definitive treatment of Mobitz type II second degree AV block, high grade AV block, or third degree (complete) AV block involves permanent pacemaker placement in most patients. (See 'Second degree AV block, high grade AV block, or third degree (complete) AV block' above.) ACKNOWLEDGMENT The UpToDate editorial staff acknowledges the late Mark E. Josephson, MD, who contributed to an earlier version of this topic review. Use of UpToDate is subject to the Terms of Use. REFERENCES 1. S nchez-Quintana D, Cabrera JA, Farr J, et al. Sinus node revisited in the era of electroanatomical mapping and catheter ablation. Heart 2005; 91:189. 2. Rosenbaum M, Elizari MV, Lazzari JO. The Hemiblocks, Tampa Tracings, Tampa 1970. 3. Uhley HN. Some controversy regarding the peripheral distribution of the conduction system. Am J Cardiol 1972; 30:919. 4. Hecht HH, Kossmann CE, Childers RW, et al. Atrioventricular and intraventricular conduction. Revised nomenclature and concepts. Am J Cardiol 1973; 31:232. 5. Demoulin JC, Kulbertus HE. Histopathological examination of concept of left hemiblock. Br Heart J 1972; 34:807. 6. Zimetbaum PJ, Josephson ME. Use of the electrocardiogram in acute myocardial infarction. N Engl J Med 2003; 348:933. https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 18/34 7/5/23, 10:34 AM Conduction abnormalities after myocardial infarction - UpToDate 7. Stiles MK, Brooks AG, Roberts-Thomson KC, et al. High-density mapping of the sinus node in humans: role of preferential pathways and the effect of remodeling. J Cardiovasc Electrophysiol 2010; 21:532. 8. Boyett MR, Honjo H, Kodama I. The sinoatrial node, a heterogeneous pacemaker structure. Cardiovasc Res 2000; 47:658. 9. Wong CK, Stewart RA, Gao W, et al. Prognostic differences between different types of bundle branch block during the early phase of acute myocardial infarction: insights from the Hirulog and Early Reperfusion or Occlusion (HERO)-2 trial. Eur Heart J 2006; 27:21. 10. Go AS, Barron HV, Rundle AC, et al. Bundle-branch block and in-hospital mortality in acute myocardial infarction. National Registry of Myocardial Infarction 2 Investigators. Ann Intern Med 1998; 129:690. 11. Stenestrand U, Tabrizi F, Lindb ck J, et al. Comorbidity and myocardial dysfunction are the main explanations for the higher 1-year mortality in acute myocardial infarction with left bundle-branch block. Circulation 2004; 110:1896. 12. Meine TJ, Al-Khatib SM, Alexander JH, et al. Incidence, predictors, and outcomes of high- degree atrioventricular block complicating acute myocardial infarction treated with thrombolytic therapy. Am Heart J 2005; 149:670. 13. Gang UJ, Hvelplund A, Pedersen S, et al. High-degree atrioventricular block complicating ST- segment elevation myocardial infarction in the era of primary percutaneous coronary intervention. Europace 2012; 14:1639. 14. Auffret V, Loirat A, Leurent G, et al. High-degree atrioventricular block complicating ST segment elevation myocardial infarction in the contemporary era. Heart 2016; 102:40. 15. Kim HL, Kim SH, Seo JB, et al. Influence of second- and third-degree heart block on 30-day outcome following acute myocardial infarction in the drug-eluting stent era. Am J Cardiol 2014; 114:1658. 16. Harikrishnan P, Gupta T, Palaniswamy C, et al. Complete heart block complicating ST- segment elevation myocardial infarction. JACCEP 2015; 1:529. 17. Singh SM, FitzGerald G, Yan AT, et al. High-grade atrioventricular block in acute coronary syndromes: insights from the Global Registry of Acute Coronary Events. Eur Heart J 2015; 36:976. 18. Kosmidou I, Redfors B, Dordi R, et al. Incidence, Predictors, and Outcomes of High-Grade Atrioventricular Block in Patients With ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention (from the HORIZONS-AMI Trial). Am J Cardiol 2017; 119:1295. https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 19/34 7/5/23, 10:34 AM Conduction abnormalities after myocardial infarction - UpToDate 19. Misumida N, Ogunbayo GO, Kim SM, et al. Frequency and Significance of High-Degree Atrioventricular Block and Sinoatrial Node Dysfunction in Patients With Non-ST-Elevation Myocardial Infarction. Am J Cardiol 2018; 122:1598. 20. Feigl D, Ashkenazy J, Kishon Y. Early and late atrioventricular block in acute inferior myocardial infarction. J Am Coll Cardiol 1984; 4:35. 21. Aplin M, Engstr m T, Vejlstrup NG, et al. Prognostic importance of complete atrioventricular block complicating acute myocardial infarction. Am J Cardiol 2003; 92:853. 22. Hindman MC, Wagner GS, JaRo M, et al. The clinical significance of bundle branch block complicating acute myocardial infarction. 1. Clinical characteristics, hospital mortality, and one-year follow-up. Circulation 1978; 58:679. 23. Kusumoto FM, Schoenfeld MH, Barrett C, et al. 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol 2019; 74:e51. 24. American College of Emergency Physicians, Society for Cardiovascular Angiography and Interventions, O'Gara PT, et al. 2013 ACCF/AHA guideline for the management of ST- elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2013; 61:e78. 25. Link MS, Berkow LC, Kudenchuk PJ, et al. Part 7: Adult Advanced Cardiovascular Life Support: 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2015; 132:S444. 26. Altun A, Kirdar C, Ozbay G. Effect of aminophylline in patients with atropine-resistant late advanced atrioventricular block during acute inferior myocardial infarction. Clin Cardiol 1998; 21:759. 27. Zei PC, Eckart RE, Epstein LM. Modified temporary cardiac pacing using transvenous active fixation leads and external re-sterilized pulse generators. J Am Coll Cardiol 2006; 47:1487. 28. Brignole M, Auricchio A, Baron-Esquivias G, et al. 2013 ESC Guidelines on cardiac pacing and cardiac resynchronization therapy: the Task Force on cardiac pacing and resynchronization therapy of the European Society of Cardiology (ESC). Developed in collaboration with the European Heart Rhythm Association (EHRA). Eur Heart J 2013; 34:2281. 29. Yu CM, Chan JY, Zhang Q, et al. Biventricular pacing in patients with bradycardia and normal ejection fraction. N Engl J Med 2009; 361:2123. https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 20/34 7/5/23, 10:34 AM Conduction abnormalities after myocardial infarction - UpToDate 30. Curtis AB, Worley SJ, Adamson PB, et al. Biventricular pacing for atrioventricular block and systolic dysfunction. N Engl J Med 2013; 368:1585. 31. Gregoratos G, Cheitlin MD, Conill A, et al. ACC/AHA guidelines for implantation of cardiac pacemakers and antiarrhythmia devices: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Pacemaker Implantation). J Am Coll Cardiol 1998; 31:1175. 32. Goldberg RJ, Zevallos JC, Yarzebski J, et al. Prognosis of acute myocardial infarction complicated by complete heart block (the Worcester Heart Attack Study). Am J Cardiol 1992; 69:1135. 33. Harpaz D, Behar S, Gottlieb S, et al. Complete atrioventricular block complicating acute myocardial infarction in the thrombolytic era. SPRINT Study Group and the Israeli Thrombolytic Survey Group. Secondary Prevention Reinfarction Israeli Nifedipine Trial. J Am Coll Cardiol 1999; 34:1721. 34. Berger PB, Ruocco NA Jr, Ryan TJ, et al. Incidence and prognostic implications of heart block complicating inferior myocardial infarction treated with thrombolytic therapy: results from TIMI II. J Am Coll Cardiol 1992; 20:533. 35. Clemmensen P, Bates ER, Califf RM, et al. Complete atrioventricular block complicating inferior wall acute myocardial infarction treated with reperfusion therapy. TAMI Study Group. Am J Cardiol 1991; 67:225. 36. Abidov A, Kaluski E, Hod H, et al. Influence of conduction disturbances on clinical outcome in patients with acute myocardial infarction receiving thrombolysis (results from the ARGAMI-2 study). Am J Cardiol 2004; 93:76. 37. Kawamura Y, Yokoyama H, Kitayama K, et al. Clinical impact of complete atrioventricular block in patients with ST-segment elevation myocardial infarction. Clin Cardiol 2021; 44:91. 38. Godman MJ, Lassers BW, Julian DG. Complete bundle-branch block complicating acute myocardial infarction. N Engl J Med 1970; 282:237. 39. Hindman MC, Wagner GS, JaRo M, et al. The clinical significance of bundle branch block complicating acute myocardial infarction. 2. Indications for temporary and permanent pacemaker insertion. Circulation 1978; 58:689. 40. Scheinman MM, Gonzalez RP. Fascicular block and acute myocardial infarction. JAMA 1980; 244:2646. 41. Dubois C, Pi rard LA, Smeets JP, et al. Short- and long-term prognostic importance of complete bundle-branch block complicating acute myocardial infarction. Clin Cardiol 1988; 11:292. https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 21/34 7/5/23, 10:34 AM Conduction abnormalities after myocardial infarction - UpToDate 42. Sgarbossa EB, Pinski SL, Topol EJ, et al. Acute myocardial infarction and complete bundle branch block at hospital admission: clinical characteristics and outcome in the thrombolytic era. GUSTO-I Investigators. Global Utilization of Streptokinase and t-PA [tissue-type plasminogen activator] for Occluded Coronary Arteries. J Am Coll Cardiol 1998; 31:105. 43. Guerrero M, Harjai K, Stone GW, et al. Comparison of the prognostic effect of left versus right versus no bundle branch block on presenting electrocardiogram in acute myocardial infarction patients treated with primary angioplasty in the primary angioplasty in myocardial infarction trials. Am J Cardiol 2005; 96:482. 44. Ricou F, Nicod P, Gilpin E, et al. Influence of right bundle branch block on short- and long- term survival after acute anterior myocardial infarction. J Am Coll Cardiol 1991; 17:858. 45. Brilakis ES, Wright RS, Kopecky SL, et al. Bundle branch block as a predictor of long-term survival after acute myocardial infarction. Am J Cardiol 2001; 88:205. 46. Al Rajoub B, Noureddine S, El Chami S, et al. The prognostic value of a new left bundle branch block in patients with acute myocardial infarction: A systematic review and meta- analysis. Heart Lung 2017; 46:85. 47. Xiang L, Zhong A, You T, et al. Prognostic Significance of Right Bundle Branch Block for Patients with Acute Myocardial Infarction: A Systematic Review and Meta-Analysis. Med Sci Monit 2016; 22:998. 48. Melgarejo-Moreno A, Galcer -Tom s J, Consuegra-S nchez L, et al. Relation of New Permanent Right or Left Bundle Branch Block on Short- and Long-Term Mortality in Acute Myocardial Infarction Bundle Branch Block and Myocardial Infarction. Am J Cardiol 2015; 116:1003. 49. Widimsky P, Roh c F, St sek J, et al. Primary angioplasty in acute myocardial infarction with right bundle branch block: should new onset right bundle branch block be added to future guidelines as an indication for reperfusion therapy? Eur Heart J 2012; 33:86. 50. Vivas D, P rez-Vizcayno MJ, Hern ndez-Antol n R, et al. Prognostic implications of bundle branch block in patients undergoing primary coronary angioplasty in the stent era. Am J Cardiol 2010; 105:1276. Topic 45 Version 29.0 https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 22/34 7/5/23, 10:34 AM Conduction abnormalities after myocardial infarction - UpToDate GRAPHICS Action potentials generated by different parts of conduction system The sinoatrial (SA) and atrioventricular (AV) nodes generate a slow action potential, mediated by calcium ions. In comparison, the tissues of the atria, ventricles, and the His-Purkinje system generate a fast action potential mediated by sodium ions. Sequential activation of these structures results in the characteristic waveforms visible on the surface electrocardiogram (ECG). The AV node and bundle of His are small structures; as a result, no electrical activity is recorded on the surface ECG during their activation. Graphic 61989 Version 4.0 https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 23/34 7/5/23, 10:34 AM Conduction abnormalities after myocardial infarction - UpToDate Normal conduction system Schematic representation of the normal intraventricular conduction system (His- Purkinje system). The Bundle of His divides into the left bundle branch and right bundle branch. The left bundle branch divides into anterior, posterior, and, in some cases, median fascicles. AV: atrioventricular; RA: right atrium; LA: left atrium; RV: right ventricle; LV: left ventricle. Graphic 63340 Version 6.0 https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 24/34 7/5/23, 10:34 AM Conduction abnormalities after myocardial infarction - UpToDate Coronary artery anatomy Graphic 70956 Version 2.0 https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 25/34 7/5/23, 10:34 AM Conduction abnormalities after myocardial infarction - UpToDate Relationship between fast sodium-mediated myocardial action potential and surface electrocardiogram Each phase of the myocardial action potential (numbers, upper panel) corresponds to a deflection or interval on the surface ECG (lower panel). Phase 4, the resting membrane potential, is responsible for the TQ segment; this segment has a prominent role in the ECG manifestations of ischemia during exercise testing. ECG: electrocardiogram. Graphic 64133 Version 4.0 https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 26/34 7/5/23, 10:34 AM Conduction abnormalities after myocardial infarction - UpToDate Electrocardiogram showing Mobitz type I (Wenckebach) atrioventricular block Single-lead electrocardiogram showing Mobitz type I (Wenckebach) second-degree atrioventricular block with 5:4 conduction. The characteristics of this arrhythmia include: a progressively increasing PR interval until a P wave is not conducted (arrow), a progressive decrease in the increment in the PR interval, a progressive decrease in the RR interval, and the RR interval that includes the dropped beat (0.96 sec) is less than twice the RR interval between conducted beats (0.53 to 0.57 sec). Courtesy of Morton Arnsdorf, MD. Graphic 73051 Version 6.0 Normal rhythm strip Normal rhythm strip in lead II. The PR interval is 0.15 sec and the QRS duration is 0.08 sec. Both the P and T waves are upright. Courtesy of Morton F Arnsdorf, MD. Graphic 59022 Version 3.0 https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 27/34 7/5/23, 10:34 AM Conduction abnormalities after myocardial infarction - UpToDate Electrocardiogram (ECG) showing concurrent Mobitz type I (Wenckebach) atrioventricular (AV) block and inferior myocardial infarction (MI) This rhythm strip shows a Mobitz type I (Wenckebach) atrioventricular block with 4:3 and 3:2 conduction and progressive prolongation of the PR intervals of conducted beats. The marked ST segment elevation suggests acute inferior wall ischemia or infarction that may be responsible for the arrhythmia. Courtesy of Ary Goldberger, MD. Graphic 62040 Version 3.0 Normal rhythm strip Normal rhythm strip in lead II. The PR interval is 0.15 sec and the QRS duration is 0.08 sec. Both the P and T waves are upright. Courtesy of Morton F Arnsdorf, MD. Graphic 59022 Version 3.0 https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 28/34 7/5/23, 10:34 AM Conduction abnormalities after myocardial infarction - UpToDate Electrocardiographic and electrophysiologic features of Mobitz type II second-degree atrioventricular block The PR and RR intervals are constant, but the third atrial beat (A) is not conducted (arrow). His bundle electrocardiography (HBE) shows constant AH (85 msec) and HV (95 msec) intervals and normal AH but no HV conduction in the nonconducted beat. The last finding indicates that the block is distal to the His bundle, in contrast with the more proximal location of Mobitz type I atrioventricular block. Adapted from: Josephson ME, Clinical Cardiac Electrophysiology: Techniques and nd Interpretations, 2 ed, Lea & Febiger, Philadelphia 1993. Graphic 79539 Version 7.0 Normal rhythm strip Normal rhythm strip in lead II. The PR interval is 0.15 sec and the QRS duration is 0.08 sec. Both the P and T waves are upright. Courtesy of Morton F Arnsdorf, MD. Graphic 59022 Version 3.0 https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 29/34 7/5/23, 10:34 AM Conduction abnormalities after myocardial infarction - UpToDate 12-lead electrocardiogram (ECG) showing bifascicular block with right bundle branch block and left anterior fascicular block The 12-lead ECG from a patient with a history of an anteroseptal myocardial infarction (Q waves seen in lead V1-V3) shows bifascicular block with RBBB and LAFB. A typical RBBB is seen with a QRS duration of 0.16 seconds and an rSR' configuration in lead V1 and a deep S wave in V6. The QRS complexes in leads II, III, and avF are negative, with a rS morphology, diagnostic of a pathologic left axis deviation, known as LAFB. ECG: electrocardiogram; RBBB: right bundle branch block; LAFB: left anterior fascicular block. Reproduced with permission by Samuel Levy, MD. Graphic 69886 Version 4.0 https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 30/34 7/5/23, 10:34 AM Conduction abnormalities after myocardial infarction - UpToDate Treatment of peri-myocardial infarction conduction abnormalities ECG: electrocardiogram; AV: atrioventricular; MI: myocardial infarction; PPM: permanent pacemaker. https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 31/34 7/5/23, 10:34 AM Conduction abnormalities after myocardial infarction - UpToDate Transcutaneous pacing is frequently the quickest way to provide temporary cardiac pacing, but is unreliable for extended periods of treatment and uncomfortable for the patient. While transcutaneous pacing may be initially successful in stabilizing the patient, central venous access should be established and transvenous pacing provided in the vast majority of patients requiring temporary cardiac pacing. The initial dose of atropine is 0.5 mg IV. This dose may be repeated every three to five minutes to a total dose of 3 mg. If the patient does not respond promptly and/or clinically deteriorates, proceed directly to temporary pacing. The typical aminophylline dose is 250 mg IV bolus. In patients with a prior heart transplant, a higher weight-based dose is preferred (6 mg/kg IV mixed in 100 to 200 mL of IV fluid adminstered over 20 to 30 minutes). Refer to UpToDate content on management of acute MI. In general, a waiting period of several days should be employed to determine potential reversibility of AV block, particularly in patients with acute inferior MI. If no reversible causes are present, definitive treatment involves PPM placement in most patients. Graphic 120722 Version 1.0 https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 32/34 7/5/23, 10:34 AM Conduction abnormalities after myocardial infarction - UpToDate Adult bradycardia algorithm 2020 update Reprinted with permission. ACLS Provider Manual. Copyright 2020 American Heart Association, Inc. Graphic 130748 Version 10.0 https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 33/34 7/5/23, 10:34 AM Conduction abnormalities after myocardial infarction - UpToDate Contributor Disclosures Peter J Zimetbaum, MD Consultant/Advisory Boards: Abbott Medical [Lead extraction]. All of the relevant financial relationships listed have been mitigated. Joseph E Marine, MD, FACC, FHRS No relevant financial relationship(s) with ineligible companies to disclose. Bradley P Knight, MD, FACC Grant/Research/Clinical Trial Support: Abbott [Electrophysiology]; Atricure [Electrophysiology]; Biosense Webster [Electrophysiology]; Biotronik [Electrophysiology]; Boston Scientific [Electrophysiology]; BSCI [Electrophysiology]; MDT [Electrophysiology]; Philips [Electrophysiology]. Consultant/Advisory Boards: Abbott [Electrophysiology]; Atricure [Electrophysiology]; Biosense Webster [Electrophysiology]; Biotronik [Electrophysiology]; Boston Scientific [Electrophysiology]; BSCI [Electrophysiology]; CVRx [Heart failure]; MDT [Electrophysiology]; Philips [Electrophysiology]; Sanofi [Arrhythmias]. Speaker's Bureau: Abbott [Electrophysiology]; Biosense Webster [Electrophysiology]; Biotronik [Electrophysiology]; Boston Scientific [Transeptal catheterization]; BSCI [Electrophysiology]; MDT [Electrophysiology]. All of the relevant financial relationships listed have been mitigated. Bernard J Gersh, MB, ChB, DPhil, FRCP, MACC Consultant/Advisory Boards: Bain Institute [CRO for trials involving Edwards percutaneous valve devices]; Cardiovascular Research Foundation [Data safety monitoring board (RELIEVE-HF Trial)]; Caristo Diagnostics Limited [Imaging and inflammation/atherosclerosis]; Philips Image Guided Therapy Corporation [Imaging]; Sirtex Med Limited [General consulting]; Thrombosis Research Institute [Data safety monitoring board (GARFIELD study)]. All of the relevant financial relationships listed have been mitigated. James Hoekstra, MD No relevant financial relationship(s) with ineligible companies to disclose. Susan B Yeon, MD, JD, FACC No relevant financial relationship(s) with ineligible companies to disclose. Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence. Conflict of interest policy https://www.uptodate.com/contents/conduction-abnormalities-after-myocardial-infarction/print 34/34