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REVIEW ARTICLE Table of Contents   
Year : 2010  |  Volume : 13  |  Issue : 1  |  Page : 7-15
Cardiac pacing in left bundle branch/ bifascicular block patients


Department of Anesthesia, Royal Hospital, PB. No: 1331, PC: 111, Seeb, Muscat

Click here for correspondence address and email

Date of Submission26-Dec-2008
Date of Acceptance15-Jul-2009
Date of Web Publication11-Jan-2010
 

   Abstract 

The primary concern in patients with bifascicular block is the increased risk of progression to complete heart block. Further, an additional first-degree A-V block in patients with bifascicular block or LBBB might increase the risk of block progression. Anesthesia, monitoring and surgical techniques can induce conduction defects and bradyarrhythmias in patients with pre-existing bundle branch block. In the setting of an acute MI, several different types of conduction disturbance may become manifest and complete heart block occurs usually in patients with acute myocardial infarction more commonly if there is pre-existing or new bundle branch block. The question that arises is whether it is necessary to insert a temporary pacing catheter in patients with bifascicular block undergoing anesthesia. It is important that an anesthesiologist should be aware of the indications for temporary cardiac pacing as well as the current recommendations for permanent pacing in patients with chronic bifascicular and trifascicular block. This article also highlights the recent guidelines for temporary transvenous pacing in the setting of acute MI and the different pacing modalities that are available for an anesthesiologist.

Keywords: Anesthesia, complete heart block, pacemaker

How to cite this article:
Maddali MM. Cardiac pacing in left bundle branch/ bifascicular block patients. Ann Card Anaesth 2010;13:7-15

How to cite this URL:
Maddali MM. Cardiac pacing in left bundle branch/ bifascicular block patients. Ann Card Anaesth [serial online] 2010 [cited 2018 Dec 17];13:7-15. Available from: http://www.annals.in/text.asp?2010/13/1/7/58828


During the perioperative period, anesthesiologists usually face dilemma regarding the need for cardiac pacing (temporary or permanent) in patients with bifascicular block. Non-invasive modalities like transcutaneous and transesophageal cardiac pacing have strengthened the armamentarium of an anesthesiologist to handle unforeseen eventualities perioperatively in patients with intracardiac conduction abnormalities.

The term 'bifascicular block' refers to an electrocardiographic picture of complete right bundle branch block [RBBB] with anterior or posterior left hemi block or of complete left bundle branch block [LBBB] alone. The term 'trifascicular' block means impaired conduction in all three branches at the same time, or at different times, although it has also been used to describe bifascicular block together with first degree atrioventricular (AV) block. [1]

Alternating (bilateral) bundle branch block is diagnosed when there is clear evidence of block in all three fascicles in different leads of the electrocardiogram (ECG) or on successive ECG tracing; for example, RBBB in one lead and LBBB in another. [2]


   Incidence Top


The bundle branch block has been found to increase with age. In population aged over 35 years the incidence is estimated at ~one per cent and at 80 years of age it is higher at ~17%. [1] In addition, patients with bundle branch blocks often have other cardiac diseases like coronary artery disease or hypertensive heart disease which explains their higher mortality (2-14%) due to the underlying diseases. [1]

Syncope is usually seen in patients with delayed conduction in left and right branch bundles although the risk of progression to high-degree AV block varies. The annual incidence of progression to high-degree AV block in unselected patients is estimated to be one to four per cent, and syncope could be the sole predictive factor. In patients with syncope, the annual incidence of block progression to high-degree AV block is 5-11% where as in patients without syncope, the incidence is just 0.6-0.8%. [1]

According to some authors, the incidence of progression from bifascicular to complete heart block can vary from two to five per cent per year. [3] In patients with bundle branch block, there is no single clinical or laboratory variable, including bifascicular block, which can identify patients at a higher risk of death from a future bradyarrhythmia. [4]

To completely understand the principles and concepts involved in cardiac pacing, a brief review of the anatomy and physiology of the specialized conduction system may be beneficial [Figure 1].


   Anatomy Top


Sinoatrial node

The sinoatrial (SA) node is located at the junction of the right atrium and superior vena cava is often found within the adventitia of the large SA nodal artery, a proximal branch of the right coronary artery (55%),or the left circumflex coronary artery. Histologically, the SA node consists of a dense framework of collagen that contains the principal pacemaker (P) cells; and Purkinje-like fiber tracts, extending through the perinodal area and into the atrium. Once the impulse exits the sinus node, it traverses the atrium to the AV node. [3]

AV node

The AV node is a small subendocardial structure within the interatrial septum and is located at the convergence of the specialized conduction tracts that course through the atria. The AV node has an abundant blood supply from AV nodal artery, a branch of the right coronary artery (in 90% of patients), or from the left circumflex artery (10%). Histologically, the AV node contains mainly P cells (although not nearly as many as in the SA node) and Purkinje cells in a loose collagenous network. [3]

His bundle

Purkinje fibers emerging from the distal AV node area converge to form the His bundle. His bundle traverses the membranous septum to the crest of the muscular septum where it divides into bundle branches. His bundle has ample blood supply originating from both AV nodal artery and septal branches of the left anterior descending artery. The rapid conduction of electrical impulses across the His-Purkinje system results in almost simultaneous activation of the right and left ventricles. [3]

Bundle branches The bundle branch system is formed by a network of interlacing Purkinje fibers. It usually starts as one or more large fiber bands that split and fan out across the ventricles. These fiber bands finally terminate in a Purkinje network that interfaces with the myocardium. The bundle branches, in some cases, conform to a trifascicular or quadrifascicular system and in other cases the delineation into separate fascicles is not seen. The right bundle is usually a single, discrete structure that extends down the right side of the interventricular septum to the base of the anterior papillary muscle where it divides into three or more branches. The left bundle more commonly originates as a very broad band of interlacing fibers that spread out over the left ventricle, sometimes in two or three distinct fiber tracts. The bundle branch system has extensive blood supply from both the right and left coronary systems. [3]


   Physiology Top


The SA node, under ordinary circumstances, is the major generator of cardiac impulses as it has the highest rate of spontaneous depolarization (automaticity). Its unique location astride the large SA nodal artery provides for continuous monitoring and instantaneous adjustment of heart rate to meet the body's changing metabolic needs. The major functions of the AV node include; to delay the passage of impulse under normal circumstances by approximately 0.04 seconds, serve as a subsidiary impulse generator; and in the event of atrial tachyarrhythmias act as a filter and limit ventricular rates. [3]

The separation of His bundle into longitudinally distinct compartments by the collagenous framework allows for longitudinal dissociation of electrical impulses. Thus a localized lesion below the bifurcation of the His bundle may cause a specific conduction defect (e.g. left anterior fascicular block). Disease within any aspect of the His bundle branch system may cause conduction defects that can affect AV synchrony or prevent synchronous right and left ventricular activation. The accompanying hemodynamic consequences have considerable clinical relevance. These consequences have provided the impetus for some of the advances in pacemaker technology. [3]

Under certain circumstances, electrophysiological studies help identify intracardiac conduction defects for which terms like A-H, H-V and H-Q intervals are used. A-H interval is the time from the initial rapid deflection of the atrial wave to the initial rapid deflection of the His bundle potential. It approximates conduction time through the A-V node and is normally 50-120 msec. H-V interval is the time from the initial deflection of the His bundle potential and the onset of ventricular activity (normally 35-45 msec). A few authors use the term H-Q interval rather than H-V interval to diagnose intraventricular conduction disturbances. On surface ECG the H-wave occurs between P-wave and Q-wave, about 50 msec preceding the R-wave peak. The H-Q interval is measured from the onset of the H- wave to the onset of the surface ECG QRS complex. The normal range of H-Q interval is 35-55 msec. [5]


   Diagnostic Criteria Top


The criteria to diagnose bifascicular block, bundle branch block, hemi block, and AV blocks are based on recommendations of the Criteria Committee of the New York Heart Association: [6]

Bifascicular block: RBBB with left anterior or left posterior fascicular block.

RBBB: QRS duration greater than or equal to 0.12 s and the QRS complex in V 1 has rsR' configuration or is a solitary notched R wave.

LBBB: QRS duration of greater than or equal to 0.12 s and QRS complex is notched and splintered in leads 1 and V6 and has a QS or rS deflection in lead V1

Left anterior fascicular block: Frontal plane QRS axis minus 45 to minus 90΀.

Left posterior fascicular block: Frontal plane QRS axis plus 90 to plus 120΀.

First-degree A-V block: P-R interval greater than 0.21 s and one-to-one A-V conduction.

Second-degree A-V block: In the presence of sinus rhythm, some P waves are followed by QRS complexes. Others are not.

Second-degree A-V block, Mobitz Type I: PR intervals of conducted beats vary according to Wenckebach periodicity.

Second-degree A-V block, Mobitz type II: PR intervals of conducted beats are normal or prolonged but constant.

Third-degree A-V block: Atrioventricular dissociation and idioventricular rhythm.

Risk assessment in bundle branch block patients

In a retrospective, cohort-controlled study, Dorman and colleagues found no difference in mortality between patients with and without bundle-branch block while investigating the clinical significance of bundle-branch block [RBBB or LBBB] as a perioperative risk factor. Bundle branch block alone was not found to be an independent risk factor for cardiac complications following surgery.

More than half of the patients with bundle-branch block presenting for elective surgery had hypertension and 10.3% had a history of congestive heart failure; both conditions were more common in patients exhibiting LBBB. In addition, they found that RBBB was more common in men while LBBB was more common among women. Multivariate analysis of men with RBBB did not demonstrate an increased likelihood of a cardiovascular abnormality, whereas women with LBBB or RBBB were more likely to suffer cardiovascular diseases. The same authors suggested that patients with LBBB might not tolerate the stress of perioperative noncardiac complications such as severe sepsis probably secondary to poor myocardial reserve and may be at a higher risk for postoperative morbidity and mortality. [7]

Data from the Framingham study indicate that appearance of bundle branch block is almost always clinically silent and often associated with the presence of cardiovascular abnormalities [hypertension (60%), coronary artery disease (10%), and congestive heart failure (4%)]. [8] In patients with newly acquired left or right bundle branch block, there is an increased likelihood of development of coronary artery disease and congestive heart failure with a three to four-fold higher mortality rate than in general population. [7],[8]

Goldman et al. noted cardiac death in five per cent of patients with intraventricular conduction abnormalities. However, a multivariate analysis did not indicate bundle branch block to be an independent predictor of cardiac death. [9] Berg and Kotler observed a higher mortality rate (10%) in surgical patients with bundle-branch block [RBBB with left axis deviation or LBBB with first degree heart block]. [10] Many clinicians consider LBBB to be a marker of cardiovascular dysfunction. As a corollary of this assumption, patients with LBBB are often thought to be at increased risk for perioperative cardiac complications. [7]


   Indications for Pacing Top


Any patient with acute hemodynamic compromise caused by bradycardia and/or episodes of asystole should be considered for temporary cardiac pacing. This is generally undertaken in the setting of surgical or other intervention; either the patient has the potential for transient bradycardia as a result of their underlying pathology or the procedure to be undertaken is likely to produce transient or permanent bradycardia.

The primary concern in patients with bifascicular or trifascicular block is that they are at an increased risk of progression to complete heart block. Anesthetics, combinations of antiarrhythmic agents with anesthetics, regional anesthesia, disturbances of blood gases or electrolytes, endotracheal intubation, central venous or pulmonary catheterization, surgical manipulation, hypothermia, or myocardial ischemia or infarction can induce conduction defects and bradyarrhythmias in patients with pre-existing bundle branch block. In patients with LBBB or bifascicular block, an additional AV conduction disorder in the remaining unaffected conducting fascicles may be precipitated by anesthesia and surgery and thereby degenerate to complete heart block. [11]

Gauss et al. studied 103 patients scheduled for surgery under general anesthesia or regional anesthesia; 56 had bifascicular block and 47 had trifascicular block. Significant bradycardia occurred in eight patients and all patients responded to pharmacotherapy. There was no incidence of a complete heart block. [11] Nonetheless, in their literature review, Gauss et al. found that during a one-year observation period perioperative progression of asymptomatic bifascicular block to complete heart block occurred in five patients. This suggested the potential importance of this complication. [11]

An additional first-degree AV block (caused by dysfunction within the AV node) in patients with bifascicular block or LBBB might increase the risk of block progression. Hence a first-degree AV block in the surface ECG could indicate an increased risk for this disorder. Apprehending this, although there is little evidence to support the need for this approach, some authors recommended use of a temporary perioperative pacemaker for all patients with bifascicular block or LBBB with an additional first-degree AV block [12],[13],[14] during anesthetic procedures.

Mikell et al. studied 76 surgical patients with bifascicular block and prolonged PR interval among whom four were cases of serious bradycardia but no complete heart block. [15] Atropine and isoprenaline were used to treat the bradycardia without recourse to pacing. Prophylactic insertion of temporary pacing wires in these patients was also not recommended by Atlee and Roizen. [16],[17]

Gauss et al. found that the presence of PR prolongation in patients with bifascicular block did not make a difference in terms of block progression or the occurrence of severe bradyarrhythmias and therefore they did not recommend routine prophylactic insertion of a temporary pacemaker. [18] They recommended pharmacotherapy as the first line of management in such patients with the caveat that temporary pacemaker equipment should be readily available in case pharmacotherapy fails. [18]

However, in patients with bifascicular block and type II second degree AV block, the risk of development of high-grade AV block is higher and the insertion of a temporary pacemaker was recommended. [3]

The significance of left axis deviation in patients with bifascicular block is unclear. A first-degree heart block in patients with RBBB and left axis deviation suggests abnormality of the H-V interval. LBBB and P-R interval prolongation in patients is frequently associated with prolonged H-Q interval. [18] Pastore et al. analyzed 44 patients with right bundle branch block and left axis deviation undergoing surgery and found one case of transient complete heart block that occurred at tracheal intubation due to parasympathetic discharge. [19]

However, Rooney et al. found no case of complete heart block [20] during 44 anesthetics in patients with right bundle-branch block and marked left axis deviation. Prophylactic temporary pacing was not recommended in this sub sect of patients.

It is essential to take a detailed medical history to exclude symptomatic bundle branch block. There is a higher risk of development of high-grade AV block in patients with bifascicular or trifascicular block with associated symptoms of syncope/presyncope. Prophylactic permanent pacing is indicated if the cause of syncope in the presence of bifascicular or trifascicular block cannot be determined with certainty or if treatment used (such as drugs) may exacerbate AV block as syncope may have been due to transient third degree AV block. [2,4]

Electrophysiological studies help in determining the need for permanent pacing in patients. Task Force of the American College of Cardiology/American Heart Association (ACC/AHA) identified PR and HV intervals as possible predictors of complete heart block and sudden death. [21]

In asymptomatic patients with bifascicular or trifascicular block, electrophysiological studies have shown that permanent pacing is considered appropriate for those who exhibit intermittent second- or third-degree AV block, or signs of a severe conduction disturbance below the level of the AV node (HV greater than100 ms, or intra- or infra-Hisian block during rapid atrial pacing). Occurrence of infra Hissian block after atrial pacing is considered an indication for pacing by a few authors. [4] However, apart from preventing future symptoms, pacemaker treatment may have no beneficial effect on survival. [1]

In patients who have a markedly prolonged HV interval (greater than 100 ms) and syncope not attributable to other causes, permanent pacing is warranted. In patients with LV systolic dysfunction, advanced heart failure and bundle branch block, especially LBBB, and a QRS interval greater than 120-130 ms, defibrillators with biventricular pacing have been shown to improve symptoms from heart failure and reduce mortality. [3] Patients with alternating bundle branch block have a high mortality rate and a significant incidence of sudden death if pacing therapy is not provided. [2]

The appearance of new bifascicular block in the immediate postoperative period should raise suspicion of an intraoperative MI and lead to insertion of a temporary pacemaker. The general availability of transcutaneous pacing has made it an acceptable alternative to temporary transvenous pacing in lower risk individuals, although poor patient tolerance is often a limitation. [3]


   Recommendations for Temporary Cardiac Pacing Top


Indications for temporary pacing can be considered in two broad categories: emergency (usually associated with acute myocardial infarction) or elective.

As a general rule, patients who may require permanent pacing should have interim temporary transvenous pacing wires placed to cover anesthetic requirements, if they have suffered syncope at rest, are hemodynamically compromised by the bradycardia or have ventricular tachyarrhythmias in response to bradycardia.

The American College of Cardiology/American Heart Association (ACC/AHA) guidelines for the management of acute myocardial infarction provide indications graded according to weight of evidence for benefit of pacing [Table 1]. [22]

[Table 2] gives indications for temporary transvenous pacing. During administration of general anesthesia, First degree AV block with bifascicular block and first degree AV block and LBBB were recommended as elective indications for temporary pacing although there is little evidence to support the need for this approach.In the setting of an acute MI, several different types of conduction disturbance may become manifest. They include abnormalities of sinus impulse formation or conduction, disorders of AV conduction, and disorders of intraventricular conduction. The ways of identifying the patient populations at greatest risk for the development of a significant bradyarrhythmia during acute MI, and in whom temporary pacing should be performed prophylactically, are discussed below.

Multiple studies have shown that patients with acute myocardial infarction and bundle branch block have a four to five-fold increased risk of progression to high-grade AV block (an increase from 4 to 18%). [3] The mortality of patients with bundle branch block and acute myocardial infarction is 30-40%, compared with 10-15% in patients without bundle branch block. [3] The risk of developing a high grade AV block in patients during acute myocardial infarction is shown in [Table 3] . [3]

Patients with a new bundle branch block and first-degree AV block or old bifascicular block and first-degree AV block are at intermediate risk of progression (19-29%) to high-grade AV block; they may undergo prophylactic pacing depending on the availability of facilities for emergency placement of a temporary pacemaker. As the greatest risk of progression to complete heart block occurs in the first five days following infarction, these decisions should be made promptly so that temporary pacing may be instituted.

The Multicenter Investigation of the Limitation of Infarct Size (MILIS) study has suggested a simpler method of risk stratification. A "risk score" for the development of complete heart block was devised. Patients with any of the following conduction disturbances were given one point each: first-degree AV block, type I second-degree AV block, type II second-degree AV block, left anterior fascicular block, left posterior fascicular block, RBBB, and LBBB. The presence of no risk factors was associated with a 1.2% risk of third-degree AV block, one risk factor with a 7.8% risk, two risk factors with a 25% risk, and three risk factors with a 36.4% risk of complete heart block [Table 3]. These findings were validated by testing the risk score in over 3000 patients from previously published studies. The risk score appears to be an alternative to risk stratification using combinations of conduction disorders. [3]

The most recent AHA guidelines for temporary transvenous pacing in the setting of acute MI are as shown in [Table 4] . [23]


   Recommendations for Permanent Cardiac Pacing Top


In chronic bifascicular and trifascicular block

In addition to ACC/AHA classification of weight of evidence for indications for pacing mentioned in [Table 1], the level of evidence was graded according to predefined scales as outlined in [Table 5] . [1]

The recommendations for permanent pacing in chronic bifascicular and trifascicular block as per ACC/AHA/NASPE Practice Guidelines are shown in [Table 6]. [3],[4]

In the year 2007, the European Society of Cardiology published the European Heart Rhythm Association Guidelines for cardiac pacing and cardiac resynchronization therapy. [1] Neuromuscular diseases with any degree of fascicular block, with or without symptoms considered as Class IIb indication according to ACC/AHA/NASPE recommendation, is Class IIa indication in the European guidelines.

Anesthetic implications

A number of medications may produce transient bradycardia that may require temporary pacing until the drug has been stopped. Some commonly used medications that may cause sinus node dysfunction or AV block are:

  • Digitalis (especially in the setting of hypokalemia)
  • Antihypertensive agents (clonidine, methyldopa, guanethidine)
  • Beta-adrenergic blockers (inderal, metoprolol, nadolol, atenolol), and administration as eye drops
  • Calcium channel blockers (verapamil, diltiazem)
  • Type 1A antiarrhythmic drugs (quinidine, procainamide, disopyramide)
  • Type 1C antiarrhythmic drugs (flecainide, propafenone)
  • Type III antiarrhythmic drugs (amiodarone, sotalol)
  • Psychotropic medications


Tricyclic antidepressants

Phenothiazines

Lithium hydrochloride

Phenytoin sodium

Cholinesterase inhibitors

These drugs may cause sinus node dysfunction and/or AV block; if used in combination; their effects may become more potent and exacerbate mild or latent conduction system disease. If long-term therapy with these agents is necessary for an underlying disorder and a substitute cannot be found, permanent pacing may be required. Recent studies have suggested that at least some patients with transient drug-related bradycardia may experience recurrent bradycardia requiring a pacemaker, even after the drug related to the bradycardia is stopped.

Certain circumstances can influence the incidence and course of perioperative bradyarrhythmias during anesthesia. One should take cognizance of the fact that in patients with underlying conduction abnormalities, concomitant circumstances like acute myocardial infarction, pre-existing severe cardiovascular disease combined with LBBB, and pulmonary artery catheterization in patients with LBBB are prone to precipitate perioperative bradyarrhythmias. [24]

It is important that vagal stimulation and combination of drugs likely to cause bradycardia should be avoided while administering anesthesia to these patients. Atropine, epinephrine, and isoprenaline should be prepared prior to induction of anesthesia in any case and temporary pacemaker equipment (pulse generator, pacing leads, connecting cables etc) must be readily available. The general availability of transcutaneous pacing has made it an acceptable alternative to temporary transvenous pacing in lower risk individuals, although poor patient tolerance is often a limitation. [3]


   Complications of Temporary Pacing Top


Complications of transvenous pacing may relate to the venous access, mechanical effects of the lead within the heart, the electrical performance of the pacemaker lead, or infection or thromboembolism caused by the presence of a foreign body. Complications can be expected in around 14-20% of patients and the majority of these will be manifest as development of a pericardial rub, ventricular arrhythmias produced during electrode positioning, or infection. [25]

Failure to capture with transcutaneous pacing may be related to electrode placement or to a barrel-shaped chest. [26] If pharmacotherapy is ineffective and transcutaneous pacing fails transesophageal pacing may be tried. Transesophageal pacing is a minimally invasive technique and may be useful in the perianesthetic care of patients with asymptomatic but potentially complete AV block. Transesophageal pacing is usually recommended only for atrial pacing, although previous reports have demonstrated that it may be applied for ventricular pacing. [26]

In conclusion, administration of a temporary pacemaker is not mandatory in patients with asymptomatic bifascicular block, even if first degree AV block is present. There is no difference in the occurrence of block progression or of severe bradyarrhythmias between patients with and without an additional PR prolongation. However, temporary pacemaker equipment should be readily available in case antiarrhythmic therapy fails. [18] Transcutaneous pacing offers a "bridge" to transvenous approach and may be useful in the perianesthetic care of patients who are asymptomatic but develop a potentially complete heart block or when staff with transvenous pacing experience is not immediately available.

 
   References Top

1.Vardas PE, Auricchio A, Blanc JJ, Daubert JC, Drexler H, Ector H, et al. Guidelines for cardiac pacing and cardiac resynchronization therapy: The task force for cardiac pacing and cardiac resynchronization therapy of the European Society of Cardiology. Developed in collaboration with the European Heart Rhythm Association. Eur Heart J 2007;28:2256-95.  Back to cited text no. 1      
2.Gregoratos G. Indications and recommendations for pacemaker therapy. Am Fam Physician 2005;71:1563-70.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]  
3.Peters RW, Vijayaraman P, Ellenbogen KA. Indications for permanent and temporary cardiac pacing. Cardiac Pacing and ICDs, 5 th edition. Edited by Kenneth A. Ellenbogen and Mark A. Wood. ͹ 2008 Blackwell Publishing, ISBN: 978-1-4051-6350-7.  Back to cited text no. 3      
4.Gregoratos G, Abrams J, Epstein AE, Freedman RA, Hayes DL, Hlatky MA et al. ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices--summary article: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (ACC/AHA/NASPE Committee to Update the 1998 Pacemaker Guidelines). J Am Coll Cardiol 2002;40:1703-19.  Back to cited text no. 4      
5.Narula OS, Samet P. Significance of first degree A-V block.Circulation 1971;43:772-4.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]  
6.The Criteria Committee of the New York Heart Association: Nomenclature and criteria for diagnosis of diseases of the heart and great vessels, 9 th ed. Boston. Little, Brown and Company; 1994. pp. 174-255.  Back to cited text no. 6      
7.Dorman T, Breslow MJ, Pronovost PJ, Rock P, Rosenfeld BA. Bundle-branch block as a risk factor in noncardiac surgery. Arch Intern Med 2000;160:1149-52.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]  
8.Schneider JF, Thomas HE, Sorlie P, Kreger BE, McNamara PM, Kannel WB. Comparative features of newly acquired left and right bundle branch block in the general population: the Framingham Study. Am J Cardiol 1981;47:931-40.  Back to cited text no. 8      
9.Goldman L, Caldera DL, Southwick FS, Nussbaum SR, Murray B, O'Malley TA, et al. Cardiac risk factors and complications in non-cardiac surgery. Medicine 1978;57:357-70.   Back to cited text no. 9  [PUBMED]  [FULLTEXT]  
10.Berg GR, Kotler MN. The significance of bilateral bundle branch block in the preoperative patient. Chest 1971;59:62-7.  Back to cited text no. 10  [PUBMED]  [FULLTEXT]  
11.Gauss A, Hόbner C, Radermacher P, Georgieff M, Schόtz W. Perioperative risk of bradyarrhythmias in patients with asymptomatic chronic bifascicular block or left bundle branch block: does an additional first-degree atrioventricular block make any difference? Anesthesiology 1998;88:679-87.  Back to cited text no. 11      
12.Boezaart AP, Clinton CW, Stanley A. Pre-operative prophylactic transvenous cardiac pacing for bifascicular heart block. S Afr J Surg 1989;27:103-5.  Back to cited text no. 12  [PUBMED]  [FULLTEXT]  
13.Zaidan JR. Electrocardiography, Clinical Anesthesia, 2nd ed. Edited by PG Barash, BF Cullen, RK Stoelting. Philadelphia, JB Lippincott; 1992. pp. 771-805.  Back to cited text no. 13      
14.Ford BM, Weich HFH, Coetzee AR. Pre-operative assessment of cardiac patients for non-cardiac surgery. S Afr Med J 1984;65:235-9.  Back to cited text no. 14      
15.Mikell FL, Weir EK, Chesler E. Perioperative risk of heart block in patients with bifascicular block and prolonged PR interval. Thorax 1981;36:14-7.  Back to cited text no. 15  [PUBMED]  [FULLTEXT]  
16.Atlee JL. Temporary perioperative pacing, Perioperative Management of Pacemaker Patients, 1 st ed. Edited by JL Atlee, H Gombotz, KH Tscheliessnigg. Berlin, Springer; 1992. pp. 127-37.  Back to cited text no. 16      
17.Roizen MF. Anesthetic implications of concurrent diseases, Anesthesia, 4 th ed. Edited by RD Miller. New York, Churchill Livingstone; 1994. pp. 903-1014.  Back to cited text no. 17      
18.Gauss A, Hόbner C, Meierhenrich R, Rφhm HJ, Georgieff M, Schόtz W. Perioperative transcutaneous pacemaker in patients with chronic bifascicular block or left bundle branch block and additional first-degree atrioventricular block. Acta Anaesthesiol Scand 1999;43:731-6.  Back to cited text no. 18      
19.Pastore JO, Yurchak PM, Janis KM, Murphy JD, Zir LM. The risk of advanced heart block in surgical patients with right bundle branch block and left axis deviation. Circulation 1978;57:677-80.  Back to cited text no. 19  [PUBMED]  [FULLTEXT]  
20.Rooney SM, Goldiner PL, Muss E. Relationship of right bundle-branch block and marked left axis deviation to complete heart block during general anesthesia. Anesthesiology 1976;44:64-6.  Back to cited text no. 20  [PUBMED]  [FULLTEXT]  
21.Dreifus LS, Fisch C, Griffin JC, Gillette PC, Mason JW, Parsonnet V. Guidelines for implantation of cardiac pacemakers and antiarrhythmia devices. A report of the American College of Cardiology/American Heart Association Task Force on Assessment of Diagnostic and Therapeutic Cardiovascular Procedures (Committee on Pacemaker Implantation). J Am Coll Cardiol 1991;18:1-13.  Back to cited text no. 21      
22.Ryan TJ, Anderson JL, Antman EM, Braniff BA, Brooks NH, Califf RM, et al. ACC/AHA guidelines for the management of patients with acute myocardial infarction. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Acute Myocardial Infarction). J Am Coll Cardiol 1996;28:1328-428.  Back to cited text no. 22      
23.Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction-executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 1999 guidelines for the management of patients with acute myocardial infarction). J Am Coll Cardiol 2004;44:671-719.  Back to cited text no. 23      
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Correspondence Address:
Madan Mohan Maddali
Senior Consultant, Department of Anesthesia, Royal Hospital, PB. No: 1331, PC: 111, Seeb, Muscat

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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9784.58828

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  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]

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