ACC-AHA 2018 2018 ACC/AHA/HRS Guideline on the Evaluation and Management of Patients With Bradycardia and Cardiac Conduction Delay
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| 頁 | クラス | レベル | 推奨文 | 表 |
|---|---|---|---|---|
| p.11 | I | C-EO | Downloaded from http://ahajournals.org by on October 7, 2026 | |
| p.11 | I | B-NR | Recommendation-Specific Supportive Text 1. The history should outline the frequency, timing, duration, severity, longevity, circumstances, triggers and alleviating factors of symptoms suspicious for bradycardia or conduction disorders. The relationship of the symptoms to medications, meals, medical interventions, emotional distress, physical exertion, positional changes, and triggers (eg, urination, defecation, cough, prolonged standing, shaving, tight collars, and head turning) can help narrow the broad differential diagnosis. Because of the propensity of some commonly prescribed medications (and nutraceuticals) to elicit or exacerbate bradyarrhythmias, a thorough review of both prescription and over-the-counter medications is essential (Table 4 and Table S1 in the Web Supplement). Bradycardia and conduction | |
| p.16 | IIa | C-LD | Downloaded from http://ahajournals.org by on October 7, 2026 | |
| p.16 | I | B-NR | Recommendation-Specific Supportive Text 1. Exercise electrocardiographic testing is integral to the diagnosis of chronotropic incompetence, a condition broadly defined as an inability to increase heart rate commensurate with the increased metabolic demands of physical activity.S4.2.2-6 Chronotropic incompetence, often considered as failure to achieve 80% of age-predicted maximal heart rate but in practice much more difficult to define particularly in the presence of comorbidities can contribute to exercise intolerance and connotes an adverse prognosis.S4.2.2-1,S4.2.2-2,S4.2.2-7 Although estimates of prevalence range broadly from 9% to 89% it appears to be common in individuals with cardiovascular disease, including one-third of those with congestive heart failure.S4.2.2-6 | |
| p.18 | I | B-NR | Downloaded from http://ahajournals.org by on October 7, 2026 | |
| p.19 | IIa | C-LD | Downloaded from http://ahajournals.org by on October 7, 2026 3. Cardiac MRI and computed tomography can be helpful in carefully selected patients to identify conditions known to contribute to conduction disturbance or SND. Specifically, MRI can be helpful in diagnosing infiltrative processes, including sarcoidosis, hemochromatosis, and amyloidosis.S4.2.4-16–S4.2.4-19,S4.2.4-40–S4.2.4-56 Cardiac computed tomography can be similarly helpful, particularly when MRI is contraindicated or unavailable. It offers superior information regarding calcification of cardiac structures and has some advantages in evaluating coronary artery anatomy when epicardial coronary atherosclerotic disease is suspected.S4.2.4-14,S4.2.4-57 Both computed tomography and MRI offer high-quality information regarding cardiovascular structure in the setting of congenital heart disease.S4.2.4-21,S4.2.4-57 Cardiac nuclear imaging techniques can be useful to detect and/or discriminate amongst infiltrative cardiomyopathies, most notably in distinguishing between wild-type transthyretin and light chain cardiac amyloidosis and diagnosing cardiac sarcoidosis using fluorodeoxyglucose positron emission tomographic imaging.S4.2.4-15,S4.2.4-20 Transesophageal echocardiography can be a useful adjunct for endocar- | |
| p.20 | IIb | C-EO | Downloaded from http://ahajournals.org by on October 7, 2026 | |
| p.21 | I | B-NR | CLINICAL STATEMENTS AND GUIDELINES | |
| p.21 | IIa | B-NR | Downloaded from http://ahajournals.org by on October 7, 2026 | |
| p.23 | IIb | C-LD | CLINICAL STATEMENTS AND GUIDELINES | |
| p.25 | IIa | C-LD | Table 7. Common Potentially Reversible or Treatable Causes of SNDS5.3.1-1 CLINICAL STATEMENTS AND GUIDELINES Acute myocardial ischemia or infarctionS5.3.1-2–S5.3.1-4 Athletic trainingS5.3.1-5 Atrial fibrillationS5.3.1-6 Cardiac surgery Valve replacement,S5.3.1-7,S5.3.1-8 maze procedure,S5.3.1-7 coronary artery bypass graftS5.3.1-9,S5.3.1-10 Drugs or toxins* Toluene, organophosphates, tetrodotoxin, cocaineS5.3.1-11 Electrolyte abnormality | |
| p.25 | IIb | C-LD | Hyperkalemia,S5.3.1-12 hypokalemia,S5.3.1-13 hypoglycemiaS5.3.1-14 Heart transplant:S5.3.1-15 Acute rejection, chronic rejection, remodelingS5.3.1- 16,S5.3.1-17 HypervagotoniaS5.3.1-18,S5.3.1-19 Hypothermia Therapeutic (post-cardiac arrest coolingS5.3.1-20) or environmental exposureS5.3.1-21 Downloaded from http://ahajournals.org by on October 7, 2026 HypothyroidismS5.3.1-22 Hypovolemic shockS5.3.1-23 Hypoxemia, hypercarbia, acidosisS5.3.1-24 Sleep apnea, respiratory insufficiency (suffocation, drowning,S5.3.1-25 stroke,S5.3.1-26 drug overdose) InfectionS5.3.1-27 Lyme disease,S5.3.1-28 legionella, psittacosis, typhoid fever, typhus, listeria,S5.3.1-29 malaria, leptospirosis, Dengue fever, viral hemorrhagic fevers, Guillain-BarreS5.3.1-30 | |
| p.28 | IIa | C-LD | Downloaded from http://ahajournals.org by on October 7, 2026 | |
| p.28 | IIa | C-LD | 2. In patients with bradycardia associated with symptoms or hemodynamic compromise attributable to digoxin toxicity, dialysis is not recommended for removal of digoxin.S5.3.2.3-9 III: No Benefit C-LD Synopsis | |
| p.28 | IIa | C-LD | Digoxin-specific antibody (Fab) is a monovalent immunoglobulin that rapidly binds to intravascular digoxin.S5.3.2.3-2 Each vial of 40 mg of digoxin Fab binds approximately 0.5 mg of digoxin, and dosage is usually dependent on the estimated amount of the digitalis preparation ingested. Repeat dosing may be necessary, particularly in the setting of chronic use attributable to the large volume of distribution. Clinical response rates to digoxin Fab are as high as 80% to 90%, particularly in the acute setting.S5.3.2.3-2 Patients with hyperkalemia or arrhythmias in the setting of digoxin serum levels of >2 mcg/L are at increased risk of death.S5.3.2.3-10 Signs and symptoms of toxicity can manifest at lower serum levels. Adverse events attributable to digoxin Fab therapy are rare and usually clinically insignificant; potassium levels should be monitored. Use of any treatment directed specifically to digoxin toxicity will depend primarily on the presence or likelihood of developing significant toxicity (Table 8). The evidence base and specific treatment considerations for digoxin mediated bradycardia are the same for SND and atrioventricular block. | |
| p.29 | IIa | C-LD | 1. Sinus bradycardia is common after heart transplant, and sinus rates of <70 to 80 bpm may be inadequate for postoperative demand. Chronotropic incompetence usually improves in the early postoperative period but can be clinically significant and require therapy in a few patients. Atropine is ineffective for treatment of post-heart transplant SND because of denervation.S5.3.2.4-16–S5.3.2.4-18 The use of terbutaline to treat sinus bradycardia after heart transplant has also been described, but data are more limited. Four small observational studies have shown improved heart rate and sinus node function after transplant using the methylxanthines aminophylline or theophylline. In 2 studies of 15 and 29 patients, oral theophylline was associated with restoration of a sinus rate of 90 bpm, and 1 study showed a reduction in PPM implantation compared with historical controls.S5.3.2.4-2,S5.3.2.4-4 The evidence for aminophylline is more limited; in invasive EPS, aminophylline infusion had variable effects on sinus node function and heart rate in heart transplant recipients.S5.3.2.4-1,S5.3.2.4-3 | |
| p.29 | IIb | C-LD | 2. Sinus bradycardia requiring medical therapy is a common complication of spinal cord injury and can be persistent and refractory to atropine and other adrenergic drugs. Although an inciting cause is not always noted, common triggers for bradycardia episodes are tracheal suctioning and turning the patient.S5.3.2.4-14,S5.3.2.4-19 Although | |
| p.32 | IIb | C-EO | 5.4.2. Transient/Reversible Causes (Including Medications) of Bradycardia Attributable to SND Recommendation for Transient/Reversible Causes of Sinus Bradycardia COR LOE Recommendation 1. Patients presenting with symptomatic SND secondary to a reversible cause should first be managed by directing the therapy at eliminating or mitigating the offending condition. | |
| p.32 | IIb | C-EO | Synopsis Patients may present with symptomatic sinus bradycardia attributable to reversible causes (Table 7).S5.4.2-1 Medications are frequent culprits. Negative chronotropic drugs such as beta blockers, calcium channel blockers, and digoxin are frequently prescribed drugs that can decrease the sinus rate. Sodium-channel and potassium-channel blocking antiarrhythmic drugs can also exacerbate bradycardia in patients with preexisting SND. Hypothyroidism can cause clinically significant bradycardia.S5.4.2-2–S5.4.2-5 Such cardiovascular abnormalities respond well to replacement therapy with thyroxine (T4).S5.4.2-6 Metabolic abnormalities such as severe systemic acidosis or hypokalemia can uncommonly cause sinus bradycardia in acute settings. Reversible physiological disturbances should be considered and treated first. | |
| p.33 | I | C-EO | CLINICAL STATEMENTS AND GUIDELINES | |
| p.33 | IIa | C-EO | a different indication or reason such as evaluation of inducibility of ventricular arrhythmia or presence of His-Purkinje conduction abnormality often in the setting of syncope or nonsustained ventricular tachycardia with reduced left ventricular function.S5.4.3-8,S5.4.3-9 In such cases, sinus node function could be evaluated at little to no added risk to the patient and can provide adjunctive information in patients with symptoms suggestive of bradycardia. 2. Patients with suspected SND sometimes do not have a definitive diagnosis even after undergoing a battery of initial noninvasive tests. EPS can be considered in such cases to help support or refute the diagnosis of SND, and the findings can be used to guide the therapy, provided that the data are used in conjunction with other clinical findings. The most well-known method to assess sinus node function is the measurement of SNRT. In brief, the atrium is paced using a properly positioned catheter at a predetermined rate for a given duration (30- 60 s) of time. The interval to the first spontaneous atrial depolarization from the last paced beat is measured after the pacing is stopped. Corrected SNRT is an indexed value obtained by subtracting the baseline R-R interval from the longest obtained SNRT. An abnormal corrected SNRT is considered to be any value >500 to 550 ms.S5.4.3-4 The SACT is less commonly used but can be calculated by either continuous pacing at different intervals, with premature atrial stimuli, or direct recording of sinus node electrograms.S5.4.3-10 | |
| p.33 | IIb | C-LD | Downloaded from http://ahajournals.org by on October 7, 2026 | |
| p.34 | I | B-R | 4. Chronotropic incompetence describes an inappropriately blunted heart rate response to physiologic need associated with physical activity but is difficult to define by simple age dependent formulas. The diagnosis is typically suggested by ambulatory heart rate monitoring (provided that symptom diaries are accurately kept), or exercise electrocardiographic testing. Cardiac pacing with sensor-based rate-responsive feature has been used to increase the heart rate in times of sensed physical activity. There are different types of sensors that can track various physiologic parameters such as body motion and minute ventilation. One RCT, however, did not demonstrate any benefit in patients with SND.S5.4.4-13 At 6 months follow-up, there was no difference in total exercise time between the dualchamber paced group and the dual-chamber paced group with additional rate adaption algorithms programmed “on.” group. At one-year follow-up, | |
| p.38 | IIa | B-NR | 6.2 Clinical Presentation | |
| p.38 | IIb | C-LD | Symptoms related to atrioventricular block vary and depend largely on the degree of atrioventricular block, the ventricular rate, and the frequency of its occurrence.S6.2-1 Profound first-degree atrioventricular block can lead to symptoms of fatigue or exertional intolerance if the PR interval is long enough to allow for loss of atrioventricular synchrony that results in a decrease in cardiac output and an increase pulmonary capillary wedge pressure (often called “pseudo pacemaker syndrome” and may occur with PR interval >300 ms).S6.2-2–S6.2-4 Second-degree atrioventricular block type I (Wenckebach) is often asymptomatic and seen in active, healthy patients with no history of heart disease. However, if occurring frequently or during exercise, it can cause symptoms of exertional intolerance or dizziness. Patients who present with complaints of syncope and have a negative initial workup such as a negative physical examination, ECG, and echocardiogram are sometimes found to have intermittent episodes of atrioventricular block with long-term monitoring.S6.2-5–S6.2-7 Intermittent complete atrioventricular block causing syncope or presyncope is more typically seen in patients with underlying heart disease or an underlying bundle branch block at baseline but can also be seen in patients with no baseline heart disease or evident conduction abnormalities. One study found that 8% of syncope patients with a normal ECG and echocardiogram had paroxysmal idiopathic atrioventricular block with no identifiable underlying cause.S6.2-5 Other studies evaluating patients with syncope and underlying bundle branch block or bifascicular block found that 61% had significant, clinically relevant His Purkinje conduction abnormalities identified at EPS.S6.2-8,S6.2-9 Patients with atrioventricular block that conducts in a 2:1 pattern can also have symptoms of fatigue and dizziness particularly if it persists during exertion. | |
| p.39 | IIb | B-NR | 2. Medications that slow or block atrioventricular conduction are commonly used in the treatment of hypertension, arrhythmias, heart failure, and other cardiac disease. Common examples are beta blockers, nondihydropyridine calcium channel blockers, and class I and III antiarrhythmic medications. Therefore, patients may commonly present with atrioventricular block while taking ≥1 of these medications. Moreover, these medications are sometimes part of an essential pharmacologic regimen that should not be interrupted. Although these scenarios may occasionally represent a reversible cause of atrioventricular block, several case series suggest that it is unusual for atrioventricular block to reverse with cessation of medications when used at therapeutic doses and even when reversal of atrioventricular block is observed acutely, later implant of a PPM is often necessary.S6.3.1-6–S6.3.1-9 The decision for whether to proceed with permanent pacing must account for the potentially deleterious effect of high amounts of right ventricular pacing and whether alternate medications without atrioventricular slowing could be used. 3. Cardiac sarcoidosis is an infiltrative/inflammatory cardiomyopathy that is often associated with atrioventricular block and ventricular arrhythmias.S6.3.1-15 Limited, small, nonrandomized studies of patients with cardiac sarcoidosis and atrioventricular block treated with corticosteroids found that only a few patients (13%–47%) had any reversibility of atrioventricular block.S6.3.1- Downloaded from http://ahajournals.org by on October 7, 2026 | |
| p.39 | IIb | C-LD | 10,S6.3.1-11 Moreover, cardiac sarcoidosis may have a waxing and waning or progressive course and initial improvement in atrioventricular conduction may later reverse. Given the known risks of delay in implantation of PPMs in patients with atrioventricular block, it is often reasonable to proceed to implantation without further delay in this clinical scenario.S6.3.1-16 Because of the risk of ventricular arrhythmias in patients with cardiac sarcoidosis, a CIED with defibrillator capability is often considered in patients who require permanent pacing.S6.3.1-17 | |
| p.40 | IIa | B-NR | 1. Atropine is a parasympatholytic drug that enhances atrioventricular nodal conduction and automaticity, generally given in 0.5- to 1.0-mg IV increments. Current advanced cardiac life support recommendations advise early use of atropine for medical treatment of hemodynamically significant bradycardia, including atrioventricular block. Uncontrolled cohort studies suggest efficacy and clinical benefit, particularly in the setting of acute inferior MI.S6.3.2-1–S6.3.2-3 Atropine is unlikely to improve atrioventricular block at the His bundle or His-Purkinje level and isolated reports have suggested occasional worsened atrioventricular conduction and/or hemodynamic compromise in such patients. For this reason, atropine should be used judiciously in patients with atrioventricular block and wide QRS complexes that suggest the presence of significant His Purkinje disease. Adverse effects of atropine include dry mouth, blurred vision, anhidrosis, urinary retention, and delirium. Excessive increase in heart rate may be problematic, particularly in patients with acute MI. 2. Beta-adrenergic agonists such as isoproterenol, dopamine, dobutamine, and epinephrine exert direct effects to enhance atrioventricular nodal and, to a lesser degree, His-Purkinje conduction. These drugs may also enhance automaticity of subsidiary atrioventricular junctional and ventricular pacemakers in the setting of complete atrioventricular block. Clinical efficacy of dopamine was shown to be equivalent to transcutaneous pacing in 1 small randomized trial of patients with unstable bradycardia unresponsive to atropine in the prehospital setting.S6.3.2-7 Isoproterenol was shown to elicit an escape rhythm in 68% of pacemaker-dependent patients undergoing generator replacement.S6.3.2-4 Other data come from cohort studies of limited design.S6.3.2-3,S6.3.2-5,S6.3.2-6 Adverse effects of beta-adrenergic agonists may include elicitation of ventricular arrhythmias and induction of coronary ischemia, particularly in the setting of acute MI or unstable coronary artery disease. In addition, isoproterenol may exacerbate hypotension because of the vasodilatory effects. 3. Aminophylline is a methylxanthine compound that is a nonselective adenosine receptor antagonist and phosphodiesterase inhibitor. It is used clinically as a bronchodilator and as a reversal drug for dipyridamole, adenosine, and regadenoson in pharmacologic nuclear stress testing. Experimental evidence suggests a role of Downloaded from http://ahajournals.org by on October 7, 2026 | |
| p.43 | I | C-LD | Recommendation-Specific Supportive Text 1. In patients who have second-degree Mobitz type I (Wenckebach) or 2:1 atrioventricular block but with symptoms of dizziness or presyncope or even syncope that do not temporally correspond to the episode of atrioventricular block, it is unclear whether permanent pacing will improve symptoms or alleviate them. If the level of the block is at the atrioventricular node, then sudden progression to a higher degree of atrioventricular block is unlikely.S6.4.1-1,S6.4.1-3 If the symptoms do not correlate with the episodes of first-degree or second-degree Mobitz type I atrioventricular block, the episodes would be considered unrelated and a pacemaker would not be indicated.S6.4.1-1,S6.4.1-3 | |
| p.45 | IIa | B-R | CLINICAL STATEMENTS AND GUIDELINES | |
| p.45 | IIb | C-LD | Downloaded from http://ahajournals.org by on October 7, 2026 | |
| p.46 | I | B-NR | help identify the presence of His bundle extrasystoles as a cause of bradycardia that presents as atrioventricular block on ECG. 4. Carotid sinus massage and medication challenges can be used to identify the presence of paroxysmal atrioventricular block or determine the level of block in patients with second-degree block where the level of block is uncertain by electrocardiographic analysis alone (eg, 2:1 atrioventricular block or Mobitz type I atrioventricular block in the setting of a wide QRS complex). One study showed that in patients with bifascicular block on ECG, a 15-ms increase in the His-ventricular (HV) interval or induced infranodal atrioventricular block with procainamide challenge was considered abnormal and possibly indicative of underlying infra-Hisian block.S6.4.3-11 The sensitivity of a procainamide challenge for distal conduction disease is low. However, it could be potentially useful in cases where the HV interval is borderline or atrioventricular block cannot be induced.S6.4.3- | |
| p.46 | IIa | B-NR | Downloaded from http://ahajournals.org by on October 7, 2026 | |
| p.46 | IIa | B-NR | 11,S6.4.3-17 Atropine shortens the refractoriness of the atrioventricular node but has little effect on infranodal conduction tissues.S6.4.3-10 Atropine will improve or have no change in atrioventricular conduction block if the block is at the level of the atrioventricular node but will worsen atrioventricular conduction block in the presence of intra-His or distal conduction disease.S6.4.3-8,S6.4.3-18 Isoproterenol can also be used to unmask underlying pathologic His-Purkinje disease by enhancing atrioventricular nodal and sinus conduction and precipitating heart block with faster heart rates.S6.4.3-12,S6.4.3-19 Similar to atropine, worsening atrioventricular block with isoproterenol infusion would be suggestive of infranodal block. Conversely, improvement of atrioventricular conduction with carotid sinus massage may be observed in patients with infranodal atrioventricular block.S6.4.3-10 All provocative testing should be done with careful monitoring, particularly when using a drug, because the pharmacologic effects can be prolonged. | |
| p.46 | IIb | C-LD | 6.4.4 Permanent Pacing Recommendations for Permanent Pacing for Chronic Therapy/ Management of Bradycardia Attributable to Atrioventricular Block Referenced studies that support recommendations are summarized in Online Data Supplements 34, 39, and 40. COR LOE Recommendations 1. In patients with acquired second-degree Mobitz type II atrioventricular block, highgrade atrioventricular block, or third-degree atrioventricular block not attributable to reversible or physiologic causes, permanent pacing is recommended regardless of symptoms.S6.4.4-1–S6.4.4-7 | |
| p.48 | I | A | 7. First-degree atrioventricular block and seconddegree Mobitz type I (Wenckebach) atrioventricular block, when above or at the level of the atrioventricular node, are not concerning for progression to a higher degree atrioventricular block. They are also typically asymptomatic. However, in some patients, severe first-degree atrioventricular block can cause symptoms similar to pacemaker syndrome, as well as heart failure, and exertional intolerance.S6.4.4-34,S6.4.4-37 If the PR interval is very long, atrial contraction occurs when the atrioventricular valves are closed which can lead to an increase in wedge pressure and a decrease in cardiac output.S6.4.4-50 This phenomenon has been referred to as “pseudo-pacemaker syndrome” and has also been reported in patients with dual pathway physiology of the atrioventricular node.S6.4.4-51,S6.4.4-52 In patients with second-degree atrioventricular block Mobitz type I, frequently dropped QRS complexes can lead to symptoms attributable to loss of atrioventricular synchrony even in the absence of bradycardia.S6.4.4-52 | |
| p.48 | I | B-R | 8. In patients with neuromuscular diseases that can affect the cardiac conduction system, such as myotonic dystrophy 1, the degree of the conduction abnormality can vary from mild first-degree atrioventricular block to complete heart block and it often progresses over a variable period of time.S6.4.4-10,S6.4.4-53–S6.4.4-55 Serial ambulatory electrocardiographic monitoring and EPSs have | |
| p.49 | IIa | B-R | CLINICAL STATEMENTS AND GUIDELINES Downloaded from http://ahajournals.org by on October 7, 2026 | |
| p.52 | IIa | B-NR | Downloaded from http://ahajournals.org by on October 7, 2026 | |
| p.53 | I | C-LD | Figure 8. Evaluation of conduction disorders algorithm. Colors correspond to Class of Recommendation in Table 2. See Section 7.4. for discussion. *Refer to Section 7.5., Figure 9. †Advanced imaging could include magnetic resonance imaging, computed tomography, or transesophageal echocardiography. ‡Monitor choice based on the frequency of symptoms. §Extensive conduction disease (eg, first-degree atrioventricular block combined with LBBB). ACHD indicates adult congenital heart disease; CM, cardiomyopathy; ECG, electrocardiogram/electrocardiographic; LBBB, left bundle branch block; and RBBB, right bundle branch block. a prolonged HV interval at EPS predicts a higher risk for complete heart block.S7.4-14 In another study, first-degree atrioventricular block or bundle branch block were markers for abnormal EPS findings in patients with syncope.S7.4-20 | |
| p.53 | IIa | C-LD | 5. Cardiac MRI may be considered in selected patients with LBBB and normal left ventricular function by echocardiography where sarcoidosis, connective tissue disease, myocarditis, or other dilated cardiomyopathies are suspected on clinical grounds. In 1 study, cardiac MRI detected subclinical cardiomyopathy in one-third of patients with asymptomatic LBBB and a normal echocardiogram.S7.4-15 In another study of patients | |
| p.55 | IIa | B-NR | significantly worse mortality (HR: 1.17; 95% CI: 1.00–1.36) and a decrease in LVEF to ≤35% (HR: 1.34; 95% CI: 1.09–1.63).S7.5-8 PROSPECT (Predictors of Response to CRT Trial) enrolled patients with LVEF of ≤35%, QRS interval >130 ms and Class III/IV heart failure. In a post hoc analysis, patients with an LVEF of >35% (when assessed by the core laboratory) had similar clinical and echocardiographic responses to CRT compared with patients with an LVEF of ≤35%.S7.5-9 In the REVERSE (Resynchronization Reverses Remodeling in Systolic Left Ventricular Dysfunction) trial, patients could be enrolled if they had New York Heart Association class I/II heart failure symptoms and an LVEF of <40% (although mean LVEF was 27%). Patients with QRS prolongation and LBBB morphology were markers for a clinical benefit with CRT.S7.5-20 CLINICAL STATEMENTS AND GUIDELINES | |
| p.56 | IIa | B-NR | opment of intraoperative bradycardia.S8.1.1-6–S8.1.1-8 In the setting of non-cardiac surgery, intraoperative bradycardia is most commonly attributable to SND and only rarely attributable to worsening atrioventricular conduction.S8.1.1-1,S8.1.1-8,S8.1.1-15 Certain surgical procedures such as carotid artery endarterectomy or stenting have been associated with periods of bradycardia.S8.1.1-3,S8.1.1-9–S8.1.1-12 Additionally, critical periods during surgery such as abdominal insufflation during laparoscopic surgeries or manipulation of regions innervated by the trigeminal nerve have been reported to be associated with bradycardia.S8.1.1-13,S8.1.1-14 In a study of 30 patients undergoing carotid angioplasty and stenting who underwent prophylactic transcutaneous pacing because of a high risk for angioplasty-related bradycardia, temporary transcutaneous pacing was used in 23 patients and was effective for eliminating bradycardia in all patients.S8.1.1-2 However, routine placement of transcutaneous pacing pads in patients solely for the presence of conduction disorders does not provide additional benefit.S8.1.1-15 | |
| p.56 | IIb | C-EO | Downloaded from http://ahajournals.org by on October 7, 2026 2. Although complete heart block can occur in the setting of pulmonary artery catheter placement in a patient with underlying LBBB, the incidence is low.S8.1.1-4,S8.1.1-5 Several studies have reported increased risk of ventricular arrhythmias with temporary pacing.S8.1.1-16,S8.1.1-17 Prophylactic transvenous pacing is not recommended, but the clinician should consider the likelihood of complete heart block if a pulmonary artery catheter is required for intraoperative monitoring and be prepared to manage this complication with rapid initiation of transvenous pacing or immediate transcutaneous pacing if sustained rate support is required. | |
| p.57 | IIb | C-EO | 2. The routine placement of temporary epicardial pacing wires at the time of isolated coronary artery bypass has been standard surgical practice. There is a very small risk of significant bleeding leading to morbidity and even mortality after their removal, but this risk is offset by the frequent and unpredictable need for the use of temporary pacing.S8.1.2.1-5,S8.1.2.1-10,S8.1.2.1-11 Some patients are at very low risk for needing temporary pacing after isolated coronary artery bypass. In 1 retrospective analysis, patients without diabetes mellitus, preoperative arrhythmia, or the requirement for pacing while coming off cardiopulmonary bypass had only a 2.6% need for postsurgical temporary pacing compared with 8.6% of patients in the entire cohort.S8.1.2.1-10 Patients undergoing off-pump coronary artery bypass grafting may also warrant special consideration for a strategy that does not use temporary pacing wires.S8.1.2.1-13 However, no large study has clearly identified a benefit to this approach. Temporary cardiac resynchronization using right atrial, right ventricular, and left ventricular pacing wires has been proposed for improving cardiac hemodynamic parameters in the immediate postoperative period in patients with severe left ventricular dysfunction with mixed results though may provide benefits in patients with accompanying LBBB.S8.1.2.1-14–S8.1.2.1-16 CLINICAL STATEMENTS AND GUIDELINES | |
| p.58 | IIb | C-EO | 3. Surgical left ventricular lead placement is performed as a stand-alone procedure when placement via coronary sinus is unsuccessful.S8.1.2.2-7 If a patient has an indication for cardiac resynchronization before cardiac surgery, an epicardial placement of a left ventricular lead at the time of surgery for AF may offer future benefit without significant risk of harm. In addition, placement of a nonapical, lateral epicardial lead will allow more pacing options if the patient undergoes a future atrioventricular nodal ablation. Although traditionally considered a contraindication, it may be that MRI can be performed safely in selected patients with abandoned leads under the auspices of specialized protocols.S8.1.2.2-8–S8.1.2.2-10 At the time of a future CRT procedure the operator can implant a coronary sinus lead or use the capped epicardial lead if necessary. | |
| p.59 | I | B-NR | Downloaded from http://ahajournals.org by on October 7, 2026 | |
| p.60 | IIa | C-LD | Downloaded from http://ahajournals.org by on October 7, 2026 | |
| p.60 | I | B-NR | Recommendation-Specific Supportive Text 1. Placement of temporary epicardial pacing wires at the time of tricuspid valve surgery is routine practice. The risk of postsurgical bradycardia is relatively frequent, and no study has advocated a selective approach to temporary pacing wire placement.S8.1.2.3.3-1–S8.1.2.3.3-4 | |
| p.61 | IIa | B-NR | CLINICAL STATEMENTS AND GUIDELINES | |
| p.62 | IIa | B-NR | Downloaded from http://ahajournals.org by on October 7, 2026 | |
| p.63 | I | B-NR | have not been consistent from study to study and have included preprocedure first-degree atrioventricular blockS8.1.2.5.2-1 or LBBB,S8.1.2.5.2-2 transient atrioventricular block and new RBBB after the procedure.S8.1.2.5.2-4 In 1 study, the first manifestation of atrioventricular block occurred between 2 days and 3 years in 9% of patients after alcohol septal ablation.S8.1.2.5.2-21 In another study, outpatient rhythm monitoring with implantable loop recorders was initiated after alcohol septal ablation.S8.1.2.5.2-8 Although there were episodes of ventricular fibrillation associated with complete heart block in the immediate periprocedural period, no episodes of heart block were identified after discharge.S8.1.2.5.2-8 Late development of atrioventricular block after surgical myectomy has not been reported with limited follow-up.S8.1.2.5.2-7,S8.1.2.5.2-15 CLINICAL STATEMENTS AND GUIDELINES | |
| p.63 | I | B-NR | 4. In 1 study of 172 patients who underwent simultaneous alcohol septal ablation and EPS, those patients with intact retrograde ventriculoatrial conduction did not develop late complete heart block regardless of changes in anterograde atrioventricular conduction properties associated with the alcohol septal ablation.S8.1.2.5.2-9 | |
| p.63 | IIa | B-NR | Downloaded from http://ahajournals.org by on October 7, 2026 8.1.2.6. Managing Episodes of Bradycardia Associated With Postoperative AF AF occurs commonly after cardiac surgery in adults, with a peak incidence 2 to 4 days postoperatively and an overall incidence ranging from 10% to 65%.S8.1.2.6- | |
| p.63 | IIb | B-NR | 1 Postoperative AF occurs more frequently in patients undergoing valve surgery than in those undergoing isolated coronary artery bypass graft.S8.1.2.6-2 Bradycardia may take several forms in these patients, including slow ventricular response during AF and prolonged sinus pauses after sinus rhythm is restored. A slow and regular ventricular response during AF usually indicates complete heart block, and pacing may be required if resolution does not occur.S8.1.2.6-3 The assessment of bradyarrhythmias in this setting is often complicated by the coexistence of atrial tachyarrhythmia; transient and time-dependent postoperative effects on sinus and atrioventricular node function, and the potential presence of antiarrhythmic drugs.S8.1.2.6-4 In general, bradyarrhythmias in the setting of postoperative AF should be treated similarly to those occurring in the nonoperative setting, and a period of watchful waiting rather than early PPM implantation is generally used. In occasional patients with refractory AF with rapid ventricular responses associated with significant SND limiting rate control drugs, a PPM may be required for adequate AF management. | |
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| p.66 | IIa | C-LD | 28,S8.3-29 In contrast, it is important to recognize that the use of atropine in patients with infranodal conduction disease or block can be associated with exacerbation of block and is potentially of harm. Aminophylline/theophylline has also been examined in this setting, and in the context of very limited data appears likely to be safe if atropine is ineffective.S8.3-10,S8.3-11,S8.3-30,S8.3-31 5. Given that the natural course of an MI with conduction system abnormalities is frequently associated with recovery of conduction, early and unnecessary pacing should be avoided.S8.3-1,S8.3- 4,S8.3-7,S8.3-12 Although PPM implantation is a relatively low risk cardiac procedure, complications including death range from 3% to 7% and there are significant long-term implications for pacing systems that use transvenous leads.S8.3-13–S8.3-16 | |
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